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MEDICAL SURGICAL

Overview of the Structures & Functions of Nervous System Central NS PNS ANS Brain &
spinal cord 31 spinal & cranial sympathetic NS Parasypathatic NS Somatic NS C- 8 T- 12 L- 5
S- 5 C- 1 ANS (or adrenergic of parasympatholitic response) SNS involved in fight or aggression
response Release of norepinephrine (adrenaline – cathecolamine) Adrenal medulla (potent
vasoconstrictor) Increases body activities VS = Increase Except GIT – decrease GITmotility *
Why GIT is not increased = GIT is not important! Increase blood flow to skeletal muscles, brain
& heart. Effects of SNS (anti-cholinergic/adrenergic) 1. Dilate pupil – to aware of surroundings -
medriasis 2. Dry mouth 3. BP & HR= increased bronchioles dilated to take more oxygen 4. RR
increased 5. Constipation & urinary retention

I. Adrenergic Agents – Epinephrine (adrenaline) SE: SNS effect II. PNS: Beta adrenergic
blocking agents (opposite of adrenergic agents) (all end in –‘lol’) - Blocks release of
norepinephrine. - Decrease body activities except GIT (diarrhea) Ex. Propanolol, Metopanolol
SE: B – broncho spasm (bronchoconstriction) E – elicits a decrease in myocardial contraction T
– treats HPN A – AV conduction slows down Given to angina & MI – beta-blockers to rest heart
Anti HPN agents: 1. Beta blockers (-lol) 2. Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL
3. Calcium antagonist ex CALCIBLOC or NEFEDIPINE Peripheral nervous system:
cholinergic/ vagal or sympatholitic response - Involved in fly or withdrawal response - Release
of acetylcholine (ACTH) - Decrease all bodily activities except GIT (diarrhea) I Cholinergic
agents ex 1. Mestinon Antidote – anti cholinergic agents Atropine Sulfate – S/E – SNS S/E- of
anti-hpn drugs: 1. orthostatic hpn Effect of PNS: (cholinergic) 1. Meiosis – contraction of pupils
2. Increase salivation 3. BP & HR decreased 4. RR decrease – broncho constriction 5. Diarrhea –
increased GI motility 6. Urinary frequency

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transient headache & dizziness. -Mgt. Rise slowly. Assist in ambulation. CNS (brain & spinal
cord) I. Cells – A. neurons Properties and characteristics a. Excitability – ability of neuron to be
affected in external environment. b. Conductivity – ability of neuron to transmit a wave of
excitation from one cell to another c. Permanent cells – once destroyed, cant regenerate (ex.
heart, retina, brain, osteocytes) Regenerative capacity A. Labile – once destroyed cant regenerate
- Epidermal cells, GIT cells, resp (lung cells). GUT B. Stable – capable of regeneration BUT
limited time only ex salivary gland, pancreas cells cell of liver, kidney cells C. Permanent cells –
retina, brain, heart, osteocytes can’t regenerate. 3.) Neuroglia – attached to neurons. Supports
neurons. Where brain tumors are found. Types: 1. Astrocyte 2. Oligodendria Astrocytoma – 90 –
95% brain tumor from astrocyte. Most brain tumors are found at astrocyte. Astrocyte – maintains
integrity of blood brain barrier (BBB). BBB – semi permeable / selective -Toxic substance that
destroys astrocyte & destroy BBB. Toxins that can pass in BBB: 1. Ammonia-liver cirrhosis. 2.
2. Carbon Monoxide – seizure & parkinsons. 3. 3. Bilirubin- jaundice, hepatitis,
kernicterus/hyperbilirubenia. 4. 4. Ketones –DM. OLIGODENDRIA – Produces myelin sheath –
wraps around a neuron – acts as insulator facilitates rapid nerve impulse transmission. No myelin
sheath – degenerates neurons Damage to myelin sheath – demyellenating disorders
DEMYELLENATING DSE 1.)ALZHEIMER’S DISEASE– atrophy of brain tissue due to a
deficiency of acetylcholine. S&Sx: A – amnesia – loss of memory A – apraxia – unable to
determine function & purpose of object A – agnosia – unable to recognize familiar object A –
aphasia – - Expressive – brocca’s aphasia – unable to speak - Receptive – wernickes aphasia –
unable to understand spoken words Common to Alzheimer – receptive aphasia Drug of choice –
ARICEPT (taken at bedtime) & COGNEX. Mgt: Supportive & palliative.

2.

Microglia – stationary cells, engulfs bacteria, engulfs cellular debris. II. Compositions of Cord &
Spinal cord 80% - brain mass 10% - CSF 10% - blood MONROE KELLY HYPOTHESIS: The
skull is a closed vault. Any increase in one component will increase ICP. Normal ICP: 0-
15mmHg Brain mass

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Connects R & L cerebral hemisphere - Corpus collusum Rt cerebral hemisphere, Lt cerebral
hemisphere Function: 1. Sensory 2. Motor 3. Integrative Lobes 1.) Frontal a. Controls motor
activity b. Controls personality development c. Where primitive reflexes are inhibited d. Site of
development of sense of umor e. Brocca’s area – speech center Damage - expressive aphasia 2.)
Temporal – a. Hearing b. Short term memory c. Wernickes area – gen interpretative or knowing
Gnostic area Damage – receptive aphasia 3.) Parietal lobe – appreciation & discrimation of
sensory imp - 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/
Limbec - Smell, libido, long-term memory Basal Ganglia – areas of gray matte located deep
within a cerebral hemisphere - Extra pyramidal tract - Releases dopamine- Controls gross
voluntary unit Decrease dopamine – (Parkinson’s) pin rolling of extremities & Huntington’s Dse.
Decrease acetylcholine – Myasthenia Gravis & Alzheimer’s Increased neurotransmitter =
psychiatric disorder Increase dopamine – schizo Increase acetylcholine – bipolar MID BRAIN –
relay station for sight & hearing Controls size & reaction of pupil 2 – 3 mm Controls hearing
acuity CN 3 – 4 Isocoria – normal size (equal) Anisocoria – uneven size – damage to mid brain
PERRLA – normal reaction DIENCEPHALON- between brain Thalamus – acts as a relay
station for sensation Hypothalamus – (thermoregulating center of temp, sleep & wakefulness,
thirst, appetite/ satiety center, emotional responses, controls pituitary function. BRAIN STEM- a.
Pons – or pneumotaxic center – controls respiration Cranial 5 – 8 CNS MEDULLA
OBLONGATA- controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus
Vasomotor center, spinal decuissation termination, CN 9, 10, 11, 12 CEREBELLUM – lesser
brain - Controls posture, gait, balance, equilibrium

1. Cerebrum – largest -

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Cerebellar Tests: a.) R – Romberg’s test- needs 2 RNs to assist - Normal anatomical position 5 –
10 min (+) Romberg’s test – (+) ataxia or unsteady gait or drunken like movement with loss of
balance. b.) Finger to nose test – (+) To FTNT – 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 – dymentrium Composition of brain - based on Monroe
Kellie Hypothesis - Skull is a closed container. Any alteration in 1 of 3 intracranial components
= increase in ICP Normal ICP – 0 – 15 mmHg Foramen Magnum C1 – atlas C2 – axis (+)
Projectile vomiting = increase ICP Observe for 24 - 48 hrs CSF – cushions the brain, shock
absorber Obstruction of flow of CSF = increase ICP Hydrocephalus – posteriorly due to closure
of posterior fontanel CVA – partial/ total obstruction of blood supply

INCREASED ICP – increase ICP is due to increase in 1 of the Intra Cranial components.
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 change in VS = always late symptoms Earliest Sx: a.) Change or decrease LOC –
Restlessness to confusion Wide pulse pressure: Increased ICP - Disorientation to lethargy
Narrow pp: Cardiac disorder, shock - Stupor to coma Late sign – change in V/S 1. BP increase
(systolic increase, diastole- same) 2. Widening pulse pressure Normal adult BP 120/80 120 – 80
= 40 (normal pulse pressure) Increase ICP = BP 140/80 = 140 – 80= 60 PP (wide) 3. RR is
decreased (Cheyne-Stokes = bet period of apnea or hyperpnea with periods of apnea) 4. Temp
increase Increased ICP: Increase BP Shock – decrease BP – Decrease HR Increase HR
CUSHINGS EFFECT Decrease RR Increase RR Increase Temp Decrease temp b.) Headache
Projectile vomiting Papilledima (edema of optic disk – outer surface of retina) Decorticate
(abnormal flexion) = Damage to cortico spinal tract / Decerebrate (abnormal extension) =
Damage to upper brain stem-pons/ c.) Uncal herniation – unilateral dilation of pupil. (Bilateral
dilation of pupil – tentorial herniation.) d.) Possible seizure.

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Nursing priority: 1.) Maintain patent a/w & adequate ventilation a. Prevention of hypoxia –
(decrease tissue oxygenation) & hypercarbia (increase in CO2 retention). Hypoxia – cerebral
edema - increase ICP Hypoxia – inadequate tissue oxygenation Late symptoms of hypoxia – B –
bradycardia E – extreme restlessness D – dyspnea C – cyanosis Early symptoms – R –
restlessness A – agitation T – tachycardia Increase CO2 retention/ hypercarbia – cerebral
vasodilatation = increase ICP Most powerful respiratory stimulant increase in CO2
Hyperventilate decrease CO2 – excrete CO2 Respiratory Distress Syndrome (RDS) – decrease
Oxygen Suctioning – 10-15 seconds, max 15 seconds. Suction upon removal of suction cap.
Ambu bag – pump upon inspiration c. Assist in mechanical ventilation 1. Maintain patent a/w 2.
Monitor VS & I&O 3. Elevate head of bed 30 – 45 degrees angle neck in neutral position unless
contra indicated 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. Siderails up d. Instruct patient to avoid the ff:
-Valsalva maneuver or bearing down, avoid straining of stool (give laxatives/ stool softener
Dulcolax/ Duphalac) - Excessive cough – antitussive Dextrometorpham -Excessive vomiting –
anti emetic (Plasil – Phil only)/ Phenergan - Lifting of heavy objects - Bending & stooping e.
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 – SE of 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
or precipitate 2.) Loop diuretic - Lasix (Furosemide) 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 Immediate effect of Lasix within 15 minutes. Max effect – 6
hrs due (7am – 1pm)

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S/E of Lasix

Hypokalemia (normal K-3.5 – 5.5 meg/L)


1. 2. 3. S&Sx Weakness & fatigue Constipation (+) “U” wave in ECG tracing

Nursing Mgt: 1.) Administer K supplements – ex Kalium Durule, K chloride Potassium Rich
food: ABC’s of K Vegetables Fruits A - asparagus A – apple B – broccoli (highest) B – banana –
green C – carrots C – cantalope/ melon O – orange (highest) –for digitalis toxicity also. Vit A –
squash, carrots yellow vegetables & fruits, spinach, chesa Iron – raisins, Food appropriate for
toddler – spaghetti! Not milk – increase bronchial secretions Don’t give grapes – may choke S/E
of Lasix: 1.) Hypokalemia

2.) Hypocalcemia (Normal level Ca = 8.5 – 11mg/100ml) or Tetany:


S&Sx weakness Paresthesia (+) Trousseau sign – pathognomonic – or carpopedal spasm. Put bp
cuff on arm=hand spasm. (+) Chevostek’s sign Arrhythmia Laryngospasm Administer – Ca
gluconate – IV slowly

Ca gluconate toxicity: Sx – seizure – administer Mg SO4


Mg SO4 toxcicity– administer Ca gluconate B – BP decrease U – urine output decrease R – RR
decrease P – patellar reflexes absent

3.) Hyponatremia – Normal Na level = 135 – 145 meg/L


Hypotension Signs of Dehydration: dry skin, poor skin turgor, gen body malaise. Early signs –
Adult: thirst and agitation / Child: tachycardia Mgt: force fluid Administer isotonic fluid sol 4.)
Hyperglycemia – increase blood sugar level P – polyuria P – polyphagia P – polydipsia Nsg Mgt:
a. Monitor FBS (N=80 – 120 mg/dl) 5.) Hyperurecemia – increase serum uric acid. Tophi- urate
crystals in joint. S/Sx –

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Gou

ty arthritis

kidney stones- renal colic (pain)

Cool moist skin Sx joint pain & swelling usually at great toe. 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 – excretes uric acid. Acute gout drug of choice. Kidney stones – renal colic
(pain). Cool moist skin Mgt: 1.) Force fluid 2.) Meds – narcotic analgesic Morphine SO4 SE of
Morphine SO4 toxicity Respiratory depression (check RR 1st) Antidote for morphine SO4
toxicity –Narcan (NALOXONE) Naloxone toxicity – tremors Increase ICP meds: 3.)
Corticosteroids - Dexamethsone – decrease cerebral edema (Decadrone) 4.) Mild analgesic –
codeine SO4. For headache. 5.) Anti consultants – Dilantin (Phenytoin) Question: Increase ICP
what is the immediate nsg action? a. Administer Mannitol as ordered b. Elevate head 30 – 45
degrees c. Restrict fluid d. 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 can’t pass. Need tracheostomy
onlyMagic 2’s of drug monitoring Drug D – digoxin L - lithium A – aminophylline D – Dilantin
A – acetaminophen N range .5 – 1.5 meq/L .6 – 1.2 meq/L 10 – 19 mg/100ml 10 -19 mg/100 ml
10 – 30 mg/100ml Toxicity 2 2 20 20 200 Classification cardiac glycosides antimanic
bronchodilator anticonvulsant narcotic analgesic Indication CHF bipolar COPD seizures
osteoarthritis

Digitalis – increase cardiac contraction = increase CO


Nursing Mgt 1. Check PR, HR (if HR below 60bpm, don’t giveDigoxin) Digitalis toxicity –
antidote - Digivine a. Anorexia -initial sx. b. n/v GIT c. Diarrhea d. Confusion

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e. f.

Photophobia Changes in color perception – yellow spots

(Ok to give to pts with renal failure. Digoxin is metabolized in liver not in kidney.) L – lithium
(lithane) decrease levels of norepinephrine, serotonine, acetylcholine
Antimanic agent Lithium toxicity S/Sx Anorexia n/s Diarrhea Dehydration – force fluid,
maintain Na intake 4 – 10g daily Hypothyroidism (CRETINISM– the only endocrine disorder
that can lead to mental retardation)

a.) b.) c.) d.) e.)

A – aminophyline (theophylline) – dilates bronchioles.


Take bp before giving aminophylline. S/Sx : Aminophylline toxicity: 1. Tachycardia 2.
Hyperactivity – restlessness, agitation, tremors a. b. c. d. Question: Avoid giving food with
Aminophylline Cheese/butter– food rich in tyramine, avoided only if pt is given MAOI Beer/
wine Hot chocolate & tea – caffeine – CNS stimulant tachycardia Organ meat/ box cereals – anti
parkinsonian

MAOI – antidepressant m AR plan n AR dil can lead to CVA or hypertensive crisis p AR nate 3
– 4 weeks - before MAOI 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
- Do sandwich method - Give NSS then Dilantin, then NSS! 2. Instruct the pt to avoid alcohol –
bec alcohol + dilantin can lead to severe CNS depression Dilantin toxicity: 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 Acetaminophen toxicity : 1. Hepato toxicity 2.
Monitor liver enzymes SGPT (ALT) – Serum Glutamic Piruvate Tyranase SGOT- Serum
Glutamic Acetate Tyranase 3. Monitor BUN (10 – 20) Crea (.8-1) Acetaminophen toxicity can
lead to hypoglycemia

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T – tremors, Tachycardia I – irritability R – restlessness E – extreme fatigue D – depression
(nightmares) , Diaphoresis Antidote for acetaminophen toxicity – Acetylcesteine = causes
outporing of secretions. Suction. Prepare suctioning apparatus. Question: The following are
symptoms of hypoglycemia except: a. Nightmares b. Extreme thirst – hyperglycemia symptoms
c. Weakness d. Diaphoresis

PARKINSONS DSE (parkinsonism) - chronic, progressive disease of CNS char by degeneration


of dopamine
producing cells in substancia nigra at mid brain & basal ganglia - Palliative, Supportive Function
of dopamine: controls gross voluntary motors. Predisposing Factors: 1. Poisoning (lead & carbon
monoxide). Antidote for lead = Calcium EDTA 2. Hypoxia 3. Arteriosclerosis 4. Encephalitis
High doses of the ff: a. Reserpine (serpasil) anti HPN, SE – 1.) depression - suicidal 2.) breast
cancer b. Methyldopa (aldomet) - promote safety c. Haloperidol (Haldol)- anti psychotic d.
Phenothiazide - anti psychotic SE of anti psychotic drugs – Extra Pyramidal Symptom Over
meds of anti psychotic drugs – neuroleptic malignant syndrome char by tremors (severe) S/Sx:
Parkinsonism – 1. Pill rolling tremors of extremities – early sign 2. Bradykinesia – slow
movement 3. Over fatigue 4. Rigidity (cogwheel type) a. Stooped posture b. Shuffling – most
common c. Propulsive gait 5. Mask like facial expression with decrease blinking eyes 6.
Monotone speech 7. Difficulty rising from sitting position 8. Mood labilety – always depressed –
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.) Anti parkinsonian agents - Levodopa (L-Dopa), Carbidopa
(Sinemet), Amantadine Hcl (Symmetrel) Mechanism of action Increase levels of dopa –
relieving tremors & bradykinesia S/E of anti parkinsonian - Anorexia - n/v - Confusion -
Orthostatic hypotension

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- Hallucination - Arrhythmia Contraindication: 1. Narrow angled closure glaucoma 2. Pt taking
MAOI (Parnate, Marplan, Nardil) Nsg Mgt when giving anti-parkinsonian 1. Take with meals –
to decrease GIT irritation 2. Inform pt – urine/ stool may be darkened 3. Instruct pt- don’t take
food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg - Cause B6 reverses therapeutic
effects of levodopa Give INH (Isoniazide-Isonicotene acid hydrazide.) SE-Peripheral neuritis. 2.)
Anti cholinergic agents – relieves tremors Artane mech – inhibits acetylcholine Cogentin action ,
S/E - SNS 3.) Antihistamine – Diphenhydramine Hcl (Benadryl) – take at bedtime S/E: adult–
drowsiness,– avoid driving & operating heavy equipt. Take at bedtime. Child – hyperactivity
CNS excitement for kids. 4.) Dopamine agonist Bromotriptine Hcl (Parlodel) – respiratory
depression. Monitor RR. Nsg Mgt – Parkinson 1.) Maintain siderails 2.) Prevent complications
of immobility - Turn pt every 2h Turn pt every 1 h – elderly 3.) Assist in passive ROM exercises
to prevent contractures 4.) Maintain good nutrition CHON – in am CHON – in pm – to induce
sleep – due Tryptopan – Amino Acid 5.) Increase fluid in take, high fiber diet to prevent
constipation 6.) Assist in surgery – Sterotaxic Thalamotomy Complications in sterotaxic
thalmotomy- 1.) Subarachnoid hemorrhage 2.) aneurism 3.) encephalitis

MULTIPLE SCLEROSIS (MS)


Chronic intermittent disorder of CNS – white patches of demyelenation in brain & spinal cord. -
Remission & exacerbation - Common – women, 15 – 35 yo cause – unknown Predisposing
factor: 1. Slow growing virus 2. Autoimmune – (supportive & palliative treatment only) Normal
Resident Antibodies: Ig G – can pass placenta – passive immunity. Short acting. Ig A – body
secretions – saliva, tears, colostrums, sweat Ig M – acute inflammation Ig E – allergic reactions
IgD – chronic inflammation S & Sx of MS: (everything down) 1. Visual disturbances a. Blurring
of vision b. Diplopia/ double vision c. Scotomas (blind spots) – initial sx 2. Impaired sensation to
touch, pain, pressure, heat, cold a. Numbness b. Tingling c. Paresthesia 3. Mood swings –
euphoria (sense of elation )

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4. Impaired motor function: a. Weakness b. Spasiticity –“ tigas” c. Paralysis –major problem 5.
Impaired cerebellar function Triad Sx of MS I – intentional tremors N – nystagmus – abnormal
rotation of eyes Charcots triad A – Ataxia & Scanning speech 6. Urinary retention or
incontinence 7. Constipation 8. Decrease sexual ability Dx – MS 1. CSF analysis thru lumbar
puncture - Reveals increase CHON & IgG 2. MRI – reveals site & extent of demyelination 3.
Lhermitte’s response is (+). Introduce electricity at the back. Theres spasm & paralysis at spinal
cord. Nsg Mgt MS - Supportive mgt 1.) Meds a. Acute exacerbation ACTH – adenocorticotopic
Steroids – to reduce edema at the site of demyelination to prevent paralysis Spinal Cord Injury
Administer drug to prevent paralysis due to edema a. Give ACTH – steroids b. Baclopen
(Lioresol) or Dantrolene Na (Dantrene) To decrease muscle spasticity c. Interferone – to alter
immune response d. Immunosuppresants 2. Maintain siderails 3. Assist passive ROMexercises –
promote proper body alignment 4. Prevent complications of immobility 5. Encourage fluid intake
& increase fiber diet – to prevent constipation 6. Provide catheterization die urinary retention 7.
Give diuretics Urinary incontinence – give Prophantheline bromide (probanthene)
Antispasmodic anti cholinergic 8. Give stress reducing activity. Deep breathing exercises,
biofeedback, yoga techniques. 9. Provide acid-ash diet – to acidify urine & prevent bacteria
multiplication Grape, Cranberry, Orange juice, Vit C

MYASTHENIA GRAVIS (MG) – disturbance in transmission of impulses from nerve to muscle


cell at neuro muscular
junction. Common in Women, 20 – 40 yo, unknown cause or idiopathic Autoimmune – release
of cholenesterase – enzyme Cholinesterase destroys ACH (acetylcholine) = Decrease
acetylcholine Descending muscle weakness (Ascending muscle weakness – Guillain Barre
Syndrome) Nsg priority: 1) a/w 2) aspiration 3) immobility S/ Sx:

1.) Ptosis – drooping of upper lid ( initial sign)


Check Palpebral fissure – opening of upper & lower lids = to know if (+) of MG. 2.) Diplopia –
double vision

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3.) Mask like facial expression 4.) Dysphagia – risk for aspiration! 5.) Weakening of laryngeal
muscles – hoarseness of voice 6.) Resp muscle weakness – lead respiratory arrest. Prepare at
bedside tracheostomy set 7.) Extreme muscle weakness during activity especially in the morning.
Dx test 1. Tensilon test (Edrophonium Hcl) – temporarily strengthens muscles for 5 – 10 mins.
Short term- cholinergic. PNS effect. Nsg Mgt 1. Maintain patent a/w & adequate vent by: a.)
Assist in mechanical vent – attach to ventilator b.) Monitor pulmonary function test. Decrease
vital lung capacity. 2. Monitor VS, I&O neuro check, muscle strength or motor grading scale
(4/5, 5/5, etc) 3. Siderails 4. Prevent complications of immobility. Adult-every 2 hrs. Elderly-
every 1 hr. 5. NGT feeding Administer meds – a.) Cholinergics or anticholinesterase agents
Mestinon (Pyridostigmine) Neostignine (prostigmin) – Long term - Increase acetylcholine s/e –
PNS b.) Corticosteroids – to suppress immune resp Decadron (dexamethasone) Monitor for 2
types of Crisis: Myastinic crisis A cause – 1. Under medication 2. Stress 3. Infection B S&Sx 1.
Unable to see – Ptosis & diplopia 2. Dysphagia- unable to swallow. 3. Unable to breath C Mgt –
adm cholinergic agents Cholinergic crisis Cause: 1 over meds S/Sx - PNS

Mgt. adm anti-cholinergic - Atropine SO4 - SNS – dry mouth 7. Assist in surgical proc –
thymectomy. Removal of thymus gland. Thymus secretes auto immune antibody. 8. Assist in
plasmaparesis – filter blood 9. Prevent complication – respiratory arrest Prepare tracheostomy set
at bedside.

GBS – Guillain Barre Syndrome


- Disorder of CNS - Bilateral symmetrical polyneuritis - Ascending paralysis Cause – unknown,
idiopathic - Auto immune - r/t antecedent viral infection - Immunizations S&Sx Initial : 1.
Clumsiness 2. Ascending muscle weakness – lead to paralysis 3. Dysphagia 4. Decrease or
diminished DTR (deep tendon reflexes) - Paralysis 5. Alternate HPN to hypotension – lead to
arrhythmia - complication 6. Autonomic changes – increase sweating, increase salivation.
Increase lacrimation

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Constipation 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 compl – immobility 5. Assist in passive ROM exercises 6.
Institute NGT feeding – due dysphagia 7. Adm meds (GBS) as ordered: – 1. Anti cholinergic –
atropine SO4 2. Corticosteroids – to suppress immune response 3. Anti arrhythmic agents a.)
Lidocaine /Xylocaine –SE confusion = VTach b.) Bretyllium c.) Quinines/Quinidine – anti
malarial agent. Give with meals. - Toxic effect – cinchonism Quinidine toxicity S/E – anorexia,
n/v, headache, vertigo, visual disturbances 8. Assist in plasmaparesis (MG. GBS) 9. Prevent
comp – arrhythmias, respiratory arrest Prepare tracheostomy set at bedside. INFL CONDITONS
OF BRAIN Meninges – 3-fold membrane – cover brain & spinal cord Fx: Protection & support
Nourishment Blood supply 3 layers 1. Duramater sub dural space 2. Arachmoid matter 3. Pia
matter sub arachnoid space

where CSF flows L3 & L4. Site for lumbar puncture.

MENINGITIS – inflammation of meningitis & spinal cord


Etiology – Meningococcus Pneumococcus Hemophilous influenza – child Streptococcus – adult
meningitis MOT – direct transmission via droplet nuclei S&Sx - Stiff neck or nuchal rigidity
(initial sign) - Headache - Projectile vomiting – due to increase ICP - Photophobia - Fever chills,
anorexia - Gen body malaise - Wt loss - Decorticate/decerebration – abnormal posturing -
Possible seizure Sx of meningeal irritation – nuchal rigidity or stiffness Opisthotonus- rigid
arching of back Pathognomonic sign – (+) Kernig’s & Brudzinski sign

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Leg pain

neck pain

Dx: 1. Lumbar puncture – lumbar/ spinal tap – use of hallow spinal needle – sub arachnoid space
L3 & L4 or L4 & L5 Aspirate CSF for lumbar puncture. Nsg Mgt for lumbar puncture – invasive
1. Consent / explain procedure to pt - RN – dx procedure (lab) - MD – operation procedure 2.
Empty bladder, bowel – promote comfort 3. Arch back – to clearly visualize L3, L4 Nsg Ngt
post lumbar 1. Flat on bed – 12 – 24 h to prevent spinal headache & leak of CSF 2. Force fluid 3.
Check punctured site for drainage, discoloration & leakage to tissue 4. Assess for movement &
sensation of extremeties Result 1. CSF analysis: a. increase CHON & WBC Content of CSF:
Chon, wbc, glucose b. Decrease glucose Confirms meningitis c. increase CSF opening pressure
N 50 – 160 mmHg d. (+) Culture microorganism 2. Complete blood count CBC – reveals
increase WBC 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 - N flora throat – streptococcus - N flora intestine – e coli Sx
of superinfection of penicillin = diarrhea b.) Antipyretic c.) Mild analgesic 2. Strict resp isolation
24h after start of antibiotic therapy A – Cushing’s synd – reverse isolation - due to increased
corticosteroid in body. B – Aplastic anemia – reverse isolation - due to bone marrow depression.
C – Cancer anytype – reverse isolation – immunocompromised. D – Post liver transplant –
reverse isolation – takes steroids lifetime. E – Prolonged use steroids – reverse isolation F –
Meningitis – strict respiratory isolation – safe after 24h of antibiotic therapy G – Asthma – not to
be isolated 3. 4. 5. 6. 7. Comfy & dark room – due to photophobia & seizure Prevent
complications of immobility Maintain F & E balance Monitor vs, I&O , neuro check Provide
client health teaching & discharge plan a. Nutrition – increase cal & CHO, CHON-for tissue
repair. Small freq feeding b. Prevent complication hydrocephalus, hearing loss or nerve deafness.
8. Prevent seizure.

14
Where to bring 2 yo post meningitis - Audiologist due to damage to hearing- post repair
myelomeningocele - Urologist -Damage to sacral area – spina bifida – controls urination 9.
Rehab for neurological deficit. Can lead to mental retardation or a delay in psychomotor
development.

CEREBRO VASCULAR ACCIDENT – stroke, brain attack or cerebral thrombosis, apoplexy


Partial or complete disruption in the brains blood supply 2 largest & common artery in stroke
Middle cerebral artery Internal carotid artery Common to male – 2 – 3x high risk

Predisposing factor: 1. Thrombosis – clot (attached) 2. Embolism – dislodged clot – pulmo


embolism S/Sx: pulmo embolism Sudden sharp chest pain Unexplained dyspnea, SOB
Tachycardia, palpitations, diaphoresis & mild restlessness S/Sx: cerebral embolism Headache,
disorientation, confusion & decrease in LOC Femur fracture – complications: fat embolism –
most feared complication w/in 24hrs Yellow bone marrow – produces fat cells at meduallary
cavity of long bone Red bone marrow – provides WBC, platelets, RBC found at epiphisis 2.) 3.)
Hemorrhage Compartment syndrome – compression of nerves/ arteries

Risk factors of CVA: HPN, DM, MI, artherosclerosis, valvular heart dse - Post heart surgery –
mitral valve replacement Lifestyle: 1. Smoking – nicotine – potent vasoconstrictor 2. Sedentary
lifestyle 3. Hyperlipidemia – genetic 4. Prolonged use of oral contraceptives - Macro pill – has
large amt estrogen - Mini pill – has large amt of progestin - Promote lipolysis (breakdown of
lipids/fats) – artherosclerosis – HPN - stroke 5. Type A personality a. Deadline driven person b.
2 – 5 things at the same time c. Guilty when not dong anything 6. Diet – increase saturated fats 7.
Emotional & physical stress 8. Obesity

S & Sx 1. TIA- warning signs of impending stroke attacks - Headache (initial sx), dizziness/
vertigo, numbness, tinnitus, visual & speech disturbances, paresis or plegia (monoplegia – 1
extreme) Increase ICP 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

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e.) Increase BP f.) (+) Kernig’s & Brudzinski – sx of hemorrhagic stroke g.) Focal &
neurological deficit 1. Phlegia 2. Dysarthria – inability to vocalize, articulate words 3. Aphasia 4.
Agraphia diff writing 5. Alesia – diff reading 6. Homoninous hemianopsia – loss of half of field
of vision Left sided hemianopsia – approach Right side of pt – the unaffected side Dx 1. CT Scan
– reveals brain lesion 2. Cerebral arteriography – site & extent of mal occlusion - Invasive
procedure due to inject dye - Allergy test All – graphy – invasive due to iodine dye Post 1.)
Force fluid – to excrete dye is nephrotoxic 2.) Check peripheral pulses - distal Nsg Mgt 1.
Maintain patent a/w & adequate vent - Assist mechanical ventilation - Administer O2 2. Restrict
fluids – prevent cerebral edema 3. Elevate head of bed 30-45 degrees angle. 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 - To prevent hypostatic pneumonia – after
prolonged immobility. b. Egg crate mattress or H2O bed c. Sand bag or foot board- prevent foot
drop 6. NGT feeding – if pt can’t swallow 7. Passive ROM exercise q4h 8. Alternative means of
communication - Non-verbal cues - Magic slate. Not paper and pen. Tiring for pt. - (+) To
hemianopsia – approach on unaffected side 9. Meds Osmotic diuretics – Mannitol Loop diuretics
– Lasix/ Furosemide Corticosteroids – dextamethazone Mild analgesic Thrombolytic/ fibrolitic
agents – tunaw clot. SE-Urticaria, pruritus-caused by foreign subs. Streptokinase Urokinase
Tissue plasminogen activating Monitor bleeding time Anticoagulants – Heparin & Coumadin”
sabay” Coumadin will take effect after 3 days Heparin – monitor PTT partial thromboplastin
time if prolonged – bleeding give Protamine SO4- antidote. Coumadin –Long term. monitor PT
prothrombin time if prolonged- bleeding give Vit K – Aquamephyton- antidote. Antiplatelet –
PASA – aspirin paraanemo aspirin, don’t give to dengue, ulcer, and unknown headache. Health
Teaching 1. Avoidance modifiable lifestyle - Diet, smoking 2. Dietary modification

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- Avoid caffeine, decrease Na & saturated fats Complications: Subarachnoid hemorrhage Rehab
for focal neurological deficit – physical therapy 1. Mental retardation 2. Delay in psychomotor
development

CONVULSIVE Disorder (CONVULSIONS)- disorder of the CNS char. by paroxysmal seizures


with or without loss of
consciousness, abnormal motor activity, alteration in sensation & perception & change in
behavior. Can you outgrow febrile seizure? Febrile seizure Normal if < 5 yo Pathologic if > 5 yo
Difference between: Seizure- 1st convulsive attack Epilepsy – 2nd and with history of seizure

Predisposing Factor Head injury due birth trauma Toxicity of carbon monoxide Brain tumor
Genetics Nutritional & metabolic deficit Physical stress Sudden withdrawal to anticonvulsants
will bring about status epilepticus Status epilepticus – drug of choice: Diazepam & glucose S &
Sx I. Generalized Seizure – a.) Grand mal / tonic clonic seizures With or without aura – warning
symptoms of impending seizure attack- Epigastric pain- associated with olfactory, tactile, visual,
auditory sensory experience - Epileptic cry – fall - Loss of consciousness 3 – 5 min - Tonic
clonic contractions - Direct symmetrical extension of extremities-TONIC. Contractions-
CLONIC - Post ictal sleep -state of lethargy or drowsiness - unresponding sleep after tonic clonic
b.) Petimal seizure – (same as daydreaming!) or absent seizure. - Blank stare - Decrease blinking
eye - Twitching of mouth - Loss of consciousness – 5 – 10 secs (quick & short) II.
Localized/partial seizure a.) Jacksonian seizure or focal seizure – tingling/jerky movement of
index finger/thumb & spreads to shoulder & 1 sideof the body with janksonian march b.)
Psychomotor/ focal motor - seizure -Automatism – stereotype repetitive & non-purposive
behavior - Clouding of consciousness – not in control with environment - Mild hallucinatory
sensory experience HALLUCINATIONS 1. Auditory – schitzo – paranoid type 2. Visual –
korsakoffs psychosis – chronic alcoholism 3. Tactile – addict – substance abuse III. Status
epilecticus – continuous, uninterrupted seizure activity, if untreated, lead to hyperprexia – coma
– death Seizure: inc electrical firing in brain=increased metabolic activity in brain=brain using
glucose and O2=dec glucose, dec O2. Tx:Diazepam (drug of choice), glucose

17
Dx-Convulsion- get health history! 1. CT scan – brain lesion 2. EEG electroencephalography -
Hyperactivity brain waves Nsg Mgt Priority – Airway & safety 1. Maintain patent a/w &
promote safety Before seizure: 1. Remove blunt/sharp objects 2. Loosen clothing 3. Avoid
restraints 4. Maintain siderails 5. Turn head to side to prevent aspiration 6. Tongue guard or
mouth piece to prevent biting of tongue-BEFORE SEIZURE ONLY! Can use spoon at home. 7.
Avoid precipitating stimulus – bright glaring lights & noises 8. Administer meds a. Dilantin
(Phenytoin) –( toxicity level – 20 ) SE Ginguial hyperplasia H-hairy tongue A-ataxia N-
nystagmus A-acetaminophen- febrile pt Mix with NSS - Don’t give alcohol – lead to CNS
depression b. (Tegretol) Carbamasene- given also to Trigeminal Neuralgia. SE: arrythmia c.
Phenobarbital (Luminal)- SE: hallucinations 2. Institute seizure & safety precaution. Post
seizure: Administer O2. Suction apparatus ready at bedside 3. Monitor onset & duration - Type
of seizure - Duration of post ictal sleep. The longer the duration of post ictal sleep, the higher
chance of having status epilepticus! 4. Assist in surgical procedure. Cortical resection 5.
Complications: Subarachnoid hemorrhage and encephalitis Question: 1 yo 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 (answer) d. Prepare suction Neurological assessment: 1.
Comprehensive neuro exam 2. GCS - Glasgow coma scale – obj measurement of LOC or quick
neuro check 3 components of ECS M – motor 6 V – verbal resp 5 E – eye opening 4 15 15 – 14 –
conscious 13 – 11 – lethargy 10 – 8 – stupor 7 – coma 3 – deep coma – lowest score Survey of
mental status & speech (Comprehensice Neuro Exam) 1.) LOC & test of memory

18
2.) 3.) 4.) 5.) 6.) 7.) 8.)

Levels of orientation CN assessment Motor assessment Sensory assessment Cerebral test –


Romhberg, finger to nose DTR Autonomics

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 gen body weakness, decrease body reflex 4. Coma (Comatose) light – (+) all
forms of painful stimulations Deep – (-) to painful stimulation Question: Describe a conscious
pt ? a. Alert – not all pt are alert & oriented to time & place b. Coherent c. Awake- answer d.
Aware Different types of pain stimulation - Don’t prick 1. Deep sternal stimulation/ pressure 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 5. Test of memory – considered
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 6. Levels of orientation Time Place Person Graphesthesia- can identify
numbers or letters written on palm with a blunt object. Agraphesthesia – cant identify numbers or
letters written on palm with a blunt object.

CN assessment:
I– II – III – IV – V– VI – VII – VIII – IX – X– XI– XII – Olfactory Optic Oculomotor Trocheal
Trigeminal Abducens Facial Acustic/auditory Glassopharyngeal Vagus Spinal accessory
Hypoglossal s s m m b m b b m m longest CN smallest CN largest CN b s

I. Olfactory – don’t use ammonia, alcohol, cologne irritating to mucosa – use coffee, bar soap,
vinegar, cigarette tar - Hyposmia – decrease sensitivity to smell - Diposmia – distorted sense of
smell

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- 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- test of visual acuity – Snellens chart – central or distance vision
Snellens E chart – used for illiterate chart N 20/20 vision distance by w/c person can see letters-
20 ft Numerator – distance to snellens chart Denominator – 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. a. b. c. d. Test of peripheral vision/ visual field Superiority Bitemporally Inferiorly
Nasally

Common Disorders – see page 85-87 for more info on glaucoma, etc. 1. Glaucoma – Normal 12
– 21 mmHg 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, IV, VI – tested
simultaneously - Innervates the movementt of extrinsic ocular muscle 6 cardinal gaze EOM Rt
eye IO LR SR 3 – 4 EOM IV – sup oblique VI – lateral rectus Normal response – PERRLA
(isocoria – equal pupil) Anisocoria – unequal pupil Oculomotor 1. Raising of eyelid – Ptosis 2.
Controls pupil size 2 -3 cm or 1.5 – 2 mm V – Trigeminal – Largest – consists of - ophthalmic,
maxillary, mandibular Sensory – controls sensation of the face, mucus membrane; teeth &
cornea reflex Unconscious – instill drop of saline solution Motor – controls muscles of chewing/
muscles of mastication Trigeminal neuralgia – diff chewing & swallowing – extreme food temp
is not recommended Question: 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
SO S MR E N O left eye

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VI Facial: Sensory – controls taste – ant 2/3 of tongue test cotton applicator put sugar. -Put
applicator with sugar to tip to tongue. -Start of taste insensitivity: Age group – 40 yrs old Motor-
controls muscles of facial expression, smile frown, raise eyebrow Damage – Bells palsy – facial
paralysis Cause – bells palsy pedia – R/T forcep delivery Temporary only Most evident clinical
sign of facial symmetry: Nasolabial folds VIII Acoustic/ vestibule cochlear (controls hearing) –
controls balance (kenesthesia or position sense) - Movement & orientation of body in space -
Organ of Corti – for hearing – true sense organ of hearing Outer – tympanic membrane, pinna,
oricle (impacted cerumen), cerumen Middle – hammer, anvil, stirrup or melleus, incus, staples.
Mid otitis media Eustachean ear Inner ear- meniere dse, sensory hearing loss (research parts! &
dse) Remove vestibule – meniere’s dse – disease inner ear

Archimedes law – buoyancy (pregnancy – fetus) Daltons law – partial pressure of gases Inertia –
law of motion (dizziness, vertigo) 1.) Pt with multiple stab wound - chest - Movement of air in &
Don’t touch uvula XI – Spinal Accessory - controls sternocleidomastoid (neck)♣out of lungs is
carried by what principle? - Diffusion – Dalton’s law 2.) Pregnant – check up – ultrasound
reveals fetus is carried by amniotic fluid - Archimedes 3.) Severe vertigo due- Inertia Test for
acoustic nerve: - Repeat words uttered IX – Glossopharyngeal – controls taste – posterior 1/3 of
tongue X – Vagus – controls gag reflex Test 9 – 10 Pt say ah – check uvula – should be midline
Damage cerebral hemisphere is L or R Gag reflex – place tongue depression post part of tongue
& trapezius (shoulders and back) - Shrug shoulders, put pressure. Pt should resist pressure.
Paresis or phlegia XII – Hypoglossal – controls movement of tongue – say “ah”. Assess tongue
position=midline L or R deviation - Push tongue against cheek - Short frenulum lingue – Tongue
tied – “bulol”

ENDOCRINE Fx of endocrine – ductless gland Main gland – Pituitary gland – located at base of
brain of Stella Turcica Master gland of body Master clock of body

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Anterior pituitary gland – adenohypophysis Posterior pituitary gland – neurohypophysis
Posterior pituitary: 1.) Oxytocin – a.) Promotes uterine contraction preventing bleeding/
hemorrhage. - Give after placental delivery to prevent uterine atony. b.) Milk letdown reflex with
help of prolactin. 2.) ADH – antidiuretic hormone – (vasopressin) -Prevents urination – conserve
H2O

A. DIABETIS INSIPIDUS (DI- dalas ihi) – hyposecretion of ADH


Cause: idiopathic/ unknown Predisposing factor: 1. Pituitary surgery 2. Trauma/ head injury 3.
Tumor 4. Inflammation * alcohol inhibits release of ADH S & Sx: 1. Polyuria 2. Sx of
dehydration - Excessive thirst (adult) - Agitation - Poor skin turgor - Dry mucus membrane 3.
Weakness & fatigue 4. Hypotension – if left untreated 5. Hypovolemic shock Anuria – late sign
hypovolemic shock (1st sx of dehydration in children-tachycardia)

Dx Proc: 1. Decrease urine specific gravity- concentrated urine N= 1.015 – 1.035 2. Serum Na =
increase (N=135 -145 meq/L) Hypernatremia Mgt: 1. 2. 3. 4. Force fluid 2,000 – 3,000ml/day
Administer IV fluid replacement as ordered Monitor VS, I&O Administer meds as ordered a.)
Pitresin (vasopressin) IM 5. Prevent complications Most feared complication – Hypovolemic
shock

B.) SIADH - Syndrome of Inappropriate Anti-Diuretic Hormone


- Increase ADH - Idiopathic/ unknown Predisposing factor 1. Head injury 2. Related to
Bronchogenic cancer or lung canerEarly Sign of Lung Ca - Cough –1. non productive 2.
productive 3. Hyperplasia of Pit gland Increase size of organ

22
S&Sx 1. 2. 3. 4.

Fluid retention Increase BP – HPN Edema Wt gain 5. Danger of H2O intoxication –


Complications: 1. cerebral edema – increase ICP – 2. seizure

Dx Proc: 1. Urine specific gravity increase – diluted urine 2. Hyponatremia – Decreased Na

Nsg Mgt: 1. Restrict fluid 2. Administer meds as ordered eg. Diuretics: Loop and Osmotic 3.
Monitorstrictly 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 & seizures
activity Anterior Pituitary Gland – adeno 1. Growth hormone (GH) (Somatotropic hormone) Fx:
Elongation of long bones Decrease GH – dwarfism children Increase GH – gigantism Increase
GH – acromegaly – adult Puberty 9 yo – 21 yo Epiphyseal plate closes at 21 yo Square face
Square jaw Drug of choice in acromegaly: Ocreotide (Sandostatin) SE dizziness Somatostatin
Hormone – antagonizes the release of of GH Melanocytes stimulating hormone - MSH Skin
pigmentation 3. Prolactin/luteotrpic hormone/ lactogenic hormone - Promotes development of
mammary gland (Oxytocin-Initiates milk letdown reflex) 4. Adrenocorticotropic hormone –
ACTH - Development & maturation of adrenal cortex 5. Luteinizing hormone – produces
progesterone. 6. FSH- produces estrogen 2. PINEAL GLAND 1. Secretes Melatonin – inhibits
lutenizing hormone (LH) secretion THYROID GLAND (TG) Question: Normal physical finding
on TG: a. With tenderness – thyroid never tender b. With nodular consistency- answer c. Marked
asymmetry – only 1 TG d. Palpable upon swallowing - Normal TG never palpable unless with
goiter TG hormones: T3 - Triodothyronine - 3 molecules of iodine

T4 -Tetraiodothyronine/ Tyroxine - 4 molecules of iodine

Thyrocalcitonin FX – antagonizes effects of parathormone

23
Metabolic hormone Increase metabolism brain –inc cerebration, inc v/s Hypo T3 T4 - lethargy &
memory impairment – Hyper T3 T4 - agitation, restlessness, and hallucination 7. Increase VS,
increase motility HYPOTHYROIDISM – all decreased except wt & menstruation, loss of
appetite but with wt gain menorrhagia – increase in mens HYPERTHYROIDISM - Increase
appetite – wt loss, amenorrhea all v/s down, constipation

SIMPLE GOITER – enlarged thyroid gland - iodine deficiency


Predisposing factors 1. Goiter belt area - Place far from sea – no iodine. Seafood’s rich in iodine
2. Mountainous area – increase intake of goitrogenic foods (US: Midwest, NE, Salt Lake)
Cabbage – has progoitrin – an anti thyroid agent with no iodine Example: Turnips (singkamas),
radish, peas, strawberries, potato, beans, kamote, cassava (root crops), all nuts. 3. Goitrogenic
drugs: Anti thyroid agents :(PTU) prephyl thiupil Lithium carbonate, Aspirin PASA Cobalt,
Phenyl butasone Endemic goiter – cause # 1 Sporadic goiter – caused by #2 & 3 S & Sx –
enlarged TG Mild restlessness Mild dysphagia Dx Proc. 1. Thyroid scan – reveals enlarged TG
2. Serum TSH – increase (confirmatory) 3. Serum T3, T4 – N or below N Nsg Mgt: 1.
Administer meds a.) Iodine solution – Logol’s solution or saturated sol of K iodide SSKI Nsg
Mgt Lugol’s sol – violet color 1. use straw – prevent staining teeth 2. Prophylaxis 2 -3 drops
Treatment – 5 to 6 drops Use straw – to prevernt staining of teeth 1. Lugol’s sol., 2. tetracycline
3. nitrofurantin (macrodantin)-urinary anticeptic-pyelonephritis. 4. Iron solution. B. Thyroid h /
Agents 1. Levothyroxine (Synthroid) 2. Liothyronine (cytomel) 3. Thyroid extract Nsg Mgt: for
TH/agents 1. Monitor vs. – HR due tachycardia & palpitation 2. Take it early AM – SE insomnia
3. Monitor s/e

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Tachycardia, palpitations Signs of insomnia Hyperthyroidism restlessness agitation Heat
intolerance HPN

3. Encourage increase intake iodine – iodine is extracted from seaweeds (!)


Seafood- highest iodine content oysters, clams, crabs, lobster Lowest iodine – shrimps Iodized
salt –easily destroyed by heat take it raw not cooked

4. Assist surgery- Sub total thyroidectomyComplication: 1. Tetany 2. laryngeal nerve damage


3.Hemorrhage-feeling of fullness at incision site.Check nape for wet blood. 4.Laryngeal spasm –
DOB, SOB – trache set ready at bedside. 2.) HYPOTHYROIDISM – decrease secretion of T3,
T4 – can lead to MI / Atherosclerosis Adult – myxedema Child- cretinism – only endocrine dis
lead to mental retardation Predisposing factor: 1. `Iatrogenic causes – caused by surgery 2.
Atrophy of TG due to: a. Irradiation b. Trauma c. Tumor, inflammation 3. Iodine def 4.
Autoimmune – Hashimoto disease S&Sx everything decreased except wt gain & mens increase)
Early signs – weakness and fatigue Loss of appetite – increased lypolysis – breakdown of fats
causing atherosclerosis = MI Wt gain Cold intolerance – myxedema - coma Constipation Late Sx
– brittle hair/ nails Non pitting edema due increase accumulation of mucopolysacharide in SQ
tissue -Myxedema Horseness voice Decrease libido Decrease VS – hypotension bradycardia,
bradypnea, and hypothermia Lethargy Memory impairment leading to psychosis-forgetfulness
Menorrhagia Dx: 1. Serum T3 T4 decrease 2. Serum cholesterol increase – can lead to MI 3. RA
IU – radio iodine uptake – decrease Nsg Mgt: 1. Monitor strictly V/S. I&O – to determine
presence of myxedema coma! Myxedema Coma - Severe form of hypothyroidism Hypotension,
hypoventilation, bradycardia, bradypnea, hyponatremia, hypoglycemia, hypothermia Might lead
to progressive stupor & coma Impt mgt for Myxedema coma 1. Assist mech vent – priority a/w
2. Adm thyroid hormone 3. Adm IVF replacement – force fluid

25
Mgt myxedema coma 1. Monitor VS, I&O 2. Provide dietary intake low in calories – due to wt
gain 3. Skin care due to dry skin 4. Comfortable & warm environment due to cold intolerance 5.
Administer IVF replacements 6. Force fluid 7. Administer meds – take AM – SE insomia.
Monitor HR. Thyroid hormones Levothyroxine(Synthroid), Liothyronine (cytomel) Thyroid
extracts 8. 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 Complications: 9.
Hypovolemic shock, myxedema coma 10. Hormonal replacement therapy - lifetime 11.
Importance of follow up care

HYPERTHYROIDISM - Graves dse or thyrotoxicosis ( everything up except wt and mens)


-Increased T3 & T4 Predisposing factors: 1. Autoimmune disease – release of long acting thyroid
stimulator (LATS) Exopthalmos Enopthalmos – severe dehydration depressed eye 2. Excessive
iodine intake 3. Hyperplasia of TG S&Sx: 1. Increase in appetite – hyperphagia – wt loss due to
increase metabolism 2. Skin is moist - perspiration 3. Heat intolerance 4. Diarrhea – increase
motility 5. All VS increase = HPN, tachycardia, tachypnea, hyperthermia 6. CNS changes 8.
Irritability & agitation, restlessness, tremors, insomnia, hallucinations 7. Goiter 8. Exopthalmos –
pathognomonic sx 9. Amenorrhea Dx: 1. 2. 3. Serum T3 & T4 - increased Radio iodine uptake –
increase Thyroid scan – reveals enlarged TG

Nsg Mgt: 1. Monitor VS & I & O – determine presence of thyroid storm or most feared
complication: Thyrotoxicosis 2. Administer meds a. Antithyroid agents 1. Prophylthiuracil
(PTU) 2. Methymazole (Tapazole) Most toxic s/e agranulocytosis- fever, sore throat,
leukocytosis=inc wbc: check cbc and throat swab culture Most feared complication : Thrombosis
– stroke CVS

26
3. 4. 5.

Diet – increase calorie – to correct wt loss Skin care – Comfy & cool environment 6. Maintain
siderails- due agitation/restlessness 7. Provide bilateral eye patch – to prevent drying of eyes-
exopthalmos 8. Assist in surgery – subtotal thyroidectomy Nsg Mgt: pre-op Adm Lugol’s
solution (SSKI) K iodide 9. To decrease vascularity of TG 10. To prevent bleeding &
hemorrhage Mgt post op: Complication: 1. Watch out for signs of thyroid storm or thyrotoxicosis
Triad signs of thyroidstorm; a. Tachycardia /palpitation b. Hyperthermia c. Agitation 1. 2. 3. Nsg
Mgt Thyroid Storm: Monitor VS & neuro check Agitated might decrease LOC Antipyretic –
fever Tachycardia - β blockers (-lol) Siderails – agitated

Comp 2. Watch for inadvertent (accidental) removal of parathyroid gland Secretes Para hormone
If removed, hypocalcemia - classic sign tetany – 1. .(+) Trousseau sign/ 2. Chvosteck’s sign Nsg
Mgt: Adm calcium gluconate slowly – to prevent arrhythmia Ca gluconate toxicity – antidote –
MgSO4

3.Laryngeal (voice box) nerve damage (accidental)


Sx: hoarseness of voice ***Encourage pt to talk or speak post operatively asap to determine
laryngeal nerve damage Notify physician!

4. Signs of bleeding post subtotal thyroidectomy


- “Feeling of fullness” at incision site Nsg mgt: Check soiled dressing at nape area

5. Signs of laryngeal spasm


a. DOB b. SOB Prepare at bedside tracheostomy

6. Hormonal replacement therapy - lifetime 7. Importance of follow up care


(Liver cirrhosis – bedside scissor – if pt complaints of DOB) (Cut cystachean tube to deflate
balloon)

Parathyroid gland – pair of small nodules located behind the TG

27
11. Secrets parathyroid hormone – promotes Ca reabsorption Thyrocalcitonin – antagonises
secretion of parathyroid hormone 1. 2. Hypoparthroidism – decrease of parathyroid hormone
Hyperparathroidsm

HYPOPARATHYROIDISM – decreased parathormone


Hypocalcemia (Or tetany) [If Ca decreases, phosphate increases] A. Predisposing, factors: 1.
Following subtotal thyroidectomy 2. Atrophy of parathyroid gland due to a. Irradiation b.
Trauma S&Sx: 1. Acute tetany a. Tingling sensation b. Paresthesia c. Dysphagia d.
Laryngospasm e. Bronchospasm Pathognomonic Sign of tetany: a. (+) Trousseau’s or
carpopedial spasm b. (+) Chvosteck’s sign f. Seizure g. Arrhythmia 2. most feared complication
Hyperphosphatemia

Chronic tetany a. Loss of tooth enamel b. Photophobia & cataract formation c. GIT changes –
anorexia, n/v, general body malaise d. CNS changes – memory impairment, irritability

Dx:

1. Serum calcium – decrease (N 8.5 – 11 mg/100ml) 2. Serum phosphate increase (N 2.5 – 4.5
mg/100ml)
3. 4. X-ray of long bone – decrease bone density CT Scan – reveals degeneration of basal ganglia

Nsg Mgt: 1. Administration of meds: a.) Acute tetany – Ca gluconate – IV, slowly b.) Chronic
tetany 1. Oral Ca supplements Ex. Ca gluconate

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Ca carbonate Ca lactate Vit D (Cholecalceferol) Drug Cholecalceferol diet calcidiol sunlight
calcitriol 7am – 9am

2. Phosphate binder Alumminum DH gel (ampho gel) SE constipation Antacid AAC MAD
Aluminum containing acids Aluminum OH gel

Mg containing antacids Ex. Milk or magnesia Diarrhea

Constipation Maalox – magnesium & aluminum - Less s/e 2. Avoid precipitating stimulus such
as bright lights & noise: photophobia leading to seizure 3. Diet – increase Ca & decrease
phosphorus - Don’t give milk – due to increase phosphorus Good = anchovies – increase Ca,
decrease phosphorus + inc uric acid. Tuna & green turnips- Inc Ca. 4. Bedside – tracheostomy
set –due to 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. Important fallow up care

HYPERPARATHYROIDISM - increase parathormone. Complication: Renal failure


Hypercalcemia can lead to Hypophosphatemia Bone dse Mineralization Leading to bone fracture
Ca – 99% bones 1% serum blood Predisposing Factors: 1. Hyperplasia parathyroid gland (PTG)
2. Over compensation of PTG due to Vit D deficiency Children – Rickets Vit D Adults –
Osteomalacia deficiency Sippy’s diet – Vit D diet – not good for pt with ulcer 2 -4 cups of milk
& butter Karrel’s 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: Bone fracture 1. Bone pain
(especially at back), bone fracture kidney stones

29
2. 3. 4.

Kidney stone – a. Renal colic b. Cool moist skin GIT changes – anorexia, n/v, ulcerations CNS
involvement– irritability, memory impairment

Dx Proc: 1. Serum Ca increase 2. Serum phosphorus decreases 3. X-ray long bones – reveals
bone demineralization Nsg Mgt: Kidney Stone 1. 2. 3. 4. 5. 6. Force fluids – 2,000 – 3,000/day
or 2-3L/day Isotonic solution Warm sitz bath – for comfort Strain all urine with gauze pad Acid
ash diet – cranberry, plum, grapefruit, vit C, calamansi – to acidify urine Adm meds a. Narcotic
analgesic – Morphine SO4, Demerol (Meperidine Hcl) S/E – resp depression. Monitor RR)
Narcan/ Naloxone – antidote Naloxone toxicity – tremors Siderails Assist in ambulation Diet –
low in Ca, increase phosphorus lean meat Prevent complication Most feared – renal failure
Assist surgical procedure – parathyroidectomy Impt ff up care Hormonal replacement- lifetime

7. 8.

9. 10.
11. 12. 13.

ADRENAL GLAND 12. Atop of @ kidney 13. 2 parts Adrenal cortex – outermost layer Adrenal
medulla - innermost layer 14. Secrets cathecolamines a.) Epinephrine / Norephinephrine – potent
vasoconstrictor – adrenaline=Increase BP Adrenal Medulla’s only disease:

PHEOCHROMOCYTOMA- presence of tumor at adrenal medulla


-increase nor/epinephrine -with HPN and resistant to drugs -drug of choice: beta blockers
-complication: HPN crisis = lead to stroke -no valsalva maneuver

Adrenal Cortex –

1. 2.

Zona fasiculata – secrets glucocorticoids Ex. Cortisol - Controls glucose metabolism (SUGAR)
Zona reticularis – secrets traces of glucocorticoids & androgenic hormones M – testosterone F –
estrogen & progesterone

30
Fx – promotes development of secondary sexual characteristics

3. Zona glomerulosa - secretes mineralcortisone


Ex. Aldosterone Fx: promotes Na & H2O reabsorption & excretion of potassium (SALT)

ADDISON’S DISEASE – Steroids-lifetime


Decreased 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 3. Tubercular infections S/Sx:

1. Decrease sugar – Hypoglycemia – Decreased glucocorticoids - cortisol


T – tremors, tachycardia I - irritability R - restlessness E – extreme fatigue D – diaphoresis,
depression

2. Decrease plasma cortisol


Decrease tolerance to stress – lead to Addisonian’s crisis

3. Decrease salt – Hyponatermia – Decreased mineralocorticoids - Aldosterone


Hypovolemia a.) Hypotension b.) Signs of dehydration – extreme thirst, agitation c.) Wt loss 4.
Hyperkalemia a.) Irritability b.) Diarrhea c.) Arrhythmia 5. Decrease sexual urge or libido-
Decreased Androgen 6. Loss of pubic and axillary hair To Prevent STD Local – practice
monogamous relationship CGFNS/NCLEX – condom 7. Pathognomonic sign– bronze like skin
pigmentation due to decrease cortisol will stimulate pituitary gland to release melanocyte
stimulating hormone. Dx Proc:

1. FBS – decrease FBS (N 80 – 120 mg/dL)


2. Plasma cortisol – decreased Serum Na – decreased (N 135 – 145 meg/L) 3. Serum K –
increased (N 3.5 – 5.5 meg/L) Nsg Mgt:

1.

Monitor VS, I&O – to determine presence of Addisonian crisis 15. Complication of Addison’s
dse : Addisonian crisis 16. Results the acute exacerbation of Addison’s dse characterized by :
Hypotension, hypovolemia, hyponatremia, wt loss, arrhythmia

31
17. Lead to progressive stupor & coma 1. 2. 3. Nsg Mgt Addisonian Crisis (Coma) Assist in
mechanical ventilation Adm steroids Force fluids

2.

Administer meds a.) Corticosteroids - (Decadron) or Dexamethazone - Hydrocortisone


(cortisone)- Prednisone Nsg Mgt with Steroids 1. Adm 2/3 dose in AM & 1/3 dose in PM in
order to mimic the normal diurnal rhythm. 2. Taper the dose (w/draw, gradually from drug) –
sudden withdrawal can lead to addisonian crisis 3. Monitor S/E (Cushing’s syndrome S/Sx) a.)
HPN b.) Hirsutism c.) Edema d.) Moon face & buffalo hump e.) Increase susceptibility to
infection sue to steroids- reverse isolation b.) Mineralocorticoids ex. Flourocortisone

3. 4. 5. 6. 7.

Diet – increase calorie or CHO Increase Na, Increase CHON, Decrease K Force fluid Administer
isotonic fluid as ordered Meticulous skin care – due to bronze like

HT & discharge planning a) Avoid precipitating factors leading to Addisonian crisis 1. Sudden
withdrawal crisis 2. Stress 3. Infection b) Prevent complications Addisonian crisis &
Hypovolemic shock

8. 9.

Hormonal replacement therapy – lifetime Important: follow up care

CUSHING’S SYNDROME – increase secretion of adrenocortical hormone


Predisposing Factors: 1. Hyperplasia of adrenal gland 2. Tubercular infection – milliary TB S/Sx
1. Increase sugar – Hyperglycemia 3 P’s 1. Polyuria 2. Polydipsia – increase thirst 3. Polyphagia
– increase appetite Classic Sx of DM – 3 P’s & glycosuria + wt loss 2. Increase susceptibility to
infection – due to increased corticosteroid 3. Hypernatrermia a. HPN b. Edema c. Wt gain d.
Moon face Buffalo hump

32
4.

5. 6. 7. Dx:

Obese trunk Pendulous abdomen Thin extremities Hypokalemia a. Weakness & fatigue b.
Constipation c. ECG – (+) “U” wave Hirsutism – increase sex Acne & striae Increase
muscularity of female

classic signs

1. FBS – increase↑ (N: 80-120mg/dL)


2. Plasma cortisol increase

3. Na – increase (135-145 meq/L) 4. K- decrease (3.5-5.5 meq/L)


Nsg Mgt: 1. Monitor VS, I&O 2. Administer meds a. K- sparing diuretics (Aldactone)
Spironolactone - promotes excretion of NA while conserving potassium Not lasix due to S/E
hypoK & Hyperglycemia! 3. 4. Restrict Na Provide Dietary intake – low in CHO, low in Na &
fats High in CHON & K Weigh pt daily & assess presence of edema- measure abdominal girth-
notify doc. Reverse isolation Skin care – due acne & striae Prevent complication - Most feared –
arrhythmia & DM (Endocrine disorder lead to MI – Hypothyroidism & DM) Surgical bilateral
Adrenolectomy Hormonal replacement therapy – lifetime due to adrenal gland removal- no more
corticosteroid!

5.
6.

7. 8.
9.

10.

PANCREAS – behind the stomach, mixed gland – both endocrine and exocrine gland
Acinar cells (exocrine gland) Secrete pancreatic juices at pancreatic ducts. Aids in digestion (in
stomach) Islets of Langerhans (endocrine gland ductless) α cells secrets glucagon Fxn:
hyperglycemia (high glucose) β Cells Secrets insulin Fxn: hypoglycemia Delta Cells

33
Secrets somatostatin Fxn: antagonizes growth hormone

3 disorders of the Pancreas 1. DM 2. Pancreatic Cancer 3. Pancreatitis

Overview only:

PANCREATITIS (check page 72)– acute inflammation of pancreas leading to pancreatic edema,
hemorrhage & necrosis due to
Autodigestion – self-digestion Cause: unknown/idiopathic 18. Or alcoholism Pathognomonic
sign- (+) Cullen’s sign - Ecchymosis of umbilicus (bluish color)- pasa (+) Grey turner’s sign –
ecchymosis of flank area Both sx means hemorrhage

CHRONIC HEMORRHAGIC PANCREATITIS- “bangugot”


Predisposing factors - unknown Risk factor: 1. History of hepatobiliary disorder 2. Alcohol 3.
Drugs – thiazide diuretics, oral contraceptives, aspirin, penthan 4. Obesity 5. Hyperlipidemia 6.
Hyperthyroidism 7. High intake of fatty food – saturated fats

DIABETES MELLITUS - metabolic disorder characterized by non utilization of CHO,


CHON,& fat metabolism
Classification:

I.

Type I DM (IDDM) – “Juvenile “ onset, common in children, non-obese “brittle dse”

-Insulin dependent diabetes mellitus Incidence rate 1.) 10% of population with DM have Type I
Predisposing Factor: 1. 90% hereditary – total destruction of pancreatic dells 2. Virus 3. Toxicity
to carbon tetrachloride 4. Drugs – Steroids both cause hyperglycemia Lasix - loop diuretics S/Sx:
3 P’S + G 1.) Polyuria 2.) Poydipsia 3.) Polyphagia 4.) Glycosuria 5.) Weight loss

34
6.) Anorexia 7.) N/V 8.) Blurring of vision 9.) Increase susceptibility to infection 10.) Delayed/
poor wound healing Mgt: 1. Insulin Therapy Diet Exercise Complications – Diabetic
Ketoacidosis (DKA) Diabetic Ketoacidosis (DKA) – due to increase fat catabolism or
breakdown of fats DKA –(+) fruity or acetone breath odor Kassmaul’s respiration – rapid,
shallow breathing Diabetic coma (needs oxygen)

II.

Type II DM – (NIDDM)

Adult/ maturity onset type – age 40 & above, obese Incidence Rate 1. 90% of pop with DM have
Type II Mid 1980’s marked increase in type II because of increase proliferation of fast food
chains! Predisposing Factor: 1. Obesity – obese people lack insulin receptors binding site 2.
Hereditary S/Sx: 1. 2. Tx: Asymptomatic 3 P’s and 1G

1. Oral Hypoglycemic Agents (OHA)


2. 3. Diet Exercise

Complication: HONKC H – hyper O – osmolar N – non K – ketotic C – coma III.


GESTATIONAL DM – 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 P’s & 1G Type of delivery – CS – due to large baby Sx of
hypoglycemia on infant 1. High pitched shrill cry

35
2. Poor sucking reflex IV. DM ASSOCIATED WITH OTHER DISORDER a.) Pancreatic tumor
b.) Cancer c.) Cushing’s syndrome 3 MAIN FOOD GROUPS Anabolism 1. CHON glucose 2.
CHON amino acids 3. Fats fatty acids

Catabolism glycogen nitrogen free fatty acids (FFA) – Cholesterol & Ketones

Pancreas → glucose → ATP (Main fuel/energy of cell ) Reserve glucose – glycogen Liver will
undergo – glucogenesis – synthesis of glucagons & Glycogenolysis – breakdown of glucagons &
Gluconeogenesis – formation of glucose form CHO sources – CHON & fats Hyperglycemia –
pancreas will not release insulin. Glucose can’t go to cell, stays at circulation causing
hyperglycemia. increase osmotic diuresis – glycosuria Lead to cellular starvation Lead to wt loss
stimulates the appetite/ satiety center (Hypothalamus) Polyphagia Stimulates thirst center
(hypothalamus) Polydipsia Increased CHON catabolism Lead to (-) nitrogen balance Tissue
wasting (cachexia) polyuria Cellular dehydration

Increase fat catabolism Free fatty acids Cholesterol Atherosclerosis HPN MI stroke ketones
DKA coma death

DIABETIC KETOACIDOSIS (DKA)


Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression &
Coma. Ketones- a CNS depressant

Predisposing factor:

36
1. Stress – between stress and infection, stress causes DKA more.
2. 3. S/Sx: 1. 2. 3. 4. 5. 6. Hyperglycemia Infection

3 P’s & 1G Polyuria Polydipsia Polyphagia Glycosuria Wt loss Anorexia, N/V 7. (+) Acetone
breath odor- fruity odor 8. Kussmaul's resp-rapid shallow respiration 9. CNS depression 10.
Coma

pathognomonic DKA

Dx Proc: 1. FBS increase, Hct – increase (compensate due to dehydration) N =BUN – 10 -20
mg/100ml --increased due to severe dehydration Crea - .8 – 1 mg/100ml Hct 42% (should be 3x
high)-nto hgb 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 as ordered: a.) Insulin therapy – IV
push Regular Acting Insulin – clear (2-4hrs, peak action) b.) To counteract acidosis – Na HCO3
c.) Antibiotic to prevent infection Insulin Therapy A. Sources: 1. Animal source – beef/ pork-
rarely used. Causes severe allergic reaction. 2. Human – has less antigenecity property Cause
less allergic reaction. Humulin 3. If kid is allergic to chicken – don’t give measles vaccine due it
comes from chicken embryo. Artificially compound

B. Types of Insulin 1. Rapid Acting Insulin - Ex. Regular acting I 2. Intermediate acting I - Ex.
NPH (non-protamine Hagedorn I) 3. Long acting I - Ex. Ultra lente Types of Insulin 1. Rapid 2.
Intermediate 3. Long acting color & consistency clear cloudy cloudy onset peak duration 2-4h 6-
12h 12-24h -

Ex. 5am Hemoglucose test (HGT) 250 mg/dl Adm 5 units of RA I

37
Peak 7-9am – monitor hypoglycemic reaction at this time- TIRED Nsg Mgt: upon injection of
insulin: 1.Administer insulin at room temp! – To prevent lipodystrophy = atrophy/ hypertrophy
of SQ tissues 2. Insulin is only refrigerated once opened! 3. Gently roll vial bet palms. Avoid
shaking to prevent formation of bubbles. 4. Use gauge 25 – 26needle – tuberculin syringe 5.
Administer insulin at either 45(for skinny pt) or 90° (taba pt)depending on the client tissue
deposit. 6. Don’t aspirate after injection 7. Rotate injection site to prevent lipodystrophy 8. Most
accessible site – abdomen 9. When mixing 2 types of insulin, aspirate 1st regular/ clear – before
cloudy to prevent contaminating clear insulin & to promote accurate calibration. 10. Monitor
signs of complications: a. Allergic reactions – lipodystrophy b. Somogyi’s phenomenon –
hypoglycemia followed by periods of hyperglycemia or rebound effect of insulin. 11. 1ml or cc
of tuberculin = 100 units of insulin

- - 1 cc = 100 units - - .5cc = 50 units - - .1 cc = 10 units 6 units RA Most Feared Complication


of Type II DM Hyper ↑ osmolarity = severe dehydration Osmolar Non - absence of lipolysis
Ketotic - no ketone formation Coma – S/Sx: headache, restlessness, seizure, decrease LOC =
coma Nsg Mgt; - same as DKA except don’t give NaHCO3! 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 b.) Antibiotic to prevent infection Tx: O ral H ypoglycemic A gents 19.
Stimulates pancreas to secrete insulin Classifications of OHA 1. First generation Sulfonylurear a.
Chlorpropamide (diabenase) b. Tolbutamide (orinase) c. Tolazamide (tolinase)

38
2. 2nd generation sulfonylurear a. Diabeta (Micronase) b. Glipside (Glucotrol)
Nsg Mgt or OHA 1. Administer with meals – to lessen GIT irritation & prevent hypoglycemia 2.
Avoid alcohol (alcohol + OHA = severe hypoglycemic reaction=CNS depression=coma)
Antabuse-Disufram Dx for DM 1. FBS – N 80 – 120 mg/dl = Increased for 3 consecutive times +
3 P’s & 1G 2. Oral glucose tolerance (OGTT) - Most sensitive test 3. Random blood sugar –
increased 4. Alpha Glucosylated Hgb – elevated Nsg Mgt; 1. Monitor for PEAK action of OHA
& insulin Notify Doc 2. Monitor VS, I&O, neurocheck, blood sugar levels. 3. Administer insulin
& OHA therapy as ordered. 4. Monitor signs of hyper & hypoglycemia. Pt DM –“ hinimatay”
20. You don’t know if hypo or hyperglycemia. Give simple sugar (Brain can tolerate high sugar,
but brain can’t tolerate low sugar!) Cold, clammy skin – hypo – Orange Juice or simple sugar /
warm to touch – hyper – adm insulin 5. Provide nutritional intake of diabetic diet: CHO – 50%
CHON – 30% Fats – 20% -Or offer alternative food products or beverage. -Glass of orange juice.
6. Exercise – after meals when blood glucose is rising. 7. Monitor complications of DM a.
Atherosclerosis – HPN, MI, CVA b. Microangiopathy – small blood vessels Eyes – diabetic
retinopathy , premature cataract & blindness Kidneys – recurrent pyelonephritis & Renal Failure
(2 common causes of Renal Failure : DM & HPN) c. Gangrene formation d. Peripheral
neuropathy 1. Diarrhea/ constipation 2. Sexual impotence e. Shock due to cellular dehydration 8.
Foot care mgt a. Avoid waking barefooted b. Cut toe nails straight c. Apply lanolin lotion –
prevent skin breakdown d. Avoid wearing constrictive garments 9. Annual eye & kidney exam
10. Monitor urinalysis for presence of ketones Blood or serum – more accurate 11. Assist in
surgical wound debridement 12. Monitor signs or DKA & HONKC 13. Assist surgical procedure

=confirms DM!!

39
BKA or above knee amputation

Overview: HEMATOLOGICAL SYSTEMS


I Blood II Blood vessels III Blood forming organs 1. Thymus – removed myasthenia gravis 2.
Liver – largest gland 3. Lymph nodes 4. Lymphoid organs – payers patch 5. Bone marrow 6.
Spleen – destroys RBC Blood vessels 1. Veins –SVC, IVC, Jugular vein – blood towards the
heart 2. Artery – carries blood away from the 21. Aorta, carotid 3. Capillaries Blood 45% formed
elements – 55% plasma – fluid portion of vlood. Yellow color. Serum Plasma CHON’s
(Produced in Liver) 1. Albumin- largest, most abundant plasma Maintains osmotic pressure
preventing edema FXN: promotes skin integrity 2. Globulins – alpha – transports steroids
Hormones & bilirubin β - Transports iron & copper Gamma – transport immunoglobulins or
antibodies 3. Prothrombin – fibrinogen – clotting factor to prevent bleeding

Formed Elements: 1. RBC (erythrocytes) Spleen life span = 120 days (N) 3 – 6 M/mm3 -
Anucleated - Biconcave discs - Has molecules of Hgb (red cell pigment) Transports & carries O2

SICKLE CELL ANEMIA –sickle shaped RBC. Should be round. Impaired circulation of RBC.
-immature cells=hemolysis of RBC=decreased hgb
3 Nsg priority 1. a/w – avoid deoxygenating activities - High altitude is bad 2. Fluid deficit –
promote hydration 3. Pain & comfort Hgb ( hemoglobin) F= 12 – 14 gms % M = 14-16 gms %
Hct – 3x hgb 12 x 3 = 36 (hamatocrit) F 36 – 42% 14 x 3 = 42 M 42 – 48% Average 42% - Red
cell percentage in whole red

40
Substances needed for maturation of RBC a.) Folic acid b.) Iron c.) Vit C d.) Vit B12
(cyanocobalamin) e.) Vit B6 (Pyridoxine) f.) Intrinsic factor Pregnant: 1st trimester- Folic acid –
prevent neural tube deficit 3rd tri – iron Life span of rbc – 80 – 120 days. Destroyed at spleen.
NON-GRANULOCYTES 1. Monocytes (macrophage) - largest WBC - involved in long term
phagocytes - For chronic inflammation - Other name macrophage Macrophage in CNS-
microglia Macrophage in skin – Histiocytes Macrophage in lungs – alveolar macrophage
Macrophage in Kidneys – Kupffer cells 2. Lymphocytes B Cell – L – bone marrow or bursa
dependent T cell – dev’t of immunity- target site for HIV NK cell – natural killer cell Have both
antiviral & anti-tumor properties 3.Platelets (thrombocytes) N- 150,000 – 450, 000/ mm3 it
promotes hemostasis – prevention of blood loss by activating clotting - Consists of immature or
baby platelets known as megakaryocytes – target of virus – dengue - Normal lifespan 9 – 12 days
Drug of choice for HIV Zidovudine (AZT or Retrovir) Standard precaution for HIV gloves,
gown, goggles & mask Malaria – night biting mosquito Dengue – day biting mosquito Signs of
platelet dis function: a.) Petecchiae b.) Ecchemosis/ bruises c.) Oozing or blood from
venipuncture site

WBC – leucocytes 5,000 – 10,000/mm3 GRANULOCYTES 1. Polymorphonuclearneutrophils


Most abundant 60-70% WBC - fx – short term phagocytosis For acute inflammation 2. PM
Basophils -Involved in Parasitic infection - Release of chem. Mediator for inflammation
Serotonin, histamine, prostaglandin, bradykinins 3. PM eosinophils - Allergic reactions

ANEMIA
Iron deficiency Anemia – chronic normocytic, hypocromic (pale), microcytic anemia due to
inadequate absorption of iron leading to hypoxemic injury. Incidence rate: 1. Common –
developed country – due to high cereal intake Due to accidents – common on adults 2. Common
– tropical countries – blood sucking parasites 3. Women – 15 – 35yo – reproductive yrs 4.
Common among the poor – poor nutritional intake

41
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 22. Common in tropical zone – Phil due blood sucks Predisposing factor: 1. Chronic blood
loss a. Trauma b. Mens c. GIT bleeding: i. Hematemesisii. Melena – upper GIT – duodenal
cancer iii. Hematochezia – lower GIT – large intestine – fresh blood from rectum 2. Inadequate
intake of food rich in iron 3. Inadequate absorption of iron – due to : a. Chronic diarrhea b.
Malabsorption syndrome –celiac disease-gluten free diet. Food for celiac pts- sardines c. High
cereal intake with low animal CHON ingestion d. Subtotal gastrectomy 4. Improper cooking of
food S/Sx: 1. 2. 3. 4. 5. Asymptomatic Headache, dizziness, dyspnea, palpitations, cold
sensitivity, gen body malaise, pallor Brittle hair, spoon shaped nails (KOILONYCHIA)=Dec
O2=hypoxia=atrophy of epidermal cells Atropic glossitis, dysphagia, stomatitis Pica – abnormal
craving for non edible food (caused by hypoxia=dec tissue perfusion=psychotic behavior)

Brittle hair, spoon shaped nail – atrophy of epidermal cells N = capillary refill time < 2 secs N =
shape nails – biconcave shape, 180° Atrophy of cells “Plummer Vinsons Syndrome” due to
cerebral hypoxia 1. Atropic glossiti – inflammation of tongue due to atrophy of pharyngeal and
tongue cells 2. Stomatitis – mouth sores 3. Dysphagia Dx Proc: 1. RBC 2. Hgb 3. Reticulocyte 4.
Hct 5. Iron 6. Ferritin Nsg Mgt 1. Monitor signs of bleeding of all hema test including urine &
stool 2. Complete bed rest – don’t overtire pt =weakness and fatigue=activity intolerance 3.
Encourage – iron rich food 23. Raisins, legumes, egg yolk 4. Instruct the pt to avoid taking tea -
impairs iron absorption 5. Administer meds a.) Oral iron preparation Ferrous SO4 Fe gluconate
Fe Fumarate Nsg Mgt oral iron meds:

42
1. 2. Straw 1. 2. 3. 4.

Administer with meals – to lessen GIT irritation If diluting in iron liquid prep –adm with straw

Lugol’s Tetracycline Oral iron Macrodantine

3. Give Orange juice – for iron absorption


4. a. b. c. d. e. Monitor & inform pts S/E Anorexia n/v Abdominal pain Diarrhea or constipation
Melena

If pt can’t tolerate oral iron prep – administer parenteral iron prep example: 1. Iron dextran (IV,
IM) 2. Sorbitex (IM) Nsg Mgt parenteral iron prep 1. Administer of use Z tract method to
prevent discomfort, discoloration leakage to tissues. 2. Don’t massage injection site. Ambulate to
facilitate absorption. 3. Monitor S/E: a.) Pain at injury site b.) Localized abscess (“nana”) c.)
Lymphadenopathy d.) Fever/ chills e.) Urticaria – itchiness f.) Hypotension – anaphylactic shock
Anaphylactic shock – give epinephrine

PERNICIOUS ANEMIA - megaloblastic, chronic anemia due to deficiency of intrinsic factor


leading to
Hypochlorhydria – decrease Hcl acid secretion. Lifetime B12 injections. With CNS involvement.
Predisposing factor 1. Subtotal gastrectomy – removal stomach 2. Hereditary 3. Infl dse of ileum
4. Autoimmune 5. Strict vegetable diet STOMACH Parietal or ergentaffen Oxyntic cells Fxn –
produce intrinsic factor For reabsorption of B12 For maturation of RBC Diet high caloric or
CHO to correct wt loss S/Sx: 1. Headache dizziness, dyspnea, palpitations, cold sensitivity, gen
body malaise, pallor Fxn – secrets Hcl acid Fx aids in digestion

43
GIT changes a. Red – beefy tongue – PATHOGNOMONIC – mouth sores b. Dyspepsia –
indigestion c. Wt loss d. Jaundice 3. CNS – Most dangerous anemia: pernicious due to
neuroglogic involvement. a. Tingling sensation b. Paresthesia c. (+) Romberg’s test Ataxia d.
Psychosis Dx:- Shilling’s test Nsg Mgt – Pernicious anemia 1. Enforce CBR 2. Administer B12
injections at monthly intervals for lifetime as ordered. IM- dorsogluteal or ventrogluteal. Not
given oral – due pt might have tolerance to drug 3. Diet – high calorie or CHO. Increase CHON,
iron & Vit C 4. Avoid irritating mouthwashes. Use of soft bristled toothbrush is encouraged. 5.
Avoid applying electric heating pads – can lead to burns

2.

APLASTIC ANEMIA – stem cell disorder due to bone marrow depression leading to
pancytopenia – all RBC are decreased
Decrease RBC Anemia Increase WBC leukocytocys Increase RBC polycythemia vera –
complication stroke, CVA, thrombosis Predisposing factors leading to Aplastic Anemia 1.
Chemicals – Banzene & its derivatives 2. radiation 3. Immunologic injury 4. Drugs – cause bone
marrow depression a. Broad spectrum antibiotic - Chlorampenicol - Sulfonamides – bactrim b.
Chemo therapeutic agents Methotrexate – alkylating agents Nitrogen mustard – anti metabolic
Vincristine – plant alkaloid S/Sx: 1. Anemia: a. Weakness & fatigue b. Headache, dizziness,
dyspnea c. cold sensitivity, pallor d. palpitations 2. Leucopenia – increase susceptibility to
infection 3. Thrombocytopenia – a. Peticchiae b. Oozing ofblood from venipuncture site c.
ecchymosis Dx: 1. CBC – pancytopenia 2. Bone marrow biopsy/ aspiration at post iliac crest –
reveals fatty streaks in bone marrow Nsg Mgt: 1. Removal of underlying cause 2. Blood
transfusion as ordered decrease WBC leukopenia decrease platelets thrombocytopenia

44
3. 4. 5. 6.

Complete bed rest O2 inhalation Reverse isolation due leukopenia Monitor signs of infection 7.
Avoid SQ, IM or any venipuncture site = HEPLOCK 8. Use electric razor when shaving to
prevent bleeding 9. Administer meds Immunosuppresants Anti lymphocyte globulin (Alg) given
via central venous catheter, 6 days – 3 weeks to achieve max therapeutic effect of drug. BLOOD
TRANSFUSION: Objectives: 1. To replace circulating blood volume 2. To increase O2 carrying
capacity of blood 3. To combat infection if there’s decrease WBC 4. To prevent bleeding if
there’s platelet deficiency Nsg Mgt & principles in Blood Transfusion 1. Proper refrigeration 2.
Proper typing & crossmatching Type O – universal donor AB – universal recipient 85% of
people is RH (+) 3. Asceptically assemble all materials needed: a.) Filter set b.) Isotonic or PNSS
or .9NaCl to prevent Hemolysis Hypotonic sol – swell or burst Hypertonic sol – 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. e.) Check blood unit for presence of bubbles, cloudiness, dark in color & sediments –
indicates bacterial contamination. Don’t dispose. Return to blood bank. f.) Never warm blood
products – may destroy vital factors in blood. - Warming is done if with warming device – only
in EMERGENCY! For multiple BT. - 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. h.) Avoid mixing or administering drug at BT line – leads to hemolysis i.) Regulate
BT 10 – 15 gtts/min KVO or 100cc/hr to prevent circulatory overload j.) Monitor VS before,
during & after BT especially q15 mins(local board) for 1st hour. NCLEX-q5min for 1st 15min. -
Majority of BT reaction occurs within 1h.

BT reactions S/Sx Hemolytic reaction: H – hemolytic Reaction 1. Headache, dizziness, dyspnea,


palpitation, lumbar/ sterna/ flank pain, A – allergic Reaction hypotension, flushed skin , (red)
port wine urine. P – pyrogenic Reaction C – circulatory overload A – air embolism T -
thrombocytopenia C – citrate intoxication – expired blood =hyperkalemia H – hyperkalemia Nsg
Mgt: Hemolytic Reaction: 1. Stop BT

45
2. 3.

Notify Doc Flush with plain NSS 4. Administer isotonic fluid sol – to prevent acute tubular
necrosis & conteract 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

Allergic Reaction:
S/Sx 1. 2. 3. 4. 5. Fever/ chills Urticaria/ pruritus Dyspnea Laryngospasm/ bronchospasm
Bronchial wheezing

Nsg Mgt: 1. Stop BT 2. Notify Doc 3. Flush with PNSS 4. Administer antihistamine –
diphenhydramine Hcl (Benadryl). Give bedtime.SE-Adult-drowsiness. Child-hyperactive 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 AllergicRxn, if (+) to hypotension – indicates anaphylactic shock 24. administer
epinephrine 9. Adm antipyretic & antibiotic for pyrogenic Rxn & TSB

Pyrogenic Reaction:
S/Sx

a.) Fever/ chills b.) Headache c.) Dyspnea


Nsg Mgt: 1. 2. 3. 4. 5. 6. 7.

d. tachycardia e. palpitations f. diaphoresis

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 8. Tepid sponge bath –
offer hypothermic blanket

Circulatory Overload:
Sx a. b. c. d. Dyspnea Orthopnea Rales or crackles Exertional discomfort

Nsg Mgt: 1. Stop BT 2. Notify Doc. Don’t flush due pt has circulatory overload. 3. Administer
diuretics Priority cases: Hemolytic Rxn – 1st due to hypotension – 1st priority – attend to
destruction of Hgb – O2 brain damage

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Allergic Pyrogenic Circulatory Hemolytic Anaphylitic

3rd 4th 2nd 2nd 1st priority

DIC – DISSEMINATED INTRAVASCULAR COAGULATION

25. Acute hemorrhagic syndrome char by wide spread bleeding & thrombosis due to a def of
clotting factors (Prothrombin &
Fibrinogen). Predisposing factor: 1. Rapid BT 2. Massive trauma 3. Massive burns 4. Septicemia
5. Hemolytic reaction 6. Anaphylaxis 7. Neoplasia – growth of new tissue 8. Pregnancy S/Sx 1.
2. 3. 4. 5. Petechiae – widespread & systemic (lungs, lower & upper trunk) Ecchymosis –
widespread Oozing of blood from venipunctured site Hemoptysis – cough blood Hemorrhage 6.
Oliguria – late sx

Dx Proc– 1. CBC – reveals decrease platelets 2. Stool for occult blood (+) Specimen – stool 3.
Opthalmoscopic exam – sub retinal hemorrhage 4. ABG analysis – metabolic acidosis pH pH ph
ph ph HCO3 PCO2 PCO2 HCO3 HCO3

ROME

respiratory alkalosis respiratory acidosis metabolic alkalosis metabolic acidosis

Diarrhea – met acidosis Vomitting – met alk Pyloric stenosis – met alkalosis – vomiting
Ileostomy or intestinal tubing – met acidosis Cushing’s – met alk DM met acid Chronic
bronchitis – resp acid – with hypoxemia, cyanosis Nsg Mgt DIC 1. Monitor signs of bleeding –
hema test + urine, stool, GIT 2. Administer isotonic fluid solution to prevent shock. 3.
Administer O2 inhalation 4. Administer meds

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a. 5.

Vit K aquamephyton

b. Pitressin or vasopressin – to conserve water.


NGT – lavage - Use iced saline lavage 6. Monitor NGT output 7. Provide heplock 8. Prevent
complication: hypovolemic shock Late signs of hypovolemic shock : anuria

Oncologic Nsg:
Oncology – study of neoplasia –new growth Benign (tumor) Diff - well differentiated
Encapulation – (+) Metastasis – (-) Prognosis – good Therapeutic modality surgery Malignancy
(cancer) poorly or undifferentiated (-) (+) poor 1. Chemotherapy plenty 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 - Drugs
(stillbestrol) - Uraehane - Hormones - Smoking Male 3.) Prostate cancer - common 40 & above
(middle age & above) BPH – 50 & above 1.) Lung cancer 2.) Liver cancer Female 1. Breast
cancer – 40 yrs old & up – mammography 15 – 20 mins (SBE – 7 days after mens) 2. Cervical
cancer – 90% multi sexual partners 5% early pregnancy 3. Ovarian cancer Classes of cancer
Tissue typing 1. Carcinoma – arises from surface epithelium & glandular tissues 2. Sarcoma-
from connective tissue or bones 3. Multiple myeloma – from bone marrow Pathological fracture
of ribs & back pain 4. Lymphoma – from lymph glands 5. Leukemia – from blood Warning /
Danger Sx of CA C – change in bowel /bladder habits

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A – a sore that doesn’t heal U – unusual bleeding/ Discharge T – thickening of lump – breast or
elsewhere I – indigestion? Dysphagia O – obvious change in wart/ mole N – nagging cough/
hoarseness U – unexplained anemia A - anemia S – sudden wt loss L – loss of wt Therapeutic
Modality:

1. Chemotherapy – use various chemotherapeutic agents that kills cancer cells & kills normal
rapidly producing cells – GIT,
bone marrow, and hair follicle. Classification: a.) Alkylating agents – b.) Plant alkaloids –
vincristine c.) Anti metabolites – nitrogen mustard d.) Hormones – DES Steroids e.)
Antineoplastic antibiotics S/E & mgt GIT - -Nausea & vomiting Nsg Mgt: 1. Administer anti
emetic 4 – 6h before start of chemo Plasil 2. Withhold food/ fluid before start of chemo 3.
Provide bland diet post chemo 26. Non irritating / non spicy - Diarrhea 1. Administer anti
diarrheal 4 – 6h before start of chemo 2. Monitor urine, I&O qh - Stomatitis/ mouth sores 1. Oral
care – offer ice chips/ popsickles 2. Inform pt – hair loss – temporary alopecia Hair will grow
back after 4 – 6 months post chemo. -Bone marrow depression – anemia 1. Enforce CBR 2. O2
inhalation 3. Reverse isolation 4. Monitor signs of bleeding Repro organ – sterility 1. Do sperm
banking before start of chemo Renal system – increase uric acid 1. Administer allopurinol/
xyloprin (gout) 27. Inhibits uric acid 28. Acute gout – colchicines 29. Increase secretion of uric
acid Neurological changes – peristalsis – paralytic ileus Most feared complication ff any
abdominal surgery Vincristine – plant alkaloid causes peripheral neuropathy

2. Radiation therapy – involves use of ionizing radiation that kills cancer cells & inhibit their
growth & kill N rapidly producing
cells. Types of energy emitted 1. Alpha rays – rarely used – doesn’t penetrate skin tissues 2. Beta
rays – internal radiation – more penetration 3. Gamma ray – external radiation – penetrates
deeper underlying tissues

49
Methods of delivery 1. External radiation- involves electro magnetic waves Ex. cobalt therapy 2.
Internal radiation – injection/ implantation of radioisotopes proximal to CA site for a specific
period of time. 2 types: a.) Sealed implant – radioisotope with a container & doesn’t contaminate
body fluid. b.) Unsealed implant – radioisotope without a container & contaminates body fluid.
Ex. Phosphorus 32 3 Factors affecting exposure: A.) Half life – time period required for half of
radioisotopes to decay. - At end of half life – less exposure B.) Distance – the farther the distance
– lesser exposure C. ) Time – the shorter the time, the lesser exposure D.) Shielding – rays can be
shielded or blocked by using rubber gloves – α & β gamma – use thick lead on concrete. S/E &
Mgt: a.) Skin errythema, redness, sloughing 1. Assist in battling pt 2. Force fluid – 2,000 – 3,000
ml/day 3. Avoid lotion or talcum powder – skin irritation 4. Apply cornstarch or olive oil 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 yo Stomatitis c.)
Bone marrow depression 1. Enforce CBR 2. O2 inhalation 3. Reverse isolation 4. Monitor signs
of bleeding

Overview of function & structure of the heart


HEART - Muscular, pumping organ of the body - Left mediastinum - Weigh 300 – 400 grams -
Resembles a closed fist - Covered by serous membrane – pericardium Pericardium Parietal layer
Pericardial Fluid – prevent Friction rub Visceral layer

Layer 1. Epicardium – outermost 2. Myocardium – inner – responsible for pumping action/ most
dangerous layer - cardiogenic shock 3. Endocardium – innermost layer Chambers 1. Upper –
collecting/ receiving chamber - Atria 2. Lower – pumping/ contracting chamber - Ventricles
Valves 1. Atrioventricular valves - Tricuspid & mitral valve

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Closure of AV valves – gives rise to 1st heart sound or S1 or “lub” 2. Semi lunar valve a.)
Pulmonic b.) Aortic Closure of semilunar valve – gives rise to 2nd heart sound or S2 or “dub”
Extra heart Sound S3 – ventricular Gallop – CHF S4 – atrial gallop – MI, HPN

Heart conduction system 1. Sino atrial node (SA node) (or Keith-Flock node) Loc – junction of
SVC & Rt atrium Fx- primary pace maker of heart -Initiates electric impulse of 60 – 100 bpm 2.
Atrioventicular node (AV node or Tawara node) Loc – inter atrial septum Delay of electric
impulse to allow ventricular filling 3. Bundle of His – location interventricular septum Rt main
Bundle Branch Lt main Bundle Branch 4. Purkenjie Fiber Loc- walls of ventricles-- Ventricular
contractions SA node

AV
Purkenjie Fibers Bundle of His Complete heart block – insertion of pacemaker at Bundle Branch
Metal – Pace Maker – change q3 – 5 yo Prolonged PR – atrial fib ST segment depression –
angina ST – elev – MI T wave inversion – MI widening QRS – arrhythmia

CAD – coronary artery dse or Ischemic Heart Dse (IHD) Atherosclerosis – Myocrdial injury
Angina Pectoris – Myocardial ischemia MI- myocardial necrosis ATHEROSCLEROSIS -
Hardening or artery due to fat/ lipid deposits at tunica intima. Artery – tunica adventitia – outer -
Tunica intima – innermost - Tunica media – middle ATHEROSCLEROSIS Predisposing Factor
1. Sex – male 2. Black race ARTEROSCLEROSIS - Narrowing or artery due to calcium &
CHON deposits at tunica media.

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3. Hyperlipidemia 4. Smoking 5. HPN 6. DM 7. Oral contraceptive- prolonged use 8. Sedentary
lifestyle 9. Obesity 10. Hypothyroidism Signs & Symptoms 1. Chest pain 2. Dyspnea 3.
Tachycardia 4. Palpitations 5. Diaphoresis Treatment P – percutaneous T – tansluminar C –
coronary A – angioplasty Obj: 1. 2. 3. To revascularize the myocardium To prevent angina
Increase survival rate

PTCA – done to pt with single occluded vessel . Multiple occluded vessels C – coronary A –
arterial B – bypass A –and G – graft surgery Nsg Mgt Before CABAG 1. Deep breathing cough
exercises 2. Use of incentive spirometer 3. Leg exercises

ANGINA PECTORIS- A clinical syndrome characterized by paroxysmal chest pain usually


relieved by REST or NGT
nitroglycerin, resulting fr temp myocardial ischemia. Predisposing Factor: 1. sex – male 2. black
raise 3. hyperlipidemia 4. smoking 5. HPN 6. DM 7. oral contraceptive prolonged 8. sedentary
lifestyle 9. obesity 10.hypothyroidism Precipitating factors 4 E’s 1. Excessive physical exertion
2. Exposure to cold environment - Vasoconstriction 3. Extreme emotional response 4. Excessive
intake of food – saturated fats. Signs & Symptoms

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1. Initial symptoms – Levine’s sign – hand clutching of chest
Chest pain – sharp, stabbing excruciating pain. Location – substernal -radiates back, shoulders,
axilla, arms & jaw muscles -relieve by rest or NGT 3. Dyspnea 4. Tachycardia 5. Palpitation
6.diaphoresis Diagnosis 1.History taking & PE 2. ECG – ST segment depression 3. Stress test –
treadmill = abnormal ECG 4. Serum cholesterol & uric acid - increase. Nursing Management 1.)
Enforce CBR 2.) Administer meds NTG – small doses – venodilator Large dose – vasodilator 1st
dose NTG – give 3 – 5 min 2nd dose NTG – 3 – 5 min 3rd & last dose – 3 – 5 min Still painful
after 3rd dose – notify doc. MI! 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. Meds: A. NTG- Nsg Mgt: 1. Keep in a dry place. Avoid moisture &
heat, may inactivate the drug. 2. Monitor S/E: orthostatic hypotension – dec bp transient
headache dizziness 3. Rise slowly from sitting position 4. Assist in ambulation. 5. If giving NTG
via patch: i. avoid placing it near hairy areas-will dec drug absorption ii. avoid rotating
transdermal patches- will dec drug absorption iii. avoid placing near microwave oven or during
defibrillation-will burn pt due aluminum foil in patch B. Beta blockers – propanolol C. ACE
inhibitors – captopril D. Ca antagonist - nefedipine Administer O2 inhalation Semi-fowler Diet-
Decrease Na and saturated fats Monitor VS, I&O, ECG HT: Discharge planning: a. Avoid
precipitating factors – 4 E’s b. Prevent complications – MI c. Take meds before physical
exertion-to achieve maximum therapeutic effect of drug d. Importance of follow-up care. 2.

3.) 4.) 5.) 6.) 7.)

MI – MYOCARDIAL INFARCTION – hear attack – terminal stage of CAD


Characterized by necrosis & scarring due to permanent mal-occlusion

53
Types:

1. Trasmural MI – most dangerous MI – Mal-occlusion of both R&L coronary artery 2. Sub-


endocardial MI – mal-occlusion of either R & L coronary artery
Most critical period upon dx of MI – 48 to 72h - Majority of pt suffers from PVC premature
ventricular contraction.

Predisposing factors 1. sex – male 2. black raise 3. hyperlipidemia 4. smoking 5. HPN 6. DM 7.


oral contraceptive prolonged 8. sedentary lifestyle 9. obesity 10. hypothyroidism

Signs & symptoms 1. chest pain – excruciating, vice like, visceral pain located substernal or
precodial area (rare) - radiates back, arm, shoulders, axilla, jaw & abd muscles. - not usually
relived by rest r NTG 2. dyspnea 3. erthermia 4. initial increase in BP 5. mild restlessness &
apprehensions 6. occasional findings a.) split S1 & S2 b.) pericardial friction rub c.) rales
/crackles d.) S4 (atrial gallop)

Diagnostic Exam 1. cardiac enzymes a.) CPK – MB – Creatinine Phosphokinase b.) LDH –
lactic acid dehydrogenase c.) SGPT – (ALT) – Serum Glutanic Pyruvate Transaminase-
increased d.) SGOT (AST) – Serum Glutamic Oxaloacetic - increased 2. Troponin test – increase
3. ECG tracing – ST segment increase, widening or QRS complexes – means arrhythmia in MI
indicating PVC 4. serum cholesterol & uric acid - increase 5. CBC – increase WBC

Nursing Management 1. Narcotic analgesics – Morphine SO4 – to induce vasodilation &


decrease levels of anxiety. 2. Administer O2 inhalation – low inflow (CHF-increase inflow) 3.
Enforce CBR without BP a.) Bedside commode 4. Avoid valsalva maneuver 5. Semi fowler 6.
General liquid to soft diet – decrease Na, saturated fat, caffeine 7. Monitor VS, I&O & ECG
tracings 8. Take 20 – 30 ml/week – wine, brandy/whisky to induce vasodilation. 9. Assist in
surgical; CABAG 10. Provide pt HT a.) Avoid modifiable risk factors b.) Prevent complications:
1. Arrhythmias – PVC 2. Shock – cardiogenic shock. Late signs of cardiogenic shock in MI –
oliguria 3. thrombophlebitis - deep vein 4. CHF – left sided 5. Dressler’s syndrome – post MI
syndrome -Resistant to medications -Administer 150,000 – 450,000 units of streptokinase c.)
Strict compliance to meds - Vasodilators 1. NTG 2. Isordil - Antiarrythmic 1. Lydocaine blocks
release of norepenephrine 2. Brithylium - Beta-blockers – “lol” 1. Propanolol (inderal) - ACE
inhibitors - pril

54
1. Captopril – (enalapril) - Ca – antagonist 1. Nifedipine - Thrombolitics or fibrinolytics– to
dissolve clots/ thrombus S/E allergic reactions/ uticaria 1. Streptokinase 2. Urokinase 3. Tissue
plasminogen adjusting factor

Monitor for bleeding: - Anticoagulants 1. Heparin PTT If prolonged bleeding

2. Caumadin – delayed reaction 2 – 3 days PT prolonged bleeding

Antidote antidote Vit K Protamine sulfate - Anti platelet PASA (aspirin) d.) Resume ADL – sex/
activity – 4 to 6 weeks Post-cardiac rehab 1.)Sex as an appetizer rather then dessert – Before
meals not after, due after meals increase metabolism – heart is pumping hard after meals. 2.)
Position – non-weight bearing position. When to resume sex/ act: When pt can already use
staircase, then he can resume sex. e.) Diet – decrease Na, Saturated fats, and caffeine f.) Follow
up care.

CHF – CONGESTIVE HEART FAILURE - Inability of heart to pump blood towards systemic
circulation.
- Backflow 1.) Left sided heart failure: Predisposing factors: 1.) 90% mitral valve stenosis – due
RHD, aging RHD affects mitral valve – streptococcal infection Dx: - 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 S/Sx
Pulmonary congestion/ Edema 1. Dyspnea 2. Orthopnea (Diff of breathing sitting pos –
platypnea) 3. Paroxysmal nocturnal dysnea – PNO- nalulunod 4. Productive cough with blood
tinged sputum 5. Frothy salivation (from lungs) 6. Cyanosis 7. Rales/ crackles – due to fluid 8.
Bronchial wheezing

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9. 10. 11. 12. Dx 1.

PMI – displaced lateral – due cardiomegaly Pulsus alternons – weak-strong pulse Anorexia &
general body malaise S3 – ventricular gallop

CXR – cardiomegaly 2. PAP – Pulmonary Arterial Pressure PCWP – Pulmonary


CapillaryWedge Pressure PAP – measures pressure of R ventricle. Indicates cardiac status.
PCWP – measures end systolic/ diastolic pressure PAP & PCWP: Swan – ganz catheterization –
cardiac catheterization is done at bedside at ICU (Trachesostomy – bedside) - Done 5 – 20 mins
– scalpel & trachesostomy set CVP – indicates fluid or hydration status Increase CVP – decrease
flow rate of IV Decrease CVP – increase flow rate of IV Echocardiography – reveals enlarged
heart chamber or cardiomayopathy ABG – PCO2 increase, PO2 decrease = = hypoxemia = resp
acidosis

3. 4.

2.) Right sided HF Predisposing factor 1. 90% - tricuspid stenosis 2. COPD 3. Pulmonary
embolism 4. Pulmonic stenosis 5. Left sided heart failure S/Sx Venous congestion - Neck or
jugular vein distension - Pitting edema - Ascites - Wt gain - Hepatomegalo/ splenomegaly -
Jaundice - Pruritus - Esophageal varies - Anorexia, gen body malaise Diagnosis: 1. 2. CXR –
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

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Nsg mgt: Increase force of myocardial contraction = increase CO 3 – 6L of CO 1. Administer
meds: Tx for LSHF: 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: Aminophillin (Theophyllin). Avoid giving caffeine d.)
Narcotic analgesic: Morphine SO4 - induce vasodilaton & decrease anxiety e.) Vasodilators –
NTG f.) Anti-arrythmics – Lidocaine 2. Administer O2 inhalation – high! @ 3 -4L/min via nasal
cannula 3. High fowlers 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)
Complications :shock Arrhythmia Thrombophlebitis MI Cor Pulmonale – RT ventricular
hypertrophy b.) Dietary modifications c.) Adherence to meds

PERIPHERAL MUSCULAR DISEASE Arterial ulcers 1. Thromboangiitis Obliterans – male/


feet 2. Reynauds – female/ hands venous ulcer 1. Varicose veins 2. Thrombophlebitis

1.) Thromboangiitis obliterates/ BUERGER DISEASE- Acute inflammatory disorder affecting


small to medium sized arteries & veins of lower extremities. Male/ feet Predisposing factors: -
Male - Smokers

57
S/Sx 1. Intermittent claudication – leg pain upon walking - Relieved by rest 2. Cold sensitivity &
skin color changes White Pallor bluish cyanosis red rubor

3. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis 4. Tropic changes 5.
Ulcerations 6. Gangrene formation Dx: 1. 2. Oscillometry – decrease peripheral pulse volume.
Doppler UTZ – decrease blood flow to affected extremities. 3. Angiography – reveals site &
extent of mal-occulsion. 5. Nsg Mgt: 1. Encourage a slow progression of 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 – 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. Surgery: BKA (Below the knee amputation)
2.)REYNAUD’S PHENOMENON – acute episodes of arterial spasm affecting digits of hands &
fingers Predisposing factors: 1. 2. 3. Female, 40 yrs Smoking Collagen dse a.) SLE –
pathognomonic sign – butterfly rash on face Chipmunk face – bulimia nervosa Cherry red skin –
carbon monoxide Spider angioma – liver cirrhosis Caput medusae – leg & trunk Lion face –
leprosy b.) Rheumatoid arthritis – Direct hand trauma – piano playing, excessive typing,
operating chainsaw 1. 2. Nsg Mgt: Intermittent claudication - leg pain upon walking - Relieved
by rest Cold sensitivity

poisoning umbilicus- Liver cirrhosis

4. S/Sx:

58
a. b. c. d.

Analgesics Vasodilators Encourage to wear gloves especially when opening a refrigerator. Avoid
smoking & exposure to cold environment

VENOUS ULCERS 1. VARICOSITIES / Varicose veins - Abnormal dilation of veins – lower


ext & trunk - Due to: a.) Incompetent valves leading to b.) Increase venous pooling & stasis
leading to c.) Decrease venous return Predisposing factors: a. Hereditary b. Congenital weakness
of veins c. Thrombophlebitis d. Heart dse e. Pregnancy f. Obesity g. Prolonged immobility -
Prolonged standing S/Sx: 1. Pain especially after prolonged standing 2. Dilated tortuous skin
veins 3. Warm to touch 4. Heaviness in legs Dx: 1. Venography

2. Trendelenberg’s test – vein distend quickly < 35 secs


Nsg Mgt: 1. Elevate legs above heart level – to promote venous return – 1 to 2 pillows 2.
Measure circumference of leg muscles to determine if swollen. 3. Wear anti embolic or knee
high stockings. Women – panty hose 4. Meds: Analgesics 5. Surgery: vein sweeping & ligation
Sclerotherapy – spider web varicosities S/E thrombosis

THROMBOPHLEBITIS (deep vein thrombosis) - Inflammation of veins with thrombus


formation
Predisposing factors: 1. Smoking 2. Obesity 2. Hyperlipedemia 4. Prolonged use of oral
contraceptives 5. Chronic anemia 6. DM 7. MI 8. CHF 9. Postop complications 10. Post
cannulation – insertion of various cardiac catheters S/Sx: 1. 2. 3. Pain at affected extremities
Cyanosis (+) Homan’s sign - Pain at leg muscles upon dorsiflexion of foot.

59
Dx: 1. Angiography 2. Doppler UTZ Nsg Mgt: 1. Elevate legs above heart level. 2. Apply warm,
moist packs to decrease lymphatic congestion. 3. Measure circumference of leg muscles to detect
if swollen. 4. Use anti embolic stockings. 5. Meds: Analgesics. Anticoagulant: Heparin 6.
Complication:

Pulmonary Embolism:
- Sudden sharp chest pain - Dyspnea - Tachycardia - Palpitation - Diaphoresis - Mild restlessness
OVERVIEW OF RESPIRATORY SYSTEM: I. Upper respiratory tract: Fx: 1. Filtering of air 2.
Warming & moistening 3. Humidification a. Nose – cartilage - Parts: Rt nostril separated by
septum Lt nostril Consists of anastomosis of capillaries – Kessel – Bach Plexus – site of epistaxis
b. Pharynx (throat) – muscular passageway for air& food Branches: 1. Oropharynx 2.
Nasopharynx 3. Layngopharynx 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 - site of
gas exchange (O2 & CO2)

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-

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

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Nsg Mgt: Enforce CBR Strict respiratory isolation Meds: a.) Broad spectrum antibiotics
Penicillin or tetracycline Macrolides – ex azythromycin (zythromax) b.) Anti pyretics c.)
Mucolytics or expectorants 4. Force fluids – 2 to 3 L/day 5. Institute pulmonary toileta.) Deep
breathing exercise b.) Coughing exercise c.) Chest physiotherapy – cupping d.) 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 c.) Deep breathing exercises d.) Adm bronchodilators 15 – 30
min before procedure e.) Stop if pt can’t 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 1. 2. 3.

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

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(+) 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

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

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

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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.

COPD – Chronic Obstructive Pulmonary Disease


1. 2. 3. 4. Chronic bronchitis 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

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e.) Dander f.) Lints 2. Intrinsic AsthmaCause: Herediatary Drugs – aspirin, penicillin, β 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. C – cough – non productive to productive D – dyspnea
3. W – wheezing on expiration 4. Cyanosis 5. Mild apprehension & restlessness 6. Tachycardia
& palpitation 7. Diaphoresis 1. 2. Pulmo function test – decrease lung capacity ABG – PO2
decrease

Dx:

Nsg Mgt: 1. CBR – all COPD 2. Medsa.) 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 2. Force fluid 3. O2 – all COPD low inflow to prevent resp distress 4.
Nebulize & suction 5. Semifowler – all COPD except emphysema due late stage 6. HT a.) Avoid
pred factors b.) Complications: - Status astmaticus- give epinephrine & bronchodilators -
Emphysema c.) Adherence to med

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

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Dx: 1. ABG – PO2 decrease Nsg Mgt: before bronchoscopy Consent, explain procedure – MD/
lab explain RN NPO Monitor VS Feeding after return of gag reflex Instruct client to avoid
talking, smoking or coughing Monitor signs of frank or gross bleeding Monitor of laryngeal
spasm DOB Prepare at bedside tracheostomy set

2. Bronchoscopy – direct visualization of bronchus using fiberscope.


1. 2. 3. 1. 2. 3. 4. -

Nsg Mgt after bronchoscopy

Mgt: same as emphysema except Surgery Pneumonectomy – removal of affected lung Segmental
lobectomy – position of pt – unaffected side

PULMONARY EMPHYSEMA – irreversible terminal stage of COPD


- Characterized by inelasticity of alveolar wall leading to air trapping, leading to maldistribution
of gases. - Body will compensate over distension of thoracic cavity - Barrel chest Predisposing
factor: 1. Smoking 2. Allergy 3. Air pollution 4. High risk – elderly 5. Hereditary - α 1 anti
trypsin to release elastase for recoil of alveoli. S/Sx: 1. 3. 4. 5. 6. 7. 8. Productive cough

2. 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 9. Pathognomonic: barrel
chest – increase post/ anterior diameter of chest 10. Purse lip breathing – to eliminated PCO2 11.
Flaring of alai nares Diagnosis: 1. Pulmonary function test – decrease vital lung capacity 2. ABG
– a.) Panlobular / centrolobular emphysema pCO2 increase pO2 decrease – hypoxema resp
acidosis Blue bloaters b.) Panacinar/ Centracinar pCO2 decrease pO2 increase – hyperaxemia
resp alkalosis Pink puffers Nursing Mgt: 1. CBR 2. Meds – a.) Bronchodilators

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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

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 & can’t 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 - 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

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a.) Petroleum gauze pad if dislodged Hemostan b.) If with air leakage – clamp c.) Extra bottle 4.
Meds – Morphine SO4 Antimicrobial 5. Monitor & assess for oscillation fluctuations or bubbling
a.) 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 1. DBE 2. Instruct to perform Valsalva maneuver for easy removal, to prevent entry
of air in pleural space. 3. Apply vaselinated air occlusive dressing - Maintain dressing dry &
intact GIT I. Upper alimentary canal - function for digestion a. Mouth b. Pharynx (throat) c.
Esophagus d. Stomach e. 1st half of duodenum II. Middle Alimentary canal – Function: for
absorption - Complete absorption – large intestine a. 2nd half of duodenum b. Jejunum c. Ileum
d. 1st half of ascending colon III. Lower Alimentary Canal – Function: elimination a. 2nd half of
ascending colon b. Transverse c. Descending colon d. Sigmoid e. Rectum IV. Accessory Organ
a. Salivary gland b. Verniform appendix c. Liver d. Pancreas – auto digestion e. Gallbladder –
storage of bile I. Salivary Glands 1. Parotid – below & front of ear 2. Sublingual 3. Submaxillary
Produces saliva – for mechanical digestion

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-

1200 -1500 ml/day - saliva produced

PAROTITIS – “mumps” – inflammation of parotid gland


-Paramyxo virus S/Sx: 1. 2. 3. 4. Fever, chills anorexia, gen body malaise Swelling of parotid
gland Dysphagia Ear ache – otalgia

Mode of transmission: Direct transmission & droplet nuclei Incubation period: 14 – 21 days
Period of communicability – 1 week before swelling & immediately when swelling begins.
Nursing Mgt: 1. CBR 2. Strict isolation 3. Meds: analgesic Antipyretic Antibiotics – to prevent
2° complications 4. Alternate warm & cold compress at affected part 5. Gen liquid to soft diet 6.
Complications Women – cervicitis, vaginitis, oophoritis Both sexes – meningitis & encephalitis/
reason why antibiotics is needed Men – orchitis might lead to sterility if it occur during / after
puberty. VERNIFORM APPENDIX – Rt iliac or Rt inguinal area - Function – lymphatic organ –
produces WBC during fetal life - ceases to function upon birth of baby

APENDICITIS – inflamation of verniform appendix


Predisposing factor: 1. Microbial infection 2. Feacalith – undigested food particles – tomato
seeds, guava seeds 3. Intestinal obstruction S/Sx:

1. Pathognomonic sign: (+) rebound tenderness


2. 3. 4. Low grade fever, anorexia, n/v Diarrhea / & or constipation Pain at Rt iliac region 5. Late
sign due pain – tachycardia Diagnosis: 1. CBC – mild leukocytosis – increase WBC 2. PE – (+)
rebound tenderness (flex Rt leg, palpate Rt iliac area – rebound) 3. Urinalysis Treatment: -
appendectomy 24 – 45° Nursing Mgt: 1. Consent 2. Routinary nursing measures: a.) Skin prep
b.) NPO c.) Avoid enema – lead to rupture of appendix 3. Meds: Antipyretic

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Antibiotics *Don’t give analgesic – will mask pain - Presence of pain means appendix has not
ruptured. 4. Avoid heat application – will rupture appendix. 5. Monitor VS, I&O bowel sound
Nursing Mgt: post op 1. If (+) to Pendrose drain – indicates rupture of appendix Position-
affected side to drain 2. Meds: analgesic due post op pain Antibiotics, Antipyretics PRN 3.
Monitor VS, I&O, bowel sound 4. Maintain patent IV line 5. Complications- peritonitis,
septicemia Liver – largest gland - Occupies most of right hypochondriac region - Color: scarlet
red - Covered by a fibrous capsule – Glisson’s capsule - Functional unit – liver lobules Function:
Produces bile Bile – emulsifies fats - Composed of H2O & bile salts -Gives color to urine –
urobilin Stool – stircobilin 2. Detoxifies drugs 3. Promotes synthesis of vit A, D, E, K - fat
soluble vitamins Hypevitaminosis – vit D & K Vit A – retinol Def Vit A – night blindness Vit D
– cholecalciferon - Helps calcium - Rickets, osteoarthritis 4. It destroys excess estrogen hormone
5. For metabolism A. CHO – 1. Glycogenesis – synthesis of glycogens 2. Glycogenolysis –
breakdown of glycogen 3. Gluconeogenesis – formation of glucose from CHO sources B.
CHON1. 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 –
promotes synthesis of cholesterol to neutral fats – called triglycerides 1.

LIVER CIRRHOSIS - lost of architectural design of liver leading to fat necrosis & scarring
Early sign – hepatic encephalopathy 1. Asterixis – flapping hand tremors Late signs – headache,
restlessness, disorientation, decrease LOC – hepatic coma. Nursing priority – assist in
mechanical ventilation Predisposing factor:

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Decrease Laennac’s cirrhosis – caused by alcoholism 1. Chronic alcoholism 2. Malnutrition –
decreaseVit B, thiamin - main cause 3. Virus – 4. Toxicity- eg. Carbon tetrachloride 5. Use of
hepatotoxic agents S/Sx: Early signs: a.) Weakness, fatigue b.) Anorexia, n/v 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 2. Late signs a.) Hematological
changes – all blood cells decrease Leukopenia- decrease Thrombocytopenia- decrease Anemia-
decrease b.) Endocrine changes Spider angiomas, Gynecomastia Caput medusate, Palmar
errythema c.) GIT changes Ascitis, bleeding esophageal varices – due to portal HPN d.)
Neurological changes: Hepatic encephalopathy - ammonia (cerebral toxin) Late signs: Early
signs: Headache asterexis Fetor hepaticus (flapping hand tremors) Confusion Restlessness
Decrease LOC Hepatic coma Diagnosis: 1. Liver enzymes- increase SGPT (ALT) SGOT (AST)
Serum cholesterol & ammonia increase Indirect bilirubin increase CBC - pancytopenia PTT –
prolonged Hepatic ultrasonogram – fat necrosis of liver lobules

2. 3. 4. 5. 6.

Nursing Mgt 1. CBR 2. Restrict Na! 3. Monitor VS, I&O 4. With pt daily & assess pitting edema
5. Measure abdominal girth daily – notify MD 6. Meticulous skin care

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7. 8.

Diet – increase CHO, vit & minerals. Moderate fats. Decrease CHON Well balanced diet
Complications: a.) Ascites – fluid in peritoneal cavity Nursing Mgt: 1. Meds: Loop diuretics – 10
– 15 min effect 2. Assist in abdominal paracentesis - aspiration of fluid - Void before
paracentesis to prevent accidental puncture of bladder as trochar is inserted b.) Bleeding
esophageal varices - Dilation of esophageal veins 1. Meds: Vit K Pitrisin or Vasopresin (IM) 2.
NGT decompression- lavage - Give before lavage – ice or cold saline solution - Monitor NGT
output 3. Assist in mechanical decompression - Insertion of sengstaken-blackemore tube - 3
lumen typed catheter - Scissors at bedside to deflate balloon. c.) Hepatic encephalopathy – 1.
Assist in mechanical ventilation – due coma 2. Monitor VS, neuro check 3. Siderails – due
restless 4. Meds – Laxatives – to excrete ammonia

HEPATITIS- jaundice (icteric sclera)


Bilirubin Kernicterus/ hyperbilirubinia Irreversible brain damage

Pancreas – mixed gland (exocrine & endocrine gland)

PANCREATITIS – acute or chronic inflammation of pancreas leading to pancreatic edema,


hemorrhage & necrosis due to auto
digestion. Bleeding of pancreas - Cullen’s sign at umbilicus Predisposing factors: 1. Chronic
alcoholism 2. Hepatobilary disease 3. Obesity 4. Hyperlipidemia 5. Hyperparathyroidism 6.
Drugs – Thiazide diuretics, pills Pentamidine HCL (Pentam) 7. Diet – increase saturated fats
S/Sx: 1. Severe Lt epigastric pain – radiates from back &flank area - Aggravated by eating, with
DOB 2. N/V 3. Tachycardia 4. Palpitation due to pain 5. Dyspepsia – indigestion 6. Decrease
bowel sounds

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7. (+) Cullen’s sign - ecchymosis of umbilicus 8. (+) Grey Turner’s spots – ecchymosis of flank
area

hemorrhage

9. Hypocalcemia Diagnosis: 1. Serum amylase & lipase – increase 2. Urine lipase – increase 3.
Serum Ca – decrease Nursing Mgt: 1. Meds a.) Narcotic analgesic - Meperidine Hcl (Demerol)
Don’t 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 - Ranitidin (Zantac) to decrease pancreatic
stimulation f.) Ca – gluconate 2. Withold food & fluid – aggravates pain 3. Assist in Total
Parenteral Nutrition (TPN) or hyperalimentation Complications of TPN 1. Infection 2. Embolism
3. Hyperglycemia 4. Institute stress mgt tech a.) DBE b.) Biofeedback 5. Comfy position - Knee
chest or fetal like position 6. If pt can tolerate food, give increase CHO, decrease fats, and
increase CHON 7. Complications: Chronic hemorrhagic pancreatitis GALLBLADDER – storage
of bile – made up of cholesterol. CHOLECYSTITIS/ CHOLELITHIASIS – inflammation of
gallbladder with gallstone formation. Predisposing factor: 1. High risk – women 40 years old 2.
Post menopausal women – undergoing estrogen therapy 3. Obesity 4. Sedentary lifestyle 5.
Hyperlipidemia 6. Neoplasm S/Sx: 1. Severe Right abdominal pain (after eating fatty food).
Occurring especially at night 2. Fatty intolerance 3. Anorexia, n/v 4. Jaundice 5. Pruritus 6. Easy
bruising 7. Tea colored urine 8. Steatorrhea Diagnosis: 1. Oral cholecystogram (or gallbladder
series)- confirms presence of stones Nursing Mgt: 1. Meds – a.) Narcotic analgesic -
Meperdipine Hcl – Demerol b.) Anti cholinergic - Atropine SO4 c.) Anti emetic Phenergan –
Phenothiazide with anti emetic properties

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2. 3. 4.

Diet – increase CHO, moderate CHON, decrease fats Meticulous skin care Surgery:
Cholecystectomy Nursing Mgt post cholecystectomy -Maintain patency of T-tube intact &
prevent infection

Stomach – widest section of alimentary canal - J shaped structures 1. Anthrum 2. Pylorus 3.


Fundus Valves 1. 1.cardiac sphincter 2. Pyloric sphincter Cells 1. Chief/ Zymogenic cells –
secrets a.) Gastric amylase - digest CHO b.) Gastric lipase – digest fats c.) Pepsin – CHON d.)
Rennin – digests milk products Parietal / Argentaffin / oxyntic cells Function: a.) Produces
intrinsic factor – promotes reabsorption of vit B12 cyanocobalamin – promotes maturation of
RBC b.) Secrets Hcl acid – aids in digestion Endocrine cells - Secrets gastrin – increase Hcl acid
secretion

2.

3.

Function of the stomach 1.Mechanical 2.Chem. Digestion 3.Storage of food -CHO, CHON-
stored 1 -2 hrs. Fats – stored 2 – 3 hrs

PEPTIC ULCER DISEASE – (PUD) – excoriation / erosion of submucosa & mucosal lining due
to:
a.) Hypercecretion of acid – pepsin b.) Decrease resistance to mucosal barrier Incidence Rate: 1.
Men – 40 – 55 yrs old 2. Aggressive persons Predisposing factors: 1. Hereditary 2. Emotional 3.
Smoking – vasoconstriction – GIT ischemia 4. Alcoholism – stimulates release of histamine =
Parietal cell release Hcl acid = 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 Ellisons sign

10. Microbial invasion – helicobacter pylori. Metromidazole (Flagyl)


Types of ulcers Ascending to severity 1. Acute – affects submucosal lining 2. Chronic – affects
underlying tissue – heals & forms a scar

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According to location 1. Stress ulcer 2. Gastric ulcer 3. Duodenal ulcer – most common Stress
ulcers – common among eritically ill clients 2 types 1.Curing’s ulcer – cause: trauma & birth
hypovolemia GIT schemia Decrease resistance of mucosal barriers to Hcl acid Ulcerations
2.Cushing’s ulcer – cause – stroke/CVA/ head injury Increase vagal stimulation Hyperacidity
Ulcerations

SITE PAIN

HYPERSECRETION VOMITING HEMORRHAGE WT COMPLICATIONS

HIGH RISK Diagnosis: 1. Endoscopic exam 2. Stool from occult blood 3. Gastric analysis – N –
gastric Increase – duodenal 4. GI series – confirms presence of ulceration Nursing Mgt: 1. Diet –
bland, non irritating, non spicy 2. Avoid caffeine & milk/ milk products Increase gastric acid
secretion 3. Administer meds

GASTRIC ULCER Intrum or lesser curvature -30 min – 1 hr after eating - epigastrium - gaseous
& burning - not usually relieved by food & antacid Normal gastric acid secretion common
hematemeis Wt loss a. stomach cause b. hemorrhage 60 years old

DUODENAL ULCER Duodenal bulb -2-3 hrs after eating - mid epigastrium - cramping &
burning - usually relieved by food & antacid - 12 MN – 3am pain Increased gastric acid secretion
Not common Melena Wt gain a. perforation 20 years old

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a.) Antacids AAC Aluminum containing antacids Ex. aluminum OH gel (Ampho-gel) S/E
constipation Magnesium containing antacids ex. milk of magnesia S/E diarrhea

Maalox (fever S/E) b.) H2 receptor antagonist Ex 1. Ranitidine (Zantac) 2. Cimetidine (Tagamet)
3. Tamotidine (Pepcid) - Avoid smoking – decrease effectiveness of drug Nursing Mgt:

1. Administer antacid & H2 receptor antagonist – 1hr apart


-Cemetidine decrease antacid absorption & vise versa c.) Cytoprotective agents Ex 1. Sucralfate
(Carafate) - Provides a paste like subs that coats mucosal lining of stomach 2. Cytotec d.)
Sedatives/ Tranquilizers - Valium, lithium e.)Anticholinergics 1. Atropine SO4 2. Prophantheline
Bromide (Profanthene) (Pt has history of hpn crisis With peptic ulcer disease. Rn should not
administer alka seltzer- has large amount of Na. 4. Surgery: subtotal gastrectomy - Partial
removal of stomach Billroth I (Gastroduodenostomy) Billroth II (Gastrojejunostomy) -Removal
of ½ of stomach & anastomoses of gastric stump - removal of ½ -3/4 of stomach & duodenal
bulb & anastomostoses of to the duodenum. gastric stump to jejunum. Before surgery for BI or
BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first. Nursing Mgt: 1.
Monitor NGT output a.) Immediately post op should be bright red b.) Within 36- 42h – output is
yellow green c.) After 42h – output is dark red 2. Administer meds: a.) Analgesic b.) Antibiotic
c.) Antiemetics 3. Maintain patent IV line 4. VS, I&O & bowel sounds 5. Complications: a.)
Hemorrhage – hypovolemic shock Late signs – anuria b.) Peritonitis c.) Paralytic ileus – most
feared d.) Hypokalemia e.) Thromobphlebitis f.) Pernicious anemia

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7.)Dumping syndrome – common complication – rapid gastric emptying of hypertonic food
solutions – CHYME leading to hypovolemia. Sx of Dumping syndrome: 1. Dizziness 2.
Diaphoresis 3. Diarrhea 4. Palpitations Nursing mgt: 1. Avoid fluids in chilled solutions 2. Small
frequent feeding s-6 equally divided feedings 3. Diet – decrease CHO, moderate fats & CHON 4.
Flat on bed 15 -30 minutes after q feeding

BURNS – direct tissue injury caused by thermal, electric, chemical & smoke inhaled (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 Thermal- direct contact – flames, hot grease, sunburn.
Electric, – wires Chem. – direct contact – corrosive materials acids Smoke – gas / fume
inhalation Stages:

1. Emergent phase – Removal of pt from cause of burn. Determine source or loc or burn 2.
Shock phase – 48 - 72°. Characterized by shifting of fluids from intravascular to interstitial space
=Hypovolemia S/Sx: BP decrease Urine output HR increase Hct increase Serum Na decrease
Serum K increase Met acidosis

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 tissue injury. Class: I. Partial Burn 1. 1st degree – superficial burns - Affects
epidermis - Cause: thermal burn - Painful - Redness (erythema) & blanching upon pressure with
no fluid filled vesicles 2. 2nd degree – deep burns - Affects epidermis & dermis - Cause –chem.
burns - very painful - Erythema & fluid filled vesicles (blisters) II Full thickness Burns 1. Third
& 4th degrees burn - Affects all layers of skin, muscles, bones - Cause – electrical - Less painful
- Dry, thick, leathery wound surface – known as ESCHAR – devitalized or necrotic tissue.

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Assessment findings Rule of nines Head & neck = 9% Ant chest = 18% Post chest = 18% @
Arm 9+9 = 18% @ leg 18+18 = 18% Genitalia/ perineum= 1% Total 100% Nursing Mgt 1.
Meds a.) Tetanus toxoid- burn surface area is source of anaerobic growth – Claustridium tetany
Tetany Tetanolysin Hemolysis tetanospasmin muscle spasm

b.) Morphine SO4 c.) Systemic antibiotics 1. Ampicillin 2. Cephalosporin 3. Tetracyclin 4.


Topical antibiotic : 1. Silver Sulfadiazene (silvadene) 2. Sulfamylon 3. Silver nitrate 4. Povidone
iodine (betadine) 2. Administer isotonic fluid sol & CHON replacements 3. Strict aseptic
technique 4. Diet – increase CHO, increase CHON, increase Vit C, and increase K- orange 5. If
(+) to burns on head, neck, face - Assist in intubation 6. Assist in hydrotherapy 7. Assist in
surgical wound debridement. Administer analgesic 15 – 30 minutes before debridement 8.
Complications: a.) Infection b.) Shock c.) Paralytic ileus - due to hypovolemia & hypokalemia
d.) Curling’s ulcer – H2 receptor antagonist e.) Septicemia blood poisoning f.) Surgery: skin
grafting GUT – genito-urinary tract Function: 1. Promote excretion of nitrogenous waste
products 2. Maintain F&E & acid base balance 1. Kidneys – pair of bean shaped organ - Retro
peritonially (back of peritoneum) on either side of vertebral column. Encased in Bowmans’s
capsule. Parts: 1. 2. 3. Renal pelvis – pyenophritis – infl Cortex Medulla

Nephrones – basic living unit Glomerulus – filters blood going to kidneys

78
Function of kidneys: 1. Urine formation 2. Regulation of BP Urine formation – 25% of total CO
(Cardiac Output) is received by kidneys 1. Filtration 2. Tubular Reabsorption 3. Tubular
Secretion Filtration – Normal GFR/ min is 125 ml of blood Tubular reabsorption – 124ml of
ultra infiltrates (H2O & electrolytes is for reabsorption) Tubular secretion – 1 ml is excreted in
urine 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 Ureters – 25 – 35 cm long,
passageway of urine to bladder Bladder – loc behind symphisis pubis. Muscular & elastic tissue
that is distensible - Function – reservoir or urine 1200 – 1800 ml – Normal adult can hold 200 –
500 ml – needed to initiate micturition reflex Color – amber Odor – aromatic Consistency – clear
or slightly turbid pH – 4.5 – 8 Specific gravity – 1.015 – 1.030 WBC/ RBC – (-) Albumin – (-) E
coli – (-) Mucus thread – few Amorphous urate (-) Urethra – extends to external surface of body.
Passage of urine, seminal & vaginal fluids. - Women 3 – 5 cm or 1 to 1 ½ “ - Male – 20cm or 8”
UTI increase CO increase PR

CYSTITIS – inflammation of bladder


Predisposing factors: 1. Microbial invasion – E. coli

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2. High risk – women 3. Obstruction 4. Urinary retention 5. Increase estrogen levels 6. Sexual
intercourse S/Sx: 1. Pain – flank area 2. Urinary frequency & urgency 3. Burning upon urination
4. Dysuria & hematuria 5. Fever, chills, anorexia, gen body malaise Diagnosis: 1. Urine culture
& sensitivity - (+) to E. coli Nursing Mgt: 1. Force fluid – 2000 ml 2. Warm sitz bath – to
promote comfort 3. Monitor & assess for gross hematuria 4. Acid ash diet – cranberry, vit C -OJ
to acidify urine & prevent bacterial multiplication 5. Meds: systemic antibiotics Ampicillin
Cephalosporin Sulfonamides – cotrimaxazole (Bactrim) - Gantrism (ganthanol) Urinary
antiseptics – Mitropurantoin (Macrodantin) Urinary analgesic- Pyridum 6. Ht a.) Importance of
Hydration b.) Void after sex c.) Female – avoids cleaning back & front Bubble bath, Tissue
paper, Powder, perfume d.) Complications: Pyelonephritis

PYELONEPHRITIS – acute/ chronic infl of 1 or 2 renal pelvis of kidneys leading to tubular


destruction, interstitial abscess
formation. - Lead 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 b.) Fever, anorexia, gen
body malaise c.) Urinary frequency, urgency d.) Nocturia, dsyuria, hematuria e.) Burning on
urination Chronic Pyelonephritis a.) Fatigue, wt loss b.) Polyuuria, polydypsia c.) HPN

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Diagnosis: 1. Urine culture & sensitivity – (+) E. coli & streptococcus 2. Urinalysis Increase
WBC, CHON & pus cells 3. Cystoscopic exam – urinary obstruction Nursing Mgt: 1. Provide
CBR – acute phase 2. Force fluid 3. Acid ash diet 4. Meds: a.) Urinary antiseptic – nitrofurantoin
(macrodantin) SE: peripheral neuropathy GI irritation Hemolytic anemia Staining of teeth b.)
Urinary analgesic – Peridium 2. Complication- Renal Failure

NEPHROLITHIASIS/ UROLITHIASIS- formation of stones at urinary tract


- calcium , milk oxalate, cabbage cranberries nuts tea chocolates uric acid anchovies organ meat
nuts sardines

Predisposing factors: 1. Diet – increase Ca & oxalate 2. Hereditary – gout 3. Obesity 4.


Sedentary lifestyle 5. Hyperparathyroidism S/Sx: 1. Renal colic 2. Cool moist skin (shock) 3.
Burning upon urination 4. Hematuria 5. Anorexia, n/v Diagnosis: 1. IVP – intravenous
pyelography. Reveals location of stone 2. KUB – reveals location of stone 3. Cytoscopic exam-
urinary obstruction 4. Stone analysis – composition & type of stone 5. Urinalysis – increase
EBC, increase CHON Nursing Mgt: 1.Force fluid 2.Strain urine using gauze pad 3.Warm sitz
bath – for comfort 4.Alternate warm compress at flank area 5. a.) Narcotic analgesic- Morphine
SO4 b.) Allopurinol (Zyeoprim) c.) Patent IV line d.) Diet – if + Ca stones – acid ash diet If +
oxalate stone – alkaline ash diet - (Ex milk/ milk products) If + uric acid stones – decrease organ
meat / anchovies sardines 6. Surgery a.) Nephectomy – removal of affected kidney Litholapoxy –
removal of 1/3 of stones- Stones will recur. Not advised for pt with big stones b.) Extracorporeal
shock wave lithotripsy

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7.

- Non - invasive - Dissolve stones by shock wave Complications: Renal Failure

BENIGN PROSTATIC HYPERTROPHY - enlarged prostate gland leading to


a.) b.) c.) d.) Hydro ureters – dilation of ureters Hydronephrosis – dilation of renal pelvis Kidney
stones Renal failure

Predisposing factor: 1. High risk – 50 years old & above 60 – 70 – (3 to 4 x at risk) 2. Influence
of male hormone S/Sx: 1.Decrease force of urinary stream 2.Dysuria 3.Hematuria 4.Burning
upon urination 5.Terminal bubbling 6.Backache 7.Sciatica Diagnosis: 1. Digital rectal exam –
enlarged prostate gland 2. KUB – urinary obstruction 3. Cystoscopic exam – obstruction 4.
Urinalysis – increase WBC, CHON Nursing Mgt: 1. Prostatic message – promotes evacuation of
prostatic fluid 2. Limit fluid intake 3. Provide catheterization 4. Meds: a. Terazozine (hytrin) -
Relaxes bladder sphincter b. Fenasteride (Proscar) - Atrophy of Prostate Gland 5. Surgery:
Prostatectomy – TURP- Transurethral resection of Prostate- No incision -Assist in cystoclysis or
continuous bladder irrigation. Nursing mgt: c. Monitor symptoms of infection d. Monitor
symptoms gross/ flank bleeding. Normal bleeding within 24h. 3. Maintain irrigation or tube
patent to flush out clots - to prevent bladder spasm & distention

ACUTE RENAL FAILURE – sudden immobility of kidneys to excrete nitrogenous waste


products & maintain F&E balance
due to a decrease in GFR. (N 125 ml/min) Predisposing factor: Pre renal cause- decrease blood
flow Causes: 1. Septic shock 2. Hypovolemia 3. Hypotension decrease flow to kidneys 4. CHF 5.
Hemorrhage 6. Dehydration Intra-renal cause – involves renal pathology= kidney problem 1.
Acute tubular necrosis-

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2. 3. 4.

Pyelonephritis HPN Acute GN

Post renal cause – involves mechanical obstruction 1. Stricture 2. Urolithiasis 3. BPH

CHRONIC RF – irreversible loss of kidney function


Predisposing factors: 1. DM 2. HPN 3. Recurrent UTI/ nephritis 4. Exposure to renal toxins
Stages of CRF 1. Diminished Reserve Volume – asymptomatic Normal BUN & Crea, GFR < 10
– 30% 2. Renal Insufficiency 3. End Stage Renal disease S/Sx: 1.) Urinary System 2.) Metabolic
disturbances a.) polyuria a.) azotemia (increase BUN & Crea) b.) nocturia b.) hyperglycemia c.)
hematuria c.) hyperinulinemia d.) Dysuria e.) oliguria 3.) CNS 4.) GIT a.) headache a.) n/v b.)
lethargy b.) stomatitis c.) disorientation c.) uremic breath d.) restlessness d.) diarrhea/
constipation e.) memory impairment 5.) Respiratory 6.) hematological a.) Kassmaul’s resp a.)
Normocytic anemia b.) decrease cough bleeding tendencies reflex 7.) Fluid & Electrolytes 8.)
Integumentary a.) hyperkalemia a.) itchiness/ pruritus b.) hypernatermia b.) uremic frost c.)
hypermagnesemia d.) hyperposphatemia e.) hypocalcemia f.) met acidosis Nursing Mgt: 1.
Enforce CBR 2. Monitor VS, I&O 3. Meticulous skin care. Uremic frost – assist in bathing pt 4.
Meds: a.) Na HCO3 – due Hyperkalemia b.) Kagexelate enema c.) Anti HPN – hydralazine d.)
Vit & minerals e.) Phosphate binder (Amphogel) Al OH gel - S/E constipation f.) Decrease Ca –
Ca gluconate 5. Assist in hemodialysis 1.) Consent/ explain procedure

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2.) Obtain baseline data & monitor VS, I&O, wt, blood exam 3.) Strict aseptic technique 4.)
Monitor for signs of complications: B – bleeding E – embolism D – disequilibrium syndrome S –
septicemia S – shock – decrease in tissue perfusion Disequilibrium syndrome – from rapid
removal of urea & nitrogenous waste prod leading to: a.) n/v b.) HPN c.) Leg cramps d.)
Disorientation e.) Paresthesia Avoid BP taking, blood extraction, IV, at side of shunt or fistula.
Can lead to compression of fistula. Maintain patency of shunt by: i. Palpate for thrills &
auscultate for bruits if (+) patent shunt! ii. Bedside- bulldog clip - If with accidental removal of
fistula to prevent embolism. - Infersole (diastole) – common dialisate used 7. Complication -
Peritonitis - Shock 8. Assist in surgery: Renal transplantation : Complication – rejection. Reverse
isolation 2. 3.

EYES
External parts 1. Orbital cavity – made up of connective tissue protects eye form trauma. 2. EOM
– extrinsic ocular muscles – involuntary muscles of eye needed for gazing movement. 3.
Eyelashes/ eyebrows – esthetic purposes 4. Eyelids – palpebral fissure – opening upper & lower
lid. Protects eye from direct sunlight Meibomean gland – secrets a lubricating fluid inside eyelid
b.) Stye/ sty or Hordeolum- inflamed Meibomean gland 5. Conjunctiva 6. Lacrimal apparatus –
tears Process of grieving a. Denial b. Anger c. Bargaining d. Depression e. Acceptance 2.
Intrinsic coat I. sclerotic coat – outer most a.) Sclera – white. Occupies ¾ post of eye. Refracts
light rays b.) Canal of schlera – site of aqueous humor drainage c.) Cornea – transparent structure
of eye II/ Uveal tract – nutritive care

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Uveitis – infl of uveal tract Consist of: a.) Iris – colored muscular ring of eye 2 muscles of iris: 1.
Circular smooth muscle fiber - Constricts the pupil 2.radial smooth muscle fiber - Dilates the
pupil 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) i. 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 ii. Maculla lutea – yellow spot center of retina iii. 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 4. Convergence of eyes Unit of measurements of refraction –
diopters Normal eye refraction – emmetropia ERROR of refraction 1. Myopia – near sightedness
– Treatment: biconcave lens 2. Hyperopia/ or farsightedness – Treatment: biconvex lens 3.
Astigmatisim – distorted vision – Treatment: cylindrical 4. Prebyopia – “old slight” – inelasticity
of lens due to aging – Treatment: 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 2. Esophoria – 3. Strabismus- squint
eye 4. Amblyopia – prolong squinting far vision= ciliary muscle dilates / relaxes= lens is flat

corrected by corrective eye surgery

GLAUCOMA – increase IOP – if untreated, atrophy of optic nerve disc – blindness


Predisposing factors: 1. High risk group – 40 & above 2. HPN 3. DM

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4. 5. 6. Type: 1. 2. 3. S/Sx:

Hereditary Obesity Recent eye trauma, infl, surgery 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 1. 2. 3. 4. 5. 6. 7. Loss of peripheral vision
– tunnel vision Halos around lights Headache n/v Steamy cornea Eye discomfort If untreated –
gradual loss of central vision – blindness

Diagnosis: 1. Tonometry – increase IOP >12- 21 mmHg 2. Perimetry – decrease peripheral


vision 3. Gonioscopy – abstruction in anterior chamber Nursing mgt: 1. Enforce CBR 2.
Maintain siderails 3. Administer meds a.) Miotics – lifetime - contracts ciliary muscles &
constricts pupil. Ex Pilocarpine Na (Carbachol) b.) Epinephrine eye drops – decrease secretion of
aqueous humor c.) Carbonic anhydrase inhibitors. Ex. acetapolamide (Diamox) - Promotes
increase out flow of aquaeous humor d.) Temoptics (Timolol maleate)- Increase outflow of
aquaous humor 2. Surgery: Invasive: a.) Trabeculectomy – eyetrephining – 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: Trabeculoctomy (eye laser surgery)

Nursing Mgt pre op- all types surgery 1. Apply eye patch on unaffected eye to force weaker eye
to become stronger. Nursing Mgt post op – 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 – both
eyes - post op

CATARACT – partial/ complete opacity of lens


Predisposing factor:

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1. 2. 3. 4. S/Sx:

90-95% - aging (degenerative/ senile cataract) Congenital Prolonged exposure to UV rays DM-

1. Loss of central vision - “Hazy or blurring of vision”


2. 3. 4. Painless Milky white appearance at center of pupil Decrease perception of colors

Diagnosis: Opthalmoscopic exam – (+) opacity of lens Nsg Mgt: 1. Reorient pt to environment –
due opacity 2. Siderails 3. Meds – a.) Mydriatics – dilate pupil – not lifetime Ex. Mydriacyl c.)
Cyslopegics – paralyzes ciliary muscle. Ex. Cyclogye 4. Surgery E – extra C - capsular C –
cataract L - lens E – extraction I - intra C - capsular C – cataract L - lens E – extraction 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

partial removal of lens

total removal of lens & surrounding capsules

RETINAL DETACHMENT- separation of 2 layers of retina


Predisposing factors: 1. 2. 3. 4. 5. S/Sx: 1. 2. 3. 4. 5. Severe myopia – nearsightedness Diabetic
Retinopathy Trauma Following lens extraction HPN

“Curtain –veil” like vision Flashes of lights Floaters Gradual decrease in central vision Headache

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Diagnosis- opthaloscopic exam Nursing Mgt: 1. Siderails (all visual disease) 2. Surgery: a.)
Cryosurgery b.) Scleral buckling EAR – 1. Hearing 2. Balance (Kinesthesia or position sense)
Parts: 1. 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 2. Anvil -Incus 3. Stirrups -malleus for bone
conduction -stapes disorder conductive hearing loss

b. Eustachian tube - Opens to allow equalization of pressure on both ears - Yawn, chew, and
swallow Children – straight, wide, short c.) 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 d.)
Middle ear disease char by formation of spongy bone in the inner ear causing fixation or
immobility of stapes e.) Stapes can’t transmit sound waves

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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. Weber’s 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.
Meniere’s disease – endolymphatic hydrops f.) Inner ear disease char by dilation of endo –
lympathic system leading to increase volume of endolin Predisposing factor of MENIERE’S
DISEASE Smoking Hyperlipidemia 30 years old Obesity – (+) chosesteatoma Allergy Ear
trauma & infection S/Sx: 1. TRIAD symptoms of Meniere’s disease a.) Tinnitus b.) Vertigo c.)
Sensory neural hearing loss

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2. 3. 4. 5. 6. 7.

Nystagmus n/v Mild apprehension, anxiety Tachycardia Palpitations Diaphoresis

Diagnosis: 1. Audiometry – (+) sensory hearing loss 1. 2. 3. 4. Nursing mgt: Comfy & darkened
environment Siderails Emetic basin Meds: a.) Diuretics –to remove endolymph b.) Vasodilator
c.) Antihistamine d.) Antiemetic e.) Antimotion sickness agent f.) Sedatives/ tranquilizers
Restrict Na Limit fluid intake Avoid smoking Surgery – endolymphatic sac decompression-
Shunt

5. 6. 7. 8.

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