Medical Surgical

MEDICAL SURGICAL
OVERVIEW OF THE STRUCTURES & FUNCTIONS OF THE NERVOUS SYSTEM 3 PARTS OF THE NERVOUS SYSTEM 1. Central NS Brain & Spinal cord 2. Peripheral NS 31 Spinal & Cranial 3. Autonomic NS Sympathetic NS & Parasympathetic NS C-8 T - 12 L- 5 S5 C-1
Somatic NS I. Autonomic Nervous System A. Sympathetic NS (SNS) 1. Fight or Aggression Response 2. Release of Norepinephrine (adrenaline cathecolamine) = Adrenal Medulla (potent vasoconstrictor) 3. All body activities increased except GIT (GIT decreased motility) Bodily Effects of SNS a. Mydriasis = Dilated pupil , to be aware of surroundings b. Dry mouth VS = Increase c. BP & HR c. RR d. Constipation e. Urinary Retention f. Increased BF to heart, brain, skeletal muscles 4. Adrenergic or Parasympatholitic Response Adrenergic Agents a. Epinephrine (Adrenaline) S/E : SNS Effects b. Anti-Psychotics ex. Haldol (Haloperidol) S/E : SNS Effects
B. Parasympathetic NS 1. Flight or Withdrawal Response 2. Release of Acetylcholine (ACTH) 3. All bodily activities decreased except GIT Bodily Effects of PNS
a. Meiosis = constriction of pupils

VS:decreased b. Increased salivation c. BP & HR d. RR =bronchoconstriction e. Diarrhea =Increased Motility f. Urinary Frequency Cholinergic or Vagal or Sympatholitic Response
4.
a. Beta-Adrenergic Blocking Agents (Beta-Blockers) (all end in lol) Ex. Propanolol, Metopanolol Blocks release of norepinephrine, Decrease body activities except GIT (diarrhea) S/E: B broncho spasm (bronchoconstriction) E elicits a decrease in myocardial contraction T treats HPN A AV conduction slows down Given To/As: a. Angina Pectoris b. MI beta-blockers to rest heart c. Anti HPN agents: -Beta blockers (-lol) - Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL - Calcium antagonist ex. CALCIBLOC or NEFEDIPINE
Created by Nia E. Tubio 1
b. Cholinergic agents
d. Anti-arrhythmic agents (arrhythmia= irregular contraction of the heart) Ex. Mestinon (prostigmine) given to MG to increase ACTH S/E = PNS *Antidote anti cholinergic agents Atropine Sulfate S/E SNS
Created by Nia E. Tubio
II. CNS (Brain & Spinal Cord) Part 1 : Parts: A. Cells neurons = Basic living units Properties and Characteristics a. Excitability ability of neuron to be affected by changes in the external environment b. Conductivity ability of neuron to transmit a wave of excitation from one cell to another c. Permanent cells once destroyed, can not regenerate (ex. heart, retina, brain, osteocytes) 3 Types of Cells According To Its Regenerative Capacity: 1. Labile once destroyed, can regenerate: Epidermal, GIT, lung cells, GUT cells 2. Stable capable of regeneration BUT limited survival time: salivary gland, pancreas, liver, kidney cells 3. Permanent cannot regenerate: retina, brain, heart, osteocytes & myocardial cells B. Neuroglia : can cause brain tumors Functions & its 4 Types: 1. Astrocyte = maintain integrity of blood brain barrier (semi-permeable/selective) 2. Microglia = stationary cells 3. Ependymal Cells 4. Oligodendrocytes 1. Astrocytes: # 1 type of brain tumor= Astrocytoma ( 90 95%) Toxic substance that destroys astrocyte & passes the Blood Brain Barrier a. Ammonia = a cerebral toxin , product of protein catabolism Hepatic encephalopathy (liver cirrhosis) = death of liver d/t necrosis Primary Cause : Malnutrition Major Cause : Alcoholism Early Sign : Asterixis (Flapping hand tremors) Late Sign : Headache, Restlessness, Fetor Hepaticus (ammonia-like breath) Hepatic Coma -----N.P. Airway b. Bilirubin = yellow pigment -------- jaundice (Icteric Sclerae) others: Bilivedrin = green pigment Hemosiderin = golden-brown pigment Hemoglobin = red cell pigment Hepatitis * Carotenemia = yellowish discoloration of the skin *Sign of Tumor in the Pituitary Gland * Kernicterus (Hyperbilirubinemia) - Increased bilirubin in the brain, irreversible brain damage
b. Carbon Monoxide :Tx for Carbon monoxide poisoning

= Hyperbaric Oxygenation (100%) Parkinsons Disease Early Sign: Pill-Rolling Tremors d. Lead Seizure = Antidote for lead poisoning ------ Calcium EDTA
e. Ketones - acids, CNS depressant Ketones in Blood DKA ---- Type 1 DM d/t increase fat catabolism free fatty acids Cholesterol Leads to: Atherosclerosis
Ketones ----- DKA : Early Signs = Weakness/ Weight Loss Late Signs = Acetone Breath & Kussmauls Breathing
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Leads to Coma HPN ==MI or Stroke --Death 2. Microglia = Stationary Cells ------- Phagocytosis Organ Brain Blood Kidney/Liver Lungs SC Tissues Macrophage ---------- Microglia ---------- Monocytes ---------- Kupffer Cells ---------- Alveolar Macrophages ---------- Histiocytes
3. Ependymal Cells = acts as a defense in the CNS along with microglia secretes a glue ------ Chemoattractants 4. Oligodendrocytes = produces myelin sheath: acts as a cover for neurons acts as an insulator w/c facilitates rapid nerve impulse transmission No myelin sheath degenerates neuron Damage to myelin sheath causes demyelinating disorders
DEMYELINATING DISEASE 1. ALZHEIMERS DISEASE atrophy of brain tissue due to a deficiency of acetylcholine - Degenerative disorder - A type of Dementia Predisposing Factors: 1. Aging 2. Aluminum Accumulation S&Sx: A amnesia loss of memory *Short-Term -- Anterograde Amnesia *Long-Term Retrograde Amnesia A apraxia unable to determine purpose of object thru movement A agnosia unable to recognize familiar object A aphasia 2 types: 1. Expressive Broccas aphasia inability to speak ex. (+) nodding TX: use of picture-boards - damage to frontal lobe - Broccas ---- motor speech center in the frontal lobe 2. Receptive Wernickes aphasia unable to understand spoken words ex. (+) illogical thoughts - damage to Temporal lobe - Wernickes Area --- general interpretative area - Common to Alzheimer Receptive Aphasia - Drug of choice ARICEPT or COGNEX ----- best given : at bedtime 2. MULTIPLE SCLEROSIS (MS) -Chronic intermittent disorder of CNS Characterized by white patches of demyelenation in brain & spinal cord. Remission & exacerbation Common women, 15 35 y/o Predisposing factor: 1. Idiopathic 2. Slow growing virus 3. Autoimmune (supportive & palliative treatment only) self-killing immunity Normal Resident Antibodies: 5 types IgG can pass placenta passive immunity, temporary IgA body secretions saliva, tears, colostrum IgM acute inflammation IgE allergic reactions IgD chronic inflammation S & Sx of MS: 1. Visual disturbances : a. *Blurring of vision = Initial sign b. Diplopia/ double vision c. Scotomas (blind spots) 2. Impaired sensation to touch, pain, pressure, heat, cold: a. Numbness b. Tingling c. Paresthesia 3. Mood swings common : EUPHORIA (sense of elation ) 4. Impaired motor function: a. Weakness b. Spasticity tigas c. Paralysis 5. Impaired cerebellar function Triad Sx of MS (INA) I intentional tremors N nystagmus A Ataxia - unsteady gait 6. Scanning of Speech 7. Urinary retention or incontinence 8. Constipation
CHARCOTS TRIAD (INA)
9. Decrease sexual ability Dx: 1. CSF analysis thru lumbar puncture : bet. L3 & L4 : Reveals CHON & IgG 2. MRI reveals site & extent of demyelination 3. Lhermittes Sign : confirmatory Dx of MS - continuous contraction & pain of the SC following laminectomy ( removal portion of lamina) Nsg Mgt: Supportive mgt 1.) Administer Meds as ordered a. ACTH ( adrenocorticotropic hormone) : Acute exacerbation to reduce edema at the site of demyelination to prevent paralysis - compression of spinal nerves b. Baclopen (Lioresol) or Dantrolene Na (Dantrene) : To c. Interferons to alter immune response d. Immunosuppressant e. Diuretics f. Bethanecol Chloride ( Urecholine) : N.M. muscle spasticity
Administer only SC Monitor S/E : wheezing, bronchospasm Monitor breath sounds 1 hr. after SC admin.
h. Anti-spasmodic (Prophanthelene Bromide) Pro-banthene & anti-cholinergic 2. Maintain side rails 3. Assist passive ROM exercises promote proper body alignment 4. Prevent complications of immobility (q 2 hr. elderly q 1 hr.) 5. Encourage fluid intake & increase fiber diet to prevent constipation 6. Provide catheterization d/t urinary retention 7. Avoid heat application 8.. Give diuretics 9. Increase fiber & provide acid-ash diet to acidify urine & prevent bacteria multiplication Ex. Grape, Plums, Cranberry, Orange juice, Prune juice, pineapple juice,Vit C *3 Causes of UTI In Women Shorter Urethra F= 1-2.5 inches (3-5 cm.) Poor Perineal Care Moist Vaginal Area M= 5-6-8 inches (16-20 cm)
PART II: Compositions of Cord & Spinal cord 80% - brain mass 10% - CSF 10% - blood 1st: Brain mass A. CEREBRUM Largest Part Function: Connects Right & Left cerebral hemisphere - Corpus collusum 1. Sensory 2. Motor 3. Integrative
Compose of 6 Lobes: 1.) Frontal (garbled speech) a. Controls motor activity b. Controls personality development c. Where primitive reflexes are inhibited d. Site of development of sense of Humor
e. Control higher cortical thinking f. Broccas area speech center Damage - expressive aphasia 2.) Temporal a. Hearing b. Short term memory c. Wernicke's area gen. interpretative Damage receptive aphasia 3.) Parietal lobe appreciation & discrimination of sensory impulses - Pain, touch, pressure, heat & cold 4.) Occipital vision 5.) Insula/island of reil/ Central lobe- controls visceral fx Function: - activities of internal organ 6.) Rhinencephalon/ Limbic - Smell, libido, long-term memory *Anosmia- absence of smell
Basal Ganglia areas of gray matter located deep within a cerebral hemisphere Extra pyramidal tract Releases dopamine- a neurotransmitter Controls gross voluntary unit Dopamine :Parkinsons or Huntingtons Acetylcholine :Myasthenia Gravis & Alzheimers Dopamine : Schizophrenia Acetylcholine : Bipolar Disorder
B. MID BRAIN/ MESENCEPHALON relay station for sight & hearing Controls size & reaction of pupil ( Normal: 2 3 mm) Controls hearing acuity ( Normal Hearing Acuity : 30-40 decibels) *PERRLA= Pupil dilated round & reactive to light & accommodation :Normal * Isocoria normal size (equal) *Anisocoria uneven size damage to mid brain C. DIENCEPHALON -------between brain 2 Parts: 1.Thalamus acts as a relay station for sensation 2. Hypothalamus Thermo-regulating center of temp, sleep & wakefulness, thirst, appetite/ satiety center Controls some emotional responses like fear, anxiety Controls pituitary function. D. BRAIN STEM a. PONS Pneumotaxic center controls rate & depth of respiration Cranial 5 8 CNS b. MEDULLA OBLONGATA- lowest portion of the brain -controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus -Vasomotor center - Site of Spinal Decuissation Termination, CN 9, 10, 11, 12 E. CEREBELLUM smallest part of the brain - Controls posture, gait, balance, equilibrium Cerebellar Tests: a.) R Rombergs test- needs 2 RNs to assist - Pt. in Normal anatomical position 5 10 min (+) Rombergs test is (+) ataxia or unsteady gait/drunken movement w/ loss of balance --seen in MS. b.) Finger to nose test (+) To FTNT seen in Dymetria inability to stop a movement at a desired point c.) Alternate pronation & supination Palm up & down . (+) To alternate pronation & supination or damage to cerebellum
seen in Dymetria 2nd: CerebroSpinal Fluid (CSF) 10% Blood 10% Compose of lipids Normal amount produced: 125-250 ml /day Produced at the Choroid Plexus Composition: Clear, colorless, odorless: (+) glucose, protein,WBC but not RBC Fx: cushions the brain Alters if there is obstruction in the flow of CSF = Increase ICP Enlargement of the skull posteriorly d/t early closure of the posterior fontanel----Hydrocephalus 3rd: Blood Stroke: partial/total obstruction in brain blood supply : 2 Commonly Affected artery: 1. ICA or Internal Carotid Artery 2. MCA or Middle Cerebral Artery
*Composition of brain - based on Monroe Kellie Hypothesis o Skull is a closed container. Any alteration in 1 of 3 intracranial components = increase in ICP *Normal ICP 0 15 mmHg Foramen Magnum = the hole in the skull where spinal cord enters C1 atlas : carrying the entire skull C2 axis ------------After C1 is the location of the medulla oblongata Brain Herniation = when the medulla forced thru in the foramen : Observe for signs of ICP (+) Projectile vomiting , irregular respiration & HR Observe for 24 hrs. before MRI DISORDER:
1. INCREASED ICP increase IC bulk is due to increase in 1 of the IC components

A. Predisposing factors: 1.) Head injury 2.) Tumor 3.) Localized abscess 4.) Hemorrhage (stroke) 5.) Cerebral edema 6.) Hydrocephalus 7.) Inflammatory conditions - Meningitis, encephalitis
B. S&Sx Earliest Sx: a.) Change or decrease LOC Restlessness to confusion (conscious, lethargy, stupor, coma) - Disorientation to lethargy *conscious = awake - Stupor to coma Late Sx: a. Change in V/S : always a late sx 1. BP (systolic increase, diastole- same) Normal adult BP 120/80 : 40 (normal PP) 2. Widening pulse pressure Ex. Increase ICP = BP 140/80 = 140 80= 60 PP (wide) 3. RR : Cheyne-Stokes =rapid respiration w/ periods of apnea 4. Temperature increase DIFFERENCE BET. SHOCK : & INCREASE ICP: Decrease BP Increase BP Increase HR Decrease HR CUSHINGS EFFECT Increase RR Decrease RR Decrease Temp Increase temp Narrowing PP Widening PP b.) Headache c.) Projectile vomiting d.) Papilledima (edema of optic disk outer surface of retina) e.) Abnormal Posturing 1. Decorticate = abnormal flexion of arms = damage to cortico spinal tract 2. Decerebrate = abnormal extension of arms = damage to upper brainstem, cerebrum, midbrain & pons Except: Flaccid = loss of muscle tone, damage to the lower brain, medulla
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f. Uncal herniation unilateral dilation of pupil g. Possible seizure Nursing Management: 1.) Maintain patent a/w & adequate ventilation a. Prevention of hypoxia =decrease tissue oxygenation & hypercarbia =increase in CO2 retention Hypoxia cerebral edema - increase ICP Early Sx: R restlessness A- agitation T- tachycardia Late Sx: B bradycardia RAT E extreme restlessness D dyspnea C cyanosis =late BEDC
* Powerful respiratory stimulant : CO2 ---an
CO2 retention/ hypercarbia ---stimulate medulla O.
stimulate lungs to Hyperventilate 2. Before & after suctioning, hyperventilate 100% - decrease CO2 excrete CO2 Suctioning 10-15 seconds, max 15 seconds Ambu bag pump upon inspiration 3. Assist in mechanical ventilation 4. Monitor VS & I&O, neuro check 5. Positioning -- Elevate head of bed 30- 45 degrees angle neck in neutral position unless C/I to promote venous drainage 4. Limit fluid intake 1,200 1,500 ml/day (FORCE FLUID means: Increase fluid intake/day 2,000 3,000 ml/day)- not for inc ICP. 5. Prevent complications of immobility 6. Prevent increase ICP by: a. Maintain quiet & comfy environment b. Avoid use of restraints lead to fractures c. Maintain side rails up d. Instruct patient to avoid activities leading to:Valsalva maneuver or bearing down -Avoid straining of stool(give laxatives/ stool softener Dulcolax/ Duphalac) - Excessive cough antitussive (Dextrometorpham) -Excessive vomiting anti emetic (plasil) - Avoid Lifting of heavy objects, Bending & stooping - Avoid clustering of nursing activities 7. Administer meds as ordered: 1.) Osmotic diuretic Mannitol/Osmitrol: promotes cerebral diuresis by decompressing brain tissue Nursing considerations: Mannitol 1. Monitor BP S/E: hypotension 2. Monitor I&O every hr. report if < 30cc out put 3. Administer via side drip 4. Regulate fast drip to prevent formation of crystals/precipitate 5. Inform client, will feel flushing sensation as drug is introduced 2.) Loop diuretic - Lasix (Furosemide) in ampule Nursing Mgt: Lasix Same as Mannitol except - Lasix is given via IV push (expect urine after 10-15mins) should be in the morning. If given at 7am. Pt will urinate at 7:15 Action of Lasix within 15 minutes. Max effect 6 hrs due (7am 1pm) S/E of LASIX 1. Hypokalemia (Normal K-3.5 5.5 meg/L) S&Sx : Compared to Hyperkalemia: 1. Weakness & fatigue 1. Irritability & Agitation 2. Constipation 2. Diarrhea, abdominal cramps 3. (+) U wave in ECG tracing 3. Peaked T-wave both will lead to arrhythmia Nursing Mgt: 1. Administer K supplements ex. Kalium Durule, Oral Kcl Potassium Rich food: ABCs of K Vegetables Fruits A - asparagus A apple B broccoli (highest) B banana green (highest)
C cantaloupe/ melon O orange (increase) Vit A squash, carrots yellow vegetables & fruits, spinach, chesa Iron raisins, *Food appropriate for toddler spaghetti! Not milk increase bronchial secretions, no grapes may choke S/E of Lasix: 2. Hypocalcemia or Tetany: life-threatening (Normal level Ca = 8.5 11mg/100ml) S&Sx : Weakness Paresthesia (+) Trousseau sign or carpo-pedal spasm pathognomonic (+) Chvosteks sign Complications: Arrhythmia Laryngospasm N. M. - Administer Ca gluconate IV slowly Ca gluconate toxicity: Sx : seizure administer Mg SO4 Mg SO4 toxicity administer Ca gluconate : BURP B BP decrease U urine output decrease R RR decrease P patellar reflexes absent
C carrots
(Normal Na level = 135 145 meg/L) Hypotension Signs of Dehydration Early signs thirst and agitation for adults --------------children: tachycardia, dry mucous m. Mgt: force fluid 2-3 L/day Administer isotonic fluid sol 4. Hyperglycemia Increase blood sugar level P polyuria P polyphagia 3 Ps of Hyperglycemia P polydipsia Nsg Mgt: a. Monitor FBS (Normal =80 120 mg/dl) *Lasix can be given to DM but strict FBS monitoring 5. Hyperurecemia increase serum uric acid = by product of purine metabolism kidney stones- renal colic (pain) Cool moist skin Sx joint pain & swelling ----great toe affected ----gouty arthritis Nsg Mgt of Gouty Arthritis a.) Cheese (not sardines, anchovies, organ meat) (Not good if pt taking MAO) b.) Force fluid c.) Administer meds Allopurinol/ Zyloprim inhibits synthesis of uric acid drug of choice for gout: Colchicene acute gout drug of choice ---promotes excretion of uric acid Kidney stones renal colic (pain). Cool moist skin Mgt: 1.) Force fluid 2.) Meds narcotic analgesic Morphine SO4 3.) Strain all urine using gauze pads S/E of Morphine SO4 toxicity Respiratory depression (check RR 1st) Antidote for morphine SO4 toxicity Narcan (NALOXONE) Naloxone toxicity tremors Gouty arthritis
3. Hyponatremia S/Sx:
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Cont. Increase ICP meds 3.) Corticosteroids - Dexamethsone decrease cerebral edema (Decadrone) *Steroids best given: 2/3 dose am & 1/3 dose pm - to mimic normal diurnal rhythm 4.) Mild analgesic codeine SO 5.) Anti consultants Dilantin (Phenytoin) Increase ICP what is the immediate nsg action? Administer Mannitol as ordered Elevate head 30 75 degrees Restrict fluid Avoid use of restraints *Nsg Priority ABC & safety Pt. suffering from epiglotitis. What is nsg priority? a. Administer steroids least priority b. Assist in ET temp, a/w c. Assist in tracheotomy permanent (Answer) d. Apply warm moist pack? Least priority Rationale: Wont need to pass larynx due to larynx is inflamed. ET cant pass. Need tracheostomy onlyMagic 2s of Drug Monitoring Toxicity Level: DLADA Drug D digoxin L - lithium A aminophylline D Dilantin A acetaminophen Normal Range .5 1.5 meq/L .6 1.2 meq/L 10 19 mg/100ml 10 -19 mg/100 ml 20 10 30 mg/100ml Toxicity 2 2 20 200 Classification Cardiac glycosides Antimanic Bronchodilator Anticonvulsant Narcotic analgesic Indication CHF Bipolar Disorder COPD Seizures Osteoarthritis
D- Digitalis (Digoxin)
increase cardiac contraction = increase CO
Cardiac Glycosides
Nursing Mgt: 1. Check PR, HR (if HR below 60bpm, dont giveDigoxin) Increase force of cardiac contraction Digitalis toxicity antidote - Digibind a. Anorexia increase cardiac output b. n/v GIT c. Diarrhea d. Confusion e. Photophobia f. Changes in color perception yellow spots-----Xantopsia L lithium (lithane) decrease levels of norepinephrine, serotonin, and acetylcholine Anti-manic agent Lithium toxicity S/Sx a. Anorexia *N.M. 1. Force Fluid b. n/s 2. Increase intake in diet 4-10g/d c. Diarrhea d. Dehydration force fluid, maintain Na intake 4 10g daily e. Hypothyroidism f. Fine Tremors CRETINISM the only endocrine disorder that can lead to mental retardation A aminophyline (Theophylline) ---dilates the bronchial tree *Seizure= 1st attack *Febrile seizure= normal 5 y/o S/Sx : Aminophylline toxicity: * Epilepsy = succeeding attacks 1. Tachycardia
2. Hyperactivity restlessness, agitation, tremors (CNS excitability) N.M. ---Avoid giving food with Aminophylline a.Cheese/butter food rich in tyramine, avoided only if pt is given MAOI b. Beer/ wine c. Hot chocolate & tea caffeine CNS stimulant tachycardia d. Organ meat/ box cereals anti parkinsonian MAOI antidepressant m AR plan n AR dilcan lead to CVA or hypertension crisis p AR nate 3 4 weeks - before will take effect Anti Parkinsonian agents Vit B6 Pyridoxine reverses effect of Levodopa D dilatin (Phenytoin) anti convulsant/seizure Nursing Mgt: 1. Mixed with plain NSS or .9 NaCl to prevent formation of crystals or precipitate o Do sandwich method o Give NSS then Dilantin, then NSS! 2. Instruct the pt to avoid alcohol bec. alcohol + dilantin can lead to severe CNS depression Dilantin toxicity: GHAN *Osteoarthritis: Sign Heberdens nodes S/Sx: G gingival hyperplasia swollen gums i. Oral hygiene soft toothbrush ii. Massage gums H hairy tongue A - ataxia N nystagmus abnormal movement of eyeballs A acetaminophen/ Tylenol non-opoid analgesic & antipyretic febrile pts a. Acetaminophen toxicity : 1. Hepato toxicity : Monitor liver enzyme SGPT (ALT) Serum Glutamic Pyruvate Transaminase SGOT- Serum Glutamic Oxaloacetic Transaminase 2. Monitor BUN (10 20) *Creatinine (.8-1)most reliable, indicative for kidney clearance b. Acetaminophen toxicity can lead to hypoglycemia:TIRED T tremors / Tachycardia I irritability R restlessness E extreme fatigue D depression Diaphoresis/Nightmares *Antidote for acetaminophen toxicity Acetylcesteine ---- Prepare suctioning apparatus Exercise: The following are symptoms of hypoglycemia except: a. Nightmares b. Extreme thirst hyperglycemia symptoms c. Weakness d. Diaphoresis
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PARKINSONS DISEASE (Parkinsonism)
Chronic, progressive disease of CNS characterized by degeneration of dopamine producing cells in substancia nigra at mid brain & basal ganglia (produces dopamine)
Mngt: Palliative & Supportive Only Predisposing Factors: 1. Poisoning (lead & carbon monoxide) 2. Hypoxia 3. Arteriosclerosis 4. Encephalitis 5. Drug Overdose High doses of the ff: a. Reserpine (serpasil)-----than only anti-HPN with S/E of depression -----suicidal ----- only HPN known to be link to breast cancer ----- promote safety b. Methyldopa (aldomet)---Anti-HPN c. Haloperidol (Haldol) - anti psychotic d. Phenothiazine - anti psychotic S/E of anti-psychotic drugs Extra Pyramidal Symptom Over medication of anti psychotic drugs neuroleptic malignant syndrome characterized by tremors (severe) S/Sx: Parkinsonism: 1. Pill-rolling tremors of extremities 1st Sign 2. Bradykinesia slow movement-----2nd Sign 3. Over fatigue 4. Rigidity (cogwheel type) ------- a. Stooped posture b. *Shuffling c.Propulsive gait 5. Mask like facial expression with decrease blinking of the eyelids 6. Monotone speech 7. Difficulty rising from sitting position 8. Mood labilety Depression suicide Nsg priority: Promote safety 9. Increase salivation drooling type 10. Autonomic signs: Increase sweating Increase lacrimation Seborrhea (increase sebaceous gland) Constipation Decrease sexual activity Nsg. Mgt. 1.) Administer Meds:Anti-parkinsonian agents Levodopa (L-Dopa)-------short-acting Carbidopa (Sinemet), Amantadine Hcl (Symmetrel)----long-acting Mechanism of action: Increase levels of dopa relieving tremors & bradykinesia S/E of anti-parkinsonian Anorexia n/v Confusion *Orthostatic hypotension Hallucination Arrhythmia, GIT irritation ( administer with meals) Contraindication: 1. Pt. with glaucoma----because L-dopa intra-ocular pressure (N: 12-21 mmHg) 2. Pt. taking MAOI (Parnate, Marplan, Nardil) MAOI = Monoamine Oxydase Inhibitor ( anti-depressant)
= Takes effect : 2-6 wks. =If on MAOI avoid: Tyramine, tryptophan rich foods ex. aged cheese, liver, beer, alcohol----leads to hypertensive crisisstroke Nsg. Mgt. when giving anti-parkinsonian a. Take with meals to decrease GIT irritation b. Inform pt urine/ stool may be darkened c. *Instruct pt. not to take food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg Because Vit. B6 reverses therapeutic effects of levodopa Only increase intake of Vit. B6 in taking INH (isoniazid, anti-TB) Isonicotinic Acid Hydrazide-----effect-----peripheral neuritis
2.) Anti- cholinergic agents relieves tremors *Artane mechanism inhibits acetylcholine *Cogentin action ---S/E - SNS 3.) Antihistamine Diphenhydramine Hcl (Benadryl) take at bedtime---relieves tremors S/E: adult drowsiness avoid driving & operating heavy equipment. Child Hyperactivity (CNS excitability) 4.) Dopamine agonist: Bromocriptine Hcl (Parlodel)---relieves rigidity, bradykinesia S/E: CNS depression, Check RR Nsg. Mgt. 1.) 2.) Maintain siderails to prevent falls Prevent complications of immobility - Turn pt every 2h - Turn pt every 1 h elderly -Turn affected extremity every 30 minutes Assist in passive ROM exercises to prevent contractures Maintain good nutrition: Protein CHON in am CHON in pm to induce sleep d/t Tryptopan ex. milk Increase fluid in take, high fiber diet to prevent constipation Assist in surgery Stereotaxic Thalamotomy Common complications: a. Subarachnoid hemorrhage b. Encephalitis c. Aneurysm Assist in ambulation
3.) 4.)
5.) 6.)
7.)
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MYASTHENIA GRAVIS (MG) A neuromuscular disorder characterized by a disturbance in transmission of impulses from nerve to muscle cell at neuro muscular junction leading to descending muscle weakness. Predisposing Factors: Common in Women, 20 40 y/o, Unknown cause or idiopathic Autoimmune release of cholenesterase (enzyme that destroys acetylcholine) Pathophysiology: Cholinesterase destroys ACTH ACTH Descending muscle weakness M.G.
S/ Sx: 1.) Ptosis drooping of upper lid ( initial sign) Palpebral fissure normal opening of upper & lower lids 2.) Diplopia (double vision) 3.) Mask-like facial expression 4.) Dysphagia 5.) Weakening of laryngeal muscles hoarseness of voice 6.) *Respiratory muscle weakness lead respiratory arrest. Prepare at bedside tracheostomy set 7.) Extreme muscle weakness during activity especially in the morning. Priority: to watch out for: a. A/W b. Aspiration c. Physical immobility Dx. Test: 1. Tensilon test (Edrophonium Hcl) an anti-cholinesterase/cholinergic agent----short-acting only) Administer to pt. for temporary relief for 5 10 mins. (+) for M.G. 2. CSF analysis- reveals cholinesterase Nsg Mgt. 1. Maintain patent a/w & adequate ventilator by: a.) Assist in mechanical ventilator attach to ventilator b.) Monitor pulmonary function test using spirometer 2. Monitor VS, I&O neuro check, muscle strength or motor grading scale (4/5, O/S, etc) 3. Siderails up 4. Prevent complications of immobility 5. NGT feeding to prevent complications 6. Administer medication as ordered a. Cholinergics or anticholinesterase agents Mestinon (Pyridostinine) Action: Increases ACTH Neostignine (prostigmin) S/E : PNS b. Steroids, Corticosteroids to suppress immune response Decadron (dexamethasone) Monitor for 2 types of Crisis: Myastinic crisis Cholinergic crisis 1. Under medication Cause: Over medication 2. Stress 3. Infection S/Sx - PNS S&Sx: 1. Unable to see Ptosis & diplopia Mgt. 2. Dysphagia Administer anti-cholinergic 3. Unable to breath 1. Atropine SO4 Mgt.: Administer cholinergic agents: Mestinon S/E: SNS dry mouth 7. Assist in surgical procedure Thymectomy (removal of thymus) 8. Assist in plasmapheresis filtering of blood 9. Prevent complication Respiratory arrest----prepare tracheostomy set at bedside Cause:
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GBS GUILLIAN BARRER SYNDROME
Predisposing Factors:
A disorder of the CNS characterized by bilateral symmetrical polyneuritis leading to ascending paralysis Polyneuritis ----- inflammation of the peripheral nerves Can leadto slow but complete recovery 1. Cause unknown, idiopathic 2. Auto immune 3. *R/t antecedent viral infection (from LRTI) 4. Immunizations
S&Sx 1. 2. 3. Clumsiness -------- Initial sign of GBS Ascending muscle weakness lead to paralysis Dysphagia Decrease or diminished DTR (deep tendon reflexes) -----Paralysis *Alternate HPN to hypotension complication: Can lead to arrhythmia Autonomic changes: a. Increase sweating b. Increase lacrimation c. Increase salivation d. Constipation
4.
5. 6.
Dx: Most important: CSF analysis thru lumbar puncture reveals increase in : IgG & CHON---same with MS Nsg Mgt. 1. Maintain patent a/w & adequate vent a. Assist in mechanical vent b. Monitor pulmonary function test 2. Monitor vs., I&O neuro check, ECG tracing due to arrhythmia 3. Siderails 4. Prevent complicarions immobility 5. Assist in passive ROM exercises 6. Institute NGT feeding 7. Administer medications as ordered: 1. Anti-cholinergic Atropine SO4 2. Corticosteroids to suppress immune response 3. Anti arrhythmic agents: a.) Lidocaine /XylocaineS/E: confusion & agitation b.) Bretyllium------blocks release of norepinephrine c.) Quinidines/Quinitine anti malarial agent & anti-arrythmic > Toxic effect Cinchonism Quinidine toxicity: S/E anorexia, n/v, headache, vertigo, visual disturbances 8. *Malaria ---king of tropical disease----antidote----Queen (Quinidine) Assist in plasmapheresis Prevent complications a. Arrhythmias b. Respiratory arrest
9.
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INFLAMMATORY CONDITIONS OF THE BRAIN Anatomy: Meninges a 3-fold membrane that covers the brain & spinal cord Fx: 1. Protection & support 2. Nourishment 3. Blood supply 3 layers: 1. Duramater (outermost 2. Arachmoid matter (middle) 3. Pia matter (outermost) 1. MENINGITIS An inflammation of the meninges of the brain & spinal cord Etiology: a. b. c. d. Meningococcus---most dangerous type Pneumococcus Hemophilous influenza common to children Streptococcus a type of adult meningitis in bet. is sub dural space sub arachnoid space where CSF flows L3 & L4
MOT: S&Sx
Direct transmission via droplet nuclei (airborne)
Stiff neck or Nuchal Rigidity ------Initial Sign of meningeal irritation Headache Projectile vomiting Photophobia Fever chills, anorexia General body malaise Weight loss Decorticate/decerebration abnormal posture Possible seizure Opisthotonus (arching of the back)-----2nd intital sign (+) Kernigs & Brudzinski sign Leg pain Neck pain
*Pathognomonic Sign:
Dx: 1. Lumbar Puncture: lumbar/ spinal tap use of hallow spinal needle Aspiration in the sub arachnoid space between L3 & L4 or L4 & L5.
Nsg Mgt . For Lumbar Puncture------- invasive 1. Consent / explain procedure to pt RN will explain if laboratory exams MD will explain if operation procedure Empty bladder, bowel promote comfort Arch back to clearly visualize L3, L4
17
2. 3.
Nsg Mgt. Post Lumbar: 1. 2. 3. 4. Result: 1. CSF analysis: Confirms Meningitis a. Increase CHON & WBC b. Decrease glucose c. Increase CSF opening pressure d. (+) Culture microorganism *Flat on bed 12 24 h to prevent spinal headache & leak of CSF Force fluid Check punctured site for drainage, discoloration & leakage to tissue, discomfort Assess for movement & sensation of extremities
(Normal: 50 160 mmHg)
2. Complete blood count CBC reveals increase WBC (Leukocytosis) Mgt: 1. Adm meds a.) Broad-spectrum antibiotic: Penicillin S/E : 1. GIT irritation take with food 2. Hepatotoxicity, nephrotoxcicity 3. Allergic reaction 4.* Super infection alteration in normal bacterial flora Normal flora: throat streptococcus Normal flora : intestine E. Coli Diarrhea
Sx: of superinfection of penicillin b.) Antipyretic c.) Mild analgesic for headache
2. Strict respiratory isolation 24 hrs. after start of antibiotic therapy 3. Comfy & dark room due to photophobia & seizure 4. Prevent complications of immobility 5. Maintain F & E balance 6. Monitor VS, I&O , neuro check 7. Provide client health teaching & discharge plan a. Nutrition Increase CHON & CHO but Small freq feeding b. *Prevent complication of Hydrocephalus & Nerve Deafness 8. Institute measures to prevent Increase ICP & seizures 9. Rehabilitation for residual deficit ( mental retardation & delayed psychomotor development) Exercise: Where to bring 2 y/o post meningitis ? Audiologist due to damage to post repair myelomeningocele Urologist -Damage to sacral area controls urination
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REVIEW: 3 Types of ISOLATION: 1. Strict Isolation 2. Reverse Isolation 3. Enteric Ex. Pt. with -Cushings syndrome reverse isolation -Aplastic anemia reverse isolation------ bone marrow depletion----pancytopenia -Cancer any type reverse isolation -Post-Liver transplant reverse isolation -Prolonged use steroids reverse isolation -Meningitis strict isolation -Asthma not to be isolated - Hepatitis A - Enteric - Measles Strict - Mumps Strict - Pneumonia Strict - PTB -Strict REVIEW: *Thrombosis & Stroke Initial sign: Late sign: * Anemia : Blood: Leukopenia Anemia Thrombocytopenia WBC RBC Platelets Leukocytosis Polycythemia Thrombocytosis Headache Pruritus -----leads to atherosclerosis
Initial sign: Weakness & Fatifue
19
CEREBRO VASCULAR ACCIDENT : Or Stroke, Brain Attack or Cerebral Thrombosis, Apoplexy A partial or complete disruption in the brains blood supply 2 largest & common artery in stroke : a. Middle cerebral artery b. Internal carotid artery Common to male 2 3x high risk, increases as you grow older
Predisposing factor: 1. 2.
3.
Thrombosis clot (attached)-----------No. 1 cause of Stroke Hemorrhage Embolism dislodged clot pulmo embolism---2nd cause S/Sx: Pulmonary Embolism 1. Sudden sharp chest pain 2. Unexplained dyspnea, SOB 3. Tachycardia, palpitations, diaphoresis & mild restlessness S/Sx: Cerebral Embolism 1. Headache, disorientation, confusion & decrease in LOC----lead to coma
4. *Compartment Syndrome compression of nerves/ arteries

Test Analysis: *Femur Fracture Fx. Complications:> Fat embolism most feared complication w/in 24hrs >Hemorrhage *Yellow bone marrow produces fat cells at medullary cavity of long bone *Red bone marrow provides WBC, platelets, RBC found at epiphysis Risk factors of CVA: a. b. c. d. e. HPN DM MI Artherosclerosis Valvular heart disease Post cardiac surgery-----*Mitral valve replacement Lifestyle: 1. Smoking nicotine potent vasoconstrictor 2. Sedentary lifestyle 3. Hyperlipidemia genetic-genes that easily binds to cholesterol h. Obesity ------20% of BW Overweight -----10% of BW i. Prolonged use of oral contraceptives - Macro pill has large amount of estrogen - Mini pill has large amount of progestin Mini-pill---- Promote lipolysis artherosclerosis HPN stroke j. Type A personality
f.
g.
2 types:
a. Deadline driven person b. 2 5 things at the same time c. Guilty when not dong anything k. Diet increase saturated fats -----ex. whole milk l. Emotional & physical stress S & Sx: 1. Transient Ischemic Attack ( TIA)- 1st sign of Impending stroke attacks o o Headache initial sing of TIA Dizziness/ vertigo, numbness, tinnitus, visual & speech disturbances, paresis or phlegia (monoplegia 1 extreme) (Paraplegialower extremeties) Increase ICP, *Temporary memory loss
2. Stroke in evolution progression of S & Sx of stroke 3. Complete stroke resolution of stroke a.) Headache b.) *Cheyne-Stokes Resp c.) Anorexia, n/v d.) Dysphagia e.) Increase BP f.) (+) Kernigs & Brudzinski Sx of Hemorrhage Stroke g.) Focal & neurological deficit 1. Phlegia 2. Dysarthria inability to vocalize 3. Aphasia 4. Agraphia difficulty in writing 5. Alexia difficulty in reading 6. Homonymous Hemianopsia loss of half of field of vision Left sided hemianopsia approach Right side of pt the unaffected side Nsng. Dx. = Unilateral Neglect Dx. 1. 2. Computerized Tomography Scan reveals brain lesion Cerebral Arteriography rveals site & extent of mal-occlusion Invasive procedure due to inject dye Allergy test *All Dx ending in graphy/gram are invasive: injection of a dye, ask if allergic to seafoods Post-CT Scan 1.) Force fluid to excrete dye because it is nephrotoxic---check BUN & Creatinine 2.) Check peripheral pulse 3.) Check Fluid imbalance----dye is an osmotic diuretic Nsg. Mgt. 1. Maintain patent a/w & adequate vent - Assist mechanical ventilation - Administer O2 inhalation 2. Restrict fluids prevent cerebral edema 3. Instruct client to avoid valsalva maneuver 4. Monitor vs., I&O, neuro check 5. Prevent compl of immobility by: a. Turn client q2h Elderly q1h To prevent decubitus ulcer/ bed sores To prevent Hypostatic pneumonia type of pneumonia r/t long immobility b. Egg crate mattress or H2O bed c. Sand bag or foot board- prevent foot drop
6. NGT feeding if pt cant swallow 7. *Passive ROM exercise q4h to prevent contractures & to promote proper body alignment 8. Alternative means of communication - Use Non-verbal cues - Magic slate - (+) To hemianopsia approach on unaffected side 9. Position pt.: elevate heat 30 degrees angle/ semi-fowlers 10. Maintain siderails 11.Meds a. Osmotic diuretics Mannitol ( Osmitrol) ---Side-dripfast drip ----S/E: decrease BP b. Loop diuretics Lasix/ Furosemide-----IV push 3. Corticosteroids Dextamethazone (ends in one) 4. Mild analgesic------codeine Sulfate-------S/E: Respiratory Depression 5. Thrombolytic/ fibrolitic agents tunaw clot Ex. Streptokinase-----S/E: Allergic Reaction Urokinase---------S/E: Hypertension Tissue Plasminogen Activating Factor ( TPAF)----S/E: Chest Pain *Monitor bleeding time 6. Anti-coagulants Heparin & Coumadin---- sabay Why : Coumadin will take effect after 3 days---long-acting Anti-Coagulants Heparin (Short-Acting) Monitor: PTT (Partial Thromboplastin Time) If prolonged, indicates bleeding Antidote: Protamine Sulfate Coumadin or Warfarin (Long-Acting) PT (Prothrombin Time) if prolonged, indicates bleeding Vitamin K (Aquamephyton)
7. Anti-platelet (PASA) aspirin paraanemo aspirin -the only NSAID that has anti-platelet property - Do not give to pts. With Dengue, Ulcer & Headache - Aspirin----- No. 1 ulceronegenic agent S/E: Tinnitus, Anemia, Heartburn & Dyspepsia *EPISTAXIS/ nose bleeding--- parameter that indicates effectiveness of thrombolytic therapy Health Teachings: 1. Avoidance of modifiable lifestyle - Diet, smoking 2. Dietary modification - Avoid caffeine, decrease Na & decrease saturated fats 3. Prevent Complications: *Subarachnoid hemorrhage 4. Rehab for focal neurological deficit 1. Mental retardation 2. Delay in psychomotor development
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CONVULSIVE Disorder (CONVULSIONS)
o A disorder of the CNS characterized by paroxysmal seizures with or w/o loss of consciousness,
abnormal motor activity, alteration in sensation & perception & changes in behavior. Exercise: Can you outgrow febrile seizure? Febrile seizure Normal if < 5 y/o Pathologic if > 5 y/o Predisposing Factor: a. Head injury d/t birth trauma------ No .1 cause of convulsions b. Toxicity of carbon monoxide c. Brain tumor d. Genetics e. Nutritional & metabolic deficit f. Physical stress g. Sudden withdrawal to anticonvulsants-----No .1 of status epilepticus Status epilepticus Drug of Choice: Diazepam & glucos S & Sx. Of Epilepsy dependent upon stages: I. Generalized Seizure 1.) Grand mal / tonic clonic seizures-----most common type of seizure - With or w/o Aura warning symptoms of impending seizure attack Epigastric pain ---1st sign of aura This is associated with olfactory, tactile, visual, auditory sensory experience Epileptic cry fall *Loss of consciousness 3 5 minutes Tonic-clonic contractions Tonic - Direct symmetrical extension of extremities Clonic - contractions Post ictal (state of lethargy or drowsiness) sleep- unresponding sleep after tonic clonic
2.) Petit mal seizure (same as daydreaming!) - Blank stare - Decrease blinking eye - Twitching of mouth - *Loss of consciousness 5 10 seconds (quick & short) - *Common to children II. Localized/partial seizure 1. Jacksonian seizure or Focal seizure tingling/jerky movement of index finger/thumb & spreads to shoulder & 1 side of the body with janksonian march 2. Psychomotor/ Focal-motorseizure -*Automatism stereotype repetitive & non-purposive behavior - Clouding of consciousness not in contact with environment - Mild hallucinatory sensory experience
3 Types of HALLUCINATION: 1. 2. 3. Auditory schitzophrenia paranoid type Visual Korsakoffs psychosis chronic alcoholism Tactile addict substance abuse
III. Status Epilecticus Continuous, uninterrupted seizure activity leading to hyperpyrexia coma death Drug of Choice : Diazepam & Glucose Pathophysiology: Status Epilepticus Increase electrical firing in the brain: if left untreated Increase Heat production -------hyperpyrexia Increase metabolism using glucose & O2 ------need for glucose therapy Coma------Death Dx: For All Types: 1. 2. 3. CT scan revealsbrain lesion EEG electroencephalography --revealsHyperactivity brain waves ECT therapy
Nsg. Mgt. Priority Airway & Safety 1. *If with seizure: S/E is PNS Maintain patent a/w & promote safety Before seizure: 1. Remove blunt/sharp objects 2. Loosen clothing of pt. 3. Avoid restraints----can lead to fracture 4. Maintain siderails 5. Turn head to side to prevent aspiration 6. Tongue guard or mouth piece to prevent biting of tongue (emergencyclean piece of cloth) 7. Avoid precipitating stimulus bright glaring lights & noises, drafts 8. Administer meds a. Dilantin (Phenytoin) ( toxicity level 20 ) S/E: Gingival hyperplasia H-hairy tongue A-ataxia N-nystagmus b. Acetaminophen- febrile pt Mix only with NSS, sandwich method - Dont give alcohol lead to CNS depression c. (Tegretol) Carbamazepine d. Phenobarbital (Luminal) -------common S/E: hallucination & mild arrythmia e. Diazepam 2. Institute seizure & safety precaution By Post seizure: Administer O2 inhalation. Suction apparatus ready at bedside 3. Monitor onset & duration of - Type of seizure
- Duration of post ictal sleep----the longer the duration, the danger of status epilepticus 4. Assist in surgical procedure - Cortical resection Exercise: 1 y/o grand mal immediate nursing action = a/w & safety a. Mouthpiece 1 yr old little teeth only b. Adm o2 inhalation post! c. Give pillow safety d. Prepare suction Neurological Assessment: 4 Objectives of Neurological Assessment: 1. To know the exact neurological deficit 2. To localized lesion 3. For rehabilitation 4. Guidance in nursing care 2 Types of N.A.
1. Glasgow Coma Scale (GCS) objective measurement of LOC or quick neuro check
3 components of ECS (MVE) M motor 6 V verbal response 5 E eye opening 4 15---- highest score Scaling: 15 14 Conscious 13 11 Lethargy 10 8 Stupor 7 Coma 3 Deep coma lowest score ( no 0 score on any response, lowest is only 1) 2. Comprehensive Neuro Exam A. Survey of Mental status & speech (Comprehensice Neuro Exam) 1.) LOC & Test of memory 2.) Levels of orientation 3.) Cranial Nerve assessment 4.) Motor assessment 5.) Sensory assessment 6.) Cerebral test Romhberg, finger to nose 7.) DTR 8.) Autonomics 1. a. Levels of consciousness (LOC) 1. Conscious (conscious) awake levels of wakefulness 2. Lethargy (lethargic) drowsy, sleepy, obtunded 3. Stupor (stuporous) awakened by vigorous stimulation Pt. has general body weakness, decrease bodily reflex 4. Coma (Comatose) Light (+) all forms of painful stimulations Deep (-) to painful stimulation *Watch out for the rise & fall of the chest b. Different types of pain stimulation o Dont prick 1. Deep sternal pressure/stimulation: 3x fist knuckle With response light coma Without response deep coma 2. Pressure on great toe 3x 3. Orbital pressure pressure on orbits only below eye 4. Corneal reflex/ blinking reflex *Wisp of cotton used to illicit blinking reflex among conscious patients *Instill 1-drop saline solution unconscious pt if (-) response pt is in deep coma
c. Test of memory consider educational background a. Short term memory What did you eat for breakfast? Damage to temporal lobe (+) antero grade amnesia b. Long term memory (+) Retrograde amnesia damage to limbic system (rhinencephalon) 2. Levels of orientation: 1st: Time 2nd:: Person 3rd: Place Exercise: Describe a conscious pt ? a. Alert not all pt are alert & oriented to time & place b. Coherent c. Awake d. Aware 3. Cranial Nerve Assessment: 12 pairs of cranial nerves I II III IV V VI VII VIII IX X XI XII Olfactory Optic Oculomotor Trocheal Trigeminal Abducens Facial Acoustic/auditory (V) Glossopharyngeal Vagus Spinal accessory Hypoglossal Old Opie Occasionaly Tries Trigonometry And Feels Very Gloomy Vague And Hypoactive s s m m b m b s b b m m Some Say Marry Money But My Brother Says Bad Business Marry Money
smallest CN largest CN
longest CN
I. Olfactory dont use ammonia, alcohol, cologne irritating to mucosa use coffee granules, vinegar * Hyposmia decrease sensitivity to smell *Diposmia distorted sense of smell *Anosmia absence of sense of smell *Either of 3 might indicate head injury damage to cribriform plate of ethmoid bone where olfactory cells are located or indicate inflammation condition sinusitis II Optic (Sensory or Vision) 1. Test of visual acuity or central or distance vision (test of near vision) Use Snellens Chart: a. Snellens Alphabet -----used for literate client b. Snellens E chart --------used for illiterate c. Animal Chart -----used for children Normal: 20/20 vision 20 numerator is constant: 20 ft (6-7 m) distance from the chart 20 denomenator ---vision distance the person can see the letters OD Rt eye 20/20 =20/200 blindness cant read E biggest OS left eye 20/20 OU both eye 20/20 2. Test of Peripheral Vision/ visual field: facing the client a. Superiorily b. Bitemporally
c. Inferiorly d. Nasally Common Disorders 1. Glaucoma (Normal 12 21 mmHg intra-ocular pressure) - Increase IOP - Loss of peripheral vision tunnel vision 2. Cataract opacity of lens - Loss of central vision, Blurring or hazy vision 3. Retinal detachment curtain veil like vision & floaters 4. Macular degeneration black spots III Oculomotor, IV (Throclear), VI (Abducens) Tested simultaneously because it controls or innervates the movement of extrinsic ocular muscle *6 Cardinal Gaze Extrinsic Ocular Movement Rt eye IO LR SR Throclear controls superior oblique (1) Abducens - lateral rectus (1) 9. Oculomotor- controls the size & response of pupil (Pupil size 2 -3 cm or 1.5 2 mm) - controls opening of the eyelids - controls the 4 gaze V Trigeminal Largest nerve consists of - ophthalmic, maxillary & mandibular branch 1. Sensory controls sensation of the face, mucus membrane; teeth & corneal reflex Unconscious instill drop of saline solution 2. Motor controls muscles of chewing/ muscles of mastication *Trigeminal neuralgia difficulty in chewing & swallowing - damage to the trigeminal nerve - Drug of Choice: Tegritol -Extreme food temperatire is not recommended -Avoid hot or cold preparation Exercise: Trigeminal neuralgia, RN should give a. Hot milk, butter, raisins b. Cereals c. Gelatin, toast, potato all correct but d. Potato, salad, gelatin salad easier to chew a. Sensory controls taste anterior 2/3 of tongue: Test cotton applicator with sugar. -Put applicator with sugar to tip to tongue. -Start of taste insensitivity: Age group 40 yrs old b. Motor- controls muscles of facial expression, smile frown, raise eyebrow if Damage causes --------Bells palsy or facial paralysis Cause of Bells palsy in children---No 1 cause : R/T forcep delivery Temporary only, resolve w/in 4-6 months *Most evident clinical sign of facial symmetry: Nasolabial folds VIII Acoustic/ Vestibulocochlear a. Cochlear ----controls hearing
SO MR
N O S E
left eye
VI Facial:
b. Vestibule-----controls balance (kinesthesia /position sense) -----Movement & orientation of body in space ------located in the inner earif it movesthe head moves too--kinesthesia
*Menieres Disease----only disease of the inner ear----loss of balance---Nsg. Priority: Safety Parts of Ears: Outer tympanic membrane, pinna, oricle (impacted cerumen), cerumen Middle hammer, anvil, stirrup or melleus, incus, staples. Mid otitis media Eustachean ear Inner ear- meniere ear, sensory hearing loss Remove vestibule menieres dse disease inner ear *Archimedes law --Bouyancy *Daltons law Partial pressure of gases (Diffusion) *Inertia law of motion (dizziness, vertigo) Exercise: 1.) Pt. with multiple stab wound in the chest - Movement of air in & out of lungs is carried by what principle? - Diffusion Daltons law 2.) Pregnant check up ultrasound reveals fetus is carried by amniotic fluid - Archimedes 3.) Severe vertigo d/t Inertia Test for acoustic nerve: ---------Repeat words uttered IX Glossopharyngeal X Vagus controls taste the posterior portion 1/3 of the tongue controls gag reflex
Test 9 10 Pt say ah check uvula (in the middle tonsils) should be midline If there is deviation from L to R ----Damage to cerebral hemisphere Gag reflex place tongue depression post part of tongue Dont touch uvula Gag reflex----vagal stimulation -----PNS Effect XI Spinal Accessory - controls sternocleidomastoid (neck) & trapezius Shrug shoulders, put pressure. Pt should resist pressure. Paresis or phlegia
XII Hypoglossal - movement of tongue say ah If L or R deviation-----damage to the cerebral hemisphere - Push tongue against cheek. Normal= tongue in midline, if (-) disorder called ------- Short frenulum lingue or tongue tied bulol
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EYES
A. External Parts: 1. Orbital cavity made up of connective tissue, protects eye from trauma. 2. EOM (Extrinsic Ocular Muscles ) involuntary muscles of eye, needed for gazing movement. 3. Eyelashes/ eyebrows aesthetic purposes 4. Eyelids palpebral fissure opening upper & lower lid. Protects eye from direct sunlight Meibomean gland secrets a lubricating fluid inside eyelid a.) Stye/ sty or Hordeolum- inflamed Meibomean gland Conjunctiva Lacrimal apparatus tears
5. 6.
B. Intrinsic Coat I. Sclerotic coat outer most a.) Sclera white. Occupies posterior of eye. Refracts light rays b.) Canal of sclera site of aqueous humor drainage c.) Cornea transparent structure of eye II. Uveal Tract provides nutritive care Uveitis inflammation of the uveal tract Consist of: a.) Iris colored muscular ring of the eye 2 Muscles of Iris: 1. Circular smooth muscle fiber 2.radial smooth muscle fiber 2 Chambers of the Eye: 1. Anterior a.) Vitereous Humor maintains spherical shape of the eye b.) Aqueous Humor maintains intrinsic ocular pressure (Normal IOP= 12-21 mmHg) II. Retina (innermost layer) a. Optic discs or blind spot nerve fibers only No auto receptors Cones (daylight/ colored vision) Phototopic vision Rods night, twilight vision Scotopic vision = Vit. A deficiency rods insufficient b. Maculla lutea yellow spot center of retina c. Fovea centralis area with highest visual acuity oracute vision Physiology of Vision: 4 Physiological Processes for Vision to occur: 1. Refraction of light rays bending of light rays 2. Accommodation of lens 3. Constriction & dilation of pupils
- Constricts the pupil - Dilates the pupil
4. Convergence of eyes *Unit of measurements of refraction Diopters *Normal eye refraction Emmetropia *PERRLA ---Normal Reaction ERROR of Refraction: 1. 2. 3. 4. Myopia - near sightedness Tx: biconcave lens Hyperopia - farsightedness Tx: biconvex lens Astigmatisim -distorted vision Tx: cylindrical Presbyopia - old slight inelasticity of lens d/t aging Tx: bifocal lens or double vista
*Accommodation of lenses based on Thelmholtz Theory of accommodation Near vision: -Ciliary muscle contracts -Lens bulges Convergence of the Eye: Error: 1. Exotropia 1 eye normal Esophoria Strabismus- squint eye Amblyopia prolong squinting Far vision: - Ciliary muscle dilates / relaxes -Lens is flat
2. 3.
4.
corrected by corrective eye surgery
1. GLAUCOMA
An increase Intra Ocular Pressure if untreated, atrophy of optic nerve disc blindness - Preventable but not curable Predisposing Factors: 1. 2. 3. 4. 5. Type: 1. 2. 3. S/Sx: 1. *Loss of Peripheral Vision a Tunnel-like vision 2. *Halos/Rainbows around lights 3. Headache & Dizziness 4. n/v 5. Steamy cornea 6. Eye discomfort 7. *Ocular Pain 7. If untreated gradual loss of central vision blindness Diagnosis: 1. *Tonometry reveals increase IOP >12- 21 mmHg 2. Perimetry reveals decrease peripheral visual field 3. *Gonioscopy reveals abstruction in anterior chamber Nursing mgt: 1. Enforce CBR 2. Maintain siderails 3. Administer meds a.) *Miotics lifetime ------ contracts ciliary muscles & constricts pupil.
High risk group 40 y/o & above HPN Hereditary Obesity Recent eye surgery, trauma, inflammation
Chronic -------- (open angle G.) *most common type Obstruct in flow of aqueous humor at trabecular meshwork of canal of schlema Acute --------- (close angle G.) *Most dangerous type Forward displacement of iris to cornea leading to blindness. Chronic--------- (closed angle) - Precipitated by acute attack
Ex. Pilocarpine Na (Carbachol) b.) Epinephrine eye drops ------decrease formation & production of aqaueous humor c.) Carbonic anhydrase inhibitors. ----- Promotes increase out flow of aquaeous humor(drainage) Ex. Acetazolamide (Diamox) 2. d.) Timoptics (Timolol maleate)- Increase outflow of aquaous humor (drainage) Surgery: Invasive: a.) Trabeculectomy --- eye-trephining removal of trabelar meshwork of canal or schlera to drain aqueous humor b.) *Peripheral Iridectomy portion of iris is excised to drain aqueous humor Non-invasive: a. Trabeculotomy (eye laser surgery)
Nursing Mgt.: Pre operative for all types of surgery: 1. Apply eye patch on unaffected eye to force weaker eye to become stronger. Nursing Mgt. Post-operative all types of surgery 1. Position unaffected/ unoperated side - to prevent tension on suture line. 2. Avoid valsalva maneuver 3. Monitor symptoms of IOP a.) Headache b.) n/v c.) Eye discomfort d.) Tachycardia 2. Eye patch for both eyes post-operatively
2. CATARACT
A partial/ complete opacity of lens, can lead to blindness Predisposing Factor: 1. 2. 3. 4. S/Sx: Aging : 90-95% (degenerative/ senile cataract)---60 y/o & above Congenital (very rare) Prolonged exposure to UV rays DM
1. *Loss of Central Vision - Hazy or blurring of vision

2. 3.
4.
Dx:
Painless Milky white appearance at center of pupil *Decrease perception of colors *Elderly can only see Red & Green
1. Opthalmoscopic exam reveals (+) opacity of lens Nsg Mgt: 1. Reorient pt. to environment due opacity 2. Siderails 3. Medications a.) *Mydriatics dilate pupil not lifetime Ex. Mydriacyl b. ) Cycloplegics paralyzes ciliary muscle. Ex. Cyclogyl c.) Atrophine 4. Surgery a. E extra C - capsular C cataract L - lens E extraction I - intra C - capsular C cataract L - lens E extraction
Partial removal of lens
b.
Total removal of lens & surrounding capsules
Complications of Lens Extraction: Hemorrhage

Retinal Detachment Endopthalmitis Nursing Mgt: 1.Position unaffected/ unoperated side - to prevent tension on suture line. 2.Avoid valsalva maneuver 3.Monitor symptoms of IOP a.) Headache b.) n/v c.) Eye discomfort d.) Tachycardia 4.Eye patch both eyes - post op
3. RETINAL DETACHMENT
- The separation of 2 layers of retina, can lead to blindness Predisposing factors: 1. 2. 3. 4. 5. S/Sx: 1. 2. 3. 4. *Curtain veil like vision Flashes of lights *Floaters d/t seepage of blood (Photopsia) Gradual decrease in central vision *Severe myopia near sightedness Diabetic Retinopathy Trauma *Following lens extraction HPN
Dx: Opthaloscopic exam Drug of Choice: Cycloplegics Nursing Mgt: 1. 2. Siderails (all visual disease) Surgery: a.) Cryosurgery (cold application) b.) *Scleral buckling c.) Diathermy ------heat application
4. MACULAR DEGENERATION
-----the appearance of black spots in the eyes
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33
Addisons Disease Angina Pectoris Appendicitis Asthma Bulimia Nervosa Cataract (loss of central vision) Cholecyctitis Cholera Cushings Disease Dengue Diptheria Down Syndrome Down Syndrome Emphysema Glaucoma (peripheral vision)
PATHOGNOMONIC SIGNS Bronze-Like Skin Levines Sign Rebound Tenderness Wheezing On Expiration Chipmunk Face Hazy Vision (+) Murphys Sign Rice-Watery Stool Moon Face Appearance Petechiae Pseudomembrane Protrusion Of Tongue Simean Creases on Palms Barrel Chest Tunnel-like Vision Exopthalmus Jaundice Carotenemia ( yellowish skin) Strawberry Tongue Leioning Face Spider Angioma Chills Kopliks spot (+) Kernigs & Brudzinskis Sign Ptosis (+) Cullens Sign (ecchymosis of umbilicus) (+) Grey-Turners (ecchymosis of flank) Pill-Rolling Tremors Machine-like Murmur Beefy Red Tongue Rusty Sputum Low-Grade Fever Olive Shape Mass Curtain Veil-Like Vision Butterfly rash Risus Sardonicus (+) Trousseau & (+) Chvostek Sign Clubbing of Fingers (+) Homans Sign Rose Spots in Abdomen
Graves Disease (Hyperthyroidism) Hepatitis Hyperpituitarism ( Acromegaly) Kawasaki Disease Leprosy Liver Cirrhosis Malaria Measles Meningitis Myasthenia Gravis Pancreatitis( Ectopic Pregnancy) Parkinsons Disease Patent ductus Arteriosus Pernicious Anemia Pneumonia PTB Pyloric Stenosis Retinal Detachment Systemic Lupus Erythematosus Tetanus Tetany Tetralogy Of Fallot Thombophlebitis Typhoid Fever
34
RELATED DISORDERS: 1. COPD = # 1 cause: Smoking ----- 4 Types: ---- all needs bronchodilators BRONCHITIS Blue bloaters Dyspnea on Exertion Lead to cor pulmonale ASTHMA Wheezing on Expiration Cause by allergens Hereditary Reversible BRONCHOIECTASIS Hemoptysis Undergo Pneumonectomy Bronchoscopy EMPHYSEMA Barrel Chest Pink Puffers Dyspnea at Rest Lead to Cor Pulmonale Cause by Allergens Hereditary CO2 narcosis Purse Lip Breathing Irreversible Terminal Stage
35
To Prevent STD Local practice monogamous relationship CGFNS/NCLEX condom
ENDOCRINE SYSTEM
The endocrine system integrates body functions by the synthesis & release of hormones. Hypothalamus: link between the nervous system & the endocrine system.
ENDOCRINE GLANDS: Secrete their products directly into the bloodstream Different from exocrine glands Exocrine glands: secrete through ducts unto epithelial surfaces or into the GIT Parts: Pituitary Gland Adrenal Glands Pancreas Thyroid Glands
Parathyroid Glands Gonads
HORMONES: - Are chemical substances that are secreted by the endocrine glands. - Can travel moderate to long distances or very short distances. - Acts only on cells or tissues that have receptors for the specific hormone. - Target Organ: The cell or tissue that responds to a particular hormone - Regulation of Hormones: Negative Feedback Mechanism When the hormone concentration rises, further production of that hormone is inhibited. When the hormone concentration falls, the rate of production of that hormone increases.
2 BASIC PATHOPHYSIOLOGICAL DISORDER OF THE ENDOCRINE
A. Hyposecretion/ Hypoactivity D/T 1. Congenital absence of glands Ex. No pancreas 2. Surgical removal of glands Ex. Total Thyroidectomy Primary Disease Problem in target gland; autonomous Parts: I. PINEAL GLAND Function: Secretes Melatonin Inhibits leutenizing hormone (LH) secretion Regulates body clock, sleeping pattern or circadian rhythm
B. Hypersecretion / Hyperactivity D/T 1. Tumor w/n or outside the gland Ex. Tumor in adrenal gland
Secondary disease problem outside the target gland; Most often d/t a problem in pituitary gland
II. PITUITARY GLAND (Hypophysis Cerebri) The main gland located at base of the brain at Sella Turcica Fx: Master gland of body/ Master clock of body---it controls all the metabolic activity of the body 2 Divisions: Anterior Pituitary Gland Adenohypophysis A. ANTERIOR PITUITARY GLAND Function: 1. Responsible for Growth Hormone (GH) (Somatotropic Hormone) Function: For elongation of long bones *Puberty age: 9 y/o 21 y/o & the Epiphysial plate closes at 21 y/o DISORDER: Hypopituitarism *Dwarfism -- Children 1. Frohlicks Syndrome
Posterior Pituitary Gland Neurohypophysis
GH
Hyperpituitarism Acromegaly -- Adult 1. Gigantism

37
hH
-Dwarf w/ obesity - Mentally retarded - Loss of reproductive ability d/t genital atrophy 2. Simmonds Disorder/ Pituitary Cachexia - Appearance of a wizened old man - Premature senility, Skin dry & wrinkled - Mental retardation - Male: Absence of spermatogenesis - Female: Amenorrhea Dx: - X-ray, MRI or CT scan: pituitary tumor - Plasma hormone levels: decreased Tx:
- If s/s appear before closure of epiphyseal plate - rapid growth of long bones 2. Acromegaly - If s/s appear after closure of epiphyseal plate - Hyperthrophy of soft tissue & bone thickness - Disproportional growth Enlargement of cartilage ( nose & ears) Enlargement of larynx (deep voice) Progmatism: Protrusion of jaw Square face & jaw Macroglossia Obstructive Sleep Apnea Drug of Choice in acromegaly: Octreotide (Sandostatin) --S/E: Seizure & GIT irritation Somatostatin Hormone - antagonizes the release of GH
2. Melanocytes Stimulating Hormone (MSH) Function: For skin pigmentation DISORDER: *Albinism ---hyposecretion of MSH ----prone to develop skin cancer & blindness *Vitiligo -----hypersecretion of MSH
3. Prolactin/ Lactogenic Hormone Initiates milk let-down reflex with help of oxytocin Promotes development of mammary gland/breast tissue Disorder: Prolactin Deficiency : Failure to lactate 4. Adrenocorticotropic Hormone ACTH Development & maturation of adrenal cortex S & Sx in Deficiency: - Results in diminished cortisol secretion. - Weakness, fatigue, weight loss, and hypotension. 5. LH -----Progesterone 6. FSH----Estrogen B. POSTERIOR PITUITARY GLAND: secretes---1.) Oxytocin a. Promotes uterine contractions-----preventing bleeding/ hemorrhage. - Best time to administer Oxytocin: after placental delivery to prevent uterine atony. b. Initiates the Milk let-down reflex with help of prolactin. 2.) Anti-Diuretic Hormones (ADH) /ADH-replacement ---Vasopressin or Pitressin Function: Prevents urination conserve H2O Regulates water metabolism Released during stress or in response to an increase in plasma osmolality to stimulate reabsorption of water & decreased urine output DISORDERS OF THE POSTERIOR PITUARY GLAND 1. DIABETIS INSIPIDUS (DI) The hyposecretion of ADH Disorder w/ massive polyuria d/t either lack of ADH or kidneys insensitivity to it Cause: Idiopathic/ unknown Predisposing factor: PITT 1. Pituitary surgery
2. Inflammation 3. Trauma 4. Tumor Pathophysiology :
Diabetes Insipidus
Disorder of H20 metabolism * Alcohol inhibits release of ADH
ADH
Prevents renal tubules from reabsorbing H20 S &Sx: POLYURIA (excessive urine output 5-29 L/24 hrs.)
Polydipsia Dehydration Other S & Sx:
F & E imbalance
Diluted Urine
Urine Specific gravity
2. Sx of Dehydration: Excessive thirst, Agitation, Poor skin turgor, Dry mucus membrane 3. Weakness & Fatigue 4. Hypotension if left untreated 5. Hypovolemic shock *Anuria Late sign hypovolemic shock 6. Weight loss Dx:
1.Decrease urine specific gravity- concentrated urine 2.Serum Na = Increase d/t compensation to attract more H2o
Mgt:
(N = 1.015 1.035) (N =135 -145 meq/L)
1. Force fluid 2,000 3,000ml/day 2.Administer IV fluid replacement as ordered ( Isotonic fluid solution) 3. Monitor VS, I&O 4.Administer meds as ordered (Commercially-Prepared ADH) a. Pitressin Tannate Oily preparation: Give deep I.M. b. Vasopressin Tannate May cause lipodystrophy , rotate site of administration Will cause vasoconstriction--Monitor BP before & after c. Desmopressin Acetate Given by Nasal Spray d. Lypressin 5. Prevent complications: Most feared complication Hypovolemic shock 2. SYNDROME OF INAPPROPRIATE ANTI-DIURETIC HORMONE (SIADH) - An increase production of ADH or Hypersecretion of ADH - Idiopathic/ unknown Predisposing Factor: 1.
2.
Head injury R/T Bronchogenic cancer or lung cancerEarly Sign of Lung Ca : Cough productive, non productive
3. Hyperplasia of Pituitary gland 4. Increase size of organ d/t increase # of cells S&Sx 1. 2. 3. 4. Fluid Retention Increase BP HPN Edema Wt gain Danger of Water Intoxication
5.
(The only Endocrine Gland with Water Intoxication)

39
Cerebral Edema
Increase ICP Complications of SIADH Seizure Activity
Dx : 1. Urine specific gravity increase: Reveals a diluted urine 2. Serum Na ----Decrease 3. Low serum osmolality 4. High urine osmolality (urine osmolality >100 mosmol/kg) 5. Normal renal function (low BUN <10 mg/dL), absence of hypothyroidism & glucocorticoid deficiency & recent diuretic therapy. Nsg Mgt:
1.Restrict fluid. (<1,000 ml/day)

Takes 3-10 days to work 2. Administer meds as ordered If the patient has evidence of fluid overloading, a history of CHF, or is resistant to treatment, loop diuretics (Furosemide) may be added as well. a. Diuretics-----both ----Osmotic (Mannitol)---for the Increase ICP (side-drip) ----Loop (Lasix)---------for edema----IV push b. Chronic treatment: lithium or demeclocycline which inhibit ADH action. 3. Monitor strictly V/S, I&O, neuro check increase ICP 4. Weigh daily 5. Assess for presence edema 6. Provide meticulous skin care 7.Prevent complications : Increase ICP & Seizure 8. Maintain sodium balance Increase sodium intake If the serum sodium is below 120 or if the patient is seizing, emergency treatment: 3% NaCl. May be followed by Furosemide. Excessively rapid correction of hyponatremia may cause central pontine myelinolysis. Patients with a plasma sodium concentration greater than 125 mmol/l rarely need specific therapy for hyponatremia. III. ADRENAL GLAND
Located at the top of the kidney 2 Parts:
A. Adrenal Cortex (Outermost layer) 1. Zona Fasiculata secrets glucocorticoids Ex. Cortisol, Corticosterone --Controls glucose metabolism (SUGAR) Increase blood glucose levels by increasing rate of gluconeogenesis Increase protein catabolism Increase mobilization of fatty acids Promote sodium and water retention Anti-inflammatory effect Aid the body in coping with stress Zona Reticularis secrets traces of glucocorticoids & androgenic hormones M Testosterone F Estrogen & progesterone
40
2.
Fx: Promotes development of secondary sexual characteristics 3. Zona Glomerulosa - secretes mineralocortisone/mineralocorticoids Ex. Aldosterone, corticosterone, Deoxycorticosterone Fx: Promotes Na & H2O reabsorption & excretion of potassium (SALT) Regulate fluid and electrolyte balance Stimulate reabsorption of sodium, chloride and water Stimulate potassium excretion Under the control of the Renin-Angiotensin-Aldosterone system Summary: Adrenal Cortex Hormones Sugar Salt Sex B. Adrenal Medulla (Innermost layer) Secrets cathecolamines a. Epinephrine b. Norephinephrine (Potent vasoconstrictor) Released during fight or flight situations SYMPATHETIC effect
DISORDERS OF THE ADRENAL CORTEX: CODE: 3 Ss Addisons Disease
S
Glucocorticoid Mineralcoritcoid Androgen
ugar alt ex
Cushings Syndrome
Hypoglycemia Hyponatermia Loss of pubic CONNS DISEASE 1. ADDISONS DISEASE
Hyperglycemia Hypernatremia Hirsutism
- Hyposecretion of adrenocortical hormones leading to: a. Metabolic Disturbances (sugar) b. F&E Imbalances- Na, H2O, K c. Deficiency of neuromuscular function (salt & sex) Predisposing Factors: 1. Atrophy of adrenal gland 2. Fungal infections Sx of 3. Tubercular infections Hypoglycemia Pathophysiology : T tremors, tachycardia I irritability R - restlessness E extreme fatigue D diaphoresis & Tolerance To Stress ---- Addisonians Crisis Hyperpigmentation (discoloration of skin & m. m.) Tan - Decreased Volume Salt = BRONZE-SKINNED
S
- Hypoglycemia - Decreased Plasma cortisol Sugar Melanocyte secreting hormone
Hypovolemia --- Hypotension

41
- Hyponatremia ---- Dehydration (Extreme thirst & agitation)----Weight Loss
- Hyperkalemia influence cardiac polarization Arrythmia ---Cardiac Arrest Sex
Sx of Hyperkalemia I irritability D diarrhea
- Decrease sexual hormone ---- libido & sexual urge Loss of axillary & pubic hair Breast atrophy
S & Sx: 1. Hypoglycemia 2. Hyponatremia Hypovolemia a. Hypotension b. Dehydration c. Weight loss 3. Hyperkalemia 4. Decrease libido & loss pf pubic hair/axilla * Pathognomonic Sign = Bronze-like skin pigmentation d/t decrease cortisol w/c will stimulate pituitary gland to release MSH Dx : 1. 2. 3. 4. FBS decrease FBS (N 80 120 mg/dL) Plasma cortisol decreased Serum Na decreased Serum K increased Normal Na = 135 -145 meq/L K = 3.5 5.5
Nsg Mgt: 1. Monitor VS, I&O to determine presence of Addisonian crisis 2. Administer isotonic fluid as ordered 3. Diet increase calorie or CHO Increase Na, Increase CHON, Decrease K 4. Force fluid d/t hyponatremia & dehydration 5. Meticulous skin care d/t bronze-like skin 6. Maintain patent IV line 7. Administer meds as ordered a.) Steroids supplementation : Corticosteroids - (Decadron) or Dexamethazone Hydrocortisone (cortisone)- Prednisone Betamedasone
Nsg. Mgt. with Steroids
1. Administer 2/3 dose in AM & 1/3 dose in PM in order to mimic the normal diurnal rhythm.
2. 3. 4. 5. 6. 7. 8. 9. Give on full stomach, after meal or w/ milk or w/ antacid ( gastric irritants) Monitor blood sugar level ( will cause hyperglycemia) Limit fluid intake ( will cause retention of water) Monitor body weight at least once a day Give calcium preparation ( can cause osteoporosis) Avoid any form of skin trauma/injury ( Steroids increases capillary fragility-----ecchymosis) Not given to children---can cause growth retardation Monitor S/E (Cushings syndrome S/Sx) a. HPN b. Hirsutism c. Edema d. Moon face & buffalo hump
10. Taper the dose (withdraw gradually from drug) to prevent complication of Addisons Crisis
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Sudden withdrawal--------- Acute exacerbation of Addisons Crisis characterized by : Sudden hypoglycemia, severe Hypotension Hypovolemia, severe Hypocalcemia Weight loss Sudden severe Hypokalemia------ Arrhythmia Cardiac arrest Leads to progressive stupor & coma Nsg Mgt: Addisonian Crisis (Coma) 1. Assist in mechanical ventilation 2. Administer steroids 3. Force fluids 11. Can suppress immune response-------prone to infection Avoid sources of infection Avoid crowded areas, people with RTI Place on reverse isolation b.) Mineralocorticoids. 8. Ex. Flurocortisone
HT & Discharge planning a. Avoid precipitating factors leading to Addisonian crisis 1. 2. 3. Sudden withdrawal crisis Stress Infection
b. Prevent complications 1. Addisonian crisis 2. Hypovolemic shock 9. Hormonal Replacement Therapy lifetime 10. Important follow up care 2. CUSHINGS SYNDROME Hypersecretion/ increase secretion of adrenocortical hormone Predisposing Factors: 1. Hyperplasia of adrenal gland
2. Tubercular infection: spread of infection to adjacent organs Milliary TB (TB of the Adrenal Gland)
Pathophysiology: Hyperglycemia (3 Ps)
- Hyperglycemia Sugar -
polyuria polydipsia polyphagia
Lead to DM
Buffalo Hump & Moon Face d/t abnormal fat distribution Increase steroids w/c WBC Increase susceptibility to infection (reverse isolation) Sx of Hypokalemia W eakness & Fatigue
Salt
- Hypokalemia
43
Arrythmia ---Cardiac Arrest - Hypernatremia--- fluid retention Edema Anasarca Obese Trunk w/ thin extremities Sex S & Sx: 1. 2. Hyperglycemia ( Difference From DM: 3 Ps + Glycosuria + Weight Loss)---Complication of Cushings: DM Hypernatremia a. HPN b. Edema c. Wt gain d. Moon face (oily w/ acne) Buffalo hump Obese trunk Classic Signs Pendulous abdomen Thin extremities Hypokalemia Easy Bruising FBS increase Plasma cortisol increase Na increase K - decrease Monitor VS, I&O Weigh patient daily & assess presence of edema Reverse isolation Restrict Na Administer meds as ordered a. K- Sparing Diuretics (Aldactone) spironolactone - Promotes excretion of NA while conserving potassium - Not lasix due to S/E hypoK & Hyperglycemia! - Virility, Hirsutism, Muscularity of female Striae & Acne, Enlarged clitoris Hypervolemia (Increase intravascular volume) HPN
3. 4. Dx: 1. 2. 3.
4.
Nsg Mgt: 1. 2. 3. 4.
5.
6. Provide Dietary intake Low in CHO, low in Na & fats

High in CHON & K
7. Skin care d/t acne & striae

8. Prevent complication - Most feared arrhythmia & DM - Endocrine disorder lead to MI Hypothyroidism & DM
9. Hormonal Replacement Therapy : Lifetime

Receive Cortisol Inhibitor Ex. Aminogluthetemide Metotane Trilostane *Metyrapone
10. Surgery: a. Surgical Removal: Bilateral Adrenolectomy

b.
Destruction:
Cobalt Therapy
44
3. CONNS DISEASE/ PRIMARY ALDOSTERONISM - Results from adenoma ( benign tumor of the adrenal cortex) Increase aldosterone HPN, Increase ADH, General Edema DISORDER OF THE ADRENAL MEDULLA: 4. PHEOCHROMOCYTOMA - Benign tumor of the adrenal medulla Hyperactive All lead to 5 Hs Increase catecholamines Epi/Nore SNS response
H
Goal: Dx : IV. THYROID GLAND
Hypertension Headache Hyperglycemia Hypermetabolism Hyperhidrosis & Other S/Sx
1. Cobalt Therapy 2. Adrenalectomy VMA ( Vanillylmandellic Acid) Done to evaluate the level of catecholamines in the blood & urine Normal: Blood 0.2 0.9 mg % Urine 0.2 7 mg % for 24 hrs. urine sample Abnormal Physical Findings: a. With tenderness b. No nodular consistency c. Marked asymmetry d. Palpable upon swallowing Anatomy: Thyroid Glands secretes 3 hormones: T3 Tri-indotyronine 3 molecules of iodine Function: Effects: CNS: GIT: T4 -Tetraiodothyronine/ Tyroxine 4 molecules of iodine Thyrocalcitonin Function: Inhibits effects of parathormone Promotes Calcium reabsorption Normal: Not tender - With nodular consistency - Only 1 - Never palpable unless with goiter
Metabolic or Calorigenic hormone Increase metabolism brain Motility

45
Physiology: Essential Elements In The Production Of Thyroid Hormones Plasma Iodide + Tyrosine Thyroglobulin T3 & T4 Through the Feedback mechanism Ex. APG ------secretes Trophic Hormones ( any hormone that stimulate a target organ) TSH ------target organ-----Thyroid gland------- T3 & T4 ACTH---------------target organ-----Adrenal cortex------ Steroids (Adrenocothropic hormone) (iodine iodized in plasma by active transport) (derived from CHON in diet + amino acid) (in storage form) Released in blood circulation in the form of
Normal: T3 = 70 -170 % mg T4 = 4.7 11 ug%
THYROID DISORDERS 1. SIMPLE GOITER Enlargement of the thyroid gland d/t iodine deficiency - No increase in T3 T4, below or Normal Toxic Goiter : If there is an increase in T3 T4 Predisposing Factors: *A non-toxic goiter can lead to Toxic goiter anytime if: > Prolonged exposure to cold weather > Stress > Infection All can cause an increase in
1. Goiter Belt area ------ Endemic Goiter ---cause by goiter belt area
a. Place far from sea no iodine seafoods rich in iodine
2. Mountainous area results to an increase intake of goitrogenic foods Ex. Baguio/Cordilllera

Ex. Turnips (singkamas) radish, peas, strawberries, sweet potato, beans, kamote, cassava (root crops), nuts, broccoli
3. Goitrogenic Drugs that contains progoitrin--- an anti-thyroid agent that has no iodine
Ex. Anti thyroid agents (PTU) prephyl thiupil Lithium carbonate, Aspirin PASA, Cobalt, Phenyl butasone Sporadic Goiter if caused by goitrogenic drugs or from an increase intake of goitrogenic foods S & Sx : 1. Enlarged TG 2. Mild restlessness 3. Mild dysphagia
Dx.
1. Thyroid Scanning Reveals enlarged TG 2.

3. Done to evaluate the amount of Iodine 131 accumulated by the thyroid gland *Serum Thyroid Stimulating Hormone (TSH) Result: Increase (Confirmatory Dx of Goiter) T3, T4 Determination More reliable test, more potent & rapid effect on metabolism Result : Serum T3, T4 will Normal or below N 1. Administer meds as ordered: a. Iodine solution Logols solution or Saturated Solution of K iodide (SSKI) - Violet/Purple Color Nsg Mgt For Lugols Solution
Nsg Mgt:
1. Use straw to prevent staining of teeth 2. Prophylaxis 2 -3 drops , Treatment 5 to 6 drops

b. Thyroid Hormone / Agents 1. Levothyroxine (Synthroid) 2. Liothyronine (cytomel) 3. Thyroid extract Nsg Mgt for Thyroid Hormones/agents
Drugs Given Using Straw To Prevent Staining 1. Tetracycline 2. Iron preparation 3. Nitrofurantoin (Macrodantin)
1. Monitor VS HR d/t tachycardia & palpation 2. Take it early AM S/E : Insomnia 3. Monitor S/E:
Tachycardia, palpations Insomnia Restlessness agitation Heat intolerance HPN 4. Signs of Hyperthyroidism
Encourage increase intake iodine 1. Seaweeds highest source 99% 2. Seafood: Highest iodine content: 1st: Oysters 2nd: Crabs 3rd: Lobster 3. Iodized salt easily destroyed by heat, take it raw not cooked 5. Assist surgery: Sub-Total Thyroidectomy 2. HYPOTHROIDISM
Least iodine: Shrimps
The Hyposecretion of T3, T4 leading to MI, Atherosclerosis, HPN & stroke. Classified According To Onset of S & Sx: 1. CRETINISM appear during childhood / only endocrine d/o that leads to mental retardation 2. MYXEDEMA appear in adulthood (both pitting & non-pitting edema) Classified According To Cause: 1. PRIMARY failure of thyroid to secrete T3 T4 2. SECONDARY failure of APG to secrete TSH 3. TERTIARY - failure of Hypothalamus to secrete TRH (Thyroid Releasing Hormone) Predisposing Factors:
1. Iatrogenic causes disease caused by medical intervention or surgery 2.Atrophy of TG d/t:

a. b.
c.
Irradiation Trauma Tumor & Inflammation

47
3.Iodine deficiency 4.Autoimmune Hashimoto disease

Pathophysiology: Hypothalamus APG secretes-----TSH---stimulate----Thyroid Gland---secrete--- T3 T4 Any disorder of T.G. will decrease T3 T4 Leading to Tertiary causes or Hypothyroidism Altered Metabolism Hypometabolic Hypoactive Memory Impairment Decrease O2 in metabolism Weight Gain Decrease VS Unable to tolerate Cold weather S&Sx: Everything decreased except weight gain & menstruation w/c are both increase Early Sx : Weakness & Fatigue Loss of appetite Weight gain Cold Intolerance Myxedema - Coma Constipation Dry skin Brittle hair/ nails Non pitting edema d/t increase accumulation of mucopolysacharide in SQ tissue Hoarseness of voice only endocrine d/o that can be Dx thru telephone conversation Decrease libido Decrease VS Hypotension, Bradycardia, Bradypnea & Hypothermia Lethargy Memory Impairment leading to Psychosis Menorrhagia (high)
Late Sx :
Dx:
1. T3 T4 Determination: Serum T3 T4 Decrease 2. Serum Cholesterol: Increase can lead to MI 3. Radio Iodine Uptake (RAIU): Decrease
- Use to evaluate the amount of radiation RAI 131 accumulated by the T.G. & excreted by the kidneys - Most reliable Diagnostic Test Normal Uptake : 15 - 40 % Urine : 40 80% of the administered dose Result: Directly proportional to Uptake, inversely proportional to urine 2 Endocrine D/O that leads to Cardiac Complications 1. DM 2. Hypothyroidism
Nsg Mgt In RAIU: 1. No iodine in diet prior to test 2. Taken P.O. RAI 131 cocktail (liquid) Nsg Mgt:
1. Monitor strictly V/S. I&O to determine presence of Myxedema Coma

A severe form of hypothyroidism Characterized by:
Hypotension Hypoventilation Bradycardia Bradypnea, Hyponatremia & Hypoglycemia That can lead to progressive stupor & coma Important Mgt For Myxedema Coma:
1. Assist in mechanical ventilator 2. Administer thyroid hormone 3. Administer IVF replacement

2. Monitor VS, I&O
3. Provide dietary intake : Low in calories d/t weight gain 4. Skin care d/t dry skin 5. Comfortable & warm environment d/ to cold intolerance that can lead to Coma
6. 7.
8.
Administer IVF replacements Force fluid Administer meds as ordered Take AM Supplement Thyroid Hormones/Extract Synthetic: Levothyroxine S/E: Constipation
Thyroid Extracts: Proloid ( Thyroglobulin) Cytomel Synthroid Euthroid Thyrolar Eltroxime 9. Health teaching & discharge plan a. Avoidance precipitating factors leading to myxedema coma: 1. Exposure to cold environment 2. Stress 3. Infection 4. Use of sedative, narcotics, anesthetics not allowed CNS depressants V/S already down
b. Prevent Complications: Hypovolemic shock, Myxedema coma, HPN, LHF, MI, Stroke
c. Hormonal replacement therapy - lifetime d. Importance of follow up care 3. HYPERTHYROIDISM GRAVES DISEASE or THYROTOXICOSIS TOXIC GOITER/ BASEDOU/ PARRYS DISEASE Predisposing Factors: The hypersecretion of T3 & T4
1. Autoimmune Disease Release of LATS

2. Exopthalmos Enopthalmos severe dehydration depressed eye Excessive iodine intake Hyperplasia of TG d/t increase # of cells 1. Theory Of LATS: (Long Acting Thyroid Stimulator) In blood, there is gamma globulin that causes Iodine Accumulation Thyroid Hyperplasia
3.
Pathophysiology:
W/c will manifest the TRIAD SYMPTOMS:

1. GOITER d/t iodine accumulation 2. EXOPTHALMOS (eye signs seen in EPS) 3. HYPERTHYROIDISM (seen in EPS) 2. EPS ( Exopthalmus Producing Substance) APG -----releases EPS----responsible for the Triad S & Sx Proptosis (downward displacement of eyeball) Lid lag (sleepy eyes) Infrequent blinking Fixed stare DALYRIMPLE SIGN Peri-orbital Edema Von Graefe ------------ failure of eyelids to follow movement of eyes when looking down 3. Hyperthyroidism ---------- Hyperactive, Voracious but losing weight, hypermetabolic T3 T4 ------the cause is over-excitability of SNS Tremors S & Sx: Hallucinations Diaphoresis Palpitation Nervousness Irritability Insomnia
1. Increase appetite : Hyperphagia but weight loss d/t increase metabolism

2. 3. 4. Skin is moist Heat intolerance Diarrhea most common gastric complications of Graves Disease All VS increase = HPN, Tachycardia, Tachypnea, Hyperthermia CNS changes Goiter Exopthalmos Constipation common in advanced Amenorrhea graves disease d/t constant increase in T3
5.
6. 7. 8. 9. Dx:
1. Serum T3 & T4 - Increased 2. RAIU : Increase 3. Thyroid Scanning: Reveals an enlarged TG

Nsg Mgt: 1. Monitor VS & I & O To determine presence of thyroid storm or most feared complication: Thyrotoxicosis 2. Administer meds as ordered
a. Antithyroid Agents 1. Prophylthiouracil (PTU)

2. 3. Methimazole (Tapazole) Neomercazole ( Carbimazole) Most Toxic S/E for prolonged Used: Agranulocytosis Common S/S: Complications R/T infections - Fever, Sore throat, Mild Leukocytosis Dx Test To Check For Toxicity: Differential Platelet Count If not available, Monitor CBC Throat Swab & Culture Most feared complication : Thrombosis ----Stroke CVS b. Adrenergic Blocking
To control the symptoms brought about by the over-excitability of SNS - Propanolol, Inderal, Betaloc, Neobloc, Metoprolol, Nadol, Visken, Aptin, Sotalex, Corgard 3. Diet Increase caloric intake to correct weight loss 4. Skin care 5. Comfy & cool environment 6. Maintain siderails d/t restlessness 7. Provide bilateral eye patch (dry material) to prevent drying of eyes 8. Hormonal Replacement Therapy 10. Importance of follow-up care 11. Assist in surgery Subtotal Thyroidectomy Tx: 1. RAI 131 To reduce size of T.G. Isotope: Risk of genetic abnormalities or genetic mutation 2. Surgery : Subtotal Thyroidectomy Nsg Mgt: Peri-Operative 1. Administer Lugols solution (SSKI) K iodide Function: To decrease vascularity of TG To prevent bleeding & hemorrhage during & after surgery To increase firmness Promote T3 T4 storage 2. Diet : a. High in calories Increase CHO Increase CHON Increase in polyunsaturated fats To satisfy increase in appetite & restore loss of glycogen reserve b. Avoid stimulant in diet (No colas, caffeine) c. Increase fluid intake d. Monitor body weight e. Provide physical & mental rest to reduce metabolism f. Provide quiet & calm environment to decrease irritability 3. If (+) for exopthalmus -----dryness of the cornea ----corneal ulceration---blindness Nsg Mgt: 1. Cover eyes w/ bilateral eye patch 2. Instill saline to moisten eyes ( Drug: Methylcellulose OD) 3. Elevate head on pillow to promote drainage & reduce peri-orbital edema 4. Give psychological preparation by telling pt. that eye signs will remain even after surgery Nsg Mgt: Post-Operative Thyroidectomy Complication: 1. Watch out for signs of Thyroid Storm or Thyrotoxicosis - If no emotional preparation pre-operative: Stress - Post-opt wound infection Pathphysiology: Pre-opt (euthyroid state----post-opt----thyroid compensates for T3 T4 production (Hyperthyroid d/t stress, infection) Increase PR, Increase BP Triad Signs of Thyroid Storm: HAT a. Hyperthermia b. Agitation c. Tachycardia ----------Early Sign: Fever w/ Tachycardia Nsg Mgt Thyroid Storm: 1.
Monitor VS & neuro check

51
Agitated might decrease LOC 2. Antipyretic fever/ TSB Tachycardia - blockers (-lol) 3. Siderails agitated Complication 2. Watch for inadvertent (accidental) removal of parathyroid gland Secretes Parathormone (Calcium Reabsorption) TETANY : Hypocalcemia If 1 removed If 2 removed If 3 or more removed No sign of tetany Mild signs of tetany - Classic Sx of Tetany: (+) Trousseau sign & (+) Chvostecks sign (Twitching of fingers) (Facial paralysis)
Nsg Mgt: 1. Administer calcium gluconate Slowly to prevent arrhythmia Ca gluconate toxicity antidote MsSO4 Complication 3. Watch out for accidental Laryngeal nerve damage Sx: Hoarseness of Voice Aphonia (no voice) 2 recurrent laryngeal nerves that control vocal cords (bilateral laryngeal) Responsible for voice production
If 1 removed whispery, hoarseness If Trauma only Whispery, Hoarseness Edema on glottis Whispery, Hoarseness If 2 removed Aphonia -----start speech therapy Nsg Mgt: 1. Encourage pt to talk or speak postoperatively 2. Notify physician immediately 4. Watch out for Signs of Laryngeal Spasm--------- Inflammation of Larynx Sx: DOB SOB Narrow opening ---- O2 cannot enter
Laryngeal Spasm Nsg Mgt: 1. Prepare at bedside tracheostomy 5. Watch Out for Signs of bleeding Post-Subtotal Thyroidectomy D/T : Failure to administer Loguls Solution (SSKI) pre-opt Failure to tie/ ligate blood vessels --------bring back to OR for emergency operation Sx: Feeling of fullness at incision site Feeling of Choking sensation BP -------- Rapid, feeble, thready pulse Rapid but shallow respiration Cold, Clammy diaphoretic skin Nsg Mgt: 1. Check soiled dressing at nape area (Slip hand under neck to check for dampness) 2. Evaluate VS 3. Notify Physician immediately Bleeding can lead to-------------- 1. Respiratory Obstruction D/T blood occlusion & Hematoma Accumulation of Tracheobronchial secretions
Can also lead to Laryngospsam/Laryngoedema Prepare for Emergency Tracheostomy OTH ER DIAGNOSTIC TEST FOR THYROID DISORDERS: 1. Protein Bound Iodine (PBI) - Done to evaluate amount of iodine attached to protein molecule of the blood Normal: 4-8 ug % Nsg. Care: 1. 2-3 days prior to test, no taking of foods & drugs containing iodine Ex. Seafoods, iodized salt, No cough syrup, ASA Estrogenic Preparations: Pills, Dyes, X-ray 2. Basal Metabolic Rate (BMR) - Done to evaluate O2 consumption when client is at rest Nsg Mgt: 1. At night, NPO for 12 hrs. 2. Ensure client had a good night sleep to decrease anxiety level Procedure: 1. When client no activity yet, no food yet 2. Clamp nose, breathe through tube connected to a tank w/ machine evaluating O2 consumption 3. TBMR (Theoretical) - Compute pulse pressure + PR/ minute 111 - Not conclusive, but if s/s submit to other test Summary: HYPOTHYROIDISM Lethargy Memory Impairment Diarrhea Decrease VS ALL DECREASE Except: Wt: Weight Gain Menstruation: Menorrhagia V. PARATHYROID GLAND ( Normal: 20-30)
T3 T4
HYPERTHYROIDISM Agitation & Restlessness Hallucination Constipation Increase VS ALL INCREASE Except: Weight Loss Amenorrhea
Anatomy:
A pair of small nodules located behind the Thyroid Gland There are 4 Parathyroid glands PTH------secretes---- PARATHORMONE Function: Essential to the absorption of Calcium & secretion of Phosphorus by renal tubules Promotes reabsorption of Calcium Regulates cardiac rythmicity Essential for blood coagulation *Thyrocalcitonin Antagonizes secretion of parathyroid hormone
CODE: CALCIUM DISORDERS OF THE PARATHYROID GLAND
53
1. HYPOPARATHYROIDISM Hypoactive PTH or a decreased secretion of parathormones HYPOCALCEMIA (TETANY) Uncontrolled spasm/Hyperactivity Predisposing Factors: 1. Following subtotal thyroidectomy d/t accidental removal of PTH 2. Atrophy of parathyroid gland due to a. Inflammation b. Tumor S&Sx: HYPERPHOSPHOTEMIA [If Ca decreases, phosphate increases]
1. Acute Tetany
a. b. c. d. e. f. g. Tingling sensation Paresthesia Dysphagia Laryngospasm Bronchospasm Seizure Most feared complications Arrhythmia
Pathognomonic Sign of Tetany:
a. (+) Chvostecks Sign : Tap facial nerve, if facial spasm of facial muscle (+) b. (+) Trousseaus /Carpopedial spasm: Occlude blood flow to vascular extremity (legs)
Use tourniquet Test for 1-2 min. & observe for carpopedial spasm 2. Chronic tetany a. Loss of tooth enamel b. Photophobia & cataract formation c. GIT changes : Anorexia, N/V & generalized body malaise d. CNS changes : Memory impairment, Irritability
Dx:
1. 2. 3. 4.
Nsg Mgt: 1.
Serum Calcium Serum Phosphate X - ray of long bone CT Scan Administration of meds: a. Acute Tetany:
Decrease (N 8.5 11 mg/100ml or 4.5 -5.5 mEq/L) Increase (N 2.5 4.5 mg/100ml) Increase bone density Reveals degeneration of basal ganglia
Administer Ca gluconate IV, slowly to prevent cardiac arrest b. Chronic tetany 1. Give Oral Ca supplements Ex. Ca gluconate - Calci-aid Ca carbonate - Calsan Ca lactate Ca chloride 10% - Caltrate
2. Give Vit. D for calcium to be readily absorb

Vitamin D (Cholecalceferol) Drug Cholecalceferol Diet Calcidiol Sunlight Calcitriol 7am 9am
Commercially-Prepared: *Calciferol Hytakerol Calcidiol *Rocatriol Dihydrotachysterol 3. Give Phosphate binder for excretion of phosphate Ex. Aluminum OH gel (ampho gel) S/E: Constipation Antacid AAC Aluminum Containing Acids Aluminum OH gel Constipation MAD Magnesium Containing Antacids Milk or Magnesia Diarrhea
*Maalox: Magnesium & Aluminum With Lesser S/E 2. Avoid precipitating stimulus such as bright lights & noise to prevent seizure 3. Diet : Increase Ca & decrease phosphorus - Dont give milk due to increase phosphorus Diet : Also For Osteoporosis a. Baked Salmon b. Dilis/Anchovies c. Green Turnips (Singkamas) 4. Bedside: Tracheostomy set d/t laryngospasm 5. Encourage to breath with paper bag in order to produce mild respiratory acidosis To promote increase ionized Ca levels 6. Most feared complication : Seizure & arrhythmia 7. Hormonal Replacement Therapy: Lifetime 8. Institute Seizure & safety precautions 9. Important follow up care 2. HYPERPARATHYROIDISM / Von Reclinghausen - Increase secretion of parathormones - HYPERCALCEMIA -------w/c can lead to Hypophosphotemia Pathophysiology: PTH Increase bone resorption Normal: Ca 99% bones 1% blood Hypercalcemia Hypophospotemia Calcium loss from bones Reverse effect: Ca in bone goes to blood
Bone Demineralization bones are brittle Leads to bone fracture
Hypercalciuria Formation of Calcium crystals in Urine Nidus/ Nucleus

55
Forms Kidney Stones Predisposing Factors: 1. Hyperplasia of the parathyroid gland 2. Over compensation of PTG d/t Vit D deficiency Children Rickets Adults Osteomalacia Vitamin D deficiency *Sippys diet Vit D diet not good for pt with ulcer: 2 -4 cups of milk & butter *Karrels diet Vit D diet not good for pt with ulcer: 6 cups of milk & whole cream *Food rich in CHON eggnog combination of egg & milk S/Sx: 1. Bone fracture a. Bone pain (especially at back) 2. Kidney Stones a. Renal colic b. Cool moist skin & body malaise 3. GIT changes: Anorexia, N/V, Ulcerations ----- only endocrine D/O that causes ulceration 4. CNS involvement: Irritability, Memory impairment Dx :
1. Serum Ca: Increase 2. Serum phosphorus: Decreases 3. X-ray of long bones : Reveals bone demineralization
Tx: 1. Removal of the gland - Parathyroidectomy 2. Destruction of the gland Cobalt Therapy 3. Drug of Choice: Calcitonin ---- inhibits resorption Nsg Mgt: Kidney Stone
Hypo : Replacement w/ commercial preparation Hyper: Removal or Destruction of
ACID-ASH DIET 3 Cs Cranberry Calamansi Vit. C Grapefruit
1. Force fluids : 2,000 3,000/day or 2-3L/day

Isotonic solution Warm sitz bath for comfort Strain all urine with gauze pad 5. Acid Ash diet to acidify urine 6. Adm meds as ordered a. Narcotic analgesic Morphine SO4, Demerol S/E Respiratory Depression Antidote - Narcan/ Naloxone Naloxone toxicity Tremors 7. Siderails 8. Assist in ambulation 9. Diet low in Ca, increase phosphorus lean meat 10. Prevent complication of Parathyroidectomy : Most Feared Renal Failure 11. Hormonal Replacement Therapy: Lifetime 12. Importance of follow up care VI. PANCREAS - Located behind the stomach , a mixed gland Pancreas: Consists of 2. 3. 4. 1G
Acinar Cells (Exocrine gland) Secrete Pancreatic juices Flows in the pancreatic duct Cells
Islets of Langerhans (Endocrine Gland: Ductless) Secretes 3 Types of Cells Cells Delta Cells
56
Aids in digestion (in stomach)
Secretes Glucagon Fx: Hyperglycemia
Secretes Insulin Fx: Hypoglycemia
Secretes Somatostatin Fx: Antagonizes Growth Hormones
DISORDER OF THE PANCREAS 1. PANCREATITIS Acute inflammation of the pancreas leading to Pancreatic Edema, Hemorrhage & Necrosis d/t Cause: Unknown/idiopathic Alcoholism Obstruction in the pancreatic duct ---- backflow of pancreatic juice to the pancreas Will cause autodigestion Pathognomonic Sign: (+) Cullens Sign (+) Grey Turners Spots - Ecchymosis of umbilicus (bluish color) - Ecchymosis of flank area Autodigestion (Self-digestion )
Both Signs Means Hemorrhage
2. CHRONIC HEMORRHAGIC PANCREATITIS Bangugot Predisposing Factors: Unknown Risk factor: History of hepatobiliary disorder Alcohol 3. Drugs: Thiazide diuretics Oral contraceptives Aspirin Penthan 4. Obesity 5. Hyperlipidemia 6. Hyperthyroidism 7. High intake of fatty food Saturated fats 3. DIABETES MELLITUS - A metabolic disorder characterized by non-utilization of CHO, CHON,& fat metabolism d/t 1. Absolute Insulin Deficiency - Cause is unknown but the islets of langerhans do not produce insulin - Congenital - Beta-Cell damage by VIRUS ----- Human Leukoantigin----Human Leuko Antibodies (Chicken Pox) Autoimmune: Destroys B-cells 2. Relative Insulin Deficiency - Capable of producing insulin but not used efficiently d/t Blocked by chemical antagonist at site of production
1. 2.
Epinephrine Physiology:
Thyroxin
Glucogen
Glucagon
All causes Glucogenolysis
Pancreas glucose ATP (Main fuel of cell) (reserve glucose glycogen) Glucogenesis ( synthesis of glucagons) Glycogenolysis ( breakdown of glucagons) Liver will undergo Gluconeogenesis (formation of glucose from CHO sources CHON & fats)
Pathphysiology: DIABETES MELLITUS Little or No Supply of Insulin
CHO Metabolism CHO utilization of glucose

Cell Starvation
CHON metabolism breakdown of stored glucose Cell to Tissue Starvation Stimulate Satiety Center (Hypothalamus) Hyperlipidemia POLYPHAGIA (excessive hunger) Blood Osmolarity
Lipolysis
Oxidation of fatty acid
Cell weakness d/t cellular starvation Weight loss
Hyperglycemia Glucose go to blood
Ketone Production DKA (Diabetic
Ketoacidosis) (result from increase breakdown of fats) kidney Kidneys tubular secretion Coma (needs O2) Glucose in blood Act as osmotic diuretic (Increase) Renal tubules fail to reabsorb glucose HONKC GLYCOSURIA Irritate perineal area Fungi in the area (-) Nitrogen Balance Pruritus A. CLASSIFICATION: 1. TYPE 1 IDDM Brittle Disease Juvenile Onset Common among children Non- obese Weight loss Symptomatic Absolute Deficiency
POLYURIA
Stimulate thirst center
Death
Diabetic
ECF dehydration POLYDIPSIA (excessive thirst) DKA Early Sx: Weight loss Weakness Late Sx: Acetone-breath odor Kausmauls Respiration
Tissue Wasting (Cachexia) 2. NIDDM Adult/ Maturity onset 40 y/o & Above Obese Weight gain Asymptomatic Relative Deficiency
58
TYPE II
Tx: Insulin Administration Diet Exercise Complications: Diabetic Ketoacidosis (DKA) Metabolic Acidosis Tx: Sodium Bicarbonate Incidence Rate: - 10% of population with DM have Type I Predisposing Factor:
Tx: OHA (Oral Hypoglycemic Agents) Diet Regimen Exercise Complication: H hyper O osmolar N non K ketotic C coma Incidence Rate: - 90% of population w/ DM have Type II Mid 1980s increase in type II d/t fast food chains Predisposing Factors: 1. Obesity lack insulin receptors binding site - # 1 cause of Type 2 DM 2. Hereditary
1. 90% hereditary total destruction of pancreatic dells 2. Virus 3. Toxicity to carbon tetrachloride (CC14) 4. Drugs Steroids Lasix - Loop diuretics DIABETES S/Sx: MELLITUS 1. 3 PS + G 2. Weight loss 3. Anorexia 4. N/V 5. Blurring of Vision 6. Increase susceptibility to infection 7. Delayed/ poor wound healing 3. GESTATIONAL DM
ia
S/Sx: 1. 3 Ps + G 2. Asymptomatic
Polyuria Polydips Polyphagia
Occurs during pregnancy & terminates upon delivery of child Predisposing Factors: 1. Unknown/ idiopathic 2. Influence of maternal hormones S/Sx : Same as type II 1. Asymptomatic 2. 3 Ps & 1G Mgt: 1. Type of delivery: CS d/t macrosomia (large baby) Sx of Hypoglycemia on Newborn: 1. High pitched shrill cry 2. Poor sucking reflex B. COMPLICATIONS OF DIABETES MELLITUS 1. HYPERLIPIDEMIA Formation of atheromatous plaques (atherosclerosis) in the arteries Narrowed arterial lumen ( blood flow) -----result to thickening of BV--- inelastic blood vessels
Formation of vascular lesion ( micro/macro-angiopathy)

Vascular Degeneration
Cerebral blood flow vessels Coronary arteries Retinal Blood Vessels Renal blood vessels Peripheral blood
Brain CVA
Heart Myocardial Ischemia In 30 minutes Irreversible M.I.
Eyes
Kidney
Lower extremities Tissue Ischemia Peripheral Neuritis
Retinopathy Nephropathy (Kimmiel-Stiel Wilson Syndrome) Cataract
RENAL FAILURE Retinal Hemorrhage Exudation
Tissue Necrosis
Diabetic Gangrene Hardening of renal tubules Ischemia KSW Sx: Proteinuria Edema Puffiness of eyelids 1st d/t Ischemia PERIPHERAL NEURITIS Sx: Numbness of exremity Coldness of extremity Tingling sensation of
Aggregation of CHON In Retinal Molecules Opacified 3 Pathies of DM Nephropathy Retinopathy Diabetic Cataract
Sx of Nephropathy is a progressive destruction of glomeruli --RF 2. DIABETIC KETOACIDOSIS (DKA) - Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression & Diabetic Coma. Predisposing Factors: 1. Stress ------ # 1 cause of DKA Nsg Mgt: 2. Hyperglycemia 3. Infection 1. Can lead to coma: assist in mechanical ventilation 4. Missed dose/Omitting dose of insulin 2. Administer .9NaCl isotonic solution Sx: 3 Ps & 1 G Followed by .45 NaCl hypotonic solution Early Sx: To counteract dehydration. Weight loss 3. Monitor VS, I&O, blood sugar levels Weakness 4. Administer meds as ordered: Late Sx: a. Insulin therapy IV push Anorexia, N/V, Dim Vision Regular Acting Insulin : Clear Acetone-breath odor (2-4hrs, peak action) Kausmauls Respiration b. To counteract acidosis Na HCO3 (rapid, shallow breathing) CNS depression, Coma 5. Antibiotic to prevent infection Cherry Red Lips Dx : 1. FBS: Increase 2. Hct: Increase (compensate d/t dehydration) C. DIAGNOSTIC PROCEDURES FOR DIABETES MELLITUS:
1. FBS/ FPG (Fasting Plasma Glucose) NPO 6-8 hrs. or NPO 12 hrs. with sips of water
60
2. RBS (Random Blood Sugar) No NPO, anytime Test 1-5 Use to Diagnosed Glycemia
3. PPBS ( Post Prandial Blood Sugar) Determination NPO 2 hrs. after diet of 100 gm CHO
4. Hgt (Hemaglukotest) Finger prick or Capillary Blood Glucose Determination (CBg)
5. OGTT ( Oral Glucose Tolerance Test) - NPO 6-8 hrs. then collect fasting specimen (am) Administer p.o. 100 gms: Urine Glucose + fruit juice Blood
After 1 hr. -----extract venous blood ---- Rise glucose Increase BS (Normal) 2 hrs. --- next extraction ---- start to normalized Decreased BS Final 3 hrs. --- next extraction ---- w/in normal BS (+) Diabetic if: Rise glucose till the 3rd extraction still not normal & there is sugar in urine
6. BT, CT (Benedicts Test) (Clini Test) - Double voided or 2nd voided specimen = accurately test presence of glucose in urine - Discard 1st void, offer 1-2 glass of H20 after 1 hr. or 30 minutes collect urine 7. Acetest
Test For Glycosuria
To test for presence of ketone bodies in urine (Ketonuria) (Result from incomplete breakdown of fats) How? Get acutest tablet (creamy/white/ off-white in color) ---drop in urine If there is no change (-), if color changes to purple (+) for ketonuria
8. Glycosylated HgB
(HgBAC)
- To evaluate the amount of glucose attached to the hemoglobin of the blood for the previous 120 days---lifespan of HgB
D. MANAGEMENT OF DIABETES MELLITUS: Supportive & Palliative 1. TYPE 1 DM INSULIN THERAPY A. Sources:
1. Animal source beef/ pork : rarely given because it causes allergic reaction
2. 3.
Human has less antigenetic property Ex. Humulin most commonly used If kid is allergic to chicken dont give measles vaccine, it comes from chicken embryo. Artificially compound
B. Types of Insulin Types of Insulin Onset Peak Given Color & Consistenc y Clear Durati on 6-8 hrs.
1. Rapid Acting Insulin - Regular Acting - Humulin R - Semi-Lente - Crystallized Zinc - Velosulin - Novolin R - MC Actrapid 2. Intermediate Insulin - NPH (Non-protamine Hagedorn 1) - Humulin N - Monotard - Lente - Globin - Novolin L 3. Long Acting Insulin - Ultra Lente - PZI (Protamine Zinc Insulin) - Humulin U
30 minutes after administrati on
2-4 hrs.
3x/day
1-2 hrs
8-16 hrs.
OD
Cloudy
24 hrs.
3-4 hrs.
16-24 hrs.
Cloudy, Mixed
36 hrs.
5 Rs Of Insulin Administration 1. Right Patient: Give insulin only if there are signs of glycosuria & hypergylcemia 2. Right Drug : Administer right type of Insulin 3. Right Route: Not given P.O., insulin destroyed in the GIT by proteinase Given: SQ, IM, I.V. Humulin R Crystalline Zinc Regular Insulin 4. Incorporated w/ water, given by drip (IVF)
Right Time: Best time given 60-90 minutes before meal or an hour before meal Physiologic effect of insulin will parallel the absorption of glucose
Right Dose: Know stock dose of insulin 10 ml vial 40 units/ml or 80 units/ml or 100 units/ml Nsg Mgt For Insulin Therapy: 1. Administer insulin at room temperature. Do not expose to sunlight Refrigerate insulin once opened only Before administration, gently roll vial between palms. Avoid shaking to prevent formation of bubbles
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5.
2. Use gauge 25 26 needle : Tuberculin syringe 3. Administer insulin at either 45 or 90 depending on the client tissue deposit. 5. Dont aspirate after injection Rotate injection site to prevent lipodystrophy (atrophy/ hypertrophy of SQ tissue) Deltoid Rectus Femoris R & L Vastus Lateralis Gluteus Maximus IM Upper Arm R & L Below breast Lower Central Abdominal Wall Lateral thigh R & L Below scapula R & L Buttocks R & L
SQ
6. Most accessible site abdomen 7. When mixing 2 types of insulin, aspirate 1st regular/ clear before cloudy to prevent contaminating clear insulin & to promote accurate calibration. 8. In giving insulin: Before meals but if pt. eating already: Give insulin If pt. already eaten 2 hrs. : Do not give, repeat CBC> MD will adjust the dose 9. 1ml or cc of tuberculin = 100 units of insulin - - 1 cc = 10 units = 100 units - - .5cc = 5 units = 50 units - - .1 cc = 1 unit = 10 units 6 units RA 10. Monitor for signs of complications: a. Allergic reactions b. Lipodystrophy c. Somogyis Phenomenon Rebound Effect of Insulin characterized by hypoglycemia followed by periods of hyperglycemia (Insulin Shock, Hyperinsulinism, Insulin Overdose, Hyperglycemia) d/t Sx: Occurs w/ insulin overdose Prolonged NPO, vomiting Long interval of insulin from the serving of food * If allowed to eat, give anything to eat an hour after administration of insulin 4-8 ounces of softdrinks 4-8 ounces of fruitjuice 1 tbs. of sugar ---best alternative, put in oral cavity 5 ml of honey 5 ml of karo syrup 2-4 pcs. Of candies 2 slices of graham crackers
Hunger Pangs Double Vision Pallor, cold clammy skin Tremors 1. Give 20-30 gm of carbo 2. Drugs
Mgt:
Epinephrine 1.1000 SQ Glucagon 1-2 mg IM *IV glucose H20 ---- D50% by IV push ---- D5W by venoclysis 2. TYPE 2 DIABETES MELLITUS Most Feared Complication of Type II DM Hyper Osmolar
osmolarity = severe dehydration

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Non Ketotic Coma Dx :
- absence of lipolysis - no ketosis S/Sx: headache, restlessness, seizure, decrease LOC Normal: BUN = 10-20 mg/100ml Creatinine = .8 1 mg/100ml Hgb: Female = 12-14 gm % Male = 14-16 gm% Average = 42 % Female = 36-42 %
1. FBS: N 80 120 mg/dl 2. 3. 4.

Increase , 3 consecutive times 3 Ps & 1G = confirmed DM Oral Glucose Tolerance (OGTT) Most sensitive test Random Blood Sugar : Increased Alpha Glucosylated Hgb : Elevated (Normal: <9 %) - Same as DKA except dont give NaHCO3!
Hct:
Nsg Mgt: 1. Can lead to coma assist mechanical ventilation 2. Administer .9NaCl isotonic solution, followed by .45NaCl hypotonic solution to counteract dehydration. 3.Monitor VS, I&O, blood sugar levels 4.Administer meds a.) Insulin therapy IV Regular Acting Insulin clear b.) Antibiotic to prevent infection Tx: 1. Give OHA O ral H ypoglycemic A gents Classifications of OHA: Fx: Stimulates pancreas to secrete insulin
1.
1st Generation Sulfonylureas Fx: Given to stimulate B-cell to secrete endogenous insulin a. Chlorpropamide (Diabenase) b. *Tolbutamide (Orinase) c. Tolazamide (Tolinase) d. *Acetonexamide (Dymelor) e. Glibenclamide (Euglucon) f. Gliclazide (Diamicron) g. Glipizide (Minidiab) C/I: Pregnant Women Surgery Allergy Infection Stress Kidney/liver damage *Presence of any of these even if pt. is NIDDM insulin is required
Monitor For: GI upset Headache Paresthesia Weakness Tinnitus
2.
2nd Generation Sulfonylureas a. Diabeta (Micronase) b. Glipside (Glucotrol)
3. Biquanides - Increase uptake of glucose by the cell but prolonged use may cause lactic acidosis Ex. Metformin Glucophage Nsg Mgt or OHA: 1. Administer with meals to lessen GIT irritation & prevent hypoglycemia 2. Avoid alcohol (alcohol + OHA = severe hypoglycemic reaction) ---leads to antabuse (Disulfiram) toxicity Nsg Mgt For DM: 1. Monitor for PEAK action of OHA & insulin
3. 4.
5.
Monitor VS, I&O, neurocheck, blood sugar levels. Administer insulin & OHA therapy as ordered. Monitor signs of hyperglycemia & hypoglycemia. -Pt DM hinimatay - You dont know if hypo or hyperglycemia - Give simple sugar (Brain can tolerate high sugar, but brain cant tolerate low sugar!) *Cold, clammy skin Hypoglycemia Orange Juice or simple sugar *Warm to touch, dry Hyperglycemia Administer insulin
6. Provide nutritional intake of Diabetic Diet: 7.
DIABETIC DIET
8.
-Or offer alternative food products or beverage. CHO = -Lots of orange juice. 50% Exercise after meals to promote increase glucose utilization CHON = - After strenuous exercise, glucose is already consumed even w/o insulin Pre-breakfast insulin: For pt. who exercised alreadydecrease dose of insulin Athletes: Take snacks in between exercise Monitor complications of DM a. Atherosclerosis HPN, MI, CVA b. Can affect the small minute capillaries of eyes & kidney leading to : Microangiopathies (thickening) c. Eyes Diabetic retinopathy , Premature cataract & blindness d. Kidneys Recurrent pyelonephritis & Renal Failure 2 Major Cause of e. Gangrene formation Renal Failure f. Peripheral Neuropathy - Diarrhea/ Constipation 1. DM - Sexual impotence (Complication of HPN & DM) g. Shock
9. Foot Care Mgt d/t delayed wound healing especially of extremities

a. b. c. d. e. f. g. Avoid waking barefooted Cut toe nails straight Apply lanolin lotion prevent skin breakdown Avoid wearing constrictive garments No Crossing of legs Avoid local cold application in extremities Never elevate legs on pillow to prevent tissue ischemia unless there are sx of leg edema
10. Encourage annual eye & kidney exam

11. Avoid smoking d/t vasoconstriction 12. Monitor urinalysis for presence of ketones or Blood or serum more accurate 13. Assist in surgical wound debridement 14. Monitor signs of DKA & HONKC 15. Assist surgical procedure: BKA or above knee amputation D. DM ASSOCIATED WITH OTHER DISORDER a.) Pancreatic tumor b.) Cancer c.) Cushings syndrome Increase Fat Catabolism Free Fatty Acids Cholesterol Atherosclerosis HPN MI Stroke Ketones DKA Coma Death
3 Main Food Groups Anabolism Catabolism 1. CHON Glucose Glycogen 2. CHON Amino Acids Nitrogen 3. FATS Fatty Acid Free Fatty Acid (Choles terol & Ketones)
HEMATOLOGICAL SYSTEMS
Overview: I . BLOOD-FORMING ORGANS 1.Thymus removed myasthenia gravis 2. Liver largest gland (occupies most of the right hypochondriac region) 3. Lymph nodes 4. Lymphoid organs Payers Patches (located between the small intestine- site of salmonella thypi) 5. Bone marrow 6. Spleen Ex. Varicosities Deep Vein Thromboplehbities
II. BLOOD VESSELS
1. Veins SVC, IVC, Jugular vein, superficial blood towards the heart 2. Artery deep seated, carries blood away from the
- 2 largest artery : Aorta, carotid 3. Capillaries Ex. Aneurysm Buergers Disease Raynauds Disease
III. BLOOD Blood Formed Elements Cellular Components: 1. RBC (Erythrocytes) - largest (Normal: 4 6 M/mm3) - Anucleated (no nucleus) - Biconcave discs - Has molecules of Hgb (red cell pigment) - Transports & carries O2 Hgb: % gms % F = 12-14 gms M = 14-16 45 % 55% Plasma & Serum Plasma CHONs (Liver) 1. Albumin - largest, most abundant plasma Fx: Maintains osmotic pressure preventing edema, If decrease albumin- Ascites Promotes skin integrity 2. Globulins a. Alpha Transports steroids, hormones & bilirubin b. - Transports iron & copper c. Gamma Transport immunoglobulins or antibodies 3. Prothrombin (CF2) Fibrinogen (CF1)
Hct : 3x Hgb F = 36-42 % M = 42-48 %
CLOTTING FACTOR 1-13

CF 1 = Fibrinogen CF 2 = Prothombin CF 3 = Thrombin CF 4 = Ca # CF 5/6 = Proaccelerin - Labile factor CF 7 = Procenvertion - Stable Factor CF 8 = Anti- HFA CF 9 = Christmas Factor/ Anti-hemophilia CF 10 = Stuart-Prower CF 11 = Plasma Thromboplastin CF 12 = Hageman CF 13 = Fibrin Stabilizing Factor
From Pakistan To China People Power Against Communism Start Peace Hate Fire
COAGULATION PATHWAY/CASCADE Intrinsic Factor EF TF CF 12 CF 9 CF 11 CF 9--------------------------------------------------CF 10 ------------------------------------------ CFS Creates------Prothrombinase----------------- CF 2 Product of Stage 1 Thrombin Stage 3 CF 1 Fibrin Clot -------- --Clot dissolved Tissue Plasminogen Activator Plasminogen Plasmin Stage 4 Stage 2 Stage 1 Extrinsic Factor TF (CF3) F
I. DISORDERS OF THE BLOOD

Pathophysiology: BLOOD DYSCRASIA
Production of blood cells (PANCYTOPENIA)
Production of both normal & defective cells
Spleen Disorder Life span of RBC 8-120 days
Defect in Coagulation Mechanism
1. ANEMIA - A condition in which the hemoglobin concentration is lower than normal - Results from : 1. 2. 3. 4. Decreased Erythropoiesis (Formation-maturation process of RBC) Increased Hemolysis Bone Marrow Depression Blood loss 1st Sign of ANEMIA:
Pathophysiology:
Hgb Count Reduction in the O2 carrying capacity of the blood TISSUE HYPOXIA
Hallmark & Basis of Anemia All symptoms cause
Brain Restlessness Headache, Irritability Syncope, Vertigo
Heart Anginal Pain PR Fatigability Palpitation
Respiratory RR Dyspnea
GIT Anorexia Angular Cheilosis Lesions at the corner of the mouth
Skin Mucus Membrane
D/T compensation of the body
D/T decreased Hgb that gives color to skin KOILONYCHIA d/t atrophy of epidermal cells D/T decreased RBC
Pallor Brittle nails & hair (Spoon-shaped nails)
Intolerance to Cold
Normal shape of nails = Biconcave & 180 Substances Needed For Maturation Of RBC: CAUSES:
1. CHON formation of all tructure/membrane 2. Iron/Fe - formation of pigment hemoglobin 3. Vit. B 12 - responsible for synthesis of nucleic acid 4. Folic Acid - matures the cell
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I. DECREASED ERYTHROPOIESIS Production maturation of RBC Absence of any one of the factors For RBC maturation will cause Type I: A. IRON DEFECIENCY ANEMIA
- Cells are microcytic (small) & hypochronic d/t inadequate absorption of iron leading to hypoxemic injury
HYPOCHROMIC ANEMIA HYPOPROLIFERATIVE ANEMIA Pathophysiology: The body stores of iron decrease, leading to depletion of hemoglobin synthesis Incidence Rate: 1. Common in developed country d/t high cereal intake & accidents 2. Common in tropical countries blood sucking insects 3. Women 15 45 y/o of reproductive yrs 4. Common among the poor d/t poor nutritional intake Predisposing Factors: Common: Suicide - common in teenager Poisoning common in children (aspirin) Aspiration common in infant Accidents common in adults Choking common in toddler SIDS common in infant in US Bleeding: Hematemesis vomiting of blood Melena passage of dark stool - Bleeding in Upper GIT - Doudenal Cancer Decreased O2 Atrophy of cells 1. Asymptomatic
1. Chronic blood loss- most common cause

a. Trauma b. Menstruation c. GIT bleeding 2. 3. Inadequate intake of food rich in iron
Inadequate absorption or iron d/t : a. Chronic diarrhea (Metabolic Acidosis) b. Malabsorption syndrome (Celiac Disease) c. High cereal intake with low animal CHON ingestion d. Subtotal gastrectomy 4. Improper cooking of food/ Alcoholism S/Sx:
2. General body malaise 3. All Sx of Anemia + PICA

+ Dx : 1. 2. 3. 4. 5. 6. 7. Tx:
Cerebral Hypoxia abnormal appetite or craving for non-edible food Ex. Chalk Atropic Glossitis inflammation of tongue Stomatitis mouth sores Dysphagia
PLUMMER VINSONS SYNDROME
RBC Hgb Reticulocyte Hct Iron Ferritin Bone Marrow Aspiration = Most Definitive
Nsg Dx: Activity Intolerance
1. Blood Transfusion = Packed RBC

Nsg Mgt:
1. Monitor signs of bleeding of all hematologic test including urine, stool & GIT
2. 3.
4. 5.
Complete bed rest dont overtire pt Encourage iron rich food Instruct the pt to avoid taking tea (Tannates - impairs iron absorption) Administer meds: Hematinic Agents or drugs that will increase blood heme a.) Oral iron preparation Ferrous SO4 Fe gluconate 300 mg OD Fe Fumarate Fortifier Fergon, Feorol, Iberet *Liquid Preparations: W/ brassy taste, disguise by chilling
IRON-RICH FOOD: 1ST: organ meat, liver 2nd: eggyolk 3rd: raisins, legumes dried fruits nuts
Nsg Mgt Of Oral Iron Medication:
1. Administer w/ meals to lessen GIT irritation/or 0ne hours before meals 2. If diluting in iron liquid prep administer w/ straw
3. 4. Give Orange juice for absorption Monitor & inform pts S/E
5. If pt cant tolerate oral iron preparation

Administer parenteral iron preparation 1. Iron dextran (IV, IM) 2. Sorbitex (IM only) 3. Inferon, Jectofer Nsg Mgt Parenteral Iron Preparation:
IRON Side-Effects: Anorexia N/V Abdominal Pain Diarrhea/ Constipation Melena
1. Administer using Z tract method to prevent discomfort, discoloration leakage to tissues.

2. 3. Dont massage injection site. Ambulate to facilitate absorption. Monitor S/E: a.) Pain at injury site b.) Localized abscess (nana) c.) Lymphadenopathy d.) Fever/ chills e.) Urticaria itchiness f.) If (+) to Hypotension ------------Anaphylactic shock Give epinephrine (SNS Effect) B. FOLATE DEFICIENCY ANEMIA - Cell is macrocytic, hypochromic anemia - A form of MEGALOBLASTIC ANEMIA - Anemias characterized by abnormal large RBC 2nd to impaired DNA synthesis d/t deficiency of Folic acid Pathophysiology: Folic acid impaired DNA synthesis in the bone marrow impaired RBC development, impaired nuclear maturation but cytoplasmic maturation continues large size Causative Factors: 1. Alcoholism 2. Mal-absorption 3. Diet deficient in uncooked vegetables Sx: All symptoms of Anemia
C. PERNICIOUS ANEMIA - A megaloblastic chronic anemia characterized by deficiency of intrinsic factor secreted by the parietal cells leading to Hypochlorhydria---------decrease Hcl acid secretion - A Vit. B12 deficiency Predisposing Factors: 1. Subtotal Gastrectomy partial removal of the stomach 2. Atrophy of gastric mucosa (elderly) ------ # 1 cause 3. Hereditary 4. Inflammatory disorder of ileum 5. Autoimmune 6. Strict vegetarian diet 7. Gastrointestinal malabsorption----Crohns Disease/ Cancer of stomach
Largest part of GIT = Large Intestine Widest part of GIT = Stomach
Pathophysiology:
STOMACH (composed of different cells) Parietal or ergentaffen Oxyntic cells
Function: Produce Intrinsic Factor INTRINSIC FACTOR Binds w/ Vit. B12 to promote absorption For maturation of RBC Disorder in the Process
Function: Secrets Hcl acid HYDROCHLORIC ACID Aids in digestion Decreased Digestion ----- Dyspepsia & Weight Loss Diet: High caloric Intake to correct Wt loss
Immature RBC Killed by Spleen Heme----Globin Ferroes------------Ferretin = Bilirubin ----- Jaundice S/Sx: 1. 2. All Sx of Anemia + GIT changes a. RED BEEFY TONGUE = PATHOGNOMONIC SIGN b. Dyspepsia indigestion c. Wt loss, mild diarrhea d. Jaundice CNS Most dangerous anemia d/t neurologic involvement d/t deficiency in Vit. B 12 a. Tingling sensation b. Paresthesia (numbness) in extremities c. (+) Rombergs test = Ataxia d. Psychosis 1. Peripheral Blood Smear = shows giant RBCs, WBCs w/ giant hypersegmented nuclei 2. Very High MCV 3. Shillings Test = reveals inadequate absorption of Vit. B 12 4. Intrinsic Factor Antibody Test Common Route: Dorsogluteal 1. Vit. Supplementation : Folic Acid 1 mg daily Ventro2. Diet Supplementation
3.
Dx:
Tx:
3. Lifetime monthly injection of IM Vit. B 12 as ordered -----not oral---pt. may developed drug toleranceNo S/E Nsg Mgt :
1.
Enforce CBR
2. Diet high calorie or CHO----Increase CHON, iron & Vit C 3. Avoid irritating mouthwashes. Use of soft bristled toothbrush is encourage
4. Avoid applying electric heating pads can lead to burns II. INCREASE HEMOLYSIS/ HEMOLYTIC ANEMIA - Destruction of RBC greater than the rate of formation ----all + Hyperbilirubinemia-----JAUNDICE + TEA-COLORED URINE Causes: 1. 2. 3. Type II: A. SICKLE CELL ANEMIA - A severe chronic incurable hemolytic anemia that results from heritance of the sickle hemoglobin gene. Causative Factor: 1. Genetic inheritance of the sickle gene- HbS gene Pathophysiology: Decreased O2, Cold, Vasoconstriction can precipitate sickling process Factors cause defective Hgb to acquire a rigid, crystal-like C-shaped configuration Sickled RBCs adhere to endothelium pile up & plug the vessels ischemia results pain, swelling & fever Sx: 1. Jaundice 2. Enlarged skull & facial bones 3. Tachycardia, murmurs & cardiomegaly Primary sites of thrombotic occlusion: spleen, lungs & CNS 4. Chest pain, dyspnea Complications: 1. Sickle Cell Crises = Results from tissue hypoxia & necrosis 2. Acute Chest Syndrome = Manifested by a rapidly falling Hgb level, tachycardia, fever & chest infiltrates in the CXR Tx: 1. Bone marrow transplant 2. Hydroxyurea = Increases the Hgb 3. Long term RBC transfusion = Packed RBC Surgery For Hemolytic anemia = Spleenectomy Nsg Mngt: 3 Nursing Priority: 1. Manage the pain Support & elevate acutely inflamed joint 1. A/W Avoid deoxygenating Relaxation techniques activities Analgesics 2. Prevent and manage infection - High altitude is bad Monitor status of patient 2. Fluid Deficit Promote Initiate prompt antibiotic therapy hydration 3. Promote coping skills 3. Pain & Comfort Provide accurate information Allow patient to verbalize her concerns about medication, prognosis & future pregnancy 4. Monitor and prevent potential complications Provide always adequate hydration Avoid cold, temperature that may cause vasoconstriction 5. Monitor and prevent potential complications Leg ulcer
Post-viral injection Exposure to ionizing radiation Prolong use of toxic drugs & medications (penicillin, chloramphenicol)
Aseptic technique Priapism = Sudden painful erection Instruct patient to empty bladder, then take a warm bath B. POLYCYTHEMIA - Refers to an INCREASE volume of RBCs -----reverse of sickle cell anemia - The hematocrit is ELEVATED to more than 55%
Classified as Primary or Secondary
1. POLYCYTHEMIA VERA - Primary Polycythemia - A proliferative disorder in which the myeloid stem cells become uncontrolled
Causative Factor: Unknown
Pathophysiology: The stem cells grow uncontrollably The bone marrow becomes HYPERcellular & all the blood cells are increased in number The spleen resumes its function of hematopoiesis and enlarges Blood becomes thick & viscous causing sluggish circulation Overtime, the bone marrow becomes fibrotic Sx: 1. Skin is ruddy 2. Splenomegaly 3. Dizziness, blurred vision, HA 5. Angina, dyspnea & thrombophlebitis Dx: 1. CBC- shows elevated RBC mass 2. Normal oxygen saturation 3 Elevated WBC & Platelets Complications: 1. Increased risk for thrombophlebitis, CVA MI 2. Bleeding d/t dysfunctional blood cells Tx: 1. To reduce the high blood cell mass- PHLEBOTOMY 2. Allopurinol 3. Dipyridamole 4. Chemotherapy to suppress bone marrow Nsg Mngt: 1. Primary role of the nurse is EDUCATOR 2. Regularly assess for the development of complications 3. Assist in weekly phlebotomy 4. Advise to avoid alcohol & aspirin 5. Advise tepid sponge bath or cool water to manage pruritus
POLYCYTHEMIA Earliest Sign : Headache Late Sign: Pruritus Complication: Stroke, Thrombosis
III. BONE MARROW DEPRESSION/ HYPOPLASTIC ANEMIA - Inadequate abnormal cells-------Hypoplastic anemia/Aplastic Anemia - All Sx + decreased WBC --------------Leukopenia ----------risk for infection + decreased PLATELETS--- Thrombocytopenia----- bleeding
when all 3 are present ----- PANCYTOPENIA
WBC (Leucocytes 5,000 10,000/mm3) GRANULOCYTES 3 Types: 1. Polymorphonuclearneutrophils (PMNs) - Most abundant 60-70% WBC - Lifespan of 24-48 hrs. Function: Short-term Phagocytosis For acute inflammation 2. Polymorphous Basophils (PMBa) -Involved in Parasitic infection - Release of chemical mediator for inflammation (Serotonin, Histamine, Prostaglandin, Bradykinins) -Absorbs large fat particles after ingestion of high fat meal 3. Polymorphous Eosinophils (PMEo) - Involved in Allergic reactions HIV Window Period: 6 months Incubation: 6 months to 5 yrs. Sx: Kaposi Sarcoma Dx Test: Western Blot Test Drug of Choice: Zidovudine ( AZT or SIGNS OF PLATELET DYFUNCTION 1. Petecchiae 2. Ecchymosis/bruises 1. B Cell L Bone marrow or bursa dependent - Arises from bone marrow 2. T Cell Devt of immunity - From thymus - Target cell of HIV 3. NK Cell Natural killer cell -Have both antiviral & anti-tumor properties C. Platelets (Thrombocytes) (Normal: 150,000 450, 000/ mm3) - Promotes homeostasis prevention of blood loss by activating clotting - Consists of immature or baby platelets known as Megakaryocytes Target of Dengue Virus Normal lifespan 9 12 days NON-GRANULOCYTES A. Monocytes (Macrophage) -Largest WBC - Involved in long term phagocytosis - For chronic inflammation - Other name macrophage Macrophage in CNS- Microglia Macrophage in skin Histiocytes Macrophage in lungs Alveolar macrophage Macrophage in Kidneys Kupffer cells B. Lymphocytes 3 Types:
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A. APLASTIC ANEMIA A condition characterized by decreased number of RBC as well as WBC & platelets - Common among clients undergoing chemotherapy, Cobalt therapy, Radiation therapy - Stem cell disorder d/t bone marrow depression leading to pancytopenia all RBC are decreased Decrease RBC Anemia Decrease WBC Leucopenia Susceptibility to infection Fever Decrease platelets Thrombocytopenia No clotting Bleeding
Petechia (Purpura) Predisposing Factors :
Ecchymosis
Bruising
Environmental Toxins & Chemicals Pesticides, Benzene & its derivatives 2. radiation 3. Immunologic injury 4. Certain drugs causes bone marrow depression a. Chemotherapeutic agents, = Methotrexate, Nitrogen Mustard (anti-metabolite), Vincristine b. Broad Spectrum antibiotic =Chlorampenicol, Sulfonamides bactrim (Pt severe isolation) c. Phenybutazones 5. Heavy Metals Pathophysiology: Toxins cause a direct bone marrow depression acellular bone marrow decreased production of blood elements Sx: 1. All Sx of Anemia + 2. Leucopenia increase susceptibility to infection 3. Thrombocytopenia 4. Splenomegaly 5. Retinal hemorrhages Dx: 1. CBC- decreased blood cell numbers 2. Bone marrow aspiration at posterior iliac crest: Confirms the anemia- hypoplastic or acellular marrow replaced by fats Fatty streaks in bone marrow Tx: Bone Marrow Transplantation 1. Bone Marrow Transplantation 1. Syngeneic BMT 2. Immunosuppressant drugs donor from twins 3. Rarely, steroids 2. Allogenic BMT 4. Blood transfusion = Fresh Whole blood Related or unrelated as Nsg Mgt: long 1. Removal of underlying cause as compatible (Human 2. Blood transfusion as ordered leukocyte antigen) 3. CBR 3. Autologous BMT 4. O2 inhalation Own self 5. Reverse isolation d/t leukopenia - harvest marrow during 6. Monitor signs of infection 7. Avoid SQ, IM or any venipuncture site 8. Use electric razor when shaving to prevent bleeding 9. Administer meds: Immunosuppressant
1.
Anti lymphocyte globulin (Alg) given via central venous catheter, 6 days 3 weeks to achieve max therapeutic effect of drug. IV. BLOOD LOSS - Cells are normocytic (normal size), normochronic (normal content) but d/t surgery, menstruation------anemia - All Sx + Hypovolemia - Blood Transfusion = Fresh Whole blood OTHER BLOOD RELATED PROBLEMS 1. DISSEMINATED INTRAVASCULAR COAGULATION (DIC) - Acute hemorrhagic syndrome characterized by wide spread bleeding & thrombosis d/t a deficiency of clotting factors (Prothrombin & Fibrinogen). Predisposing Factor:
1. Rapid BT d/t hemolysis

2. 3. 4. Massive trauma Massive burns Septicemia R/T Hemolytic reaction & Anaphylaxis Neoplasia new growth of new tissue (tumor) Pregnancy Septicemia
5. 6.
7. 8. S/Sx: 1. 2. 3. 4. 5.
6.
Dx : 1. 2. 3. 4.
Petechiae widespread & systemic (lungs, lower & upper trunk) Ecchymosis widespread Oozing of blood from venipunctured site Hemoptysis cough blood Hemorrhage Oliguria---------------LATE SIGN
CBC reveals decrease platelets Stool for occult blood (+) Specimen stool Opthalmoscopic exam sub retinal hemorrhage ABG analysis metabolic acidosis
Nsg Mgt:
1. Monitor signs of bleeding All hematologic test + urine, stool, GIT

2. 3.
4.
a.
Administer isotonic fluid solution Administer O2 inhalation Administer meds: Vit K aquamephyton
b. Pitressin or vasopressin -----t o conserve H20 & has vasoconstriction effect----Most Common S/E: Chest Pain
5. NGT lavage - Use iced saline lavage 1st to induce vasoconstriction inside the stomach
6. Monitor NGT output 7. Provide heplock 8. Prevent complication: Hypovolemic shock----Early Sign: Restlessness & Cool moist Skin Late Sign of hypovolemic shock : Anuria 9. Give Heparin-----short-acting
DIAGNOSTIC TEST FOR BLOOD DYSCRASIAS 1. CBC, Hgb, Hct 2. BT, CT, PT 3. ERYTHROCYTE INDEX MCV = Mean Corpuscolar Volume -----to evaluate size of RBC MCH = Mean corpuscular Hgb -----------to evaluate the Hgb content of RBC MCHC = Mean corpuscular Hgb Concentrationto evaluate Hgb content of Pack RBC (in grams /100ml) (Normal: 30-36 grams/100ml)
4. COOMBS TEST - To evaluate the presence of immune bodies that adheres to RBC causing hemolysis/agglutinization of RBC (Rh Incompatibility, ABO Incompatibility)
RBC Normal Size: 80-94 cu micron < 80 ---- Microcytic Cell ANISOCYTOSIS > 94 ----- Macrocytic Cell (abnormal size) Normal Hgb content of RBC: 22-28 micromicrogram < 22
5. SCHILLING TEST - To evaluate rate of absorption of Vit. B12 (Cyanocobalamine) - Use to diagnosed Pernicious Anemia Procedure: Administer P.O. radioactive Vit. B12 ------24 hr. urine Check (+) (-) of Vit. B12 ------ if (-) Pernicious Anemia (do not give P.O. give parenterally) ------ if (+) in urine ---normal Common in Pts. Who undergone gastrectomy/ cancer----they do not have intrinsic factor
6. BONE MARROW ASPIRATION/PUNCTURE/TAP POIKILOCYTOSIS = abnormality in shape of RBC METARUBRICYTE = abnormal RBC w/
- To evaluate size, shape, character of RBC cells - Invasive (consent) - Local anesthesia (lidocaine 1-2%) - Sites: Sternum ------ Position: Supine A & P Iliac Crest ------ Position: Supine (A) & Prone/Lateral (P) - Pediatric pts. --- use the long bones (femur, humerus)-----as we grow older the # of marrows in long bones decreases - Apply pressure dressing over site to prevent bleeding
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7. LYMPH NODE BIOPSY - Site : Cervical LN, Axilla LN, Inguinal LN
IV. BLOOD TRANSFUSION: Objectives: 1. 2. 3. 4. To replace circulating blood volume To increase O2 carrying capacity of blood To combat infection if theres decrease WBC To prevent bleeding if theres platelet deficiency Packed RBC = 250 ml Refrigerated = 3-5 days
Nsg Mgt & Principles in Blood Transfusion 1. Proper refrigeration Proper typing & cross matching Type O universal donor AB universal recipient 85% of people are RH (+) Aseptically assemble all materials needed: a.) Filter set b.) Isotonic or PNSS or .9NaClfor flushing to prevent Hemolysis Hypotonic solution Cell swells or burst Hypertonic solution Cell will shrink or crenate c.) Needle gauge 18 - 19 or large bore needle to prevent hemolysis. d.) Instruct another RN to recheck the following . Pts name, blood typing & cross typing expiration date, serial number Most important e.) Check blood unit for bubbles, cloudiness, dark in color & sediments indicates bacterial contamination. Return to blood bank, do not dispose f.) Never warm blood products may destroy vital factors in blood. - Warming is done if with warming device only in EMERGENCY! - Within 30 mins room temp only! g.) Blood transfusion should be completed < 4hrs because blood that is exposed at room temp for > 2h causes blood deterioration------can lead to bacterial contamination h.) Avoid mixing or administering drug at BT line leads to hemolysis i.) Regulate BT 10 12 gtts/min KVO or 100cc/hr to prevent circulatory overload j.) Monitor VS before, during & after BT especially q15 mins for 1st hour - Majority of BT reaction occurs within 1h. BLOOD TRANSFUSION REACTIONS: BT REACTIONS: 1. HEMOLYTIC REACTION Sx: Headache Dizziness Dyspnea Palpitation Lumbar/Sternal flank pain Hypotension, Flushed Skin---red port wine urine Nsg Mgt:
2.
3.
H A P C A T C H expired
Hemolytic Reaction Allergic Reaction Pyrogenic Reaction Circulatory Reaction Air Embolism Thrombocytopenia Citrate Intoxication Hyperkalemia d/t blood
1. Stop BT 2. Notify Doc 3. Flush with plain NSS 4. Administer isotonic fluid sol to prevent acute tubular necrosis & counteract shock 5. Send blood unit to blood bank for reexamination 6. Obtain urine & blood samples of pt & send to lab for reexamination 7. Monitor VS & Allergic Rxn 2. ALLERGIC REACTION S/Sx: 1. 2. 3. 4. 5. Fever/ chills Urticaria/ pruritus Dyspnea Laryngospasm/ bronchospasm Bronchial wheezing
Nsg Mgt: 1. 2. 3. 4. Stop BT Notify Doc Flush with PNSS Administer antihistamine diphenhydramine Hcl (Benadryl) If (+) Hypotension anaphylactic shock administer epinephrine 5. Send blood unit to blood bank 6. Obtain urine & blood samples send to lab 7. Monitor VS & IO 8. Adm. Antihistamine as ordered for Allergic Rxn, if (+) to hypotension indicates anaphylactic shock Shock -----administer epinephrine 9. Administer antipyretic & antibiotic for pyrogenic Rxn & TSB
3. PYROGENIC REACTION: S/Sx:
a.) Fever/ chills b.) Headache c.) Dyspnea

Nsg Mgt: 1. 2. 3. 4. 5. 6. 7. 8.
d.) Tachycardia e.) Palpitations f.) Diaphoresis (Pyrogens -----fever-producing agents)
Stop BT Notify Doc Flush with PNSS Administer antipyretics, antibiotics Send blood unit to blood bank Obtain urine & blood samples send to lab Monitor VS & IO Tepid sponge bath offer hypothermic blanket
PRIORITY CASES Hemolytic Reaction = 1st d/t Hypotension---attend to destruction of Hgb ------ O2----- Brain Damage Circulatory Reaction = 2nd Allergic Reaction = 3rd Pyrogenic Reaction = 4th But: Anaphylactic = 1st priority Hemolytic = 2nd
4. CIRCULATORY OVERLOAD Sx: Dyspnea

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Orthopnea Rales or crackles Exertional discomfort
Nsg Mgt: 1. 2. 3. Stop BT Notify Doc Administer diuretics
ONCOLOGIC NURSING
Oncology study of neoplasia new growth Benign (tumor) Well differentiated Encapulation (+) Metastasis (-) Prognosis good Surgery Malignancy (cancer) Poorly or undifferentiated (-) (+) Poor prognosis 1. Chemotherapy Many S/E 2. Radiation 3. Surgery most preferred treatment 4. Bone marrow transplant - Leukemia only
Predisposing Factors: (Carcinogenesis) G genetic factors I immunologic factors V viral factors a. Human Papiloma Virus causing warts b. Epstein Barr Virus E environmental Factors 90% a. Physical irradiation, UV rays, nuclear explosion, chronic irritation, direct trauma b. Chemical factors - Food additives (nitrates - Hydrocarbon vesicants, alkalies Warning / Danger Sx of CANCER - Drugs (stillbestrol) - Urethane C change in bowel /bladder habits - Hormones A a sore that doesnt heal - Smoking U unusual bleeding/ Discharge Male: st T thickening of lump breast or 1 Lung Cancer Bronchogenic d/t smoking nd elsewhere 2 Liver Cancer Hepatic d/t alcohol rd I indigestion/Dysphagia 3 Prostate cancer 40 y/o & above (middle age & above) th O obvious change in wart/ mole 4 Testicular Cancer 30 y/o N nagging cough/ hoarseness BPH 50 & above U unexplained anemia A - anemia Female: S sudden wt loss 1st Breast Cancer 40 yrs old & up Mammography 15 20 mins (SBE 7 days after mens) 2nd Cervical Cancer 90% Multi-sexual partners 5% Early Pregnancy 3 LS TRIAD 3rd Ovarian Cancer common to squamous cell type Sx 4th Uterine Cancer Large Lump Loaded
CLASSES OF CANCER: Tissue Typing:

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1. 2. 3.
Carcinoma arises from surface epithelium & glandular tissues Sarcoma- from connective tissue or bones Multiple myeloma from bone marrow Pathological fracture of ribs & back pain
4. Lymphoma from lymph glands 5. Leukemia from blood 1. LEUKEMIA Cancer of the WBC Uncontrolled abnormal proliferation ---------------immature WBC known as Blast Cells activity of cell Proliferation of BLAST CELLS cellular metabolism prone to infection Temperature
Pathology:
Invade/Infiltrate vital organs Spleen Spleenomegaly Liver Hepatomegaly Kidney RF Brain ICP
Crowd/ Congest/Accumulate Joint Pain, Swell Hinder/Prevent Production of Cells RBC Platelets
CLASSIFICATION: ONSET 1. ACUTE LEUKEMIA Sudden DURATION Short < 6 months CELLS Immature blast cells Mature WBC
2. CHRONIC LEUKEMIA Gradual long duration - Characterized by periods of remission (absence) & exacerbation (recurrence)
PREDOMINANT CELLS PRESENT IN BLOOD: 1. Acute/Chronic Lymphocytic Leukemia = 2. Acute/ Chronic Myelocytic Leukemia = Lymphocytes & monocytes ---- ALL (common to children)
myeloblasts ----- CML (common to Adult)
Cells Derived 1. Bone Marrow Granulocyte

2. Lymphoid Tissue Agranulocyte

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Agranulocyte
Immature Myeloblast Myelocyctes
immature Monoblast Monocyte
immature mature Lymphocyte
2. BREAST CANCER Predisposing Factors: 1. Family Hx (mother/sister) 2. Obesity 3. Unmarried at age 40 y/o 4. Married w/o children 5. Married w/ children but did not breastfeed 6. Women w/ prolonged menstruation 7. Early menarche at 11 y/o 8. Late menopause at 52 y/o 9. 1st pregnancy at age 35 y/o Prevention: Sx: 1. Dimpling of skin 2. Orange skin 3. Asymmetry of breast 4. Discharges of nipple Dx: 1. Mammography 2. Breast Biopsy = Best confirmatory Dx Tx: 1. Surgery: Lumpectomy Modified Mastectomy mass, tissue, pectoralis major or minor at axillary Radical Mastectomy - leave either pectoralis major or minor muscle SBE = 7-10 days after menstruation = after menopause----- 1x/month Late Sign of Breast Ca: MASTOIDYNA = breast pain
Early Sign of Breast Ca: Non-tender Non-mobile Painless breast mass/lump
Common Site Of Breast Ca UPPER OUTER QUADRANT LEFT
3. ONCOLOGIC EMERGENCIES Obstructive or Compressive Disorders Superior vena cava syndrome Pericardial effusion/cardiac tamponade Leukostasis Spinal Cord Compression Metabolic Disorders Hypercalcemia Symptoms of SIADH Tumor lysis syndrome 3. Disruptions of hematologic/im-munologic function
PROGNOSIS Lung = 6 yrs Breast = 2-6 yrs. Colon = 2-6 yrs. Pancreatic = 3-6 months Liver = 3 mnths
DIC Septic shock
3. BRAIN TUMOR Location: 1. Supratentorial Cerebrum, anterior 2/3 of the brain 2. Infratentorial Cerebellum, brainstem, posterior 1/3 of the brain *Both will manifest Increased ICP Both will undergo Brain Surgery: a. CRANIOTOMY/CRANIECTOMY - Use general endotracheal anesthesia (For all brain surgery) If surgery lasts for more than 2 hrs, assured of patent airway - Type of incision: Coronal or Butterfly - Skin Preparation: Shaving of head done at stage 3 of anesthesia Nursing Management: DONTS POST-OPERATIVE: 1. Do not put client on Trendelenberg position---- it will increase ICP & abdominal content will compress stomach 2. If pt. in shock: Supine w/ pillow, head turned to one side 3. If pt. not in shock: Supratentorial---- elevate head 45 degrees (SF) ---- to promote venous return to heart Infratentorial ---- elevate head 10-15 degrees ------ to prevent compression of brain stem --- turn head to one side, unoperated side especially if bone flap not returned --- allowed on affected side but not more than 20 minutes to prevent ischemia 4. Do not give narcotic agent/analgesic No Demerol------ respiratory depressant 5. No suctioning---- mere suction will trigger coughing----- Increased ICP --- If needed: Oropharyngeal suctioning only --- Nasal suctioning will damaged nasal mucosa---leakage of CSF 6. Do not restrain client -- Makes client agitated --- Increased ICP 7. No rectal tube, rectal movement or manual extraction of feces. -- Vagal stimulation------Bradycardia Treatment Modality: 1. Radiotherapy Early Sign of Brain Tumor: PAPILLEDEMA (tumor compress on optic chiasm)
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Therapeutic Modality: 1. CHEMOTHERAPY Use various chemotherapeutic agents that kills cancer cells & kills normal rapidly producing cells GIT, bone marrow, and hair follicle. Classification of Cytotoxic Agents: Cell-Cycle Non-specific 1. Alkylating Agents Action: Binds w/ DNA & prevents cell replication Nitrogen Mustard Cyclophosphamide (Cytoxan) Chlorambucil (Leukeran) Nitrosureas Carmustine Lomustine Alkylating-like agents Busulfan (Myeleran) Carboplatin Cisplatin (Platinol)* common Thiotepa Ifex (Ifosfamide) 2. Antitumor/Anti-Neoplastics Antibiotics Action: Inhibits cell division by interfering w/ synthesis of nucleic acid Bleomycin Doxorubicin Dactinomycin Mitomycin Idarubicin Adriamycine (Doxorubicin) Mithramycin Plimcamycin Actinomycin Action: Foster cell death by interfering w/ the cellular metabolic process Cytarabine (Cytosar/Ara C) 5-fluorouracil (5-FU) Hydroxyurea 6-mercaptopurine (Purinethol) Methotrexate (Mexate) Classification of Cytotoxic Agents: Cell-Cycle Specific 1. Antimetabolite (S phase) Classification of Cytotoxic Agents 1. Hormones & Steroids Action: Reduces cellular metabolism by providing a non-favorable environment for growth of Ca cells Estrogens DES (Post-menopausal) (Diethylstibestrol) Ethinyl estridiol Antiestrogens Tamoxifen Raloxifene Others Aminogluthetimide Asparaginase Leuprolide Mitotane Androgens (Pre-menopausal) Fluoxymesterone Testosterone Propionate Halotestin Antiandrogens Bicalutamide Flutamide Progestins Medroxyprogesterone Megestrol acetate
2. Vinca/Plant Alkaloids (M phase) Action: Mitotic Inhibitors Docetaxel Etoposide (Toposar) Vinblastine (Velban,Velbie) Vincristine (Oncovin)
Side-Effects: 1. GIT - -Nausea & Vomiting Nsg Mgt:

PROTOCOL IN THERAPY 6 cycle of Chemotherapy Interval of 28 days

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Administer anti-emetic (Plasil) 4 6h before start of chemotherapy Ex. Ondansetrone Zofran Alprazolan - Zanax 2. Withhold food/ fluid before start of chemo 3. Provide bland diet post chemotherapy: Avoid spic foods---irritants Ex. Non irritating / non spicy 4. Avoid bulky course diet 5. Advise Neutropenic Diet : Avoid raw foods, raw vegetable - Diarrhea 1. Administer anti diarrhea 4 6h before start of chemo 2. Monitor urine, I&O qh - Stomatitis/ Mouth Sores Doxorubicin -Toxic to myocardium - Do not give if client is not hooked up to a cardiac monitor
1.
1. Oral care offer ice chips/ popsickles Use alkalanizer for mouth sores 2. Inform patient that 10-15 days after chemotherapy there will be hair loss Temporary Alopecia - Loss from other hair of the body - Hair will grow back after 4 6 months post chemo. -Bone Marrow Depression --------Leukopenia/Anemia 1. Enforce CBR 2. O2 inhalation 3. Reverse isolation 4. Monitor signs of bleeding 5. Inform pt. it will last only for 21 days 2. Reproductive Organ Sterility 1. Do sperm banking before start of chemo
3. Renal System Increase uric acid 1. Administer allopurinol/ xyloprin (gout) Fx: Inhibits uric acid Acute gout colchicines Increase secretion of uric acid
3. Neurological Changes peristalsis paralytic ileus Most feared complication following any abdominal surgery Vincristine plant alkaloid causes peripheral neuropathy Mngt: 1. Cancer drugs can be very potent------- it can destroy normal cells 2. Protect yourself from Ca drugs that can destroy the skin: cover everything 3. Increase fluid intake post-chemo d/t drugs are hepato-toxic 4. Avoid exposure of Ca drugs to light----reduces the potency of the drug---cover w/ carbon paper, dim lights REVERSE ISOLATION TECHNIQUE 1. Private room, laminar air flow (positive pressure room) 2. Sterile linen, sterile hygiene equipment 3. Dedicated equipment 4. Put on shoe covers, mask & cap, sterile gown & gloves. 5. Low bacteria diet: no fresh fruits & vegetables; avoid drinking water allowed to stand for more than 15 min. 6. No fresh flowers or potted plants 7. Institute prophylactic oral hygiene regimen before, within 30 minutes after each meal & q2Hq4H during waking hours 8. May use tsp salt, pinch of baking soda & 8 oz. of H2O or saline 9. Avoid alcohol- or glycerine-based mouthwash
10. Use softbristled toothbrush 11. Use foam stick moistened with mouthwash to remove debris from mucosa 12. May apply topical anesthetic, as prescribed 13. Encourage fluid intake of 2000 ml/day 14. Encourage bland diet high in CHON to promote healing. Avoid hard or spicy food Avoid citrus juices 15. If patient has difficulty in eating & maintaining fluid intake, parenteral nutrition may be necessary 16. Assess the need for use of antifungal or antibacterial agents 2. RADIATION THERAPY Involves use of ionizing radiation that kills cancer cells & inhibit their growth & kill rapidly producing cells. Types of Energy Emitted:
1. Alpha rays 2. Beta rays 3. Gamma ray

2 Methods of Delivery:
rarely used doesnt penetrate skin tissues internal radiation more penetration external radiation penetrates deeper underlying tissues
1. External Radiation
- Involves electro magnetic waves Ex. Cobalt Therapy, Teletherapy, External Beam Radiation
Nursing Responsibility: a. c. d. e. f. g. h. Explain that it is a painless procedure Tell pt. not to erase markings & cleanse area only w/ H2O. No soap. Pat dry. Avoid sunlight over site Avoid pressure over the site Avoid hot/cold application over site Avoid use of oil cream solution/lotion to prevent skin reaction Observed for S/S of RADIATION SICKNESS Systematically - Leukopeniabone marrow - Sterility---- Gonadsboth sensitive to radiation
b. During procedure: Pencil Markings on skin indicating area to be radiated
Locally Manifested - Erythema - Dryness of skin - Loss of skin hair - Blister formation - Skin desquamation
2. Internal Radiation
Injection/ implantation of radioisotopes proximal to CA site for a specific period of time. - Form of wire, seed, needle - Isotope inside clients body
Administering ISOTOPE: a. Implant or Intracavitary Implantation - Insert isotope into body cavity - Radium seed/Radom seed (sealed) b. Brachytherapy - Intralesion/ intratumor - Cesium 135 (sealed) c. P.O. - RAI 135, RAI 131 (unsealed liquid) d. Intra-arterial Perfusion
- RA Gold 198 (liver cancer) - RA Phosphorus (bone cancer) 2 Types: a. Sealed Implant b. Unsealed Implant Nursing Responsibility: 1. Isolate patient. 2. Offer diversional therapy 3. Post at door radiation sign 4. Separate set of utensils 5. articles not needed in room should be removed 6. In Unsealed: All excreta, vomitus are considered contaminated. Throw directly to toilet bowl 7. Observe for Time: Longer exposure means more radiation Not more than 5 minutes/exposure, 30 minutes/shift Distance: 3-8 ft. from site Shielding: Stay at the farthest part/ use lead apron 8. Prevent accidental dislodgement of the radium: Place on CBR NO bed pan, insert indwelling catheter Give diet constipation: Decreased fiber & roughage Once dislodge, pick-up w/ long forcep, put in lead container 9. Use scanner, Geiger counter to detect remaining traces of radiation 10. Tell partner to resume sex, once edema has subsided 11. Tell pt. if dysuria & burning in urination: SUSPECT URETHRAL ATHROPHY Meatus, Urinary bladder---- CYSTITIS, HEMATURIA 3 Factors Affecting Exposure: a. Half life b. Distance c. Time d. Shielding S/E & Mgt: a.) Skin errythema, redness, sloughing Time period required for half of radioisotopes to decay. - At end of half life less exposure The farther the distance lesser exposure The shorter the time, the lesser exposure Rays can be shielded or blocked by using rubber gloves & gamma use thick lead on concrete. Radioisotope with a container & doesnt contaminate body fluid. Ex. Radium Seed, Radom Seed, Cesium 135 Radioisotope without a container & contaminates body fluid. - Liquid given either P.O. or Intra-arterial Ex. Phosphorus 32, RAI, RA
1. Assist in bathing pt
2. 3. 4. Force fluid 2,000 3,000 ml/day Avoid lotion or talcum powder skin irritation Apply cornstarch or olive oil Stomatitis
b.) GIT Nausea / Vomiting /
1. Administer antiemetic 4 6h before start of chemo - Plasil 2 Withhold food/ fluid before start of chemo 3. Provide bland diet post chemo Non irritating / non spicy Dysglusia decrease taste sensitivity -When atrophy papilla (taste buds) 40 y/o
c.) Bone Marrow Depression 1. 2. 3. 4. Enforce CBR O2 inhalation Reverse isolation Monitor signs of bleeding
CARDIOVASCULAR SYSTEM
OVERVIEW: HEART: -
Muscular, pumping organ of the body Occupies most of the Left mediastinum Weigh 300 400 grams Microscopic Resembles a closed fist Covered by a serous membrane Pericardium 2 Parts
Cardio Physiology: The main functions of this system are: To transport oxygen, hormones & nutrients to the tissues To transport waste products to the
Parietal layer
Pericardial Space Fluid prevent Friction rub
Visceral layer
CONSISTS OF 3 LAYERS:
1. Epicardium 2. Myocardium 3. Endocardium

2 CHAMBERS:
Outermost - ( Essential, coronary arteries arelocated here) --------- M.I. & AP Inner Responsible for pumping action/ Most dangerous layer -- Cardiogenic shock & RHD Innermost layer Connected to Tunica Intica ------------------------ Endocarditis
1. Upper Collecting/ Receiving chamber - Atria 2. Lower Pumping/ Contracting chamber Ventricles
VALVES & HEART SOUNDS:
1. Atrioventricular Valves - Tricuspid & Mitral Valve

Closure of AV valves gives rise to 1st heart sound or S1 or lub
2. Semi-lunar Valve Pulmonic & Aortic

Closure of semilunar valve gives rise to 2nd heart sound or Extra heart Sound:
S2 or dub
S3 d/t Increased Ventricular Filling -Ventricular Gallop S4 d/t Forceful Atrial Contraction - Atrial Gallop
Left CHF, Left ventricular hypertrophy MI, HPN, Pulmonic Stenosis, Aging
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CORONARY ARTERIES: The Blood supply of the heart comes from the Coronary arteries a. Right coronary artery b. Left coronary artery Both supply the myocardium with blood 1.Arises from the base of the aorta : RMCA & LMCA CONDUCTION SYSTEM OF THE HEART: 1. Sino atrial node (SA node) (or Keith-Flock node) Location: Junction of SVC & Right Atrium Function: Primary pace maker of heart Initiates electric impulse of 60 100 bpm
2. Atrioventicular Node (AV node or Tawara node)

Location: Inter atrial septum Delay of electric impulse to allow ventricular filling of 0.8 milliseconds Slowest conduction 3. Bundle of His Location: Interventricular septum Branches out into: Rt main Bundle Branch & Lt main Bundle Branch Purkenjie Fiber Location: Walls of ventricles-- Ventricular contractions Fastest conduction
4.
Physiology The intrinsic conduction system causes the heart muscle to depolarize in one direction The rate of depolarization is around 75 beats per minute (60-100/min) The SA node sets the pace of the conduction This electrical activity is recorded by the Electrocardiogram (ECG) Sympathetic system INCREASES HR Parasympathetic system (Vagus) DECREASES HR ANATOMY OF THE HEART
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SA node
AV
Bundle of His
Septum Purkenjie Fibers
BLOOD SUPPLY: Amount of blood the heart pumps out in each beat Stroke Vol. X HR/min (Normal C.O: 4-6 L/min)
Cardiac Output Factors in Cardiac Output: 1. Systole 2. Diastole - Contraction - Relaxation
Total Peripheral Resistance
= Blood Pressure
The PRELOAD refers to the amount of blood contained in the ventricle at the end of a diastole. Degree of stretching of the heart muscle when it is filled-up with blood (reduced with hypovolemia) The AFTERLOAD force that LV has to exert in order to pump blood to the aorta. The resistance to which the heart must pump to eject the blood (increased with HPN) Control is neural (central & peripheral) & hormonal Baroreceptors in the carotid & aorta Hormones- ADH, Adrenergic hormones, Aldosterone & ANF ADH increases water retention Aldosterone increases sodium retention & water retention secondarily Epinephrine & NE increase HR & BP ANF= causes sodium excretion The vascular system consists of the arteries, veins & capillaries The arteries are vessels that carry blood away from the heart to the periphery The veins are the vessels that carry blood to the heart
The capillaries are lined with squamos cells, they connect the veins & arteries The lymphatic system also is part of the vascular system & the function of this system is to collect the extravagated fluid from the tissues & returns it to the blood IRREGULARITIES: 1. Complete Heart Block Insertion of pacemaker at Bundle Branch Metal Pace Maker change q3 5 y/o 2. ECG Tracings Prolonged PR ST segment Depression ST elevated T wave inversion Widening QRS 3. Coronary Artery Disease Atherosclerosis Angina Pectoris MI Myocardial Injury Myocardial Ischemia - Myocardial Necrosis Atrial Fibrillation Angina Pectoris MI MI Arrhythmia
DISORDERS OF THE HEART I. CORONARY ARTERY DISEASE/ ISCHEMIC HEART DISEASE Results from the focal narrowing of the large & medium-sized coronary arteries d/t deposition of atheromatous plaque in the vessel wall If 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery, becomes significant Pathophysiology: Fatty streak formation in the vascular intima T-cells & monocytes ingest lipids in the area of deposition Atherosclerosis Narrowed arterial lumen
Reduced coronary blood flow
Potential For: Thrombosis Embolism
With Coronary occlusion Myocardial Ischemia ( 8-10 seconds : Anginal Pain) Chest Pain SAVERS S sudden onset (myocardial & anginal) A anterior or substernal V by Nia E. Createdvague Tubio discomfort E exercise
Without Coronary Occlusion
Myocardial Necrosis Akinesia/Dyskinesia of the myocardium *DECREASED CARDIAC OUTPUT CARDIOGENIC SHOCK Renal Damage (Acute Renal Failure) PULMONARY EDEMA Right Ventricular Hypertrophy
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Electrical Failure Dysrrythmia Ventricular Fibrillation Sudden Heart Arrest
Right Ventricular Hypertrophy
Rales Cough Hemoptysis Orthopnea Excertional dyspnea Easy fatigability
Sx of Right CHF
Pitting Edema
Weight Gain
Ascites
Hepatomegaly
(+) Hepato-Jugular Reflux
Dyskinesia - difficult contraction of the myocardium Akinesia -temporary
Sx of Left CHF
1. ATHEROSCLEROSIS ATHEROSCLEROSIS - Narrowing of artery d/t fat/ lipid deposits at tunica intima.
ARTEROSCLEROSIS - Hardening of artery d/t calcium & CHON deposits at tunica media.
Predisposing Factor: 1. Sex male 2. Black race 3. Hyperlipidemia - Genetic 4. Smoking 5. HPN 6. DM 7. Oral contraceptive/Steroids - prolonged use 8. Sedentary lifestyle 9. Obesity >20 % of Body weight 10. Hypothyroidism Sx: 1. 2. 3. 4. 5. Tx: 1. PTCA 2. CABG (Refer to MI for management) Chest pain Dyspnea Tachycardia Palpitations Diaphoresis
LAYERS OF THE ARTERY TUNICA ADVENTITIA outer TUNICA INTIMA innermost TUNICA MEDIA - middle
2. ANGINA PECTORIS
A clinical syndrome characterized by paroxysmal chest pain d/t temporary myocardial ischemia usually relieved by REST or NGT nitroglycerin Reversible, no dead cells yet Chest pain resulting from coronary atherosclerosis or myocardial ischemia (tissue ischemia)
3 COMMON TYPES OF ANGINA 1. Stable Angina - The typical angina that occurs during exertion - Relieved by rest and drugs & the severity does not change - < 15 minutes 2. Unstable Angina -Occurs unpredictably during exertion & emotion - Severity increases with time & pain may not be relieved by rest & drug - Mimics M.I. 3. Variant angina - Prinzmetal angina, results from coronary artery VASOSPASMS - May occur at rest Pathophysiology: STERLING LAW = the greater the myocardium fiber stretch = the greater the pressure on contraction For Myocardium to survive: Supply = Demand If < then it will suffer ISCHEMIA If blood supply decreased or 8-10 seconds (partially occluded) Suffer Ischemia CHEST PAIN (Anginal Pain) If more than 30 minutes, the heart cannot withstand Myocardial Infarction/Necrosis CHEST PAIN Angina Pectoris: Predisposing Factor: Precipitating Factors: 4 Es
Variant Angina smoking Angina Decubitus when lying-down
From pain
1. 2. 3. 4.
5. 6.
7. 8. 9.
10.
Sex male Black raise Hyperlipidemia Smoking HPN DM Oral contraceptive prolonged Sedentary lifestyle Obesity Hypothyroidism
1. Excessive physical exertion 2. Exposure to cold environment (vasoconstriction) 3. Extreme emotional response Angina Sx: 4. Excessive intake of foods high in S sudden onset 1st: Levines Sx: hand clutching chest A anterior or substernal pain Type: sharp, stabbing, excruciating pain Radiates to back, shoulders, axilla, arms & jaw muscles V vague discomfort E exercise will intensify the pain R rest Relieved by rest or NGT
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Sx: Others: 1. Dyspnea 2. Tachycardia 3. Palpitation 6. Diaphoresis Dx: 1.History taking & PE 2. ECG ST segment depression 3. Stress test treadmill = abnormal ECG 4. Serum cholesterol & uric acid - increase. 5. Cardiac Catherization Nsg Mngt: To decrease Myocardial Demand
If chest pain does not radiate: Cause: Pulmonary
1. Administer prescribed medications Nitrates- to dilate the venous vessels decreasing venous return and to some extent dilate the coronary arteries NTG small doses Venodilator (sublingual) Large dose vasodilator 1st dose NTG give 3 5 min 2nd dose NTG 3 5 min Given 3x at 3-5 minutes interval 3rd & last dose 3 5 min Still painful after 3rd dose notify doc. MI! Exercise: 55 yrs old with chest pain: 1st question to ask pt: what did you do before you had chest pain. 2nd question: does pain radiate? If radiate heart in nature. If not radiate pulmonary origin Venodilator veins of lower ext increase venous pooling lead to decrease venous return. Nsg Mgt For NGT: 1. 2. Keep in a dry place. Avoid moisture & heat, may inactivate the drug. Monitor S/E: Vasodilation Orthostatic hypotension Transient headache Dizziness 3. 4. 5. Rise slowly from sitting position Assist in ambulation. If giving NTG via Patch:
a. Avoid placing it near hairy areas-will decrease drug absorption b. Avoid rotating transdermal patches- will decrease drug absorption c. Avoid placing near microwave oven or during defibrillation-will burn pt d/t aluminum foil in patch (color: blue & white) Aspirin- to prevent thrombus formation Beta-blockers- to reduce BP & HR (Propanolol) Calcium-channel blockers- to dilate coronary artery & reduce vasospasm ACE inhibitors Captopril Ca antagonist Nefedipine (anti-hypertensive) 2. Teach the patient management of anginal attacks Advise patient to stop all activities
Nursing Diagnoses For Angina Pectoris: Decreased cardiac output Altered comfort Impaired gas exchange Activity intolerance Anxiety
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3. Enforce CBR 4. Administer O2 inhalation 5. Semi-fowler 6. Diet- Decrease Na & saturated fats, low caffeine 7. Monitor VS, I&O, ECG 8. HT: Discharge Planning: a. b. Avoid precipitating factors 4 Es Prevent complications MI Instruct client to take meds before physical exertion-to achieve maximum therapeutic effect of drug Importance of follow-up care.
c.
d.
3. MYOCARDIAL INFARCTION (MI)
Anatomy: 1. 2. i. j.
A terminal stage of CAD characterized by necrosis & scarring leading to permanent mal-occlusion
Coronary Artery Right CA ---supply blood------ RA, RV, Posterior Wall Left CA Anterior Descending LCA --- supply--- RV, LV, Septum, Anterior Wall Circumflex LCA -------------- supply --- LA, LV, Lateral Wall
2 Blood vessels supplying ventricles------ventricles receive higher blood than atria LV needs more blood to pump to pulmonary circulation RV pump blood to systemic Ex. If occlusion is in Circumflex LCA-------affected LA, LV so basis of nursing DX----- systemic Circumflex---TYPES OF MI: 1. Clot RCA 2. Anterior Descending LCA 3. Circumflex LCA Zone RA, RV Posterior Wall RV, LV Septum LA LV lateral wall ECG Inferior Wall MI Posterior Wall MI Anterior Wall MI Antero-Septal MI Lateral Wall MI CO2
TYPES OF MI BY LAYERS: 1. Sub-endocardial MI 2. Myocardial Infarction 3. Trasmural MI Mal-occlusion of either R & L coronary artery, Ischemia of the inner part muscle layer affected: most common Most dangerous MI Mal-occlusion of both R&L coronary artery, Involves all layers
PATHOLOGY OF CHEST PAIN IN MI & Sx:

Myocardial Ischemia
reverse effect if occluded (KREBs CYCLE)
Anaerobic Metabolism Metabolite will release enzyme LACTIC ACID
causes Increased BP Vasodilation Alters conduction of electrical impulses Dysrrythmia Weakness: PR or PR
Irritate sensory nerve endings CHEST PAIN
Ensuing inflammatory process Causes release of increased neutrophils (1st cells to migrate when inflammation occurs) LEUKOCYTOSIS LOW GRADE FEVER (38 degree C) lasts for 3-5 days---best indicator for monitoring of MI progression or healing If responding to treatment & N.I. Neutrophils will be replaced by fibroblastic cells----result to scarring/fibrolysis---- the healing process---- Normal Temperature MYOCARDIAL INFARCTION Predisposing Factors Sex male Black raise Hyperlipidemia Smoking HPN DM Oral contraceptive Sedentary lifestyle Obesity Hypothyroidism 1. CHEST PAIN S sudden onset of pain A anterior/substernal/precordial area Excruciating, vice like, visceral pain Radiates back, arm, shoulders, axilla, jaw via afferent nerve cells pain w/ referred epigastric S/Sx Dx Exam 1. Cardiac Enzymes Go to blood following cardiac death a. CPK MB Creatinine Phosphokinase b. LDH lactic acid dehydrogenase c. SGPT (ALT) Serum Glutamic Pyruvate Transaminase d. SGOT (AST) Serum Glutamic Oxaloacetic 2. Troponin test increase 3. ECG Tracing ST segment elevation, Widening of QRS complexes means arrhythmia in MI indicating PVC 4. Serum Cholesterol & Uric acid 5. CBC increase WBC
V vague discomfort Feeling of tightness or heavy chest E exercise increases pain R rest does not relieved the pain or by NGT 2. Dyspnea 3. Erthermia 4. Initial increase in BP 5. Mild restlessness & apprehensions 6. Cool, moist, ashen skin 7. Occasional findings
Myocardial Infarction Nursing Diagnoses Pain (Altered comfort) Decreased cardiac output Impaired gas exchange Activity intolerance Altered tissue perfusion
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a. Split S1 & S2 b. Pericardial friction rub (inspiration) c. Rales /crackles d. S4 (atrial gallop)
*Most critical period after Dx of MI 6-8 hrs. d/t arrhythmia, a type of PVC premature ventricular contraction. COMPLICATIONS: (Refer to Pathophysiology of Atherosclerosis)
1. Cardiogenic Shock d/t poor contraction/akinesia .

2. 4. Renal Failure decreased CO2----decreased renal failure---renal ischemia----cessationRF Pulmonary Edema Right Ventricular Hypertrophy Left-sided HF Late Sx of Cardiogenic Right-sided HF Shock In MI Thrombophlebitis DVT Oliguria Arrhythmias PVC Dresslers Syndrome post MI syndrome - Non-resistant to Pharmacological agents -Administer 150,000 450,000 units of streptokinase
3. Ventricular Fibrillation--- heart beat very irregular, erratic & very rapid 180 bpm 5.
6. 7. 8.
9. 10.
Management of Myocardial Infarction: 1. Increase Myocardial O2 supply - Administer O2 inhalation (low-flow) - Also to prevent extension of necrosis - Monitor VS, I&O & ECG tracings 2. Relieve pt. of chest pain - Give drug of choice: Narcotic Analgesic Morphine SO4 ------ Action: Decreased preload & afterload through vasodilation Decrease level of anxiety Relieves severe intensity of pain Longer sustained effect If not available: Demerol but S/E: Hypotension
3. Relieve pt. of anginal pain - *Give NITRITES or NITRATES Action: Relax smooth muscles of the coronary artery/ also as vasodilators Ex. a. Isosorbade (Isordil) b. Isosorbide Mononitirite (Indur) c. NGT (Nitroglycerine) 5 mg SL Ex. Nitrostatic 10 mg - P.O. Patch, cream Topical Ex> Nitral Patch, Transderm Nsg. Mgnt For Nitroglycerine: 1. Explain that drug may cause S/E : Throbbing headache Flushing of skin Warm sensation & stringing, biting Burning sensation under tongue if taken SL 2. S/E : Postural hypotension d/t vasodilation Give drugs while on bed or in a sitting position 3. Keep drug in dark, opaque container because exposure to light/sun will reduce potency of nitrates 4. If topical administration: Cleanse area w/ H2O only, Avoid hairy areas, rotate administration Place on precardium: 5th ICS or site of pain 5. If SL : Advise pt. to place under tongue, allow to dissolve, swallow saliva NEVER follow it w/ H2O (interrupt sustained effect) 6. Keep away from your own skin, causes vasodilation & headache 4. R - rest - To decrease cardiac workload - To decrease work for breathing - To decrease myocardial O2 demand - To increase cardiac reserve - Enforce CBR without BRP - Provide Bedside commode - Abstain from sexual activity (4-6 wks. After MI attack) - Take nitrate prior to sex & if w/ insomnia, chest pain, SOB-----seek medical advice - Avoid valsalva maneuver - Semi fowler - Resume ADL activity - Post-cardiac rehab: 1.)Sex as an appetizer rather then dessert Before meals not after, after meals increase metabolism heart is pumping hard after meals. 2.) Assume a non-weight bearing position. *When to resume sex/ act: When pt can already use staircase, then he can resume sex. 5. D diet - To decreased caloric intake in order to decrease cardiac load - General liquid to soft diet - Low in Na 2-4 grams/day to get rid of ECF fluid excess - Avoid food high in saturated fat & avoid gas-forming foods - Avoid drugs w/ high Na like laxative - Avoid cardiac stimulant (caffeine, colas) - Increase fiber intake to avoid constipation - Avoid too hot drinks ------abdominal distention----- SOB - Avoid too cold drinks------ vagal stimulation-------- Decreased PR (Bradycardia) - Take 20 30 ml/week wine, brandy/whisky to induce vasodilation
*continue taking the drug s/s will disappear w/ the continued medication
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6. D- diuretic - To prevent reabsorption of H20 by the renal tubules-----absorption---Hypokalemia----Use K-sparing diuretics Ex. Aldactone Spironolactone Ex. Furosemide (lasix) Frusema Diuret Edecrine Mercuhydrin Sign that diuretic is effective? *Absence of rales indicates (+) effect of diuretics
7. D- digitalis - Drug categorized as CARDIAC GLYCOSIDES Ex. Digitoxin, Digoxin, Lanoxin, Gdiranid
3-FOLD ACTION OF DIGITALIS 1. Strengthen myocardial contraction-----------(+) Inotropic Effect Any drug that influences myocardial contraction has an inotropic effect 2. Increase cardiac output -------- Increase renal blood flow/renal perfusion Increase urinary output (secondary effect: Diuretic) 3. Decrease Cardiac Rate --------- (-) Chronotropic Effect Any drug that influences cardiac rate has a chronotropic effect (- or +) Nursing Management in Giving Digitalis:
1. Check CR, if below 60 do not give drug

2. 3. Monitor serum potassium d/t its secondary effect as a diuretic Check for DIGITALIS Toxicity: Anorexia-----------------most common complaint Headache w/ N/V------ Early Sx of toxicity Diarrhea Photophobia Dysrrythmia Yellow spots in eyes Gynecomastia ----- Late Sx of Toxicity Antidote: DIGIBIND or DIGOXIN IMMUNE Fab ---------bind w/ lanoxin to decrease toxicity of lanoxin
8. If patient undergoes CARDIOGENIC SHOCK: a. Prepare for vasopressor-----BP Ex. Dopamine Intropine Aramine --- Metaraminol Bitartrate Levophed Levartenenol Adrenalin /Epinephrine
b. Increase rate of impulse formation in SA node Ex. Lidocaine 1-2% Pronestyl --------Procainamide HCI Quinidine SO4 -- Quinidex Brethylium ------blocks release of norepenephrine
c. Dysrrythmia ----------- Give anti-arrhythmic drugs Ex. 1. Lydocaine blocks release of norepenephrine 2. Brithylium S/E: Confusion & Agitation If not corrected by medications: - Install artificial pacemaker or when SA node is damaged - Equipped with wire electrode & pulse generator PACEMAKER Type 1. Temporary 2. Permanent: Epicardial-------- thru Thoracotomy RV Endocardial-----Thoracotomy RV (5-6 yrs. ) Permanent SA so attach to chamber w/ thicker myocardium Nursing Management: 1. Temporary: Avoid toying w/ the pulse generator Wrapped w/ rubber gloves Avoid vigorous arm & shoulder movements Avoid lifting heavy objects Do not come closer to a microwave oven, cell site, electrical power Or any apparatus emitting power voltage Do not go through X-rays, scanner Teach pt. how to monitor PR for 1 whole minute S/S of malfunctioning pacemaker: HICCUP Bradycardia Palpitation Syncope Implanted in abdominal wall Implanted subcutaneously below the device (subclavicular) Insertion Antecubital basilic vein Wire/Electrode Tip rest on RA or RV Pulse Generator Outside
2. Permanent: Both:
9. Prevent other complications. Give medications a. Beta-blockers lol 1. Propanolol (inderal) b. ACE inhibitors - pril 1. Captopril (enalapril) c. Ca antagonist 1. Nifedipine d. Anti platelet PASA (aspirin) e. Thrombolitics or fibrinolytics to dissolve clots/ thrombus S/E allergic reactions/ uticaria Ex.
1. Streptokinase--------most common
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2. Urokinase ----------- S/E: Hypotension 3. Tissue Plasminogen Activating Factor (TPAF) ------- S/E: Chest Pain Monitor for bleeding: Anticoagulants 1. Heparin PTT If prolonged bleeding Antidote : Protamine Sulfate
2. Coumadin delayed reaction 2 3 days PT Prolonged bleeding Antidote Vit K
10. For patient w/ VENTRICULAR FIBRILLATION a. Administer: DEFIBRILLATION To terminate a life-threatening dysrrythmia thru unsynchoronous application (anytime) at any rate (200-360 joules) CARDIOVERSION - To correct dangerous dysrrythmia (sinus tachycardia) thru a synchronous application during R wave w/ 50-200 joules 11. Relieve patient of Sx of PULMONARY EDEMA: a. Rotating Tourniquet/ Dry, bloodless Phlebotomy - To reduce right atrial flow Nursing Management: Indicative of too tight Tourniquet: Absence of Peripheral
1. Only 3 extremities should be pressed at the same time 2. Tourniquet should not be applied too tight 3. Rotate tourniquet every 15 minutes 4. Rotate clockwise ---use BP cuff if not available (at Pulse pressure) 5. Remove at interval of 15 minutes 6. No single extremity should be compressed for more than 45 minutes Cause VENOUS STASIS ----- stagnation of blood in 3 extremities Decrease blood to enter RA---pulmonary system---- blood will edema
12. Treatment for patient with CORONARY ARTERY DISEASE: 1. Prepare for Revascularization Surgery to restore myocardial blood flow
a. PTCA Done to pt with single occluded vessel/simple vessel - Done under direct fluoroscopic guidance - Indicated for Angina less than 1 year & coronary artery not calcified Objective of PTCA:
PTCA P percutaneou s T transluminar

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1. To revascularize the myocardium 2. To prevent angina 3. Increase survival rate 4. To compress plaque against vessel wall increasing arterial lumen Procedure: Balloon-tipped catheter to/from femoral to CA to dilate CA or dislodge an atheroma/plaque b. CABG - For Multiple occluded vessels: - Done to improve blood flow to myocardial tissue - Uses saphinous vein/mammary artery - Done on an open heart technique & jump-graft from lower extremities Nsg Mgt Before CABG: 1. Deep breathing cough exercises 2. Use of incentive spirometer 3. Leg exercises 4. Cut at sigmoid process to umbilicus CABAG C coronary A arterial B bypass G graft surgery Feared Complications 2 Ps Pneumonia Pulmonary
- Once thoracic is opened, change in normal pressure (-) intrapleural pressure lungs will collapse Prepare for 1 way or 3 way Chest drainage
13.
CHEST DRAINAGE -Done to restore (-) intrapleural pressure of lungs to prevent collapse a. One-way H20 Sealed Chest Drainage System - Maintain an air-tight water-sealed system To patient Air vent, above H2O level (Emerson/Steidmanns Pump)
Glass rod 2-3 cm. Tip below H2O level

H2O 102
b. 3-Way Chest Drainage

To suction provides (-) pressure
To patient
H2O
H2O
H2O
Output Bottle Controlled Nursing Management For Chest Drainage:
H2O Sealed Bottle
Vacuum
1. The 3 bottles should be below chest level (18 inches) to prevent backflow 2. Bottles should be taped to the floor to prevent accidental leakage 3. Observe for OSCILLATION fluctuation, Tidalling---- rise & fall of H2O Important that there is constant communication bet. thoracic cavity & output bottle a. Observe for OSCILLATION - Favorable ---- indicates that the lungs has re-expanded Non-Favorable ---- Absence may mean: Turn client side to side, if still (-) (To dislodge adhesion to wall) Tell client to do deep breathing exercise, if still (-) Stripping/Milking of the tube----an occlusion/clot will come out b. Observe for BUBBLING - Normal in vacuum bottle connected to suction machine - If present in H2O sealed bottle----- indicates PLEURAL LEAKAGE/DAMAGE - Measure output correctly. Put tape on bottle - Change bottle when empty - Do not clamp when changing bottle---- Tension Pneumothorax - For accidental breakage: Immediately get a bottle w/ sterile H2O & immersed tube If none available----clamp - In any set-up: 1st bottle is always the output bottle - Observe aseptic technique - Removal: Do not remove test tube during inhalation. Inhale deeply then pull during expiratory phase to prevent entry of air & suction residual fluid Apply petrolatum gauze dressing (non-porous dressing0 After removal, continue observing for S/S of hypoxia 4. CONGESTIVE HEART FAILURE - Inability of the heart to pump blood towards systemic circulation d/t obstruction. - Backflow - A syndrome of congestion of both pulmonary & systemic circulation caused by inadequate cardiac function & inadequate cardiac output to meet the metabolic demands of tissues - Inability of the heart to pump sufficiently - The heart is unable to maintain adequate circulation to meet the metabolic needs of the body This can happen acutely or chronically Acute as in Myocardial infarction Chronic as in cardiomyopathies
Classified according to the major ventricular dysfunction1.Left Ventricular failure 2. Right ventricular failure Etiology of CHF 1. CAD 2. Valvular heart diseases 3. Hypertension 4. MI 5. Cardiomyopathy 6. Lung diseases 7. Post-partum 8. Pericarditis & cardiac tamponade Systemic Circulation *Inferior Vena Cava & UnO2 Right Atrium Tricuspid Valve RSHF Blood goes back to TV-circulation Right Ventricles Pulmonary Artery Lungs (For Oxygenation) Superior Vena cava Aorta Left Ventricles Mitral Valve Left Atrium Pulmonary Veins LSHF blood goes back to PV
A. RIGHT-SIDED HF -#1 Cause: Tricuspid Valve Stenosis S/S: Jugular Vein Distention Pitting Edema---IVC from toes Ascites Weight Gain Hepatospleenomegaly Jaundice Pruritus---Urticaria Esophageal Varices Anorexia
B. LEFT-SIDED HF -#1 Cause: Mitral Valve Stenosis S/S: Pulmonary Edema/ congestion Dyspnea Paroxysmal Nocturnal Dyspnea 2 pillows/High-fowlers Orthopnea Productive Cough (blood-tinged sputum) Frothy Salivation Rales/Crackles Bronchial Wheezing Pulsus Alterans (weak-strong pulse) Anorexia & generalized body malaise S3 (Ventricular Gallop) Cyanosis PMI is displaced laterally : 4th -5th ICSMCL -----if below 5th ---cardiomegaly
1. LEFT-SIDED HEART FAILURE: Predisposing Factors: 1. 90% Mitral Valve Stenosis d/t RHD, Aging RHD affects mitral valve streptococcal infection Dx: 1. ASO Titer (Anti-Streptolysine O) > 300 total units - Steroids - Penicillin - Aspirin Complication:
RS-CHF Aging degeneration / calcification of mitral valve Ischemic heart disease HPN, MI, Aortic stenosis Dx:
1. CXR Reveals Cardiomegaly

2. 3. PAP Pulmonary Arterial Pressure PCWP Pulmonary Capillary Wedge Pressure PAP PCWP Measures pressure of R ventricle. Indicates cardiac status. Measures end systolic/ diastolic pressure
PAP & PCWP: Swan Ganz Catheterization cardiac catheterization is done at bedside at ICU (Tracheostomy bedside) - Done 5 20 mins scalpel & tracheostomy set CVP Indicates fluid or hydration status Increase CVP decrease flow rate of IV Decrease CVP increase flow rate of IV 4. 5. Tx: M A D D O G - Morphine SO4 (to induce vasodilation) - Aminophylline - Digoxin - Diuretics - O2 - Monitor Blood Gases ----------- PO2 Respiratory Acidosis Hypoxemia Cyanosis Echocardiography Reveals enlarged heart chamber or cardiomayopathy ABG PCO2 increase, PO2 decrease = = hypoxemia = respiratory acidosis
2. RIGHT-SIDED HEART FAILURE Predisposing Factor:
1. 90% - Tricuspid Stenosis

2. 3. 4. 5. S/Sx: Venous Congestion - Neck or jugular vein distension
COPD Pulmonary embolism Pulmonic stenosis Left sided heart failure
Pitting edema Ascites Wt gain Hepatomegaly/ Splenomegaly Jaundice Pruritus Esophageal Varices----- Dilation of the veins of the esophagus Anorexia, General body malaise, Nausea Pulsus alternans Nocturia = urination at night at frequent intervals as the blood moves from interstitial space to the intravascular space & is excreted
Dx:
CXR Reveals Cardiomegaly CVP Measures the pressure at R atrium Normal: 4 to 10 cm of water Increase CVP > 10 hypervolemia Decrease CVP < 4 hypovolemia Flat on bed post of pt when giving CVP Position during CVP insertion Trendelenburg to prevent pulmonary embolism & promote ventricular filling.
3. Echocardiography enlarged heart chamber / cardiomyopathy 4.Liver enzyme SGPT ( ALT) SGOT AST Nsg mgt: Increase force of myocardial contraction = increase CO 3 6L of CO 1. Administer meds: M morphine SO4 to induce vasodilatation A aminophylline & decrease anxiety D digitalis (digoxin) D - diuretics O - oxygen G - gases a.) Cardiac Glycosides Increase myocardial = increase CO Digoxin (Lanoxin) Antidote: digivine Digitoxin: metabolizes in liver not in kidneys not given if with kidney failure. b.) Loop diuretics: Lasix effect with in 10-15 min. Max = 6 hrs c.) Bronchodilators: Aminophylline (Theophyllin). Avoid giving caffeine d.) Narcotic analgesic: Morphine SO4 - induce vasodilator & decrease anxiety e.) Vasodilators NTG f.) Anti-arrhythmic Lidocaine 2. Administer O2 inhalation high! @ 3 -4L/min via nasal cannula 3. High Fowlers (2-3 pillows) 4. Restrict Na 5. Provide meticulous skin care 6. Weigh pt daily. Assess for pitting edema. Measure abdominal girth daily & notify MD 7. Monitor V/S, I&O, breath sounds 8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous return 9. Diet decrease salt, fats & caffeine 10. HT: a) Prevent Complications : Shock
Arrhythmia Thrombophlebitis MI Cor Pulmonale RT ventricular hypertrophy b.) Dietary modifications c.) Adherence to meds
CLASSIFICATION BASED ON New York Heart Association Class 1 Ordinary physical activity does NOT cause chest pain & fatigue No pulmonary congestion Asymptomatic NO limitation of ADLs Class 2 SLIGHT limitation of ADLs NO symptom at rest Symptoms with INCREASED activity Basilar crackles and S3 Class 3 Markedly limitation on ADLs Comfortable at rest BUT symptoms present in LESS than ordinary activity Class 4 SYMPTOMS are present at rest
OTHER PROBLEMS ASSOCIATED WITH THE CARDIOVASCULAR SYSTEM 1. CARDIAC TAMPONADE - A condition where the heart is unable to pump blood d/T accumulation of fluid in the pericardial sac (pericardial effusion) - This condition restricts ventricular filling resulting to decreased cardiac output - Acute tamponade happens when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac Causative Factors: 1. Cardiac trauma 2. Complication of Myocardial infarction 3. Pericarditis 4. Cancer metastasis ASSESSMENT FINDINGS 1. BECKs Triad- Jugular vein distention, hypotension & distant/muffled heart sound
2. Pulsus paradoxus 3. Increased CVP 4. Decreased cardiac output 5. Syncope 6. Anxiety 7. Dyspnea 8. Percussion- Flatness across the anterior chest
Laboratory FINDINGS 1. Echocardiogram= shows accumulate fluid in the pericardial sac 2. Chest X-ray NURSING INTERVENTIONS 1. Assist in PERICARDIOCENTESIS 2. Administer IVF 3. Monitor ECG, urine output & BP 4. Monitor for recurrence of tamponade Pericardiocentesis Patient is monitored by ECG Maintain emergency equipments Elevate head of bed 45-60 degrees Monitor for complications- coronary artery rupture, dysrhythmias, pleural laceration & myocardial trauma
2. CARDIOGENIC SHOCK - Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion - This shock occurs when the hearts ability to contract & to pump blood is impaired & the supply of oxygen is inadequate for the heart & tissues Risk factors: Coronary factor- Myocardial infarction Risks factors: NON coronary: Cardiomyopathies Valvular damage Cardiac tamponade Dysrhythmias Severe CHF
Pathophysiology: Precipitating factors will cause decreased cardiac contractility Decreased stroke volume & cardiac output leading to 3 things: Damming up of blood in the pulmonary vein will cause pulmonary congestion Decreased blood pressure will cause decreased systemic perfusion
Decreased pressure causes decreased perfusion of the coronary arteries leading to weaker contractility of the heart ASSESSMENT FINDINGS 1. HYPOTENSION 2. Oliguria (less than 30 ml/hour) 3. Tachycardia 4. Narrow pulse pressure 5. Weak peripheral pulses 6. Cold clammy skin 7. Changes in sensorium/LOC 8. Pulmonary congestion LABORATORY FINDINGS 1. Increased CVP due to pooling of blood in the venous system Normal is 4-10 cmH2O 2. Metabolic acidosis
NURSING INTERVENTIONS 1. Place patient in a modified Trendelenburg (shock ) position 2. Administer IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE These drugs will increase cardiac contractility 3. Administer O2 4. Morphine is administered to decreased pulmonary congestion & to relieve pain, relieve anxiety 5. Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz catherization & IABP 6. Monitor urinary output, BP & pulses 7. Cautiously administer diuretics & nitrates
DIAGNOSTIC PROCEDURES FOR CARDIOVASCULAR DISORDERS 1. ECG/EKG -Done To measure the electrical impulses of the heart to Dx heart rate & rhythm Pathology: SA node------starts myocardial contractions Initiates electrical (+) impulses (emikts 60-100 bpm) Goes into Intra-atrial Track-------- A-V Node (located at right side of intra-atrial septum) Bundle of His (L & R) Purkinje Fibers Ventricular Contraction

If below 60---- Sinus Bradycardia If above 100--- Sinus Tachycardia If 60-100 ------ Normal Sinus Rhythm
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DEPOLARIZATION is the myocardial contraction REPOLARIZATION Refractory Period/relaxation regaining its (-) charge Normal Refractory Period 0.15-0.30 seconds
SA NODE ----- located at posterior wall of RA close to the entrance to Vena Cava During depolarization ---- permeable to entry of Na & Cal----- influencing myocardial contraction During repolarization----- permeable to entry of K & Cl P Wave Atrial depolarization or contraction PR interval travel time of impulse from atria to ventricle ( Normal: 0.12-0.20 seconds) Any delay in flow of impulse ------heart block
QRS Complex Ventricular Repolarization (From ventricular contraction A---V to time it will be (+) charged After a brief period of resting----- (-) charge refractory period ST Segment - completion of depolarization & beginning if repolarization T Wave ventricular repolarization QT Interval entire duration of depolarization & repolarization ( lasts for 0.42-0.43 seconds) (From QRS to T)
5 IMPORTANT ECG TRACINGS 1. MYOCARDIAL INFARCTION - Inverted T wave - Elevated ST -Pathological prominent T wave 2. HYPERKALEMIA - Peaked T wave - Prolonged PR Interval - Widened QRS complex 3. HYPOKALEMIA - Flat T wave - Depressed ST - Prominent U wave ----- Pathological--- influences myocardial repolarization Decreased K ---- weakened contraction or repolarization Prolonged T wave Forming an abnormal U wave
area of ischemia ---- reversible with time area of infarction ----- irreversible, will always appear for life
4. HYPERCALCEMIA - Shortened QT interval 5. HYPOCALCEMIA - Prologed QT interval 2. 24 HOUR HOLTER MONITORING/DYNAMIC ECG - Done to monitor 24 hrs. cardiac activity - Given pen & paper to record 24 hrs. - Non-invasive 3. STRESS TEST/ THREADMILL TEST/BICYCLE/ERGOMETRIC TEST - Done to evaluate amount of activities that the heart can tolerate Nsg Responsibility: - Avoid smoking the night before the threadmill - Wear comfortable light material - Wear rubber-soled shoes - Avoid heavy meal prior to test - Allowed light snack 2 hrs. before test - Avoid hot shower 2 hrs. after test to prevent syncope - Rest after the exercise 4. PHONO-ECHOCARDIOGRAPHY - Non-invasive - Use to detect any abnormal anatomical structure & abnormal heart sounds 5. ECHOCARDIOGRAPHY - Use to evaluate changes in the cardiac dimension during the cardiac cycle 6. ELECTROLYTE STUDIES - No NPO - Na & Ca ------- Depolarization - K & Cl ------- Repolarization 7. BLOOD TEST - Use to evaluate atheromatous changes Serum Cholesterol ------ NPO 6-8 hrs. Serum Triglyceride ----- NPO 12 hrs Serum Lipids -------- NPO 12 hrs. Nsg. Responsibility: - No lipid forming drugs Ex. Salicylates Estrogen Steroids No alcohol----- influence 8. ENZYMATIC TEST - No NPO------ it is normally released by the myocardium---- if elevated enzymes----problem to the myocardium
a. SGOT
(Serum Glutamic Oxaloacitic Aminotransferase) or AST (Serum Aspartate Aminotransferase)
SGOT/AST : 5-40 u/L
b. SGPT (Serum Glutamic Pyruvic Transaminase) or ALT ( Serum Alanine Amintransfirase)
SGPT/ALT : 4-36 u/L
c. CPK mb ( Creatinine Phosphokinase ) 3 Isoenzymes MB Increases myocardial insult/damage BB Increased brain, bladder, bowel MM Increased skeletal muscle
d. SLDH (Serum Lactic Dehydrogenase)
1&2 Myocardial insult *BEST CONFIRM MI -------- SGOT
3 lung parenchymal damage
4&5 liver damage
* BEST DIAGNOSED MI -------- CPKmb *Nsg Intervention prior to blood extraction ----- No IM injection------- Increased CPK when skeletal muscle injury CARDIOVASCULAR ASSESSMENT Assessment: I. During Interview: 1. (+) Family History 2. Smoking Pathology: a.) Nicotine -----stimulates release of Catecholamines--------------------------Epinephrine Platelet Aggregation Risk for thrombus formation Increased cardiac workload b.) Carbon Monoxide ------ + Hgb (blood) ------interfere w/ O2 transport (carboxyhgb) Tissue hypoxia/hypoxemia 3. Stress 4. DM------can lead to MI 5. Atherosclerosis
Increased Myocardial O2 demand Increased cardiac workload
Vasoconstrictor HPN
6. HPN 7. Age ------- above 40 y/o 8. Sex ------- M: high risk F: high risk after menopause 9. Personality ---- high among Type A individual 10. Assess for history of easy fatigability----- 1st sign of poor cardiac reserve Ability of the heart to adjust to cardiac demand 11. History of Palpitations 2 Types: a. Physiologic ------ diet (coffee), strenuous activity, strong emotion, after eating b. Pathologic ------- clients w/ hyperthyroidism clients w/ cardiomegaly ( enlarged heart) contractions----hit cardiac wall----- palpitations Palpitations---pounding, jumping sensations for every myocardial contractions 12. Listen for normal & abnormal sounds S1 lubb ----systole S2 dub ----- diastole Abnormal: Best heard at PMI ( Point of Maximum Impulse) on the 4th-5th ICSMCLL
S3 sound -----heard on early part of diastole------ Sign of Ventricular Dysfunction Sign of Left Ventricular Hypertension S4 sound ----- heard on late part of diastole------- Seen in MI, HPN, Pulmonic Stenosis *S3 sound-----normal to children
Assess for audible sound: Murmur ------ audible vibration Thrill --------- palpable vibration Heave --------- visible vibration
Stenotic Valvular Opening/narrowing Increased velocity of bloodflow Abnormal vibrations
13. Lifestyle----- Diet ----- High in calories, saturated fats, Na & heart stimulant like caffeine, alcohol ---- ExerciseSedentary lifestyle----venous stasis---- Risk for thrombus formation 14. Assess for history of chest pain 15. Assess for Dyspnea & its cause --- Positioning: Orthopnea Time : Night (Paroxysmal Nocturnal Dyspnea) 16. Check for history of CYANOSIS 2 Types: a. Central Cyanosis----- circum-oral (lips, oral mucus membrane) Sign of decreased arterial O2 saturation b. Peripheral Cyanosis---- cyanosis of nail beds, earlobes Sign of decreased cardiac output 17. Assess for pitting edema: (Normal: 95-100%)
a. Elevate 1st the legs w/ edema, if still (+)

b. 18. Assess for HPN:
Press skin, if indentation is present = (+) Pitting Edema
Systole---- Atrio-ventricular contraction & closure of the A-V valves-----TV & BV Strength of Myocardial contractions Diastole Atrio-ventricular relaxation & closure of Semi-lunar valves---- PV & AV More dangerous because it is systematic TYPES OF HPN: 1. Systolic HPN & Diastolic HPN 2. Primary/Essential/Idiopathic - Unknown cause 2 Theory: a. R-A-A Pathology: Juxtaglomerular Cells (kidney) Renin releases Angiotensin I (activated by enzymes that converts it to) Angiotensin II ------- stimulates adrenal cortex to release aldosterone Potent vasoconstrictor HPN Fx: Fluid & Na retention & K excretion Increased IV volume Hypovolemic Shock 3. Secondary HPN - Due to pregnancy related to toxemia - Children w/ coarctation of the aorta - Pheochromocytoma ( 5 H) 4. Accelerated HPN ----- persistent high BP with signs of retinal hemorrhages + epistaxis 5. Malignant HPN ----- persistent high BP with signs of papilledema (Increased ICP) Degree of systolic arterial resistance
FLUIDS & ELECTROLYTES

1. WATER Adult: Child: 50-60% TBS 70-80% TBS
*Volume of Distribution Depends On: 1. Age - H2O decreases with age 2. Sex Male with more muscles so increase H2O 3. Adipose Tissues More Obese so more H2O *Fluid Intake: Fluid: Food 2 2.5 L/day 24 hrs. 1 -1.5 L/24 hrs. 1 L/24 hrs.
By-product of oxidation-nitrogen process = 100 ml/24 hrs.

*Avenues Of Losses/Routes: 1. Kidney 2. Skin 3. Lungs 4. GIT CELLS Intracellular Extravascular ICF ECF = 2/3 of BF 70 % = 1/3 of BF 30 % = 1-1.5 L/24 hrs = 600-700 ml/24 hrs = 400-500 ml/24 hrs = 100 ml/24 hrs BLOOD Intravascular (blood, lymph vessels) Intercellular ( interstitial space)
2. ELECTROLYTES
1. CATION (+) =
Sodium Potassium Calcium Magnesium Chloride Phosphorus Sulfate Bicarbonate K & PO4 Na & Cl
Na K Cal Mg Cl PO4 SO4 HCO3
Homeostasis--- continuous shifting of fluids in Intravascular compartment
2. ANION (-)
3.
ICF ECF
= =
FLUID SHIFTING 1. IV-ITS-IV (Normally exercised by circulatory blood)
Arteriolar End
COP = 22 mmHg
Venular End
HP = 40 mmHg Start: Fluid pushed into ITS
HP = 12 mmHg COP> HP Fluid drawn back into capillaries ITS
HP greater than COP so that fluid movement occurs 2 Governing forces for IV-ITS Shifting
1. COLLOID OSMOTIC PRESSURE - Pressure exerted by plasma protein/albumin on semi-permeable membrane 2. HYDROSTATIC PRESSURE - Pressure exerted by fluid against wall of BV
Example: 1. MALNUTRITION (Protein)
Less COP----venous HPN congestion-----fluids remains in ITS---Edema, Anasarca, Ascites 2. ABNORMAL If HP less than COP---fluid stays in the VC------ Circulatory Overload------ Hypovolemia 3. BLOOD TRANSFUSION BT/Protein/Albumin----- High COP----fluid stays in capillary---- Circulatory Overload 4. FLUID SHIFTING IC ----TO----- EC *Movement of fluids governed by Osmosis & Diffusion Solvent (H2O) Solute (Electrolyte)
* High H2O EC------ Low Na concentration-------- H2O will enter the cell If continues Cell will Swell/Burst H2O Intoxication/ Hypo-Osmolar Imbalance * Less H20 E ----- High Na-----leave the cell-----cell shrink-----Dehydration
3. BURNS Direct tissue injury caused by thermal, electric, chemical & smoke inhalation (TECS) Nursing Priority infection (all kinds of burns) Head burn-priority- a/w 2nd priority for 1st & 2nd - pain 2nd priority for 3rd - F&E CLASSIFICATION: 1. CAUSE a. Thermal b. Electric c. Chemical 4. Smoke - direct contact flames, hot grease, sunburn. -- wrapped wires direct contact corrosive materials acids-------flush with saline solution gas / fume inhalation
2. DEPTH OF TISSUE DAMAGE & AREA I. Partial Thickness Burn

1. 1st degree Superficial Partial Thickness Burns - Affects epidermis - Cause: Thermal burn/sun burn - Painful -No edema - Redness (erythema) & (+) blanching upon pressure with no fluid filled vesicles - Healing Duration : 1-2 wks. w/ any residual evidence of tissue damage 2. 2nd degree Deep Partial Thickness Burns - Affects epidermis & dermis - Cause chem. Burns - With edema - (+) Very painful - (+) Erythema & fluid filled vesicles (blisters) - Mottled (bluish & reddish) - Healing duration: 2-3 wks. w/ signs of minimal scarring II . Full Thickness Burns 1. Third & 4th Degrees Burn - Affects all layers of skin, muscles, bones - Cause electrical - Without pain or less painful - Blanched, pale, charred - Dry, thick, leathery wound surface known as ESCHAR devitalized or necrotic tissue. - Healing duration: No exact time-frame. Depends on the actual depth of tissue damage, infection
3. ACCORDING TO EXTENT OF BODY SURFACE BURNED Rule of 9 Head & Neck & Face Upper Anterior Trunk/Chest Upper Posterior Trunk/Chest @ Arm 9+9 Lower Anterior Extremity (leg) Upper Posterior Extremity (leg) Genitalia/ perineum Total = 9% = 18% = 18% = 18% = 18% = 18 % = 1% 100%
4. CLASSIFICATION AS MINOR & MAJOR 1. Minor : 2nd Degree : 2nd Degree: 3rd Degree: 2. Major: 2nd Degree: 2nd Degree: 3rd Degree:
10-20% BSA (C) 15-25 % BSA (A) 2-10 % BSA 10-20 % (C) 15-25 % (A) 2-10 %
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3. Critical: 2nd Degree: 2nd Degree: 3rd Degree
> 21 % ( C) > 25 % (A) > 10 %
STAGES:
1. Emergent Phase Removal of pt from cause of burn. Determine source or loc or burn 2. Shock Phase
S/Sx: 24 - 48. Characterized by shifting of fluids from intravascular to interstitial space = Hypovolemia
BP Decrease Urine output HR Increase Hct Elevated Serum Na Decrease Serum K Increase Metabolic Acidosis
Priority To All Types of Burn: INFECTION
3. Diuretic/ Fluid Remobilization Phase - 3 to 5 days. Return of fluid from interstitial to intravascular space 4. Recovery/ Convalescent Phase complete diuresis. Wound healing starts immediately after burn injury.
Pathophysiology Of THERMAL BURN: (2ND Stage in the 1st 24-48 hrs.) Intense heat ------------- activates a sympatho-adrenal medullary response Tissue Trauma Release of Histamine Vasodilation Increased Capillary Permeability Fluid shifts from IV to ITS (seepage of plasma fluid to ITS)
1
Edema formation HYPOVOLEMIA 3
Hyponatremia
Decreased Cardiac Output

Sluggish BF
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Thrombus Formation Hypovolemic Shock Renal Perfusion Tissue Ischemia Evaluate: 1. Decreased BP Creatinine Hematuria Hyperkalemia2. Increase Hct (Evaluate vol. % of RBC in plasma Ventricular Fibrillation hemoconcentration) 3. Decreased CVP Sudden Cardiac Arrest
Hourly Urine Output
BUN
Tissue Starvation (-) Nitrogen balance Weight loss Legend: 1 - Stage of Neurogenic Shock 2 Stage of Hypovolemic Shock/ Oligenic Shock 3 Stage of Diuresis 4 Stage of Repair COMPLICATIONS OF BURNS: 1. SODIUM (Na) (Normal: 135-145 mEq/L) a. Decrease Na system of burn victim d/t Hyponatremia Weakness
Anaerobic Metabolism Lactic Acid Production METABOLIC ACIDOSIS (Common problem)
Edema----- trapping of Na----------------- Na activated in 3 Ways/Causes Hyponatremia S/Sx: - Decreased BP - Increased rapid, weak pulse - Diaphoresis - Poor memory - Hypoactive - (-) reflexes - Oliguria-Anuria S/Sx: - Thirst - Flushed Skin - Increase temperature - Dry tongue - Dry & sticky mucus membrane - Hyperactive reflexes c. Hypovolemia - Assess for BP, Hct, CVP d. CVP - Pressure exerted by blood appropriately at the right atrium of the heart - Done to evaluate cardiac efficiency - Done to evaluate state of hydration - CVP: decrease in burn victims -If CVP, prepare for Cut-down or Venesection------prior insert 3-way polyethylene tubing e. Hypovolemic Shock (Oligenic)
1. R-AAldosterone --- Na reabsorption & K excretion 2. Prostaglandin-Renin 3. Kallikreen---Kinin--- Increase urination, Na excretion Distal tubules of the kidneys
b. Hypernatremia
Normal CVP 6-12 mmHg
Normal Hourly Urine Output: 30 60 ml/hour
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- Evaluate BP, Hct, CVP - LOC decreased - PR increased - RR increased but shallow - Skin cold & clammy (Hypo, Tachy, Tachy) BUN Creatinine ------ 10-20 mg% w/ NPO ------ 0.9 -1.5 mg % w/o NPO--- Reliable indicator of renal function Not influenced by protein content & diet Product of muscle metabolism
2. POTASSIUM (K) b. c.
(Normal: 3-5 5.5 mEq/L)
causes R-A-A Insulin/Glucose/ Glucagon ----- Increase Uptake of K----- cell
Ex. In DM pt.--- insulin decrease or none--- potassium will leave the cell (EC to IV)--- K in blood (Hyperkalemia) a. Increased K in Burns S/Sx: - Decreased PR - Abdominal cramps - Diarrhea - Muscular weakness - ECG changes b. Decreased K in Diarrhea S/Sx: - Increased PR followed by decreased PR - Weakness - Weak respiratory muscle - Shallow respiration------- Paralytic Ileus Hypo-active bowel sound (K influences intestinal tone) 3. Evaluate METABOLIC ACIDOSIS: ABG Interpretation S/Sx: Acidosis = CNS depression + Increased K Alkalosis = CNS excitability + Decreased K MANAGEMENT OF BURN VICTIMS: 1. Extinguish the flame - Roll over the pt. - If burn w/in the eyes, irrigate the eyes. - Remove clothing that can impede circulation - Get piece of cloth & place on wound 2. Hospital: - Establish patent airway - Make initial assessment including body weight---needed for fluid replacement - If (+) for hypokalemia: hook patient to a cardiac monitor - Get an open IV line for cardiac replacement - If veins are collapsed, do a cut-down or venisection - Prepare for insertion of indwelling catheter to monitor urine output - Prepare for NGT ----- to evacuate/decompress gastric content to prevent aspiration 3. Administer isotonic fluid solution 4. Strict aseptic technique 5. Diet increase CHO, increase CHON, increase Vit C, and increase K- orange 6. If (+) to burns on head, neck, face - Assist in intubation
Abdominal distention
7. Assist in surgical wound debridement. Administer analgesic 15 30 minutes before debridement 8. Prevent Complications: 1. Infection ------ Increase anerobic circulation, risk for anaerobic infection a. Prepare Tetanus Toxoid Injection------ .5 ml IM - Prevent Tetanus: Burn surface area is source of anaerobic growth Clostridium tetany Tetanus Tetanolysin Hemolysis Tetanospasmin Muscle Spasm b. Morphine SO4 2. Hypovolemic Shock - Replace fluid losses. Use solution a. EVANS FORMULA Colloid Non-Electrolyte Electrolyte 1 ml x kgBW x % BSA Ex. Isotonic solution---- NSS, LRS - 2,000 ml of glucose in H2O - 1 ml x Kg BW x % BSA
b. BROOKES FORMULA Colloid Electrolyte - 0.5 ml x Kg BW x % BSA - 1.5 ml x kg BW x % BSA
c. PARKLAND/BAXTER FORMULA 4 ml LRS x KgBW x % BSA
Ex.
Colloid Plasma Expanders ------ will increase IV volume Dextran Polyrpan Electrolyte - Isotonic solution--- NSS, LRS------ will increase IV volume
Non- Electrolyte - Glucose in H2O - D5 in H2O INDICATIONS FOR FLUID RESUSCITATION/REPLACEMENT 1. Child below 2 y/o ----- resuscitate ---- Increase 10 % BSA 2. Adult 60 y/o ------ resuscitate ------- Increase 10 % BSA Ex. Face & Neck = 45 Abdomen =9 Posterior forearm = 2.25 Whole RLE = 18 Buttocks =6 Perineum =1 Total 40.75 = 41%
33 y/o with BW 60 Using Evans Formula: Colloid = 1 x 60 x 41 = 2,460 ml/24 hrs. Electrolyte = 1 x 60 x 41 = 2,460 ml/24 hrs. Non-electrolyte = 2,000 ml/24 hrs. *Replace losses 1 hr. after incident to prevent hypovolemic shock Time 12-8pm 8-4 pm 4-12 % 1st 8 hrs. 50% 2nd 8 hrs. 25 % 3rd 8 hrs. 25 % Colloid 1,230 ml 615 615 Electrolyte 1,230 ml 615 615 Non-Electrolyte 1,000 ml 500 500
*If only 1 IV line (cut-down) ---- transfuse LRS, NSS---- piggyback glucose H2O *Maximum volume in 24 hrs. is only 10 liters (divided) * Should replaced only 50 % of body losses * No plasma in cut-down * WBC---- FWB given only to burn pt. 1 unit = 500 ml to run for 4 hrs. to prevent hemolysis 3. Paralytic ileus d/t hypovolemia & hypokalemia 4. Curlings ulcer H2 receptor antagonist 5. Septicemia blood poisoning 6. Surgery: Skin grafting 9. Management to promote wound healing: a. Diet : Increase CHON replacements & K-orange for repair of tissue damage &o promote wound healing Vitamin C ----- for formation of collagen fibers Granulation of tissue Scarring/ fibrosis Healing Process b. Cleanse wound/ dress - Use aseptic technique, use betadine or NSS c. Apply ointment as anti-microbic agent Topical antibiotic : 1. Silver Sulfadiazine (silvadene) ----- anti-microbic---promote re-epithelization of wound tissue 2. Sulfamylon 3. Silver nitrate 4. Povidone iodine (betadine) d. Systemic Antibiotic Ex. 1. Ampicillin 2. Cephalosporin 3. Tetracycline e. Dressing 1. Open/Exposure Method 2. Closed/Occlusive *Reverse isolation if open wound/method (bed cradle) f. Do hydrotherapy/Tubbing ------ to loosen the eschar
- In Hubbard Tank Done only when VS are stable & level of electrolyte is normal 2 to 3x/day for 15-20 minutes Prior to tubbing, check temperature of solution Give analgesic 30 minutes before tubbing Take VS prior to tubbing While pt. in tub, encourage ROM exercises to prevent contracture deformity If wound is severely infected, mix betadine solution
4. RELATED TO F & E BALANCE 1. BLOOD GASES
R O M E
pH pH ph ph ph
HCO3 PCO2 PCO2 HCO3 HCO3
Respiratory Alkalosis Respiratory Acidosis Metabolic Alkalosis Metabolic Acidosis
RESPIRATORY ALKALOSIS
RESPIRATORY ACIDOSIS Chronic Bronchitis
METABOLIC ALKALOSIS Vomiting Pyloric Stenosis Cushing
METABOLIC ACIDOSIS Ileostomy Intestinal Tubing DM Diarrhea
VASCULAR DISEASES
I. HYPERTENSION CLASSIFICATION OF HYPERTENSION by JNC-VII Pathophysiology: Multi-factorial etiology BP= CO (SV X HR) x TPR Any increase in the above parameters will increase BP 1. Increased sympathetic activity 2. Increased absorption of Sodium & water in the kidney Risk factors for Cardiovascular Problems in 3. Increased activity of the RAAS Hypertensive patients 4. Increased vasoconstriction of the peripheral vessels 5. Insulin resistance Major Risk factors ASSESSMENT FINDINGS
1. Smoking 2. Hyperlipidemia 3. DM 4. Age older than 60 5. Gender- Male & post menopausal Women 6. Family History
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1. Headache 2. Visual changes 3. chest pain 4. dizziness 5. N/V DIAGNOSTIC STUDIES 1. Health history & PE 2. Routine laboratory - Urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS 3. Other lab- CXR, creatinine clearance, 24-huour urine protein MEDICAL MANAGEMENT 1. Lifestyle modification 2. Drug therapy 3. Diet therapy 4. Drug therapy Drug Therapy For HPN: Diuretics Beta blockers Calcium channel blockers ACE inhibitors
NURSING INTERVENTIONS 1. Provide health teaching to patient
Teach about the disease process Elaborate on lifestyle changes Assist in meal planning to lose weight Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day Limit alcohol intake to 30 ml/day Regular aerobic exercise Advise to completely Stop smoking 2. Provide information about anti-hypertensive drugs Instruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition Instruct to avoid over-the-counter drugs that may interfere with the current medication 3. Promote Home care management Instruct regular monitoring of BP Involve family members in care Instruct regular follow-up 4. Manage hypertensive emergency & urgency properly II. ANEURYSM - Dilation involving an artery formed at a weak point in the vessel wall Types: 1. Saccular= when one side of the vessel is affected 2. Fusiform= when the entire segment becomes dilated
RISK FACTORS 1. Atherosclerosis 2. Infection= syphilis 3. Connective tissue disorder 4. Genetic disorder= Marfans Syndrome PATHOPHYSIOLOGY
Damage to the intima and media weakness outpouching Dissecting aneurysm tear in the intima and media with dissection of blood through the layers ASSESSMENT 1. Asymptomatic 2. Pulsatile sensation on the abdomen 3. Palpable bruit LABORATORY: 1. CT scan 2. Ultrasound 3. X-ray 4. Aortography Medical Management: 1. Anti-hypertensives 2. Synthetic graft Nursing Management: 1. Administer medications 2. Emphasize the need to avoid increased abdominal pressure 3. No deep abdominal palpation 4. Remind patient the need for serial ultrasound to detect diameter changes
III. PERIPHERAL VALVULAR DISEASES A. PERIPHERAL ARTERIAL OCCLUSIVE DISEASE (PAOD) - Refers to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis. - Found in males age 50 & above - The legs are most often affected Risk factors for Peripheral Arterial occlusive disease Non-Modifiable 1. Age 2. gender 3. family predisposition Risk factors for Peripheral Arterial occlusive disease Modifiable 1. Smoking
2. HPN 3. Obesity 4. Sedentary lifestyle 5. DM 6. Stress ASSESSMENT FINDINGS: 1. INTERMITTENT CLAUDICATION- the hallmark of PAOD This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same degree of exercise or activity This pain is RELIEVED by REST This commonly affects the muscle group below the arterial occlusion 2. Progressive pain on the extremity as the disease advances 3. Sensation of cold and numbness of the extremities 4. Skin is pale when elevated and cyanotic/ruddy when placed on a dependent position 5. Muscle atrophy, leg ulceration and gangrene Diagnostic Findings 1. Unequal pulses between the extremities 2. Duplex ultrasonography 3. Doppler flow studies Medical Management 1. Drug therapy Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation 2. Surgery- Bypass graft and anastomoses Nursing Interventions 1. Maintain Circulation to the extremity Evaluate regularly peripheral pulses, temperature, sensation, motor function and capillary refill time Administer post-operative care to patient who underwent surgery 2. Monitor and manage complications Note for bleeding, hematoma, decreased urine output Elevate the legs to diminish edema Encourage exercise of the extremity while on bed Teach patient to avoid leg-crossing 3. Promote Home management Encourage lifestyle changes Instruct to AVOID smoking Instruct to avoid leg crossing B. ARTERIAL ULCERS 1. BUERGERS DISEASE / THROMBOANGIITIS OBLITERANS -Acute inflammatory disorder characterized by recurring inflammation of the medium sized small arteries & veins of the lower extremities - Occurs in MEN ages 30 y/o /FEET - SMOKING! Pathophysiology: Cause is UNKNOWN Probably an Autoimmune disease Inflammation of the arteries thrombus formation occlusion of the vessels Sx:
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1. INTERMITTENT CLAUDICATION Leg PAIN upon walking but relieved by rest Foot cramps in the arch (instep claudication) after exercise Aggravated by smoking, emotional disturbance & cold chilling 2. Digital rest pain not changed by activity or rest 3. Cold sensitivity & skin color changes Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances FEET----becomes White Pallor d/t vasoconstriction Bluish Cyanosis d/t pooling of deoxygenated blood Red (W-B-R) Rubor with dependency (+) especially post-smoking d/t exaggerated reflow/hyperemia
4. Paresthesia 5. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis 6. Tropic changes 7. Ulcerations 8. Gangrene formation Dx:
1. Oscillometry 2. Doppler UTZ

3.
Reveals a decrease peripheral pulse volume. (Duplex ultrasnography) Reveals a decrease blood flow to affected extremities. Angiography (Contrast angiography) reveals site & extent of mal-occulsion.
Nsg Mgt: 1. Encourage a slow but progressive physical activity a.) Walk 3 -4 x / day b.) Out of bed 2 3 x a / day 2. Meds a.) Analgesic b.) Vasodilator c.) Anticoagulant 3. Foot care mgt like DM to prevent gangrene formation a.) Avoid walking barefoot b.) Cut toe nails straight c.) Apply lanolin lotion prevent skin breakdown d.) Avoid wearing constrictive garments 4. Avoid smoking & exposure to cold environment 5. Assist in the medical and surgical management Surgery: BKA (Below the knee amputation) Bypass graft/amputation Post-operative care: after amputation Elevate stump for the FIRST 24 HOURS to minimize edema & promote venous return Place patient on PRONE position after 24 hours Assess skin for bleeding and hematoma Wrap the extremity with elastic bandage 2. RAYNAUDS DISEASE/
- A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain & pallor of the fingertips or toes - Acute episodes of arterial spasm affecting digits of hands & fingers
Cause : UNKNOWN Predisposing Factors: 1. SLE Pathognomonic sign butterfly rash on face Chipmunk face bulimia nervosa Cherry red skin carbon monoxide poisoning Spider angioma liver cirrhosis 127 Caput medusae leg & trunk umbilicusLiver cirrhosis Lion face leprosy
1. WOMEN 16- 40 yrs

2. Smoking
2. Rheumatoid Arthritis
- Direct hand trauma
3. Collagen Disease
Sx: 1. RAYNAUDS PHENOMENON - A localized episode of vasoconstriction of the small arteries of the hands that causes color & temperature changes 2. Intermittent claudication - leg pain upon walking - Relieved by rest 3. Cold sensitivity (same with buergers) W-B-R 4. Paresthesia 5. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis 6. Ulcerations 7. Gangrene formation 8. Tingling sensation 9. Burning pain on the hands and feet Nsg Mgt: a. Analgesics to relieve pain Vasodilators -----CALCIUM channel blockers To prevent vasospasms b. Encourage to wear gloves especially when opening a refrigerator. c. Avoid smoking & exposure to cold environment Instruct patient to avoid situations that may be stressful Instruct to avoid exposure to cold & remain indoors when the climate is cold g. Instruct to avoid all kinds of nicotine h. Instruct about safety. Careful handling of sharp objects
DIFFERENTIATION: PERIPHERAL VALVULAR DISEASE
Arterial Ulcers 1. Thromboangiitis Obliterans male/ feet 2. Raynauds female/ hands
Venous Ulcer 1. Varicose veins 2. Thrombophlebitis
C. VENOUS ULCERS 1. VARICOSE VEINS / Varicosities - Abnormal dilation of veins usually in the lower extremities & trunk Pathophysiology Factors venous stasis increased hydrostatic pressure edema Due to: a.) Incompetent valves leading to b.) Increase venous pooling & stasis leading to
Veins in valve Fx: To increase venous return If incompetent valve Pump blood down Pooling of blood in veins heart Cannot return to
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c.) Decrease venous return Predisposing Factors: a. b. c. d. e. f. Hereditary Congenital weakness of veins Thrombophlebitis Cardiac diseases Pregnancy Obesity Prolonged immobility - Prolonged standing/sitting -------dorsiflex feet Constipation (for hemorrhoids) Incompetent venous valves Pain especially after prolonged standing Dilated tortuous superficial skin veins on the legs Warm to touch Leg pain & Heaviness in legs Dependent edema
g.
h. i. Sx:
Dx: 1.
Venography How: Elevate legs in 45 degrees angle. After 15-30 minutes, let pt. stand & see the varicosities
2. Trendelenbergs Test Reveals that veins distends quickly in < 35 secs.

Medical Management: 1. Pharmacological therapy 2. Leg vein stripping/ligation Sclerotherapy----------Spider Wed Varicosities (small-like) (Cold-solution injection) S/E: Thrombosis 3. Anti-embolic stockings Nsg Mgt: Consistent to all venous ulcers Elevate legs above heart level to promote venous return 1 to 2 pillows Measure circumference of leg muscles to determine if swollen. 3. Wear anti embolic or knee high stockings. Women full panty hose 4. Meds: Analgesics for pain 5. Caution patient to avoid prolonged standing or sitting 6. Provide high-fiber foods to prevent constipation 7. Teach simple exercise to promote venous return 8. Caution patient to avoid knee-length stockings & constrictive clothings 9. Avoid massage on the affected area 2. THROMBOPHLEBITIS / DVT- Deep Vein Thrombosis - Inflammation of the deep veins of the lower extremities & the pelvic veins - The inflammation results to formation of blood clots in the area 1. 2.
Predisposing Factors: 1. 2. 4. Smoking Obesity 2. Hyperlipedemia Prolonged use of oral contraceptives Chronic anemia DM
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Complication:
MI CHF Post-surgical complications Post cannulation insertion of various cardiac catheters Prolonged immobility Varicosities Traumatic procedures Diet high in saturated fats Pulmonary Embolism: Sx: - Sudden sharp chest pain - Dyspnea - Tachycardia - Palpitation - Diaphoresis - Mild restlessness
Sx: 1. 2.
3.
4. 5. 6. Dx:
Pain at affected extremities Cyanosis (+) HOMANS SIGN - Pain at leg muscles upon dorsiflexion of foot ---- Pathognomonic sign Leg tenderness Leg pain & edema Dilated tortous vein 1. 2. 3. Angiography Doppler UTZ Duplex Scan
Medical Management: Antiplatelets Vein stripping & grafting Anti-embolic stockings Analgesics. Anticoagulant: Heparin Nsg Mgt: 1. Elevate legs above heart level. 2. Apply warm, moist packs to reduce lymphatic congestion. 3. Measure circumference of leg muscles to detect if swollen. 4. Use anti embolic stockings. 5. Provide measures to avoid prolonged immobility Repositioning Q2 Provide passive ROM Early ambulation 6. Provide skin care to prevent the complication of leg ulcers 7. Monitor for signs of pulmonary embolism (sudden respiratory distress)
GASTROINTESTINAL TRACT
Overview: The GIT is composed of two general parts The main GIT starts from the mouthEsophagusStomachSILI I. Upper Alimentary Canal: Function for digestion
a. Mouth ------------------------ where digestion starts

Contains the lips, cheeks, palate, tongue, teeth, salivary glands, masticatory/facial muscles & bones Anteriorly bounded by the lips Posteriorly bounded by the oropharynx Important for the mechanical digestion of food
The saliva contains SALIVARY AMYLASE or PTYALIN that starts the INITIAL digestion of CHO b. c. Pharynx (throat) Esophagus A hollow collapsible tube Length- 10 inches Made up of stratified squamos epithelium The upper third contains skeletal muscles The middle third contains mixed skeletal and smooth muscles The lower third contains smooth muscles and the esophago-gastric/ cardiac sphincter is found here Functions to carry or propel foods from the oropharynx to the stomach
d. Stomach ---------------------- widest section of UAC: Digestion ends here e. 1st half of duodenum
II. Middle Alimentary canal Function: For Absorption * Small Intestine Absorption starts * Large Intestine - Complete absorption / 90% of water absorbed 2nd half of duodenum Jejunum Ileum 1st half of ascending colon
a.
b. c.
d.
III. Lower Alimentary Canal Function: Elimination
a. 2nd half of ascending colon

b. c. d. e. Transverse Descending colon Sigmoid Rectum
IV. Accessory Organ
a. Salivary Gland b. Verniform Appendix ---------------------- commonly inflammed c. Liver ---------------------- site of bile production
d. e. Pancreas auto digestion Gallbladder storage of bile
The GIT Physiology Absorbs water Eliminates wastes Bacteria in the colon synthesize Vitamin K Appendix participates in the immune system SYMPATHETIC Generally INHIBITORY! Decreased gastric secretions Decreased GIT motility But: Increased sphincteric tone and constriction of blood vessels PARASYMPATHETIC Generally EXCITATORY! Increased gastric secretions
Increased gastric motility But: Decreased sphincteric tone and dilation of blood vessels
Gastrointestinal Assessment : Physical Exam Sequence Inspection Auscultation Percussion Palpation
The ABDOMINAL examination The sequence to follow is: Inspection Auscultation Percussion Palpation
COMMON LABORATORY PROCEDURES 1. FECALYSIS Examination of stool consistency, color and the presence of occult blood. Special tests for fat, nitrogen, parasites, ova, pathogens and others FECALYSIS: Occult Blood Testing Instruct the patient to adhere to a 3-day meatless diet No intake of NSAIDS, aspirin and anti-coagulant Screening test for colonic cancer 2. Upper GIT study: barium swallow Examines the upper GI tract Barium sulfate is usually used as contrast Pre-test: NPO post-midnight Post-test: increase pt fluid intake, instruct that stools will turn white, monitor for obstruction, laxative is also ordered 3. Lower GIT study: barium enema Examines the lower GI tract Pre-test: Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to the test Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn white, monitor for obstruction 4. Gastric analysis Aspiration of gastric juice to measure pH, appearance, volume and contents Pre-test: NPO 8 hours, avoidance of stimulants, drugs and smoking Post-test: resume normal activities 5. EGD (Esophagogastroduodenoscopy) Visualization of the upper GIT by endoscope Pre-test: ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics
Intra-test: position : LEFT lateral to facilitate salivary drainage and easy access Post-test: NPO until gag reflex returns, place patient in SIMS position until he awakens, monitor for complications, saline gargles for mild oral discomfort 6. Lower GI- scopy Use of endoscope to visualize the anus, rectum, sigmoid and colon Pre-test: consent, NPO 8 hours, cleansing enema until return is clear Intra-test: position is LEFT lateral, right leg is bent and placed anteriorly Post-test: bed rest, monitor for complications like bleeding and perforation 7. Cholecystography Examination of the gallbladder to detect stones, its ability to concentrate, store and release the bile Pre-test: ensure consent, ask allergies to iodine, seafood and dyes; contrast medium is administered the night prior, NPO after contrast administration Post-test: Advise that dysuria is common as the dye is excreted in the urine, resume normal activities 8. Paracentesis Removal of peritoneal fluid for analysis Pre-test: ensure consent, instruct to VOID and empty bladder, measure abdominal girth Intra-test: Upright on the edge of the bed, back supported and feet resting on a foot stool 9. Liver biopsy Pretest Consent NPO Check for the bleeding parameters Intratest Position: Semi fowlers LEFT lateral to expose right side of abdomen Post-test: position on RIGHT lateral with pillow underneath, monitor VS and complications like bleeding, perforation. Instruct to avoid lifting objects for 1 week
I. ACCESSORY ORGANS DISORDER SALIVARY GLANDS Function: Produces saliva for mechanical digestion 1200 -1500 ml/day - saliva produced 3 Types of Saliva produced: Parotid below & front of ear Sublingual Submaxillary
1. PAROTITIS - Endemic Mumps - Inflammation of the parotid gland - Contagious Causative Agent: Paramyxo Virus --------- Target: Parotid Glands, Respiratory Glands & Meninges Swollen Parotid Glands Ear Ache (Otalgia)
Fever
Dysphagia
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S/Sx: 1. Fever, chills anorexia, gen body malaise 2. Swelling of parotid gland 3. Dysphagia 4. Ear ache Otalgia MOT: Direct transmission & droplet nuclei Incubation Period: 14 21 days Period of Communicability 1 week before swelling & immediately when swelling begins. Nsg Mgt: 1. CBR
2. Strict isolation (Gentan Violet for aesthetic purposes only) 3. Meds: Analgesic
4. Antipyretic Antibiotics to prevent 2 complications Alternate warm & cold compress at affected part General liquid to soft diet Prevent Complications : 1.Women Cervicitis, Vaginitis, Oophoritis 2.Both sexes meningitis & encephalitis/ reason why antibiotics is needed 3. Men Orchitis (inflammation of testes) might lead to sterility if it occur during / after puberty.
5. 6.
VERNIFORM APPENDIX Location: Right Iliac or Right Inguinal area Function : As a Lymphatic organ that produces WBC during fetal life - ceases to function upon birth of baby 1. APENDICITIS Inflamation of verniform appendix Predisposing Factor:
1. 2. 3. 4.
Microbial infection cause by bacteria Fecalith undigested food particles Ex. Tomato seeds, guava seeds Intestinal obstruction, lymphoid hyperplasia, foreign body & helminthic obstruction Kinking & external occlusion by adhesions, fibrous conditions of abdomen
Pathophysiology: Obstruction of lumen increased pressure decreased blood supply bacterial proliferation and mucosal inflammation ischemia necrosis rupture Stages: 1. Congestive 2. Suppurative 3. Gangenous 4. Perforation S/Sx:
1. Pathognomonic sign: (+) REBOUND TENDERNESS

2. Low grade fever, anorexia, n/v
134 Created by Nia E. Tubio
3. 4.
5.
6.
7.
Dx:
Diarrhea / & or constipation Pain at Rt iliac region Late sign : Tachycardia D/T pain Abdominal pain: begins in the umbilicus then localizes in the RLQ (Mc Burneys point) Abdominal rigidity (if perforated)
1. CBC : Reveals mild leukocytosis increase WBC---------- Confirmatory DX 2. PE : (+) Rebound Tenderness (flexion of Rightt leg, palpate Rt iliac area rebound) 3. Urinalysis --- Reveals (+) to acetone
4. 5. Ultrasound Abdominal X-ray
Treatment: 1. Surgical Intervention Appendectomy- Should be operated 24 48 to prevent rupture---- Peritonitis * MC BURNEYS POINT site of surgical incision for appendectomy Nsg Mgt: PRE- OPERATIVE Consent Notify MD----- local anesthesia Routinary nursing measures: a.) Skin preparation b.) NPO c.) Avoid enema lead to rupture of appendix 4. Meds: Antipyretic Antibiotics to prevent secondary infection *Dont give analgesic will mask the pain - Presence of pain means appendix has not ruptured. 4. Avoid heat application, enemas & laxative will rupture appendix. 5. Monitor VS, I&O bowel sound, fever & hydration status 6. Monitor for perforation and signs of shock 7. POSITION of Comfort: RIGHT SIDELYING in a low FOWLERS Nursing Mgt: POST-OPERATIVE 1. 2. 3. PAIN sensation an important parameter: (-) to pain : Ruptured appendix (+) to pain : Inflammation
1. If (+) to Pendrose Drain indicates rupture of appendix

Position- affected side to drain If no Penrose Drain, position based on pt. comfort 2. 3. 4. Meds: analgesic due post op pain Antibiotics, Antipyretics PRN Monitor VS, I&O, bowel sound Maintain patent IV line
5. Complications: Peritonitis & Septicemia

6. Monitor VS and signs of surgical complications 7. Maintain NPO until bowel function returns 8. If rupture occurred, expect drains and IV antibiotics 9. POSITION post-op: RIGHT side-lying, SEMI- FOWLERS to decrease tension on incision & legs flexed to promote drainage 10. Administer prescribed pain medications
COMMON GIT SYMPTOMS AND MANAGEMENT 1. CONSTIPATION - An abnormal infrequency and irregularity of defecation - Multiple causations
Pathophysiology Interference with three functions of the colon 1. Mucosal transport 2. Myoelectric activity 3. Process of defecation NURSING INTERVENTIONS 1. Assist physician in treating the underlying cause of constipation 2. Encourage to eat HIGH fiber diet to increase the bulk 3. Increase fluid intake 4. Administer prescribed laxatives, stool softeners 5. Assist in relieving stress 2. DIARRHEA -Abnormal fluidity of the stool Multiple causes Gastrointestinal Diseases Hyperthyroidism Food poisoning Nursing Interventions 1. Increase fluid intake- ORESOL is the most important treatment! 2. Determine and manage the cause 3. Anti-diarrheal drugs
LIVER
The largest internal organ Located in the right upper quadrant/ Right Hypochondriac Region Contains two lobes- the right & the left Color: Scarlet Red Covered by a fibrous capsule--------- GLISSONS CAPSULE The hepatic ducts join together with the cystic duct to become the common bile duct Functions to store excess glucose, fats and amino acids Also stores the fat soluble vitamins- A, D and the water soluble- Vitamin B12 Produces the BILE for normal fat digestion The Von Kupffer cells remove bacteria in the portal blood Detoxifies ammonia into urea Functional Unit Liver Lobules
In locating organs of the abdomen: Use the 9 regions
Function: 1. Produces bile Bile: Function is to emulsifies fats Gives color to urine Urobilin (light yellow) Stool Stircobilin (brown)
Precursor: Cholesterol water Bile salt +
2. Detoxifies toxic substances from drugs 3. Promotes synthesis of Vit A, D, E, K

Vitamin A = Retinol Vitamin D = Cholecalciferol Vitamin E = Tococalciferol Vitamin K = Phetione Excess Vit. D & K = Hypervitaminosis Deficiency Vit. A = Night Blindness
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(Fat soluble vitamins) 4. It destroys excess estrogen hormone 5. For metabolism of: A. CHO 1. Glycogenesis synthesis of glycogens 2. Glycogenolysis breakdown of glycogen 3. Gluconeogenesis formation of glucose from non- CHO sources B. CHON 1. Promotes synthesis of albumin & globulin Cirrhosis decrease albumin Albumin maintains osmotic pressure, prevents edema 2. Promotes synthesis of prothrombin & fibrinogen 3. Promotes conversion of ammonia to urea. Ammonia like breath fetor hepaticus C. FATS 1. Promotes synthesis of cholesterol to neutral fats called triglycerides
1. LIVER CIRRHOSIS / Laennecs Cirrhosis
Predisposing Factor:
Lost of architectural design of liver leading to fat necrosis & scarring A chronic, progressive disease characterized by a diffuse damage to the hepatic cells The liver heals with scarring, fibrosis and nodular regeneration
Laennacs Cirrhosis caused by alcoholism 1. Chronic alcoholism ------ Common Cause 2. Malnutrition DecreaseVit B- Thiamine - main cause 3. Virus 4. Toxicity to Carbon Tetrachloride 5. Use of hepatotoxic agents 6. Post-infection 7. Cardiac diseases 8. Schistosomiasis 9. Biliary obstruction 10. Portal Hypertension Compression of the intra-liver vessels Decreased protein (colloid pressure) Increased hydrostatic pressure S/Sx: Early signs:
a.) Weakness & Fatigue b.) Anorexia, Early mornig Nausea & vomiting, Weight loss
c.) Stomatitis d.) Urine Tea color / Stool Clay color e.) Amenorrhea
f.) Decrease sexual urge g.) Loss of pubic & axilla hair h.) Hepatomegaly i.) Jaundice j.) Pruritus or Urticaria k.) RUQ abdominal pain 2. Late signs a.) Hematological changes all blood cells decrease---- Pancytopenia Leukopenia- decrease Thrombocytopenia- decrease Anemia- decrease b.) Endocrine changes Spider Angiomas (Teleangectasis---nose), Gynecomastia Caput medusae (Abdomenloss of tortousity of the umbilicus) , Palmar errythema (redness) c.) GIT changes Ascitis, bleeding esophageal varices due to portal HPN d.) Neurological Changes: Hepatic Encephalopathy Dx: Liver enzymes- increase SGPT (ALT) SGOT (AST) Serum cholesterol & ammonia = Iincrease Indirect Bilirubin or Unconjugated Bilirubin = Increase CBC = Pancytopenia PTT = Prolonged Hepatic Ultrasonogram = Reveals fat necrosis of liver lobules Pathophysiology: CIRRHOSIS * 1-3 : Complications No production of albumin Decreases Osmotic Pressure Edema to Liver ASCITES 2 ASCITES (Fluid Accumulation in the Peritoneal cavity) Nsg Mgt: 1. Medication: Loop Diuretics (10-15 minutes) K- sparing diuretics 2. Assist in abdominal Paracentesis (Aspiration of fluid in the peritoneum) *Void before paracentesis to prevent accidental puncture of bladder as Created by Nia E. Tubio No convertion of Ammonia to urea Ammonia reabsorb back to blood HEPATIC ENCEPHALOPATHY 1 HEPATIC ENCEPHALOPATHY (accumulation of ammonia-a cerebral toxin) 1st Sign: Asterixis (Flapping Hand Tremors) Late Signs: Headache Fetor Hepaticus Restlessness Disorientation/ Confusion Decrease LOCcan lead to Hepatic Coma Nsg. Priortity: Assist In Mechanical Ventilation Nsg. Mgt: 1. Assist in mechanical ventilation d/t coma 2. Monitor VS, neuro check 3. Siderails d/t restless 4. Meds: No Prothrombin & Firinogen No clotting Factor BLEEDING 3
BLEEDING ESOPHAGEAL VARICES (d/t Portal HPNdilation of esophageal veins) Sx: Vomiting---- accompanied by blood Nsg Mgt: 1. Medication: Vit. K Pitressin or Vasopressin (IM) 2. NGT DecompressionLavage Give before lavage - ice or cold saline solution Monitor NGT output 3.Assist in Mechanical
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Liver cirrhosis bedside scissor if pt complaints of DOB Nsg Mgt: Cut cystachean tube to 1. CBR ---- Elevate the head of the bed to minimize dyspnea 2. Restrict Na before fluids 3. Monitor VS, I&O, weight, LOC & bleeding 4. With pt daily & assess pitting edema 5. Measure abdominal girth daily notify MD 6. Meticulous skin care 7. Provide Moderate to LOW-protein (1 g/kg/day) & LOW-sodium diet DIET 8. Diet Increase CHO, Vit. & minerals. Moderate fats. Well balanced diet Early Stage 9. Provide supplemental Vit. (especially K) & minerals 10. Administer prescribed: High in: CHO Diuretics= to reduce ascites & edema CHON Lactulose= to reduce NH4 in the bowel Vitamins Antacids= to prevent ulcer & bleeding Minerals Neomycin= to kill bacterial flora that cause NH production Low in : Fats 11. Avoid hepatotoxic drugs Paracetamol Late Stage: Anti-tubercular drugs High in: CHO 12. Reduce the risk of injury Vit. & Side rails reorientation Minerals Assistance in ambulation Low in : CHON Use of electric razor & soft-bristled toothbrush 13. Keep equipments ready including Sengstaken-Blakemore tube, IV fluids, Medications to treat hemorrhage PANCREAS - Mixed gland (Functions as an exocrine & endocrine gland) - A retroperitoneal gland The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi The exocrine function of the pancreas is the secretion of digestive enzymes for carbohydrates, fats & proteins Pancreatic amylase carbohydrates Pancreatic lipase (steapsin) fats Trypsin, Chymotrypsin and Peptidases proteins Bicarbonate to neutralize the acidic chyme. Stimulated by SECRETIN! Pancreas----- with acinar cells----secretes pancreatic juice going to--- pancreatic duct--- to--stomach 1. PANCREATITIS
Predisposing Factors: 1. 2. 3. 4. 5.
An Inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion Can be acute or chronic
6.
7. 8.
Chronic alcoholism Hepatobilary disease Obesity Hyperlipidemia Hypoparathyroidism Drugs Thiazide diuretics, pills, Pentamidine HCL (Pentam)---for AIDS Diet increase saturated fats Hypercalcemia
Cullens Sign at the Umbilicus: Bleeding of
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9. 10. 11. 12. 13.
Trauma Biliary tract disease Bacterial disease PUD Mumps
- cholelithiasis
Pathophysiology of Acute Pancreatitis: Self-digestion of the pancreas by its own digestive enzymes principally TRYPSIN Spasm, edema or block in the Ampulla of Vater reflux of proteolytic enzymes Auto digestion of the Pancreatic Tissue INFLAMMATION Hemorrhage----- Necrosis KININ ACTIVATION will result to increased permeability Loss of Protein-rich fluid into the peritoneum HYPOVOLEMIA S/Sx:
1. Severe Left epigastric pain radiates from back &flank area Abdominal pain- acute onset, occurring after a heavy meal or alcohol intake 2. Aggravated by eating, with DOB---- rest the GIT 2. N/V, Jaundice, Anorexia 3. Tachycardia 4. Palpitation due to pain 5. Dyspepsia indigestion 6. Decrease bowel sounds 7. (+) Cullens sign - ecchymosis of umbilicus Hemorrhage------ Chronic Hemorrhagic Pancreatitis 8. (+) Grey Turners spots ecchymosis of flank area Confirmatory Dx 9. Hypocalcemia 10. Hypotension & Hypovolemia 11. Signs of Shock Dx: 1. Serum amylase & lipase Increase---- Confirm the presence of pancreatitis 2. Urine lipase Increase 3. Serum Ca Decrease 4. Ultrasound 5. WBC 6. CT scan 7. Hemoglobin and hematocrit
Nursing Mgt: 1. Meds: Assist in pain management. Usually, Demerol is given. Morphine is AVOIDED a.) Narcotic analgesic - Meperidine Hcl (Demerol) Dont give Morphine SO4 will cause spasm of sphincter. b.) Smooth muscle relaxant/ anti cholinergic Ex. Papavarine Hcl Prophantheline Bromide (Profanthene) c.) Vasodilator NTG d.) Antacid Maalox e.) H2 receptor antagonist - Ranitidine (Zantac) To decrease pancreatic stimulation *Ranitidine ---- more common & with less S/E f.) Ca gluconate A Phosphate binder---- Antacid-----Constipation---- Amphogel
2. Withold food & fluid aggravates pain 3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation Complications of TPN: 1. Infection 2. Air Embolism -----Tape all connections to the system 3. Hyperglycemia 4. Hyponatremia 4. Institute stress mgt tech a.) DBE b.) Biofeedback 5. Comfy position - Knee chest or fetal like position to decrease pain Position patient in SEMI-FOWLERs to decrease pressure on the diaphragm 6. If pt can tolerate food, give increase CHO, decrease fats, and increase CHON 7. Assist in correction of Fluid and Blood loss 8. lace patient on NPO to inhibit pancreatic stimulation 9. NGT insertion to decompress distention and remove gastric secretions 10. Maintain on bed rest 11. Deep breathing and coughing exercises 12. Introduce oral feedings gradually- HIGH carbo, LOW FAT 13. Maintain skin integrity 14. Manage shock and other complications: Chronic hemorrhagic pancreatitis Shock Pulmonary Complications---- Pneumonia, Air embolism & Pleural effusion GALLBLADDER Located below the liver The cystic duct joins the hepatic duct to become the bile duct The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the duodenum Storage of bile (made of cholesterol) & concentrates bile Contracts during the digestion of fats to deliver the bile Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder & relaxation of the sphincter of Oddi DISORDER OF THE GALLBLADDER 1. CHOLECYSTITIS Inflammation of the gallbladder Can be acute or chronic: 1. Acute cholecystitis usually is due to gallbladder stones 2. Chronic cholecystitis is usually due to long standing gall bladder inflammation CHOLELITHIASIS - Inflammation of the gallbladder with Formation of GALLSTONES in the biliary apparatus Predisposing FACTORS: 1. 5 F Female Fat (Obesity) Forty (High Risk : 40 y/o) Fertile
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Fair 2. Post menopausal women undergoing estrogen therapy 3. Sedentary lifestyle 4. Hyperlipidemia 5. Neoplasm Pathophysiology: Supersaturated bile, Biliary stasis Stone formation Blockage of Gallbladder Inflammation, Mucosal Damage and WBC infiltration S/Sx: 1. Severe Right abdominal pain (after eating fatty food). Occurring especially at night Epigastric pain that radiates to the scapula or localized at the RUQ Mass at the RUQ 2. Fatty intolerance 3. Anorexia, n/v 4. Jaundice 5. Pruritus 6. Easy bruising 7. Tea colored urine / Dark-orange & foamy urine 8. Steatorrhea 9. Indigestion, belching and flatulence 10. Murphys sign Dx:
1. Oral cholecystogram (or gallbladder series)- Confirms presence of stones but cannot visualize the gallbladder
2. Ultrasonography- can detect the stones 3. Abdominal X-ray 4. Cholecystography WBC count increased ERCP: Revaels inflamed gallbladder with gallstone 5. Serum Lipase Increase 6. Indirect Bilirubin - Increase Tx: Analgesic- Meperidine Chenodeoxycholic acid= to dissolve the gallstones Antacids Anti-emetics Nursing Mgt: 1. Medications: Administer prescribed medications to relieve pain. a.) Narcotic Analgesic - Usually Demerol (MEPERIDINE) NOT Codeine & Morphine may cause spasm of the Sphincter increased pain. Morphine cause MOREPAIN b.) Anti cholinergic - Atropine SO4 c.) Anti emetic Metoclopramide (Plasil) Phenergan Phenothiazide with anti emetic properties
2. Diet increase CHO, moderate CHON, decrease fats 3. Meticulous skin care d/t Urticaria 4. Maintain NPO in the active phase 5. Maintain NGT decompression 6. Instruct patient to AVOID HIGH- fat diet & GAS-forming foods 7. Surgical Procedures : Cholecystectomy---removal of gallbladder Choledochotomy Laparoscopy Post-operative Nursing Interventions Cholecystectomy: 1. Monitor for surgical complications 2. Post-operative position after recovery from anesthesia- LOW FOWLERs 3. Encourage early ambulation 4. Administer medication before coughing and deep breathing exercises 5. Advise client to splint the abdomen to prevent discomfort during coughing 6. Administer analgesics, antiemetics, antacids 7. Care of the biliary drainage or T-tube drainage 8. Fat restriction is only limited to 4-6 weeks. Normal diet is resumed IMPORTANT: -Maintain patency of T-tube . Check if intact & drain to prevent infection Purpose: To prevent entry of bile into the peritoneal cavity
STOMACH
A J-shaped structure organ in the epigastrium - Capacity is 1,500 ml Contains 4 Parts: Fundus/ Anthrum Cardia Body Pylorus
Valves ------ prevents reflux or regurgitation of food 1. Cardiac Sphincter - prevents the reflux of the contents into the esophagus (bet. esophagus & stomach) 2. Pyloric Sphincter - regulates the rate of gastric emptying into the duodenum (bet. stomach & half of pylorus)
The glands & cells in the stomach secrete digestive enzymes: 1. Parietal / Oxyntic Cells Function: a. Produces intrinsic factor - promotes reabsorption of Vit. B12 promotes maturation of RBC b. HCl Acid - Aids in digestion Ph of Hydrocholoric Acid: 1-2
2. Chief Cells/ Zymogenic Cells : Secretes a. b.

Gastric amylase - digest CHO Gastric lipase digest fats

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c. d. 3. Antral G-cells- gastrin
Pepsin digests PROTEIN Rennin digests milk products
4. Argentaffin cells- serotonin 5. Mucus neck cells- mucus 6. Endocrine cells - Secrets gastrin increase Hcl acid secretion Function of the Stomach: Generally to digest the food (proteins) & to propel the digested materials into the SI for final digestion 1.Mechanical 2.Chemical Digestion 3.Storage of food
CHO & CHON : Stored in the stomach for 1 -2 hrs. FATS : Stored in stomach for 2 3 hrs
DISORDERS OF THE STOMACH 1. PEPTIC ULCER DISEASE (PUD)
An ulceration of the gastric & duodenal lining characterized by excoriation / erosion of submucosa & mucosal lining due to: a.) Hypercecretion of acid pepsin b.) Decrease resistance of mucosal barrier to HCl acid secretion - May be referred as to location as Gastric ulcer in the stomach, or Duodenal ulcer in the duodenum - Most common Peptic ulceration: anterior part of the upper duodenum Incidence Rate:
1. Men : 40 55 yrs old

2. Aggressive persons PATHOPHYSIOLOGY of PUD: Disturbance in acid secretion & mucosal protection Increased acidity or decreased mucosal resistance erosion & ulceration Infection with H. pylori------ # 1 cause of ULCER Predisposing Factors: 1. Hereditary 2. Emotional Stress 3. Smoking vasoconstriction GIT ischemia---lead to resistance of HCl----- ulceration 4. Alcoholism stimulates release of histamine = stimulates Parietal cell release Hcl acid = Hypersecretion ----Ulceration 5. Caffeine tea, soda, chocolate 6. Irregular diet 7. Rapid eating 8. Ulcerogenic drugs NSAIDS, aspirin, steroids, indomethacin, ibuprofen Indomethacin - S/E corneal cloudiness. Needs annual eye check up. 9. Gastrin producing tumor or Gastrinoma Zollinger Ellison Syndrome 10. Microbial invasion R/T helicobacter pylori. Metromidazole (Flagyl)
TYPES OF ULCERS I. Ascending to severity: 1. Acute affects submucosal lining 2. Chronic affects underlying tissue heals & forms a scar II. According to location:
Most feared complications of Bruns in GIT : Curlings Ulcer
1. Stress ulcer ---common among critically-ill patients

2.
3.
Gastric ulcer Duodenal ulcer most common----- 90% of ulcers because it has less bicarbonate ions Buffers that neutralizes acidity
A. STRESS ULCER 2 Types Of Stress Ulcer 1. CURLINGS ULCER : Cause: Trauma & Burns Bleeding Hypovolemia GIT schemia Decrease resistance of mucosal barriers to Hcl acid Ulcerations Drug Of Choice: Ranitidine (Zantax) GASTRIC ULCER DEFINITION - Ulceration of the gastric mucosa, submucosa & rarely the muscularis d/t break in the mucosal barrier w/ reduced production 2nd to incompetent pylorus. - Hypoperfusion-ischemia to gastric mucosa is also a factor. H.pylori in >90% cases RISK FACTORS (same) PATHOLOGY SITE Other Sx Stress Smoking Alcohol History of gastritis Decreased mucosal protection---------Infection with H. pylori-----Decreased blood supply to the stomach Antrum or lesser curvature 1. Nausea 2. Vomiting is more common 3. Hematemesis>melena 4. Weight loss -30 min 1 hr AFTER EATING - epigastrium - Hot , gaseous & burning - not usually relieved by food & antacid - Gnawing, sharp pain in the midepigastrium - NOT RELIEVED by food intake, Helicobacter pylori infection NSAIDS abuse Type A personality Increased gastric acidity------Infection with H pylori Duodenal bulb 2. CUSHINGS ULCER: Cause: Stroke/ CVA / Head Injury Increase vagal stimulation Hyperacidity Ulcerations
B.
DUODENAL ULCER - Ulceration of duodenal mucosa & submucosa - Usually d/t increased gastric acidity
EPIGASTRIC PAIN
-2-4 hrs after eating or during the night - mid epigastrium - Cramping & Burning PAIN - usually relieved by food intake & antacid - 12 MN 3am pain
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sometimes AGGRAVATING the pain!
GASTRIC SECRETION VOMITING HEMORRHAGE WT COMPLICATION S HIGH RISK
Normal gastric acid secretion common Hematemesis Wt loss a. Stomach Cancer b. Hemorrhage 40 - 60 y/o Incidence is high in older adults, male>female,
Increased gastric acid secretion Not common Melena Wt gain a. Perforation 20 y/o
Dx 1. EGD to visualize the ulceration 2. Urea breath test for H. pylori infection 3. Biopsy- to rule out gastric cancer d/t malignancy risk 4. Barium swallow 5. Gastric analysis = NORMAL
1. EGD & Biopsy 2. Endoscopic exam 3.Stool from occult blood 4.Gastric analysis = INCREASE 5. Upper GI series confirms presence of ulceration
NURSING INTERVENTIONS: 1. Give BLAND diet, small frequent meals during the active phase of the disease a.
b.
Diet bland, non irritating, non spicy Avoid caffeine & milk/ milk products, carbonated drinks Increase gastric acid secretion
2. Administer prescribed medications- H2 blockers, Protein pump inhibitor, mucosal barrier protectants & antacids a.) Antacids ACA Aluminum Containing Antacids Ex. Aluminum OH gel (Ampho-gel) S/E constipation Maalox (fewer S/E) MA Magnesium Containing Antacids Ex. Milk Of Magnesia S/E diarrhea
b.) H2 Receptor Antagonist

Ex.
1. Ranitidine (Zantac) lesser S/E---- Best given if OD = AM

or BID = AM & Nightime to prevent nocturnal acid gastric secretion
2. Cimetidine (Tagamet) more S/E

3. Famotidine (Pepcid)
3. Avoid smoking decrease effectiveness of drug Nursing Mgt For Both: 1. Administer antacid & H2 receptor antagonist 1hr apart -Cimetidine decrease antacid absorption & vise versa - Instruct client to avoid smoking because it decreases effectiveness of the drug
c.) Cytoprotective Agents

Ex. 1. Sucralfate (Carafate) - Provides a paste-like substance that coats mucosal lining of stomach 2. Cytotec - causes severe spasm ( abortive effect) d.) Sedatives/ Tranquilizers - Valium, lithium e.)Anticholinergics / Anti-spasmodic Agent 1. Atropine SO4 2. Prophantheline Bromide (Probanthine) (Pt has history of HPN crisis With peptic ulcer disease. Rn should not administer alka seltzer- has large amount of Na. 4. Provide teaching about stress reduction & relaxation techniques 5. Surgery: Subtotal Gastrectomy - Partial removal of stomach Billroth I (Gastroduodenostomy) -Removal of 1/3 of stomach & anastomoses of gastric stump to the duodenum. Billroth II (Gastrojejunostomy) - Removal of 1/2 -3/4 of stomach & duodenal bulb & anastomostosis of gastric stump to jejunum.
Before surgery for BI or BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first. ` 1. Nursing Mgt For B1 or B II: Monitor NGT output a.) Immediately post op should be bright red drainage b.) Within 6-8 hrs output is greenish in color c.) After 24h output is dark red d/t influence of HCI acid Administer meds: a.) Narcotic Analgesic b.) Antibiotic c.) Antiemetics Maintain patent IV line VS, I&O & bowel sounds Monitor for Complications: SURGICAL PROCEDURES FOR PUD Total gastrectomy, vagotomy, gastric resection, Billroth I & II, pyloroplasty Post-operative Nursing management 1. Monitor VS 2. Post-op position: FOWLERS 3. NPO until peristalsis returns 4. Monitor for bowel sounds 5. Monitor for complications of surgery 6. Monitor I & O- report U.O:<.5cc/kg/hr, IVF, hydrate
2.
3. 4.
5.
a. HEMORRHAGE Hypovolemic shock

Late signs anuria Nsg Interventions For BLEEDING: 1. Maintain on NPO 2. Administer IVF & medications 3. Monitor hydration status, Hct & Hgb 4. Assist with room temperature SALINE lavage (iced may lead to more mucosal damage via severe vasoconstriction-ischemia,vagal stimulation) 5. Insert NGT for decompression & lavage & assessment of GI bleeding 6. Prepare to administer blood transfusion 7. Prepare to give VASOPRESSIN to induce vasoconstriction to reduce bleeding 8. Prepare patient for SURGERY if warranted
b. PERITONITIS c. PARALYTIC ILEUS Most feared complication in all types of abdominal surgery (absence of peristalsis)
d. e.
f.
Hypokalemia Thromobphlebitis Pernicious anemia
g. DUMPING SYNDROME
Common complication Rapid gastric emptying of hypertonic food solutions CHYME leading to hypovolemia. A postprandial condition of rapid emptying of the gastric contents into the small intestine (jejunum) usually after a gastric surgery (gastrojejunostomy) without proper mixing of chyme & the normal duodenal digestive process - Symptoms occur 5-30 minutes after eating
Pathophysiology: Foods high in CHO & electrolytes must be diluted in the jejunum before absorption takes place. The rapid influx of stomach contents will cause distention of the jejunum early symptoms The hypertonic chyme will draw fluid from the blood vessels to dilute the high concentrations of CHO and electrolytes Later, there is increased blood glucose stimulating the increased secretion of insulin Then, blood glucose will fall causing reactive hypoglycemia Sx of Dumping syndrome: EARLY Sx: d/t rapid movement of extracellular fluids into the bowel to convert the hypertonic bolus to isotonic 1. Nausea and Vomiting, syncope 2. Abdominal fullness 3. Abdominal cramping 4. Palpitation, tachycardia 5. Diaphoresis, Pallor LATE Sx: 1. Drowsiness 2. Weakness & Dizziness 3. Hypoglycemia 4. Diarrhea Nursing Mgt: 1. Avoid fluids in chilled solutions Instruct to eat SMALL frequent meals, include MORE dry food items in 6 equally divided feedings Advise patient to eat LOW-carbohydrate HIGH-fat and HIGH-protein diet 2. Flat on bed 15 -30 minutes after q feeding 5. Instruct to AVOID consuming FLUIDS 1 hr before, with, 2 hrs after meals 6. Instruct to eat in semi recumbent position, LIE DOWN after meals 7. Administer sedative, anti-spasmodic medications to delay gastric emptying 2. GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD) - Backflow of gastric contents into the esophagus FACTORS: - Usually due to incompetent lower esophageal sphincter , pyloric stenosis or motility disorder - Symptoms may mimic ANGINA or MI
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Pathophysiology: incompetent lower esophageal sphincter regurgitation of acidic contents Erosion of esophageal mucosa Pain Sx: Heartburn Dyspepsia Regurgitation Epigastric pain Difficulty swallowing Ptyalism 1. Endoscopy or barium swallow 2.Gastric ambulatory pH analysis Note for the pH of the esophagus, usually done for 24 hours The pH probe is located 5 inches above the lower esophageal sphincter The machine registers the different pH of the refluxed material into the esophagus NURSING INTERVENTIONS 1. Instruct the patient to AVOID stimulus that increases stomach pressure & decreases GES pressure 2. Instruct to avoid alcohol , spices, coffee, tobacco & carbonated drinks 3. Instruct to eat LOW-FAT, HIGH-FIBER diet, BLAND DIET 4. Avoid foods and drinks TWO hours before bedtime 5. Elevate the head of the bed with an approximately 8-inch block 6. Administer prescribed H2-blockers & prokinetic meds like cisapride, metochlopromide 7. Advise proper weight reduction 3. GASTRITIS - Inflammation of the gastric mucosa May be Acute or Chronic Etiology: Acute- bacteria, irritating foods, NSAIDS, alcohol, bile & radiation Chronic- Ulceration, bacteria, Autoimmune disease, diet, alcohol, smoking Pathophysiology: Insults cause gastric mucosal damage inflammation, hyperemia and edema superficial erosions decreased gastric secretions, ulcerations & bleeding Sx: (Acute) Dyspepsia Headache Anorexia Nausea/Vomiting Chronic) Pyrosis Singultus Sour taste in the mouth Dyspepsia, N/V/anorexia, Pernicious anemia UPPER GIT
Dx: 1. EGD- to visualize the gastric mucosa for inflammation 2. Low levels of HCl 3. Biopsy to establish correct diagnosis whether acute or chronic
Dx:
NURSING INTERVENTIONS 1. Give BLAND diet 2. Monitor for signs of complications like bleeding, obstruction and pernicious anemia 3. Instruct to avoid spicy foods, irritating foods, alcohol and caffeine 4. Administer prescribed medicationsH2 blockers, antibiotics,
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1. HERNIATIONS - Abnormal protrusion of an organ/tissue/part of an organ through a structure that normally contains it through a congenital or acquired weakness of the enclosing wall (eg. Abdominal musculature) with accompanying increased pressure (valsalva, lifting, crying). Wall defect Intraabdominal Pressure Tissue/organ Protrusion Types: Descriptors: - Reducible - Incarcerated/Irreducible - Strangulated (emergency)
Medical management: - Truss Surgery: - Herniorrhapy, mesh - Laparoscopic ExtraPeritoneal herniorrhapy Nursing Management: - Preop: Health instructions, consent, let patient void - Postop: Vital signs, urine output & urine bladder status - Scrotal swelling. Ice pack over the incision. - General diet as soon tolerated by the patient. Advise no lifting for 4-6 wks - Postop Scrotal support. ESOPHAGUS 1. ESOPHAGEAL VARICES - Dilation &tortuosity of the submucosal veins in the distal esophagus ETIOLOGY: commonly caused by PORTAL hypertension secondary to liver cirrhosis This is an Emergency condition! Sx: 1. Hematemesis 2. Melena 3. Ascites 4. Jaundice 5. Hepatomegaly/splenomegaly Signs of Shock- tachycardia, hypotension, tachypnea, cold clammy skin, narrowed pulse pressure Dx: 1. Esophagoscopy
NURSING INTERVENTIONS FOR EV 1. Monitor VS strictly. Note for signs of shock 2. Monitor for LOC 3. Maintain NPO 4. Monitor blood studies 5. Administer O2 6. Prepare for blood transfusion 7. Prepare to administer Vasopressin and Nitroglycerin 8. Assist in NGT and Sengstaken-Blakemore tube insertion for balloon tamponade (scissors pls!) 9. Prepare to assist in surgical management: Endoscopic sclerotherapy, Variceal ligation, Shunt procedures
2. HIATAL HERNIA (Diaphragmatic Hernia) -Protrusion of the esophagus into the diaphragm thru an opening (esophageal hiatus) Two types: - Sliding hiatal hernia ( most common) - Axial hiatal hernia Factors: History: >/=60 y/o, female>male, history of trauma, increased intraabdominal pressure conditions Sx: 1. Heartburn (30-60min after meal) in sliding type, (-) in rolling type. 2. Regurgitation 3. Dysphagia, chestpain 4. 50%- without symptoms Pathophysiology: Weakness/ Enlarged Esophagial hiatus Increased intraabdominal pressure Protrusion of the stomach
sliding hernia LES exposed to low thoracic pressure Reflux/regurgitation & motor dysfunction manifestations Dx: 1. Barium swallow & Fluoroscopy NURSING INTERVENTIONS 1. Provide small frequent feedings 2. AVOID supine position for 1 hour after eating 3. Elevate the head of the bed on 8-inch block 4. Provide pre-op and post-op care
rolling hernia Obstruction Strangulation Volvulus
Surgical Management: -Nissen fundoplication (suturing the fundus around esophagus, most common procedure) - Angelchick prosthesis insertion Pre-op nursing: Health teaching, consent Post-op nursing: Monitor respi distress especially if chest tubes are in place. Instruct coughing and deep breathing exercises, ambulation Assess for bleeding, thrombosis and infection NGT maintained patent Diet transition, starts with fluids after 24hrs, then small frequent feeding, avoid carbonated beverages
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LOWER GIT The Small Intestine Grossly divided into the Duodenum, Jejunum & Ileum The duodenum contains the two openings for the bile & pancreatic ducts The ileum is the longest part (about 12 feet) The intestinal glands secrete digestive enzymes that finalize the digestion of all foodstuff Enzymes for carbohydrates disaccharidases Enzymes for proteins dipeptidases & aminopeptidases Enzyme for lipids intestinal lipase The Large intestine Approximately 5 feet long, with parts: 1. The cecum widest diameter, prone to rupture 2. The appendix 3. The ascending colon 4. The transverse colon 5. The descending colon 6. The sigmoid most mobile, prone to twisting 7. The rectum 1. CROHNS DISEASE -Also called Regional Enteritis - An inflammatory disease of the GIT affecting usually the small intestine Inflammatory Bowel Disease ETIOLOGY: unknown, genetics,environmental, immune defect 1. CROHNS DISEASE The terminal ileum thickens, with scarring, ulcerations, abscess formation and narrowing of the lumen Sx: 1. Fever 2. Abdominal distention 3. Diarrhea 4. Colicky abdominal pain 5. Anorexia/N/V 6. Weight loss 7. Anemia CONDITIONS OF THE LARGE INTESTINE 2. ULCERATIVE COLITIS - Ulcerative and inflammatory condition of the GIT usually affecting the large intestine - The colon becomes edematous and develops bleeding ulcerations - Scarring develops overtime with impaired water absorption and loss of elasticity Sx: 1. Anorexia 2. Weight loss 3. Fever 4. SEVERE diarrhea with Rectal bleeding 5. Anemia 6. Dehydration 7. Abdominal pain and cramping NURSING INTERVENTIONS for CD & UC 1. Maintain NPO during the active phase 2. Monitor for complications like severe bleeding, dehydration, electrolyte imbalance 3. Monitor bowel sounds, stool and blood studies 4. Restrict activities= rest and comfort 5. Administer IVF, electrolytes and TPN if prescribed Monitor complications of diarrhea 6. Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and
vegetables especially SPINACH, pepper, alcohol and caffeine 7. Diet progression- clear liquid LOW residue, high protein diet 8. Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming agents and vitamin/iron supplements 3. HEMORRHOIDS - Abnormal dilation and weakness of the veins of the anal canal - Variously classified as Internal or External, Prolapsed, Thrombosed and Reducible PATHOPHYSIOLOGY -Increased pressure in the hemorrhoidal tissue due to straining, pregnancy, etc dilatation of veins Internal hemorrhoids These dilated veins lie above the internal anal sphincter Usually, the condition is PAINLESS External hemorrhoids These dilated veins lie below the internal anal sphincter Usually, the condition is PAINFUL Sx: 1. Internal hemorrhoids- cannot be seen on the peri-anal area 2. External hemorrhoids- can be seen 3. Bright red bleeding with each defecation 4. Rectal/ perianal pain 5. Rectal itching 6. Skin tags Dx: 1. Anoscopy 2. Digital rectal examination NURSING INTERVENTIONS 1. Advise patient to apply cold packs to the anal/rectal area followed by a SITZ bath 2. Apply astringent like witch hazel soaks 3. Encourage HIGH-fiber diet and fluids 4. Administer stool softener as prescribed Post-operative care for hemorrhoidectomy 1. Position: Prone or Side-lying 2. Maintain dressing over the surgical site 3. Monitor for bleeding 4. Administer analgesics and stool softeners 5. Advise the use of SITZ bath 3-4 times a day
BOWEL OBSTRUCTION Condition where the segment of the intestine is obstructed by: Tumors Paralysis Volvolus Signs and Symptoms Abdominal pain Abdominal rigidity Increased BOWEL sound in early stage and ABSENT BOWEL sound in late stage Abdominal distention
Vomiting and fluid imbalance DX: 1. Abdominal x-ray Management: Surgery Nursing care of abdominal surgery
Quick Summary Peptic Ulcer Ulceration of mucosa; In the stomach or duodenum Outstanding Symptom: PAIN Nursing Goal: Allow ulcer to heal, prevent complication Rest: physical and Mental Eliminate certain foods Medications: antacid, H2 blockers, Proton Pump inhibitors, antibiotics, mucosal protectants Surgery: Vagotomy, Billroth 1 and 2 Quick Summary Liver Cirrhosis Destruction of liver with replacement by scars Common causes: alcoholism, post-hepatitic Manifestations related to liver derangements Jaundice, Ascites, splenomegaly, bleeding, enceph Nursing goal: Control manifestations and maximize liver function
GENITO-URINARY TRACT Overview: Function: 1. 2. I. KIDNEYS: Pair of bean shaped organ - Located Retro peritonially (back of peritoneum) on either side of vertebral column. Encased in Bowmanss Capsule. Parts: 1. Renal pelvis --------If theres inflammation----Pyelonephritis 2. Cortex
Promote excretion of nitrogenous waste products Maintain F&E & acid base balance
3.
Medulla
* Nephrons = Basic living unit * Glomerulus = Filters blood going to kidneys Function of Kidneys: 1. Urine formation Urine formation 25% of total CO (Cardiac Output) is received by kidneys
1. Filtration -------------any disorder affecting filtration results to decreased renal output

*Normal GFR/ min is 125 ml of blood /minute filtered by glomerulus 2. Tubular Reabsorption Tubular reabsorption 124ml of ultra infiltrates (Na,K,Mg,Cl, H2O) (H2O & electrolytes is for reabsorption)
3. Tubular Excretion
Tubular Excretion 1 ml is excreted in urine/minute 2. Regulation of BP: Predisposing Factor: Ex. CS hypovolemia decrease BP going to kidneys Activation of RAAS Release of Renin (hydrolytic enzyme) at juxtaglomerular apparatus Angiotensin I mild vasoconstrictor Angiotensin II Vasoconstrictor Adrenal cortex Aldosterone Increase BP Increase Na & H2O reabsorption Hypervolemia increase CO increase PR
II. URETERS

III. BLADDER
25 30 cm long, passageway of urine to bladder Capable of peristalis movement
Located behind the symphysis pubis. Consists of muscular & elastic tissue that is distensible Function: Reservoir of urine Maximum capacity: 1200 1800 ml Normal adult can hold 250 500 ml needed to initiate micturition reflex
NORMAL COMPOSITION OF URINE: Color = Odor = Consistency = Ph = Specific Gravity = WBC/ RBC = Albumin = E coli = Mucus thread = Amorphous urate = CHON = Catheters: Pediatric Female Male IV. URETHRA Extends to external surface of body. Passage of urine, seminal & vaginal fluids. Female : Male: 3 5 cm or 1 to 1 20 cm or 8 = = = 8-10 french 12-14 french 16-18 french Pale yellow toAmber Faint Aromatic Clear or slightly turbid 48 1.015 1.030 (-) (-) (-) few (-) None
Urological Assessment I. Nursing History Reason for seeking care Current illness Previous illness Family History Social History Sexual history II. Key Signs & Symptoms of Urological Problems 1. EDEMA Associated with fluid retention Renal dysfunctions usually produce ANASARCA 2. PAIN Suprapubic pain= bladder
Colicky pain on the flank= kidney 3. HEMATURIA Painless hematuria may indicate URINARY CANCER! Initial/Early-stream hematuria= urethral lesion,prostatic,seminal vesicle Terminal/Late-stream hematuria= bladder lesion,post urethra Throughout: glomerulonephritis Pneumaturia: gas in urine;bladder-bowel fistula 4. DYSURIA Pain with urination= lower UTI Normal urine output: 1cc/kg/hr or 800-1800ml/24hr 5.POLYURIA More than 2 Liters urine per day 6. OLIGURIA 100- 400 mL per day 7. ANURIA Less than 100 mL per day Urinary Urgency: sudden controllable strong desire to void Urinary retention: sense of incomplete bladder emptying(100ml left) Urinary frequency: voiding more often than every 2hrs Urinary Hesitancy: at least 10 sec delay in initiation of urination Urinary incontinence: involuntary loss of urine Nocturia: excessive urination at night Implementation Steps for selected III. PHYSICAL EXAMINATION problems Inspection Auscultation Percussion Palpation IV. Laboratory examination Urinalysis BUN and Creatinine levels of the serum Serum electrolytes Radiographic IVP KUB x-ray KUB ultrasound CT and MRI Cystography DISORDERS OF THE GUT 1. URINARY TRACK INFECTION (UTI) - Bacterial invasion of the kidneys or bladder (CYSTITIS) usually caused by Escherichia coli - Bacteria (+) 10 to the 5th in culture Predisposing Factors: Poor hygiene Irritation from bubble baths Urinary reflux Instrumentation Residual urine, urinary stasis Dehydration 1. Provide PAIN relief Assess the level of pain Administer medications usually narcotic ANALGESICS 2. Maintain Fluid and Electrolyte Balance Encourage to consume at least 2 liters of fluid per day In cases of ARF, limit fluid as directed Weigh client daily to detect fluid retention 3. Ensure Adequate urinary elimination Encourage to void at least every 2-3 hours Promote measures to relieve urinary retention: Alternating warm and cold compress Bedpan Open faucet 8.
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Pathophysiology: The invading organism ascends the urinary tract, irritating the mucosa & causing characteristic symptoms: Ureter= ureteritis Bladder= cystitis Urethra=Urethritis Pelvis= Pyelonephritis Sx: Low-grade fever Abdominal pain Enuresis Pain/burning on urination Urinary frequency Hematuria Upper UTI Fever and CHIILS Flank pain Costovertebral angle tenderness Laboratory Examination Urinalysis Urine Culture Nursing interventions: Administer antibiotics as ordered Provide warm baths and allow client to void in water to alleviate painful voiding. Force fluids. Nurses may give 3-4 liters of fluid per day if not contraindicated Encourage measures to acidify urine (cranberry juice, acid-ash diet). Provide client teaching and discharge planning concerning a. Avoidance of tub baths b. Avoidance of bubble baths that might irritate urethra c. Importance for girls to wipe perineum from front to back d. Increase in foods/fluids that acidify urine. Pharmacology for urine bacteria >100,000/ml 1. Sulfa drugs Highly concentrated in the urine Effective against E. coli! Can cause CRYSTALLURIA 2. Quinolones Not given to less than 18 because they can cause cartilage degradation 3. Pyridium= urinary antiseptic Can cause urine discoloration a. CYSTITIS Inflammation of bladder Predisposing Factors: 1. 2. 3. Microbial invasion E. coli High risk women Obstruction Urinary retention/stagnation Increase estrogen levels Sexual intercourse
4.
5. 6. S/Sx:
1. Hypogastric Pain flank area

2. 3. 4. 5. Dx:
Urinary frequency & urgency Burning upon urination Dysuria & hematuria Fever, chills, anorexia, gen body malaise
1. Urine culture & sensitivity = (+) to E. coli (80-90% cause)

Nursing Mgt:
1. Force fluid = 2000 ml-3000 ml/day

2. Warm sitz bath to promote comfort
3. Monitor & assess for gross hematuria, assess odor of urine 4. Acid Ash Diet cranberry, vit C -OJ to acidify urine & prevent bacterial multiplication
5. Meds: a. Systemic antibiotics Ampicillin Cephalosporin b. Sulfonamides cotrimaxazole (Bactrim) - Gantrism (ganthanol) c. Urinary Antiseptics Nitrofurantoin (Macrodantin) S/E: Staining of Teeth Peripheral Nephropathy GIT irritants Hemolytic Anemia ----- 1st Sign: Fever d. Urinary analgesic- Pyridum 6. Health Teaching a.) Importance of Hydration b.) Void after sex c.) Female avoids cleaning front to back Do not use Bubble bath, Tissue paper, Powder, perfume----alters the ph of vagina & irritants d.) Complications: Pyelonephritis *Ph = measures acidity of solution
b. PYELONEPHRITIS - Acute/Cchronic inflammation of 1 or 2 renal pelvis of kidneys leading to tubular destruction, interstitial abscess formation & can leadt to Renal Failure Predisposing Factor: 1. Microbial invasion a. E. Coli b. Streptococcus 2. Urinary retention /obstruction 3. Pregnancy 4. DM 5. Exposure to renal toxins S/Sx:
Acute Pyelonephritis:
a. Costovertibral angle pain & tenderness FLANK PAIN

b. c. d. e. Fever, anorexia, gen body malaise Urinary frequency, urgency Nocturia, dsyuria, hematuria Burning on urination
Chronic Pyelonephritis: a. b. c. Dx: Fatigue, wt loss Polyuuria, polydypsia HPN
1. Urine culture & sensitivity (+) E. coli & streptococcus---- (+) Cultured Microorganisms
2.
3.
Urinalysis Increase WBC, CHON & pus cells Cystoscopic exam Reveals urinary obstruction
Nursing Mgt:
1. Provide CBR acute phase. Especially during acute attack

2. 3. 4. Force fluid Acid ash diet Meds: a.) Urinary antiseptic nitrofurantoin (macrodantin) SE: peripheral neuropathy GI irritation Hemolytic anemia Staining of teeth
b.) Urinary analgesic Pyridium

2. Complication- Renal Failure
2. NEPHROLITHIASIS/ UROLITHIASIS - Formation/ Presence of stones elsewhere in the urinary tract 3 Major Types of Stone 1. Calcium Milk 2. Oxalate Cabbage Cranberries Nuts tea Chocolates 3. Uric Acid Anchovies Organ meat Nuts Sardines
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Predisposing Factors:
1. Diet large amounts of Ca & oxalate

2. 3. 4. 5. 6. Hereditary gout Obesity Sedentary lifestyle, immobility Hyperparathyroidism Increased uric acid levels(diet) Dehydration,urinary stasis
7.
Pathophysiology: Supersaturation of crystals due to stasis Stone formation May pass through the urinary tract OBSTRUCTION, INFECTION & HYDRONEPHROSIS S/Sx:
1. Renal Colic radiating to the groin

2. Cool moist skin (shock) 3. Burning upon urination 4. Hematuria 5. Anorexia, n/v Abdominal or flank pain Dx:
1. 2. 3. 4.
IVP (Intravenous Pyelography) = Identifies site of obstruction and presence of non-radiopaque stones KUB Ultrasound & X-ray = Reveals location of stone, number & size Cytoscopic exam = Reveals urinary obstruction Stone analysis = Reveals composition & type of stone 5. Urinalysis = Indicates presence of bacteria, increased protein, increased WBC and RBC (hematuria) Medical Mgt: 1. Surgery a. Percutaneous Nephrostomy: tube is inserted through skin & underlying tissues into renal pelvis to remove calculi. b. Percutaneous Nephrostolithotomy: delivers ultrasound waves through a probe placed on the calculus. 2. Extracorporeal shock-wave lithotripsy: delivers shock waves from outside the body to the stone, causing pulverization - Non-invasive - Dissolves stone through shock wave application Pain management : Morphine or Meperidine Diet modification
3. Nephrectomy Removal of affected kidney 4. Litholapoxy removal of 1/3 of stones- Stones will recur. Not advised for pt with big stones Nursing interventions 1. Strain all urine through gauze to detect stones and crush all clots. 2. Force fluids (30004000 cc/day). 3. Encourage ambulation to prevent stasis. 4. Relieve pain by administration of analgesics as ordered and application of moist heat to flank area. 5. Monitor I & O 6. Warm sitz bath for comfort 7. Alternate warm compress at flank area 8. Medications: a.) Narcotic analgesic- Morphine SO4
b.) Allopurinol (Zyloprim) to decrease uric acid production S/E : Allergic Reactions-----rashes, nasal congestion 9. Patent IV line 10. Provide modified diet, depending upon stone consistency: Calcium, Oxalate and Uric acid stones 1. Calcium Stones Limit milk/dairy products Acid-Ash Diet to acidify urine (cranberry or prune juice, meat, eggs, poultry, fish, grapes & whole grains) 2. Oxalate Stones Avoid excess intake of foods/ fluids high in oxalate (tea, chocolate, rhubarb, spinach) Alkaline-Ash Diet to alkalinize urine (Milk, milk products, vegetables; fruits except prunes, cranberries & plums) 3. Uric Acid Stones Reduce foods high in purine (liver, beans, kidneys, venison, shellfish, meat soups, gravies, legumes) Maintain alkaline urine 11. Provide client teaching and discharge planning concerning Prevention of Urinary stasis by maintaining increased fluid intake especially in hot weather & during illness; mobility; voiding whenever the urge is felt and at least twice during the night 12. Provide client teaching & discharge planning concerning: Adherence to prescribed diet Need for routine urinalysis (at least every 34 months) Need to recognize and report signs/ symptoms of recurrence (hematuria, flank pain).
3. ACUTE RENAL FAILURE (ARF) Sudden inability of the kidneys to excrete nitrogenous waste products & maintain F&E balance d/t a decrease in GFR. Most important manifestation: OLIGURIA Pathophysiology: 3 Stages/Causes:
Normal GFR = 125 ml/min
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1. Pre-Renal Cause: Decrease in GFR Causes: 1. 2. Septic shock Hypovolemia Hypotension CHF Hemorrhage Chronic Diarrhea Burns Cardiogenic Shock Anaphylaxis
3.
4. 5. 6. 7. 8. 9.
Decrease flow to kidneys
2. Intra-Renal Cause: Involves renal pathology Kidney Problem Conditions that cause damage to the nephrons: Acute tubular necrosis (ATN Endocarditis DM Malignant HPN AGN Ttumors BT Reactions Hypercalcemia Nephrotoxins (certain antibiotics, x-ray dyes, pesticides, anesthetics) Pyelonephritis 3. Post-Renal Cause: Mechanical Obstruction anywhere from the tubules to the urethra Calculi BPH Tumors Strictures Blood clots Trauma Anatomic malformation Urolithiasis Laboratory Findings: 1. Urinalysis: Urine osmo and sodium 2. BUN & Creatinine levels increased 3. Hyperkalemia 4. Anemia 5. ABG: Metabolic Acidosis
3 Phases of Acute Renal Failure 1. Oliguric Phase Urine output less than 400 cc/24 hours Duration 12 weeks Manifested by a. Dilutional Hyponatremia
4 Phases of Acute Renal Failure (Brunner & Suddarth) Initiation phase ( 0-2 days) Oliguric phase Diuretic phase Convalescence or recovery phase
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b. Hyperkalemia c. Hyperphosphatemia d. Hypocalcemia e. Hypermagnesemia f. Metabolic Acidosis Dx: BUN & creatinine elevated 2. Diuretic Phase Diuresis may occur (output 35 liters/day) d/t partially regenerated tubules inability to concentrate urine Duration: 23 week Manifested by: a. Hyponatremia b.Hyperkalemia c. Hypovolemia d. Metabolic Acidosis Dx: BUN & Creatinine slightly elevated 3. Convalescence or Recovery Phase Renal function stabilizes with gradual improvement over next 312 months. Complete Diuresis
Nursing Interventions: 1. Monitor & maintain fluid & electrolyte balance. Measure l & O every hour. note excessive losses in diuretic phase Administer IV F & E supplements as ordered. Weigh daily & report gains. Monitor lab values; assess/treat F & E & acid-base imbalances as needed 2. Monitor alteration in fluid volume. Monitor vital signs, PAP, PCWP, CVP as needed. Weigh client daily. Maintain strict I & O records. 3. Assess every hour for hypervolemia Maintain adequate ventilation. Restrict FLUID intake Administer diuretics & antihypertensives 4. Promote optimal nutritional status. Administer TPN as ordered. With enteral feedings, check for residual & notify physician if residual volume increases. Restrict protein intake to 1 g/kg/day Restrict POTASSIUM intake HIGH CARBOHYDRATE DIET, calcium supplements 5. Prevent complications from impaired mobility (pulmonary embolism, skin breakdown & atelectasis) 6. Prevent fever/infection. Assess for signs of infection. Use strict aseptic technique for wound & catheter care. 7. Support client/significant others & reduce/ relieve anxiety. Explain pathophysiology & relationship to symptoms. Explain all procedures and answer all questions in easy-to-understand terms Refer to counseling services as needed 8. Provide care for the client receiving dialysis 9. Provide client teaching & discharge planning concerning Adherence to prescribed dietary regimen Signs and symptoms of recurrent renal disease Importance of planned rest periods Use of prescribed drugs only: Sx of UTI or respiratory infection need to report to physician immediately 4. CHRONIC RENAL FAILURE (CRF) Irreversible loss of kidney function - Gradual, Progressive irreversible destruction of the kidneys causing severe renal dysfunction. The result is azotemia to UREMIA Predisposing Factors:
1. DM worldwide leading cause

Hallmark of Renal Failure: AZOTEMIA & OLIGURIA

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2. HPN -2nd cause 3. Recurrent UTI/ Pyelonephritis

4. 5.
6.
Pathophysiology:
Exposure to renal toxins Recurrent infections Urinary tract obstruction
As renal functions decline Retention of end-products of metabolism
STAGE 1= Reduced renal reserve volume (Asymptomatic) 40-75% loss of nephron function Normal BUN & Creatinine GFR <10-30% STAGE 2= Renal insufficiency, 75-90% loss of nephron function STAGE 3= End-stage renal disease, more than 90% loss. DIALYSIS IS THE TREATMENT! S/Sx: 1. Urinary System a. Polyuria b. Nocturia c. Hematuria d. Dysuria e. Oliguria 3. CNS a. Headache b. Lethargy c. Disorientation/Confusion d. Restlessness e. Memory impairment 5. Respiratory a. Kassmauls resp b. Decrease cough reflex c. Pericardial Friction rub 7. Fluid & Electrolytes a. Hyperkalemia b. Hypernatermia c. Hypermagnesemia d. Hyperposphatemia e. Hypocalcemia f. Metabolic Acidosis Diagnostic Tests: a. 24 hour creatinine clearance urinalysis b. Protein, sodium, BUN, Crea and WBC elevated c. Specific gravity, platelets, and calcium decreased d. CBC = Aanemia Medical Mgt: 1. Diet restrictions 2. Multivitamins 3. Hematinics and erythropoietin 4. Aluminum hydroxide gels 5. Anti-hypertensive 6. Anti-seizures 7. Assist in DIALYSIS DIALYSIS - A procedure that is used to remove fluid & uremic wastes from the body when the kidneys cannot function Two Methods:
2. Metabolic disturbances a. Azotemia (increase BUN & Crea) b. Hyperglycemia c. Hyperinulinemia 4. GIT a. N/V, Anorexia b. Stomatitis c. Uremic breath d. Diarrhea/ constipation 6. Hematological a. Normocytic anemia bleeding tendencies Pancytopenia/ Leukopenia 8. Integumentary a. Itchiness/ pruritus b. Uremic frost accumulation of urea in the skin 9. Cardiovascular a. Pulmonary HPN b. CHF c. Pericarditis
1. Hemodialysis 2. Peritoneal dialysis Process of: Diffusion / Osmosis / Ultrafiltration Nsg. Responsibility: 1. Assist in Hemodialysis 1.) 2.) 3.) 4.)
Weight: An important parameter that indicates effective hemodialysis
Consent/ explain procedure Obtain baseline data & monitor VS, I&O, wt, blood exam Strict aseptic technique Monitor for signs of complications: DISEQUILIBRIUM SYNDROME: B bleeding E embolism D disequilibrium syndrome S septicemia S shock decrease in tissue perfusion
-Results from rapid removal of urea & nitrogenous waste prod leading to: 1. N/V 2. HPN 3. Leg cramps 4. Disorientation 5. Paresthesia 6. Headache
5.) Avoid BP taking, blood extraction, IV, at side of shunt or fistula. Can lead to compression of fistula. 6.) Maintain patency of shunt by: Palpate for thrills & auscultate for bruits if (+) patent shunt! Bedside- Bulldog Clip to prevent embolism - If with accidental removal of fistula to prevent embolism. - Infersole (Diastole) Most common type of dialysate used 7. Meet the patient's psychosocial needs 8. Remember to avoid any procedure on the arm with the fistula (HEMO) 9. Monitor WEIGHT, blood pressure & fistula site for bleeding 10. Monitor symptoms of uremia 11. Detect complications like infection, bleeding (Hepatitis B/C and HIV infection in Hemodialysis) Peritonitis in peritoneal dialysis 12. Warm the solution to increase diffusion of waste products (PERITONEAL) 13. Manage discomfort & pain 14. To determine effectiveness, check serum creatinine, BUN & electrolytes 15. Inform client that minimal bleeding is expected because blood has been heparinized
Nursing Mgt For Chronic Renal Failure: 1. 2. 3. Enforce CBR Monitor VS, I&O Meticulous skin care. Uremic frost assist in bathing pt
DIET:
CHO = Increased CHON = Decreased FATS = Decreased
4. Meds: a.) Na HCO3 = to correct acidosis b.) Kayexelate Enema = to promote excretion of potassium c.) Anti HPN = Hydralazine d.) Vit & minerals e.) Phosphate binder (Amphogel) Al OH gel - S/E constipation f.) To Decrease Ca Ca gluconate g.) Hematinics 5. Assist in surgery: Renal transplantation : Complication rejection. Reverse isolation: Lifetime steroids 6. Complication - Peritonitis -------Early Sign: Cloudy Output - Shock
Additional Nsg. Interventions For Chronic Renal Failure: 1. Prevent neurological complications. Assess every hour for signs of uremia (fatigue, loss of appetite, decreased urine output, apathy, confusion, elevated blood pressure, edema of face and feet, itchy skin, restlessness, seizures). Assess for changes in mental functioning. Orient confused client to time, place, date, and persons Institute safety measures to protect client from falling out of bed. 2. Promote optimal GI function. Assess/provide care for stomatitis Monitor nausea, vomiting, anorexia Administer antiemetics as ordered. Assess for signs of Gl bleeding 3. Monitor/prevent alteration in fluid and electrolyte balance 4. Assess for hyperphosphatemia (paresthesias, muscle cramps, seizures, abnormal reflexes), and hydroxide gels (Amphojel) as ordered 5. Promote maintenance of skin integrity. Assess/provide care for pruritus. Assess for uremic frost (urea crystallization on the skin) and bathe in plain water 6. Monitor for bleeding complications, prevent injury to client. Monitor Hgb, hct, platelets, RBC. Hematest all secretions. Administer hematinics as ordered. Avoid lM injections 7. Promote/maintain maximal cardiovascular function. Monitor blood pressure and report significant changes. Auscultate for pericardial friction rub. Perform circulation checks routinely. Administer diuretics as ordered and monitor output. Modify drug doses 8. Provide care for client receiving dialysis administer aluminum
MALE REPRODUCTIVE DISORDERS 1. BPH 2. Prostatic cancer
167
DIAGNOSTIC PROCEDURES: 1. DIGITAL RECTAL EXAMINATION- DRE Recommended for men annually with age over 40 years Screening test for cancer Ask patient to BEAR DOWN 2. TESTICULAR EXAMINATION Palpation of scrotum for nodules and masses or inflammation BEGINS DURING ADOLESCENCE 3. Prostate specific antigen (PSA) Elevated in prostate cancer Normal is 0.2 to 4 nanograms/mL Cancer= over 4 1. BENIGN PROSTATIC HYPERPLASIA (BPH) Enlargement of the prostate gland that causes outflow obstruction leading to : 1. 2. 3. 4. Predisposing Factor: Hydro ureters dilation of ureters Hydronephrosis dilation of renal pelvis Kidney stones Renal failure
1. High Risk Men 50 years old & above

2. S/Sx: 1.Nocturia - Decrease in the volume & force of urinary stream 2.Dysuria 3.Hematuria 4.Burning upon urination 5.Terminal bubbling 6.Backache 7.Sciatica 8. Increased frequency, urgency & hesitancy Diagnosis: 1. Digital rectal exam enlarged prostate gland that is rubbery, large & NON-TENDER 2. KUB urinary obstruction 3. Cystoscopic exam obstruction 4. Urinalysis increase WBC, CHON Medical Mgt: 1. Immediate catheterization 2. Prostatectomy 3. TRANSURETHRAL RESECTION of the PROSTATE (TURP) 4. Pharmacology: alpha-blockers, alpha-reductase inhibitors. SAW palmetto NURSING INTERVENTION: TURP Maintain the three way bladder irrigation to prevent hemorrhage Only initially the drainage is pink-tinged and never reddish Administer anti-spasmodic to prevent bladder spasms NURSING INTERVENTION Nursing Mgt:
60 70 (3 to 4 x at risk) Influence of male hormone
1. 2.
3.
4.
Prostatic message promotes evacuation of prostatic fluid Limit fluid intake Provide catheterization Meds: a. Alpha-Adrenergic Blockers b. Terazozine (hytrin) - Relaxes bladder sphincter c. Finasteride (Proscar) - Atrophy of Prostate Gland
Avoid anticholinergics Prepare for surgery or TURP Teach the patient perineal muscle exercises. Avoid valsalva until healing Surgery: Prostatectomy TURP- Transurethral resection of Prostate- No incision -Assist in cystoclysis or continuous bladder irrigation. Monitor symptoms of infection 2. Monitor symptoms gross/ flank bleeding. Normal bleeding within 24h. 9. Maintain irrigation or tube patent to flush out clots - to prevent bladder spasm & distention Nursing Mgt: 1.
2. PROSTATE CANCER - A slow growing malignancy of the prostate gland - Usually an adenocarcinoma -This usualy spread via blood stream to the vertebrae Predisposing Factor: Age Assessment: 1. DRE: hard, pea-sized nodules on the anterior rectum 2. Hematuria 3. Urinary obstruction 4. Pain on the perineum radiating to the leg Dx: 1. Prostatic specific antigen (PSA) 2. Elevated SERUM ACID PHOSPHATASE indicates SPREAD or Metastasis Medical & Surgical Mgt: 1.Prostatectomy 2. TURP 3. Chemotherapy: hormonal therapy to slow the rate of tumor growth 4. Radiation therapy Nursing Interventions: 1.Prepare patient for chemotherapy 2. Prepare for surgery Nursing Interventions: Post-prostatectomy: 1. Maintain continuous bladder irrigation. Note that drainage is pink tinged w/in 24 hours 2. Monitor urine for the presence of blood clots and hemorrhage 3. Ambulate the patient as soon as urine begins to clear in color OVERVIEW OF RESPIRATORY SYSTEM: I. Upper respiratory tract:
Fx: 1. Filtering of air 2. Warming & moistening 3. Humidification Nose cartilage - Parts: Rt nostril separated by septum Lt nostril 2. Consists of anastomosis of capillaries Kessel Bach Plexus site of epistaxis Pharynx (throat) muscular passageway for air& food Branches: 1. Oropharynx 2. Nasopharynx 3. Layngopharynx
a.
b.
c. Larynx voice box Fx: 1. 2. For phonation Cough reflex
Glottis opening Opens to allow passage of air Closes to allow passage of food II. Lower Rt Fx for gas exchange a. Trachea windpipe - has cartillagenous rings - site for permanent/ artificial a/w tracheostomy b. Bronchus R & L main bronchus c. Lungs R 3 lobes = 10 segments L 2 lobes 8 segments Post pneumonectomy - position affected side to promote expansion of lungs Post segmental lobectomy position unaffected side to promote drainage Lungs covered by pleural cavity, parietal lobe & visceral lobe Alveoli acinar cells 3. site of gas exchange (O2 & CO2) 4. diffusion: Daltons law of partial pressure of gases Ventilation movement of air in & out of lungs Respiration movement of air into cells Type II cells of alveoli secrets surfactant Surfactant - decrease surface tension of alveoli Lecithin & spinogometer L/S ratio 2:1 indicator of lung maturity If 1:2 adm O2 - < 40% Concentration to prevent atelectasis & retinopathy or blindness.
I. PNEUMONIA inflammation of lung parenchyma leading to pulmonary consolidation as alveoli is filled with exudates.
Etiologic agents: 1. Streptococcus pneumoniae (pnemococcal pneumonia) 2. Hemophilus pneumoniae(Bronchopneumonia) 3. Escherichia coli 4. Klebsiella P. 5. Diplococcus P. High risk elderly & children below 5 yo Predisposing factors: 1. Smoking 2. Air pollution 3. Immuno-compromised a. AIDS PLP b. Bronchogenic CA - Non-productive to productive cough 4. Prolonged immobility CVA- hypostatic pneumonia 5. Aspiration of food 6. Over fatigue S/Sx:
1. Productive cough pathognomonic: greenish to rusty sputum

2. 3. 4. 5. 6. 7. 8. Dyspnea with prolonged respiratory grunt Fever, chills, anorexia, gen body malaise Wt loss Pleuritic friction rub Rales/ crackles Cyanosis Abdominal distension leading to paralytic ileus
Sputum exam could confirm presence of TB & pneumonia Dx: 1. Sputum GSCS- gram staining & culture sensitivity - Reveals (+) cultured microorganism. 2. CXR pulmo consolidation 3. CBC increase WBC Erythrocyte sedimentation rate 4. ABG PO2 decrease Nsg Mgt: Enforce CBR Strict respiratory isolation Meds: 1. Broad spectrum antibiotics Penicillin or tetracycline Macrolides ex azythromycin (zythromax) 2. Anti pyretics 3. Mucolytics or expectorants 4. Force fluids 2 to 3 L/day 5. Institute pulmonary toilet1. Deep breathing exercise 2. Coughing exercise 3. Chest physiotherapy cupping 4. Turning & reposition - Promote expectoration of secretions 6. Semi-fowler 7. Nebulize & suction 8. Comfy & humid environment 9. Diet: increase CHO or calories, CHON & vit C 10. Postural drainage - To drain secretions using gravity Mgt for postural drainage: a.) Best done before meals or 2 4 hrs after meals to prevent Gastroesophageal Reflux b.) Monitor VS & breath sounds Normal breath sound bronchovesicular
1. 2. 3.
c.) Deep breathing exercises d.) Adm bronchodilators 15 30 min before procedure e.) Stop if pt cant tolerate procedure f.) Provide oral care it may alter taste sensation g.) C/I pt with unstable VS & hemoptysis, increase ICP, increase IOP (glaucoma) Normal IOP 12 21 mmHg 11. HT: a.) Avoidance of precipitating factors b.) Complication: Atelectacies & meningitis c.) Compliance to meds 2. PULMONARY TUBERCULOSIS (KOCH DSE) - Inflammation of lung tissue caused by invasion of mycobacterium TB or tubercle bacilli or acid fast bacilli gram (+) aerobic, motile & easily destroyed by heat or sunlight. Predisposing factors: 1. Malnutrition 2. Overcrowding 3. Alcoholism 4. Ingestion of infected cattle (mycobacterium BOVIS) 5. Virulence 6. Over fatigue S/Sx: 1. 2. 3. 4. 5. 6. 7. Productive cough yellowish Low fever Night sweats Dyspnea Anorexia, general body malaise, wt loss Chest/ back pain Hempotysis
Diagnosis: 1. Skin test mantoux test infection of Purified CHON Derivative PPD DOH 8-10 mm induration WHO 10-14 mm induration Result within 48 72h (+) Mantoux test previous exposure to tubercle bacilli Mode of transmission droplet infection 2. Sputum AFB (+) to cultured microorganism 3. CXR pulmonary infiltrate caseosis necrosis 4. CBC increase WBC Nursing Mgt: 1. CBR 2. Strict resp isolation 3. O2 inhalation 4. Semi fowler 5. Force fluid to liquefy secretions 6. DBCE 7. Nebulize & suction 8. Comfy & humid environment 9. Diet increase CHO & calories, CHON, Vit, minerals 10. Short course chemotherapy 5. Intensive phase INH isoniazide Rifampicin - give before meals for absorption - given within 4 months, given simultaneously to prevent resistance -S/E: peripheral neutitis vit B6 Rifampicin -All body secretions turn to red orange color urine, stool, saliva, sweat & tears.
PZA Pyrazinamide given 2 mos/ after meals. S/E: allergic rxn, nephrotoxicity & hepatoxicity
Standard regimen 1. Injection of streptomycin aminoglycoside Ex. Kanamycin, gentamycin, neomycin S/E: a.) Ototoxicity damage CN # 8 tinnitus hearing loss b.) Nephrotoxicicity monitor BUN & Crea HT: a.) Avoid pred factors b.) Complications: 1.) Atelectasis 2.) Miliary TB spread of Tb to other system b.) Compliance to meds - Religiously take meds 3. HISTOPLASMOSIS- acute fungal infection caused by inhalation of contaminated dust with histoplasma capsulatum transmitted to birds manure. S/Sx: Same as pneumonia & PTB like 1. Productive cough 2. Dyspnea 3. Chest & joint pains 4. Cyanosis 5. Anorexia, gen body malaise, wt loss 6. Hemoptysis Dx: 1. 2. Histoplasmin skin test = (+) ABG pO2 decrease
Nsg Mgt: 1. CBR 2. Meds: a.) Anti fungal agents Amphotericin B (Fungizone) S/E : a.) Nephrotoxcicity check BUN b.) Hypokalemia b.)Corticosteroids c.) Mucolytic/ or expectorants 3. O2 force fluids 4. Nebulize, suction 5. Complications: a.) Atelectasis b.) Bronchiectasis COPD 6. Prevent spread of histoplasmosis: a.) Spray breading places or kill the bird.
4. COPD Chronic Obstructive Pulmonary Disease 1. Chronic bronchitis

2. 3. 4.
Bronchial asthma Bronchiectasis Pulmonary emphysema terminal stage
CHRONIC BRONCHITIS - called BLUE BLOATERS inflammation of bronchus due to hypertrophy or hyperplasia of goblet mucus producing cells leading to narrowing of smaller airways. Predisposing factors: 1. Smoking all COPD types 2. Air pollution S/Sx: 1. Prod cough 2. Dyspnea on exertion 3. Prolonged expiratory grunt 4. Scattered rales/ rhonchi 5. Cyanosis 6. Pulmo HPN a.)Leading to peripheral edema b.) Cor pulmonary respiratory in origin 7. Anorexia, gen body malaise Dx: 1. ABG PO2 PCO2 Resp acidosis
Hypoxemia causing cyanosis Nsg Mgt: (Same as emphysema) 2.) BRONCHIAL ASTHMA- reversible inflammation lung condition due to hyerpsensitivity leading to narrowing of smaller airway. Predisposing factor: 1. Extrinsic Asthma called Atropic/ allergic asthma a.) Pallor b.) Dust c.) Gases d.) Smoke e.) Dander f.) Lints 2. Intrinsic AsthmaCause: Herediatary Drugs aspirin, penicillin, blockers Food additives nitrites Foods seafood, chicken, eggs, chocolates, milk Physical/ emotional stress Sudden change of temp, humidity &air pressure 3. mixed type: combi of both ext & intr. Asthma 90% cause of asthma S/Sx: 1. 2. 3. 4. 5. 6. 7. Dx: 1. 2. C cough non productive to productive D dyspnea W wheezing on expiration Cyanosis Mild apprehension & restlessness Tachycardia & palpitation Diaphoresis Pulmo function test decrease lung capacity ABG PO2 decrease
Nsg Mgt: 1. CBR all COPD

2.
Meds-
a.) Bronchodilator through inhalation or metered dose inhaled / pump. Give 1st before corticosteroids
b.) Corticosteroids due inflammatory. Given 10 min after adm bronchodilator c.) Mucolytic/ expectorant d.) Mucomist at bedside put suction machine. e.) Antihistamine Force fluid O2 all COPD low inflow to prevent resp distress Nebulize & suction Semifowler all COPD except emphysema due late stage HT a.) Avoid pred factors b.) Complications: Status astmaticus- give epinephrine & bronchodilators Emphysema c.) Adherence to med
2.
3.
4. 5. 6. 6. 7.
BRONCHIECTASIS abnormal permanent dilation of bronchus resulting to destruction of muscular & elastic tissues of alveoli. Predisposing factors: 1. Recurrent upper & lower RI 2. Congenital anomalies 3. Tumors 4. Trauma S/Sx: 1. Productive cough 2. Dyspnea 3. Anorexia, gen body malaise- all energy are used to increase respiration. 4. Cyanosis 5. Hemoptisis Dx: ABG PO2 decrease Bronchoscopy direct visualization of bronchus using fiberscope. Nsg Mgt: before bronchoscopy 1. Consent, explain procedure MD/ lab explain RN 2. NPO 3. Monitor VS Nsg Mgt after bronchoscopy 1. Feeding after return of gag reflex 2. Instruct client to avoid talking, smoking or coughing 3. Monitor signs of frank or gross bleeding 4. Monitor of laryngeal spasm 8. DOB 9. Prepare at bedside tracheostomy set Mgt: same as emphysema except Surgery Pneumonectomy removal of affected lung Segmental lobectomy position of pt unaffected side 1. 2.
PULMONARY EMPHYSEMA irreversible terminal stage of COPD 10. Characterized by inelasticity of alveolar wall leading to air trapping, leading to maldistribution of gases. 11. Body will compensate over distension of thoracic cavity 12. Barrel chest Predisposing factor: 1. Smoking 2. Allergy 3. Air pollution 4. High risk elderly 5. Hereditary - 1 anti trypsin to release elastase for recoil of alveoli.
S/Sx: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Productive cough Dyspnea at rest due terminal Anorexia & gen body malaise Rales/ rhonchi Bronchial wheezing Decrease tactile fremitus (should have vibration) palpation 99. Decreased - with air or fluid Resonance to hyperresonance percussion Decreased or diminished breath sounds Pathognomonic: barrel chest increase post/ anterior diameter of chest Purse lip breathing to eliminated PCO2 Flaring of alai nares
Diagnosis: 1. Pulmonary function test decrease vital lung capacity 2. ABG 1. Panlobular / centrolobular emphysema pCO2 increase pO2 decrease hypoxema resp acidosis Blue bloaters 2. Panacinar/ Centracinar pCO2 decrease pO2 increase hyperaxemia resp alkalosis Pink puffers Nursing Mgt: 1. CBR 2. Meds a.) Bronchodilators b.) Corticosteroids c.) Antimicrobial agents d.) Mucolytics/ expectorants 3. O2 Low inflow 4. Force fluids 5. High fowlers 6. Neb & suction 7. Institute P posture E end E expiratory to prevent collapse of alveoli P pressure 8. HT a.) Avoid smoking b.) Prevent complications 1.) Cor pulmonary R ventricular hypertrophy 2.) CO2 narcosis lead to coma 3.) Atelectasis 4.) Pneumothorax air in pleural space 9. Adherence to meds
5. RESTRICTIVE LUNG DISORDER

PNEUMOTHORAX partial / or complete collapse of lungs due to entry or air in pleural space. Types: 1. Spontaneous pneumothorax entry of air in pleural space without obvious cause. Eg. rupture of bleb (alveoli filled sacs) in pt with inflammed lung conditions Eg. open pneumothorax air enters pleural space through an opening in chest wall -Stab/ gun shot wound 2. Tension Pneumothorax air enters plural space with @ inspiration & cant escape leading to over distension of thoracic cavity resulting to shifting of mediastinum content to unaffected side. Eg. flail chest paradoxical breathing Predisposing factors: 1.Chest trauma 2.Inflammatory lung conditions 3.Tumor S/Sx: 1. Sudden sharp chest pain 2. Dyspnea 3. Cyanosis 4. Diminished breath sound of affected lung 5. Cool moist skin 6. Mild restlessness/ apprehension 7. Resonance to hyper resonance Diagnosis: 1. ABG pO2 decrease 2. CXR confirms pneumothorax Nursing Mgt: 1. Endotracheal intubation 2. Thoracenthesis 3. Meds Morphine SO4 13. Anti microbial agents 4. Assist in test tube thoracotomy Nursing Mgt if pt is on CPT attached to H2O drainage 1. Maintain strict aseptic technique 2. DBE 3. At bedside 1. Petroleum gauze pad if dislodged Hemostan 2. If with air leakage clamp 3. Extra bottle 4. Meds Morphine SO4 Antimicrobial 5. Monitor & assess for oscillation fluctuations or bubbling 1. If (+) to intermittent bubbling means normal or intact - H2O rises upon inspiration - H2o goes down upon expiration b.) If (+) to continuous, remittent bubbling 1. Check for air leakage 2. Clamp towards chest tube 3. Notify MD c.) If (-) to bubbling 1. Check for loop, clots, and kink 2. Milk towards H2O seal 3. Indicates re-expansion of lungs When will MD remove chest tube: 1. If (-) fluctuations 2. (+) Breath sounds 3. CXR full expansion of lungs Nursing Mgt of removal of chest tube 2. DBE 3. Instruct to perform Valsalva maneuver for easy removal, to prevent entry of air in pleural space. 4. Apply vaselinated air occlusive dressing 14. Maintain dressing dry & intact EAR
1. 2. Parts: 1.
Hearing Balance (Kinesthesia or position sense) Outera.) Pinna/ auricle protects ear from direct trauma b.) Ext. auditory meatus has ceruminous gland. Cerumen c.) Tympanic membrane transmits sound waves to middle ear
Disorders of outer ear Entry of insects put flashlight to give route of exit Foreign objects beans (bring to MD) H2O - drain 2. Middle ear a.) Ear osssicle 1. Hammer -malleus 2. Anvil -Incus 3. Stirrups -stapes for bone conduction disorder conductive hearing loss
b. Eustachian tube - Opens to allow equalization of pressure on both ears - Yawn, chew, and swallow Children straight, wide, short 5. Otitis media Adult long, narrow & slanted c. Muscles 1. Stapedius 2. Tensor tympani
3. Inner ear a. Bony labyrinth for balance, vestibule Utricle & succule Otolithe or ear stone has Ca carbonate Movement of head = Righting reflex = Kinesthesia b. Membranous Labyrinth 1. Cochlea ( function for hearing) has organ of corti 2. Endolymph & perilymph for static equilibrium 3. Mastoid air cells air filled spaces in temporal bone in skull Complications of Mastoditis meningitis Types of hearing loss: 1. Conductive hearing loss transmission hearing loss Causes: a.) Impacted cerumen tinnitus & conduction hearing loss- assist in ear irrigaton b.) Immobility of stapes OTOSCLEROSIS 6. Middle ear disease char by formation of spongy bone in the inner ear causing fixation or immobility of stapes 7. Stapes cant transmit sound waves Surgery Stapedectomy removal of stapes, spongy bone & implantation of graft/ ear prosthesis
Predisposing factor: 1. Familiar tendency 2. Ear trauma & surgery S/Sx: 1. 2. Tinnitus Conductive hearing loss
Diagnosis: 1. Audiometry various sound stimulates (+) conductive hearing loss 2. Webers test Normal AC> BC result BC > AC Stapedectomy Nursing Mgt post op 1. Position pt unaffected side 2. DBE No coughing & blowing of nose - Night lead to removal of graft 3. Meds: a.) Analgesic b.) Antiemetic c.) Antimotion sickness agent. Ex. meclesine Hcl (Bonamine) 4. Assess motor function facial nerve - (Smile, frown, raise eyebrow) 5. Avoid shampoo hair for 1 to 2 weeks. Use shower cap SENSORY NEURAL HEARING LOSS/ NERVE DEAFNESS Cause: 1. Tumor on cocheal 2. Loud noises (gun shot) 3. Presbycusis bilateral progressive hearing loss especially at high frequencies elderly Face elderly to promote lip reading 4. Menieres disease endolymphatic hydrops 8. Inner ear disease char by dilation of endo lympathic system leading to increase volume of endolin Predisposing factor of MENIERES DISEASE Smoking Hyperlipidemia 30 years old Obesity (+) chosesteatoma Allergy Ear trauma & infection S/Sx: 1. TRIAD symptoms of Menieres disease a.) Tinnitus b.) Vertigo c.) Sensory neural hearing loss Nystagmus n/v Mild apprehension, anxiety Tachycardia Palpitations Diaphoresis Audiometry (+) sensory hearing loss
2. 3. 4. 5. 6. 7. Diagnosis: 1.
Nursing mgt: 1. Comfy & darkened environment 2. Siderails 3. Emetic basin

4.
Meds: a.) b.) c.) d.) e.) f.)
Diuretics to remove endolymph Vasodilator Antihistamine Antiemetic Antimotion sickness agent Sedatives/ tranquilizers
5. Restrict Na 6. Limit fluid intake 7. Avoid smoking 8. Surgery endolymphatic sac decompression- Shunt *Kawasaki : Drug of Choice : Aspirin, IgG Common to children 5 y/o below (desquamation of palms & toes) *Anatomy : URT Nose Pharynx Larynx LRT Trachea Bronchos
180

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MEDICAL SURGICAL

a. Meiosis = constriction of pupils

Created by Nia E. Tubio

b. Carbon Monoxide :Tx for Carbon monoxide poisoning

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CHARCOTS TRIAD (INA)

1. INCREASED ICP increase IC bulk is due to increase in 1 of the IC components

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* Powerful respiratory stimulant : CO2 ---an

CO2 retention/ hypercarbia ---stimulate medulla O.

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increase cardiac contraction = increase CO

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PARKINSONS DISEASE (Parkinsonism)

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GBS GUILLIAN BARRER SYNDROME

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Direct transmission via droplet nuclei (airborne)

(Normal: 50 160 mmHg)

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Initial sign: Weakness & Fatifue

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4. *Compartment Syndrome compression of nerves/ arteries

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CONVULSIVE Disorder (CONVULSIONS)

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- Constricts the pupil - Dilates the pupil

corrected by corrective eye surgery

1. *Loss of Central Vision - Hazy or blurring of vision

Partial removal of lens

Total removal of lens & surrounding capsules

Complications of Lens Extraction: Hemorrhage

Created by Nia E. Tubio

Created by Nia E. Tubio

Created by Nia E. Tubio

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To Prevent STD Local practice monogamous relationship CGFNS/NCLEX condom

Parathyroid Glands Gonads

2 BASIC PATHOPHYSIOLOGICAL DISORDER OF THE ENDOCRINE

Posterior Pituitary Gland Neurohypophysis

Hyperpituitarism Acromegaly -- Adult 1. Gigantism

2. Inflammation 3. Trauma 4. Tumor Pathophysiology :

Polydipsia Dehydration Other S & Sx:

Urine Specific gravity

(N = 1.015 1.035) (N =135 -145 meq/L)

(The only Endocrine Gland with Water Intoxication)

Increase ICP Complications of SIADH Seizure Activity

1.Restrict fluid. (<1,000 ml/day)

Located at the top of the kidney 2 Parts:

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DISORDERS OF THE ADRENAL CORTEX: CODE: 3 Ss Addisons Disease

Hypoglycemia Hyponatermia Loss of pubic CONNS DISEASE 1. ADDISONS DISEASE

Hyperglycemia Hypernatremia Hirsutism

- Hypoglycemia - Decreased Plasma cortisol Sugar Melanocyte secreting hormone

Hypovolemia --- Hypotension

- Hyponatremia ---- Dehydration (Extreme thirst & agitation)----Weight Loss

- Hyperkalemia influence cardiac polarization Arrythmia ---Cardiac Arrest Sex

Sx of Hyperkalemia I irritability D diarrhea

Nsg. Mgt. with Steroids

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polyuria polydipsia polyphagia