Renal

Renal System
enal System
enal System
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Functions of the Renal System

Excretion of waste Regulation of the acid-base balance Formation of erythropoeitin Regulation of fluid and electrolyte System balance (renin-angiotensin system) Regulation of phosphate and calcium
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Classification of Renal Disorders

Obstructive disorders Acute renal failure Chronic renal failure
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Obstructive Disorders
Can occur anywhere in the urinary tract Signs and symptoms depend on the site of location and size of obstruction
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Causes of Urinary Tract Obstruction
Lower Urinary Tract Bladder neoplasms enal System Urethral strictures Calculi Tumors Benign prostatic hypertrophy
Causes of Urinary Tract Obstruction
Ureteral Obstruction Calculi Trauma enal System Enlarged lymph nodes Congenital anomalies Kidney Calculi Polycystic kidney disease
Renal Stones
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Crystallizations of minerals around an organic matrix (blood, pus, devitalization tissue) System Usually idiopathic; major predisposing factor is infection
Renal Stones
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Composition of Renal Stones

Calcium (oxalate and phosphate) Hypercalcemia from: Hyperparathyroidism Vitamin D intoxication Immobilization Tumors System Renal tubular acidosis Intake of steroids Uric acid High purine diet, gout Chemotherapy Cystine Genetic disorder Struvite Infection-related
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Renal Stones
Epidemiology -Occur three times more often in males than females (3:1) -Age: 30-50 -Predisposing Factors Idiopathic UTI Hereditary diseases Renal tubular acidosis Hyperparathyroidism Cystinuria Lifestyle Factors Patients in mountainous, desert, or tropical regions Sedentary jobs During warmest months of the year
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Medications Protease inhibitorIndinavir sulfate (HIV drug) Carbonic anhydrase inhibitors Triamterene Laxative abuse Bone diseases Pagets disease Cancer Multiple myeloma Vitamin D intoxication Immobilization syndrome
Renal Stones
Pathophysiology . Supersaturation . enal SystemLack of inhibitors . Stasis
Renal Stones
Clinical Manifestations Asymptomatic until partial obstruction of the urinary tract occurs Pain (renal enalSystem colic) Kidney pelvis: costovertebral angle (CVA), Flank pain radiating anteroinferiorly around the abdomen, progressing toward the ipsilateral testicle or labium majorum Hematuria
Renal Stones
Clinical Manifestations
Nausea, vomiting, diaphoresis Urinary frequency, urgency System Hematuria
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--Gross/frank: due to the stones rough edges --Microhematuria: almost always present
Renal Stones
Diagnostics 1. Physical Examination 2. Laboratory Tests Urinalysis BUN Systemand Creatinine 3. Diagnostic Imaging Helical Computed Tomography/Spiral CT Computed tomography (CT) Intravenous Urography/Intravenous Pyelogram Ultrasound Plain Abdominal Radiographs (KUB) 4. Cystoscopy
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Renal Stones
Medications Pain medications Medications to decrease urinary calcium
Sodium or potassium phosphate Thiazide diuretics enal System

Medication for phosphate calculi
Ascorbic acid (to acidify urine)

Medications to decrease uric acid formation sodium bicarbonate allopurinol
Renal Stones
Surgery Ureterolithotomy Pyelolithotomy System Nephrolithotomy Litholapaxy Extracorporeal shock wave lithotripsy Percutaneous lithotripsy
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Set up of ESWL
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ESWL
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Nursing Management
1. 2. Administer medications as ordered Immediately post-lithotripsy Observe for bleeding Monitor blood pressure Initial urine output:cherry red to pink for several hours Observe for localized pain and bruising 3. Strain urine to detect passage of stones 4. Monitor intake and output 5. Encourage increase fluid intake of at least 2,500 ml/day 6. Exercise legs and arms for immobilized patients 7. Observe scrupulous aseptic technique 8. Instruct patient on how to prevent infection 9. Repost signs and symptoms of UTI 10. Regulate urine pH through diet
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Summary of Diet Principles in Renal Stone Disease

Stone Chemistry Calcium System Phosphate Oxalate Struvite Uric acid Cystine Nutrition Modification Diet Ash Urinary pH
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Low calcium (400 mg) Acid ash Low phosphorus (1-1.2 g) Low oxalate Low phosphorus (1.-1.2 Acid ash g) Low purine Low methionine Alkaline ash Alkaline ash
Acid-Ash and Alkaline-Ash Food Groups `

Acid Ash Alkaline Ash Neutral Meat Milk Sugars Whole grains Vegetables Fats Eggs Fruit (except Beverages System Cheese cranberries, Coffee Cranberries prunes, plums) Tea Prunes Plums
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Bladder Carcinoma
Etiology /Epidemiology Most common site of cancer in the urinary tract enal System Most common among 50-70 years old It affects more men than women with 3:1 ratio Common in whites than in African American
Bladder Carcinoma
Risk Factors Cigarette smoking: risk is proportional to number of pack years smoked daily and number of years of smoking Environmental carcinogens: dyes, rubber, Systemink, or paint leather, Recurrent or chronic bacterial infection of the urinary tract Bladder stones High urinary pH High cholesterol intake Pelvic radiation therapy Cancer arising from the prostate, colon, and rectum in males Abuse of phenacetin-containing analgesics
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Bladder Carcinoma
Pathophysiology Cells normally repair and reproduce themselves in an orderly way. If for some reason this process gets out of control, a GROWTH or TUMOUR will form. Tumors range from small benign papilloma to large invasive carcinomas. Most neoplasms are of the transitional cell type These neoplasms begin as papillomas Squamous cell carcinoma occurs less frequently and has poorer prognosis Other neoplasias include adenocarcinoma (often unoperable) and rhabdomyosarcoma (seen most frequently in infants)
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Bladder Carcinoma
Clinical Manifestations: Gross painless hematuria UTI (common complication) with frequency, urgency System and dysuria Any alteration in voiding or change in the urine Pelvic or back pain (may occur with metastasis) Cystitis
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Bladder Carcinoma
Diagnostics Blood Test Urinalysis Intravenous Urogram or enal System Pyelogram (IVU or IVP) Cystoscopy Biopsy CT Scan Ultrasound Scans
Bladder Carcinoma
Surgical treatment - Transurethral resection or fulguration (cauterization) - Cystectomy System Chemotherapy
Methotrexate 5-fluorouracil Vinblastin Doxorubicin (Adriamycin) Cisplatin
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Bladder Carcinoma
Topical Chemotherapy/Intravesical Chemotherapy Thiotepa Doxorubicin System Mitomycin Ethoglucid BCG Radiation Therapy Urinary Diversion Ileal Conduit Ureterosigmoidostomy Cutaneous ureterostomy Vesicostomy Nephrostomy
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Nursing Management
Maintain integrity of the stoma. Prevent skin irritation and breakdown Keep NG tube patent and in place until gastric motility returns. System Assist client to identify strengths and qualities that have a positive effect on self-concept.
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Nursing Management
Provide client teaching/discharge planning on: 1. Maintenance of stomal/peristomal skin integrity. 2. Proper application of appliance 3. Information regarding prevention of UTI 4. Control System of odor of peritonitis (abdominal pain, 5. Monitor for signs abdominal distention, fever). 6. Change stoma every 3-5 days to prevent infection. 7. Teach patient to report signs of UTI (cloudy urine, blood in urine, strong odor to urine, fever, flank pain).
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Benign Prostatic Hyperplasia
The prostate gland enlarges, extending upward into the bladder and obstructing the outflow of the urine by encroaching on the vesical orifice. enalEtiology/Epidemiology System --High prevalence (as many as 75%) that increases with age (over 50) --Changes in the size and shape of the prostate are associated with increased androgen levels --Not seen in males castrated before puberty --Is not a predisposing factor for prostatic carcinoma

Pathophysiology --nodular tissue enlargement that impinges on the urethra. --urethra elongates and compresses, causing obstruction of the urinary flow. --compensatory hypertrophy of the bands of bladder muscles --increase in trabeculation (contouring) of the bladder wall, providing pockets for urinary retention. --Bladder muscle becomes thick, lessening its capacity. --Muscle tone diminishes over time --The bladder can not empty completely at each voiding --These changes to the urethra and the bladder can result in symptoms of urinary obstruction and irritation.
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Clinical Manifestations 1. Prostate gland enlarges becoming more nodular 2. Straining on urination System 3. Hesitancy in starting urine flow 4. Decreased urine stream 5. Post-void dribbling 6. Nocturia 7. Dysuria 8. Blood in urine 9. Urgency
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Diagnostics 1. Rectal examination 2. Catheterization after voiding System 3. Intravenous urogram or abdominal ultrasound 4. Uroflowmetry 5. Cystourerthroscopy 6. Serum creatinine and BUN
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Medical Management Treatment is based on the severity of the disease and the patients age and symptoms. - Decreases the production of dihydrotestosterone . . Finasteride (Proscar) - Drugs that relax muscles and reduce straining during urination selectine alpha blockers . Prazosin (MInipress) . Doxazosin . Terazosin(Hytrin) Non-selective alpha blockers . Phenoxybenzamine (Dibenzyline)
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Diet 1. Alcohol should be avoided 2. Avoid drugs that impair System muscle function like anticholinergics and antidepressants 3. Avoid tranquilizers and nasal decongestants which usually causes urinary retention
Surgical Management It is the usual choice of treatment for recurrent and obstructive BPH problems. TransurethralProstatectom y/Transurethral Prostatic Resection (TURP) Suprapubic Prostatectomy Retropubic Prostatectomy
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Transurethral Resection Prostatectomy

Nursing Management Immediate Post-op (Prostatectomy) - Evaluate for shock and hemorrhage - Monitor for late post-op complications .Incision infection .Urinary tract infection (from catheter) .Deep vein thrombosis/pulmonary embolism .Late complications: urethral stricture, internal meatal stenosis
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Establish adequate bladder drainage - Utilize a closed sterile gravity system of drainage - Watch drainage for evidence of increased bleeding . Bright red urine: arterial bleeding . Dark red urine: venous bleeding System oral fluids . Encourage . Irrigate bladder as prescribed . Keep urinary catheter patent Monitor intake and output including the irrigated solution Administer prescribed analgesic or tranquilizer
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Discharge teaching Temporary urinary incontinence after removal of the catheter Perform Kegels exercise 10-20 times each hour Urine may be cloudy for several weeks
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Avoid vigorous physical activity, prolonged sitting, or excessive use of alcohol Drink adequate fluids (8 glassses/day) Do not take anticholinergics and diuretics Total prostatectomy results to impotence Nerve-sparing radical prostatectomy: prevents impotence Penile prosthesis: surgically implanted Sexual activity may be resumed in 6-8 weeks No fluid goes out with ejaculation (goes out with next urination) Report to physician anything unusual
Prostate Cancer
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malignant tumor of the prostate gland arises from prostate parenchyma; usually in the most posterior part most prostatic cancers are palpable on rectal System examination Etiology/Epidemiology Hormonal changes that accompany aging, seen exclusively among men over age 40 Second leading killer from cancer in American men Viral cause (cytomegalovirus) has not been proved but has been isolated from malignant transformations
Prostate Cancer
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Other risk factors 1. History of multiple sex partners 2. Episodes of STDs 3. Presence of cervical cancer in sexual partners System 4. Industrial exposure to cadmium 5. Genetic predisposition (still under investigation) 6. More prevalent in African American men 7. High-fat diet
Prostate Cancer
Pathophysiology may be confined to the gland and surrounding capsule. Limited extension of the tumor usually causes no symptoms can Systemalso be found outside the capsule boundaries and can spread to the lymphatic system and be disseminated through the vascular system. Most common site of metastasis: bone of pelvis; lumbar and thoracic spine; femur; and ribs. Organ involvement (lung, liver, kidneys) is usually seen in late stages of the disease
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Prostate Cancer
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Prostate Cancer
Clinical Manifestation Early stages rarely produce symptoms Symptoms due to obstruction of the urinary flow Hesitancy and straining on voiding, frequency, nocturia Diminution in size and force of urinary stream Symptoms due to metastasis . Pain in lumbosacral area radiating to hips and down the legs (from bone metastasis) . Perineal and rectal discomfort . Anemia, weight loss, weakness, nausea, oliguria (from uremia) . Hematuria (from urethral or bladder invasion, or both) . Lower extremity edema- occurs when pelvic node metastases compromise venous return
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Prostate Cancer
Diagnostic Evaluation Digital rectal examination Needle biopsy for histological study of tissue and/or aspirarion for cytological study System Transrectal ultrasonography Serologic markers of prostate cancer . Prostate-specific antigen (PSA) . Prostatic acid phosphates Excretory urogram Metastatic work-up: chest x-ray, intravenous urography, and bone scan for detecting skeletal metastasis
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Prostate Cancer
Digital Rectal Exam Brachytherapy
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Prostate Cancer
Medical Management Surgical Interventions (curative) Transurethral resection of the prostate (TURP) Radical prostatectomy A surgical dissection that has been refined to prevent sexual impotence by preserving the nerves that control erection Complication of radical prostatectomy: urinary incontinence, impotence, rectal injury.
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Prostate Cancer
Radiation (curative) External beam radiation (using linear accelerator) focused on the prostate- to deliver maximum radiation dose to tumor and minimal dose to surrounding tissues. enal System radiation- interstitial implantation of Interstitial radioactive substances (brachytherapy) into prostate, delivering doses of radiation directly to tumor while sparing uninvolved tissue. Complications of radiation: radiation cystitis (urinary frequency, urgency, nocturia), urethral injury (stricture), radiation enteritis (diarrhea, anorexia, nausea), radiation proctitis (diarrhea, rectal bleeding), impotence.
Prostate Cancer
Hormone manipulation (palliative) Prostate cancer is a hormone-sensitive cancer. Hormonal treatment aims to deprive tumor cells of androgens and their byproducts. . Bilateral orchiectomy (removal of testes) . Estrogen therapy (diethylstilbestrol) --Therapy can cause water retention, cardiovascular side effects, and gynecomastia --Pretreatment radiation therapy to breast can prevent gynecomastia . Other methods of achieving androgen deprivation --LHRH analogs (leuprolide) --Antiandrogen drugs (megestrol acetate; flutamide) --Ketoconazole
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Prostate Cancer
Nursing Management Administer pain medication as ordered Permit the patient to communicate his concerns and sexual needs Expect some client feeling depressed, anxious, angry and regressing Help patient use positive coping strategies Develop a trusting relationship with the patient Give repeated explanations of treatment; identify and correct misconceptions. This may help the patient gain some feeling control. Help patient/family set reachable small goals Comfort the patient with nurturing voice, touch, eye contact, and expert physical care
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Acute Renal Failure

deterioration of kidney function over hours or days resulting in the accumulation of toxic wastes and the loss of internal homeostasis damage is reversible Community-acquired ARF is approximately 100 per 1 million population Hospital-acquired ARF 4 percent of hospital admissions 20 percent o critical care admissions Mortality rate of approximately 50%
enal System Epidemiology
Acute Renal Failure

Pathophysiology Normally, the kidney receives 25 percent of the cardiac output. decrease in renal blood flow (RBF), glumerular filtration rate is depressed. System renal blood flow injures the kidney Decresed The kidney tries to adapt by preserving volume that would be lost due to the decreased reabsorptive capacity of the injured tubes Injured renal tubular cells lose their appropriate function, further depressing the glumerular filtration rate During the period of depressed renal blood flow, the kidneys are specially vulnerable to further insults Recovery from ARF is first dependent on restoration of renal blood flow
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Causes of ARF
Ischemic/Pre-renal Causes - conditions that decrease renal blood flow causing a drop in the GFR Hypovolemia Burns Diuretic therapy Dehydration Blood loss (surgery, trauma) Cardiac failure Shock
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Clinical Manifestations Nausea vomiting diarrhea decreased tissue turgor dryness of mucous membranes somnolence
Causes of ARF
Antibiotics (gentamicin, amphotericin B, neomycin) Pesticides Mushrooms Clinical Manifestations Fever Skin rash Edema
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Intrarenal -result from ischemic, toxic or immunologic mechanisms; from intrinsic disease of renal parynchema including glumerular, tubointerstitial, and vascular diseases Solvents (carbon, tetrachloride, methanol, ethylene glycol) Heavy metals (lead, arsenic, mercury)
Causes of ARF
Obstruction/Post-renal - arise from obstruction of urine flow Ureteral: calculi, blood clot, retroperitoneal tumor Bladder: prostatic hypertrophy, carcinoma, tumor Urethral: strictures, stenosis
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Clinical Manifestations Difficulty in voiding Changes in urine flow 4. Other causes: Acute glomerulonephritis malignant hypertension hemolysis Scleroderma
Phases of Acute Renal Failure

PHYSIOLOGIC EFFECT FINDINGS SYMPTOMS
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OLIGURIC PHASE Increased BUN, Inability to creatinine excrete metabolic wastes
Drowsiness, confusion, coma GI bleeding Asterixis Pericarditis Cardiac dysrythmias Kausmaulls breathing Coma
Inability to regulate electrolytes
Hyperkalemia Hyponatremia Acidosis

PHYSIOLOGIC EFFECT
Cont. OLIGURIC PHASE Inability to excrete fluid loads DIURETIC PHASE
FINDINGS
Fluid overload
SYMPTOMS
CHF Pulmonary edema Neck vein distention Hypertension
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Hypovolemia Urine output up to 4-5L/day Hyponatremia Hypotension Hypokalemia Tachycardia Improving mental alertness Weight loss Dry mucus membranes Muscle weakness Constipation
Acute Renal Failure
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Medical Management Correction of any reversible cause Attention to and correction of underlying fluid excess or deficits enal System Correction and control of biochemical imbalancestreatment of hyperkalemia Restoration/maintenance of blood pressure Maintenance of nutrition Initiation of hemodialysis, peritoneal dialysis, or continuous hemodiafiltration for patients with progressive azotemia
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Nursing Management
Monitoring and Managing Hyperkalemia 1. Evaluate for hyperkalemia correlated with ECG changes 2. Administration of sodium bicarbonate or glucose and insulin enal 3. Administer cation exchange resin (sodium System polystyrene sulfonate [Kayexalate, given as retention enema]) 4. WOF cardiac dysrhythmias (cardiac arrest) and congestive heart failure 5. Control potassium balance. 6. Prepare for dialysis
Nursing Management
Providing Electrolyte Replacement - Acidosis: sodium bicarbonate - Hyperphosphatemia: aluminum or calcium antacids Monitoring for Gastrointestinal Bleeding - Examine stools for blood System allH2-receptor antagonist (cimetidine or - Administer ranitidine) and/or antacids as prophylaxis - Prepare for endoscopy in case bleeding occurs
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Nursing Management
Correcting Fluid Volume Deficits or Overload WOF signs and symptoms of hypovolemia (dehydration) or hypervolemia . Hypovolemia: poor skin turgor, dryness of mucous membranes, hypotension, tachycardia . Hypervolemia: dyspnea, tachycardia, distended System veins, crackles, peripheral edema, neck pulmonary edema - Monitor urinary output and urine specific gravity; measure intake and output - Monitor serum and urine electrolyte concentrations. - Weigh patient daily; expected weight loss is 0.250.5 kg (1/2-1 lb. daily) - Provide skin care
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Nursing Management
Maintain rest/activity balance Provide assistance in ADLs.. Maintain strict bedrest in the acute phase Prevent injury System Keep side rails elevated and pad side rails if necessary. Protect patient from bleeding. WOF mental status changes Employ seizure precaution
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Nursing Management
Prevent infection . Maintain aseptic technique at all times. . Isolate patients from anyone with infection. . Turn weak or immobile patients frequently. . Provide meticulous skin care . Promote measures to relieve pruritus. Improving Nutritional Status . Employ moderate protein restriction during oliguric phase . Offer high-carbohydrate feedings . Restrict foods and fluids containing potassium and phosphorus (bananas, citrus fruits/juices, coffee) . Encourage a high-protein, high-caloric diet after diuretic phase`
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Chronic Renal Failure

gradual and progressive loss of the ability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes which fatally ends in uremia Damage is irreversible System Causes: Chronic systemic diseases (DM, hypertension) Polycystic Kidney Disease Long standing obstruction Chronic glomerulonephritis Obstructive Uropathy Interstitial nephritis
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Chronic Renal Failure

Pathophysiology some of the nephrons (including the glomeruli and tubules) are thought to remain intact while others are destroyed. The intact nephrons hypertrophy and produce System an increased volume of filtrate with increased tubular reabsorption despite a decreased glomerular filtration rate(GFR) This adaptive method permits the kidney function until about three fourths of the nephrons are destroyed The solute load then becomes greater than can be reabsorbed, producing an osmotic diuresis with polyuria and thirst.
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Stages of CRF
Decreased renal reserve (renal impairment)
GFR 40%-50% of normal BUN and creatinine normal Asymptomatic
GFR enal System 20%-40% normal to rise BUN and creatinine begins Mild anemia, mild azotemia Polyuria, nocturia
Renal Insufficiency
Renal Failure
GFR 10%-20% of normal BUN and creatinine increase Anemia, azotemia, metabolic acidosis Polyuria, nocturia
Stages of CRF
End-stage renal disease GFR <10% of normal BUN and creatinine severely increased Anemia, azotemia, metabolic acidosis, bleeding System Oliguria Signs of CHF Hypocalcemia, hyperphosphatemia, hyperkalemia, hyponatremia Fractures, joint pains Signs of renal failure Uremia Infertility, amenorrhea
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Initial symptoms may include the following: Unintentional weight loss Nausea, vomiting General ill feeling Fatigue Headache Frequent hiccups Generalized itching (pruritus) Later symptoms may include the following: Increased or decreased urine output Need to urinate at night Easy bruising or bleeding; May have blood in the vomit or in stools Decreased alertness drowsiness, somnolence, lethargy confusion, delirium coma
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Muscle twitching or cramps Seizures Uremic frost -- deposits of white crystals in and on the skin Decreased sensation in the hands, feet, or other areas Additional symptoms that may be associated with this disease: Excessive nighttime urination Excessive thirst Abnormally dark or light skin Paleness Nail abnormalities Breath odor High blood pressure Loss of appetite Agitation
Diagnostics
Glomerular Filtration Rate Serum creatinine and BUN Anemia Sodium and water retention Acidosis (metabolic) System Calcium and phosphorus imbalance Low serum proteins, especially albumin Urinalysis KUB-TUZ
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Medical Management
Goal: Conservation of renal function as long as possible Detection and treatment of reversible causes of renal failure Dietary regulation - low-protein diet supplemented with essential amino acids or their keto-analogues Treatment of associated conditions to improve renal dynamics - Anemia - recombinant human erythropoietin, a synthetic kidney hormone, iron, Folate and Vit B12 and blood transfusion. - Acidosis - sodium bicarbonate - Hyperkalemia - restriction of dietary potassium; administration of potassium-binding agents. - Phosphate retention - decrease dietary phosphorus (chicken, milk, legumes, carbonated beverages); administer phosphate-binding agents Maintenance dialysis or kidney transplantation when symptoms can no longer be controlled with conservative management.
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Nursing Management
Monitoring for potential complications Cardiovascular disease; congestive heart failure; pericarditis Hypertension Anemia System Chronic metabolic acidosis Hyperlipidemia Hyperurecemia Renal osteodystrophy - renal bone disease, as uremia is associated with abnormal calcium metabolism, which causes bone pathology Paresthesias; neurologic abnormalities
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Nursing Management
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Achieving fluid and electrolyte balance Assess intake and output every 8 hours. Weigh patient everyday. Assess presence and extent of edema. Auscultate breath sounds. System Monitor cardiac rhythm and blood pressure every 8 hours. Assess level of consciousness every 8 hours. Encourage patient to remain within prescribed fluid restrictions. Encourage a diet high in carbohydrates and within prescribed sodium, potassium and protein limits. Administer medications as ordered. Monitor for acidosis
Nursing Management
Maintain fluid and electrolyte balance Assess intake and output every 8 hours Weigh patient everyday Assess presence and extent of edema Auscultate enal System breath sounds Monitor cardiac rhythm and blood pressure every 8 hours Assess level of consciousness every 8 hours Encourage patient to remain within prescribed fluid restrictions Encourage high CHO diet and within prescribed Na, K, and CHON limits Administer medications as ordered Monitor for acidosis
Nursing Management
Maintaining nutrition to conserve renal function as long as possible - Protein should be of high biologic value, rich in essential amino acids (dairy products, eggs, meat) - Low-protein diet may be supplemented with essential amino acids and vitamins System function declines, protein may be - As renal restricted proportionately - Protein will be increased if patient is on a dialysis program to allow for loss of amino acids during dialysis . Ensure high calorie intake . Encourage intake of hard candy, jelly beans, jellies, and flavored carbohydrates powders. . Monitor nutritional state: body weight, anthropometric measurements, serum albumin and nitrogen balance.
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Nursing Management
Prevent infection and promote skin integrity Use measures to produce vasoconstriction; cool environment, removal of excessive bedding Provide tepid, cooling baths or cool wet dressings Eliminate irritants; apply emollient lotions Promote meticulous skin care Maintain good medical/surgical asepsis Encourage use of soft toothbrush. Protect confused person from injury. Protect person from infectious agents.
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Nursing Management
Relieving Constipation Phosphate binders cause constipation Encourage high-fiber diet, bearing in mind the potassium content of some System and vegetables. fruits - Commercial fiber supplements (Fierall; FiberMed) may be prescribed - Give stool softeners as prescribed - Avoid laxatives and cathartics that can cause electrolyte toxicities (compounds containing magnesium or phosphorus)
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Dialysis
Hemodialysis Access Peritoneal dialysis
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Arteriovenous peritoneum fistula Subclavian/femoral vein catheterization SystemArteriovenous graft
Duration
2-4 hours
36 hours exit site infection peritonitis hernias pulmonary complications
complication dysequilibrium s syndrome hypotension bleeding sepsis
Dialysis
Hemodialysis Peritoneal dialysis
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Nursing Check BP and pulse rate every 30- Monitor vital signs and interventi 60 minutes to monitor for observe for changes in ons hypotension. behavior. Weigh patient before and after Make sure that catheter dialysis. is patent. Monitor intake and output. May add procaine HCl in Monitor for signs of disequilibrium the dialysate to minimize syndrome (headache, hypertension, discomfort. restlessness, mental confusion and Observe for signs of nausea) peritonitis. Watch out for signs of bleeding. Maintain aseptic Avoid taking BP on site of AV technique during fistula. insertion of catheter and Avoid blood extraction on site of throughout the AV fistula. procedure.
Dialysis
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Dialysis
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Dialysis
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Kidney Transplantation
kidney from a living donor or human cadaver donors who are related to the patient are slightly more successful than those from cadever donors. transplanted kidney is placed in iliac fossa System anterior to the iliac crest. ureters of the newly transplanted kidney is transplanted into the bladder or anastomosed to the ureter of the recipient.
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Preoperative Management Bring the patients metabolic state to a level as close to normal as possible. Complete physical examination Tissue typing, blood typing, and antibody screening System urinary tract is studied to assess bladder The lower neck function and to detect ureteral reflux. Patient must be free of infection at the time of transplantation Psychological evaluation is also done before the surgery because corticosteroid may aggravate psychiatric conditions. Hemodialysis is done before the day of the scheduled transplantation to optimize the patients physical status.
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Preoperative Nursing Intervention Management is similar to that of the patient undergoing an elective abdominal surgery. Preoperative teaching on: . Postoperative pulmonary hygiene System . Pain management options . Dietary restrictions . Intravenous and arterial lines . Tubes (indwelling catheter and possibly a nasogastric tube) . Early ambulation
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Postoperarative Management The goal is to maintain homeostasis until the transplanted kidney is functioning well. Immunosuppressive therapy . Azathioprine (Imuran) enal System . Corticosteroid (Prednisone) . Cyclosporine (Neoral) . OKT-3 (a monoclonal antibody) . Prograf (formerly FK-506) . Mycophenolate (RS-61433) Doses of immunosuppressive agents are gradually tapered off over several weeks The patient will take an anti-rejection medication as long as he has the transplanted kidney.
Rejection concerns Hyperacute rejection - occur within 24 hours Acute - within 3 to 14 days Chronic - after Diagnostics on rejection System Ultrasound - to detect kidney enlargement Percutaneous renal biopsy - most reliable test in evaluating rejection X-ray
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Postoperative Nursing Interventions Assess for signs and symptoms of rejection . Oliguria . Edema System . Fever . Increasing blood pressure . Weight gain . Swelling or tenderness over the transplanted kidney or graft Assess for rise in the serum creatinine level and BUN Monitor leukocytes and platelets A distinction should be made between
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Monitor closely for infection 1. Protect the client from hospital staff, visitors and other patients who have active infections System hand washing is imperative; face 2. Careful mask may be worn by hospital staff and visitors. Clinical manifestations of infection include shaking chills, fever, rapid heart beat and respirations (tachycardia and tachypnea), and either an increase or a decrease in WBCs (leukocytosis or leukopenia) Practice strict aseptic technique
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UPDATE
New research from Stanford University Medical Center New approach: preventing rejection without the use of immunosuppressive drugs transplantation begins with the usual process- surgery, immunosuppressive drugs (until the completion of the next step) Given multiple small doses of radiation targeting the immune system in combination of a drug reducing the number of cells capable of an immune attack. Blood stem cells from the kidney donor is injected to the patient The newly injected stem cells find their way into the patients bone marrow where they reproduce new cells and immune cells that mix with those of the patient. After this procedure, the patients immune cells recognize the donors organ as friend rather than foe. The Stanford team monitored the recipients new hybrid immune system looking for a mixture of cells from both the recipient and the donor. These cells were tested in the laboratory and did not attack cells taken from the donor. This told the team that the new hybrid immune system would not mount an attack against the transplanted organ. At this time, the team slowly weaned the patient away from the immune-suppressive drugs.
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Electrolyte Imbalance
SODIUM Main cation in the extracellular compartment 135-145 mEq/L Functions: 1. Primary determinant of ECF osmolality 2. Generation of nerve impulses
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CAUSE
Hyponatremia sodium loss K+-sparing diuretics GI/biliary drainage Draining fistulas Addisons disease Profuse sweating water excess SIADH CHF Excessive hypotonic IV fluids
CLINICAL MANIFESTATIONS
Apprehension, irritability Postural hypotension Tachycardia Rapid thready pulse Decreased CVP Dry mucus membranes Headache, apathy, weakness Weight gain Increased BP Increased CVP Labs indicate: decrease serum and urine sodium, decrease urine specific gravity and osmolality
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CAUSE
Hypernatremia Sodium excess IV hypertonic NaCl Primary Aldosteronism Saltwater near drowning Water loss Increased insensible loss Diabetes insipidus
CLINICAL MANIFESTATIONS
Intense thirst Restless, agitation Seizures, coma Weight gain Peripheral and pulmonary edema Increased BP Dry mucous membranes, intense thirst Hypotension Seizures Weakness Hypotension Weight loss
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CAUSE CLINICAL MANIFESTATIONS
HypernatremiLabs indicate:increase sserum a sodium, decrease urine sodium, increase urine specific gravity and osmolality
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Medical Management A. Hyponatremia Sodium replacementcareful administration of sodium by mouth, nasogasrtric tube, or parenteral means. Water restrictionin patients with normal or excess fluid volume, hyponatremia is treated by restricting fluid to a total of 800 mL in 24 hours.
B. Hypernatremia -gradual lowering of the serum sodium level -hypotonic electrolyte solution (e.g., 0.3% sodium chloride) -isotonic nonsaline solution (e.g., D5W). D5W is indicated System when water needs to be replaced without sodium. POTASSIUM Main cation in the intracellular compartment 3.5-5 mEq/L Functions: maintenance of regular cardiac rhythm conduction of nerve impulses contraction of muscles
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Cause
Hypokalemia (<3.5 mEq/L) Diarrhea Vomiting Gastric suction Corticosteroid administration Hyperaldosteronism Carbenicillin Amphotericin B Bulimia Osmotic diuresis Alkalosis Starvation Digoxin toxicity
Fatigue Anorexia Nausea and vomiting Muscle weakness Decreased bowel motility Ventricular asystole or fibrillation Paresthesias Leg cramps Decrease blood pressure Ileus Abdominal distention Hypoactive reflexes ECG -flattened T waves -prominent U waves -ST depression -prolonged PR interval
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Cause
Hyperkalemia (>5.0 mEq/L) Pseudohyperkalemia oliguric renal failure Use of potassiumconserving diuretics in patients with renal insufficiency Acidosis Addisons disease Crush injury Burns Stored bank blood transfusions Rapid IV administration of potassium
Vague muscular weakness Bradycardia Dysrhythmias Flaccid paralysis Paresthesias Intestinal colic Cramps Irritability Anxiety ECG -Tall tended T waves -Prolonged PR interval and QRS duration -Absent P waves -ST depression
enal System
Medical Management Hypokalemia - increased intake in the diet (average adult intake is 50-100 mEq/L); oral or IV replacement therapy Foods high in potassium . Raisins SystemBananas . . Apricots . Oranges . Vegetables . Legumes . Whole grains . Milk . Meat
enal
Medical Management Hyperkalemia
First stepdetermine if hyperkalemia is life-threatening. Perform an ECG and administer IV calcium to ameliorate cardiac toxicity. Second stepidentify and remove sources of potassium intake . Discontinue oral and parenteral potassium supplements . Remove potassium-containing salt substitutes . Examine the patients diet. Change the diet to a low- potassium tube feed or a 2-g potassium ad-lib diet
enal System
Third step - enhance potassium uptake by cells to decrease the serum concentration . Give parenteral glucose and insulin . Correct metabolic acidosis with sodium bicarbonate . Beta-adrenergic agonists (somewhat more controversial),highly effective and preferred over alkali therapy for patients with renal failure. Fourth step - increase potassium excretion from the body administration of parenteral saline accompanied by a lop diuretuic such as furosemide . Discontinue potassium-sparing diuretics, ACE inhibitors, angiotensin receptor blockers, and other drugs that inhibit renal potassium excretion . Monitor volume status and aim to maintain euvolemia administration of aldosterone analogue such as 9-alpha fluorohydrocortisone acetate (Florinef). Florinef especially is helpful in those with hyporeninemia or hypoaldosteronism.
enal System
Gastrointestinal excretion--cation exchange resin: Kayexalate administered orally or rectally as retention enema (preferred for hyperkalemic emergencies). . Drug is much more effective if the enema is retained for an hour . Repeated enemas can be used but, occasionally, cause colon perforation . Onset of action is within 2 hours and is long lasting Emergency dialysisfor patients unresponsive to conservative measures experiencing potentially lethal hyperkalemia or for patients who have complete renal failure The final step is to determine the cause of hyperkalemia in order to prevent future episodes. . Sources of potassium intake . Causes of decreased renal excretion . Causes of impaired cellular uptake
enal System
CALCIUM 99% stored in bones regulated by PTH, Vitamin D and calcitonin present in three forms: ionized, bound to protein and complexed with phosphate, citrate Systemor carbonate calcium and phosphorus has an inverse relationship 8.5-10.5 mg/dL Functions: transmission of nerve impulses muscle contraction formation of teeth and bone blood clotting
enal
Cause
Hypocalcemia (<8.5 mg/dL) Hypoparathyroidism (may follow thyroid surgery or radical neck dissection) Malabsorption Pancreatitis Alkalosis Vitamin D deficiency Massive subcutaneous infection Generalized peritonitis Massive transfusion of citrated blood Diuertic phase of renal failure
Clinical Manifestation
Numbness Tingling of fingers, toes, and circumoral region Positive Trousseaus sign Positive Chvosteks sign Seizures Carpopedal spasms Hyperactive deep tendon reflexes Irritabilty Bronchospasm ECG Prolonged QT interval
enal System
Cause Hypercalcemia (> 10.5 mg/dL) Hyperparathyroidism Malignant neoplastic disease Prolonged immobilization Overuse of calcium supplements Vitamin D excess Oliguric phase of renal failure Acidosis Digoxin toxicity Clinical Manifestation Muscular weakness Constipation Anorexia Nausea and vomiting Polyuria and polydipsia Hypoactive deep tendon reflexes Lethargy Deep bone pain Pathologic fractures ECG Shortened QT interval Bradycardia Heartblocks
enal System
Medical Management
HYPOCALCEMIAIV administration of calcium. Parenteral calcium salts: calcium gluconate, calcium chloride,calcium gluceptate. -kept at the bedside at all times. -rapidly effective calcium solution is ionized calcium chloride (10%) -for rapid use for severe tetany, infusion is carried out every 10 minutes. -Ionized calcium chloride (10%) is administered slowly. It is highly irritating, stings, and causes thrombosis;patient experiences unpleasant burning flash of skin and of the tongue. -Too rapid calcium administration may cause cardiac arrest. -slow drip of D5W containing calcium gluconate is given until control of tetany is ensured; then intramuscular or oral administration of calcium is prescribed -Never use normal saline with calcium because it will increase renal calcium loss -Solutions containing phosphates or bicarbonates should not be used with calcium -Vitamin D is added to calcium intake.
enal System
HYPERCALCEMIA 1. Hydration with intravenous normal saline (0.9% NaCl) is the initial treatment for patients with acute hypercalcemia and clinical symptoms. 2. Pharmacotherapy a. Diuretics System b. Plicamycin or etidronate disodium (for patients who do not respond to normal saline diuresis.) Plicamysin blocks PTH and may also inhibit bone resorption. c. Calcitonin inhibits osteoclast activity and causes hypocalcemia. It has a rapid onset of action. d. Oral phosphates used for chronic hypercalcemia, which can inhibit bone resorption. e. Diphosphonates used to stimulate osteoblast activity, which increases bone uptake of calcium
enal
Nursing Management:
A. Hypocalcemia
enal System
Neuromuscular status should be assessed for patients who are at risk for hypocalcemia (post-op patients: thyroidectomy. Parathyroidectomy, radical neck dissection). Check for positive Trousseaus or Chvosteks sign Frequently assess for respiratory status in post-op recovery phase Monitor serum calcium and phosphate levels. Report indications of respiratory distress, laryngeal stridor, or cardiovascular failure. Promote high calcium diet as prescribed. Instruct patient on what signs and symptoms to report. Exercise caution in giving other medications to patient with hypocalcemia --Hypocalcemic patients are sensitive to digoxin --Cimetidine (Tagamet) interferes with normal parathyroid function, increases the risk of hypocalcemia Institute seizure precautions (airway at the bedside, padded side rails).
Nursing Management B. Hypercalcemia Prevent and detect hypercalcemia early Recognize patients at risk and monitor for signs and symptoms such as nausea and vomiting, constipation, lethargy, and anorexia. . Emphasize importance of mobility to minimize bone demineralization and constipation. . Adequately hydrate the patient Administer normal saline infusions as prescribed Administer medications as prescribed Monitor intake and output; observe for oliguria and anuria Take vital signs every 4 hours, especially apical pulse and blood pressure Monitor electrolyte values and renal function Assess mental status Assess for cardiorespiratory status for signs of fluid overload
enal System
MAGNESIUM Next to potassium, magnesium is the most abundant intracellular cation. 1.8 mg/dL 3.0mg/dL or 1.5 2.5 mEq/L Acts as an activator for many intracellular enzyme systems and plays a role in both carbohydrate and protein metabolism Directly acts on the myoneural junction affecting neuromuscular irritability and contractility.
enal System Function
Cause Hypomagnesemia (<1.8 mg/dL) Chronic alcoholism Hyperparathyroidism Hyperaldosteronism Diuretic phase of renal failure Malabsorptive disorders Diabetic ketoacidosis Refeeding after starvation Certain pharmacologic agents Gentamicin Cisplatin Clinical Manifestation Neuromuscular irritability Positive Trousseaus sign Positive Chvosteks sign Insomnia Mood changes Anorexia Vomiting
enal System
Cause Hypermagnesemia (>2.7 mg/dL) Oliguric phase of renal failure (particularly when magnesium-containing medications are administered) Adrenal insufficiency Excessive IV magnesium administration Clinical Manifestation Flushing Hypotension Drowsiness Hypoactive reflexes Depressed respirations Cardiac arrest Coma Diaphoresis ECG Tachycardiabradycardia Prolonged PR interval and QRS
enal System
Medical Management Hypomagnesemia 1. Mild magnesium deficiency can be corrected by diet alone. Dietary sources of magnesium include: . Green leafy vegetables . Nuts . Legumes . Whole grains Seafood . Peanut butter . Chocolate 2. Magnesium salts can be administered orally to replace continuous excessive losses -Diarrhea is a common complication with excessive ingestion 3. Patients receiving TPN require magnesium in the IV solution to prevent hypomagnesemia -A bolus dose given too rapidly can produce cardiac arrest 4. Calcium gluconate should be readily available to treat hypocalcaemic tetany or hypermagnesemia 5. For overt symptoms of hypomagnesemia, it is treated with parenteral magnesium. - Commonly used magnesium salt: Magnesium sulfate
enal System
Medical Management Hypermagnesemia 1. Prevention by: -avoiding administration of magnesium to patients with renal failure -carefully monitor seriously ill patients receiving magnesium salts 2. In sever cases; all parenteral and oral magnesium salts are discontinued. 3. In emergencies like respiratory depression or defective cardiac conduction, ventilatory support and IV calcium are indicated. -Hemodialysis with a magnesium-free diasylate can reduce serum magnesium to a safe level within hours -Loop diuretics and 0.45% NaCl (half-strength saline) solution can enhance magnesium excretion in patients with adequate renal function -IV calcium gluconate antagonizes the neuromuscular effects
enal System
Nursing Management A. Hypomagnesemia 1. Assess patients risk for hypomagnesemia and observe for its presence. 2. Monitor closely patients receiving digitalis because hypomagnesemia can predispose them to digitalis toxicity
3. For severe cases of hypomagnesemia, implement seizure precaution Dysphagia may occur; assess ability to swallow before oral medications or foods are offered 5. Instruct the patient on misuse of diuretic or laxative medications which causes magnesium deficits 6. Instruct the patient about the need to consume magnesium-rich foods. 7. For alcoholic patients, refer to alcohol abstinence program or other professional help
enal System
Nursing Management B. Hypermagnesemia 1. Identify and assess patients at risk for hypermagnesemia. 2. If hypermagnesemia is suspected, monitor the following: System . Vital signs noting hypotension and shallow respirations . Decreased patellar reflexes . Changes in LOC 3. Patients with compromised renal function or with renal failure are not given medications containing magnesium. 4. Check with the doctor before taking OTC drugs.
enal
PHOSPHORUS A ubiquitous intracellular anion that is essential for membrane structure and energy storage and transport in all cells. 2.5 04.5 mg/dL Presumably greater in children because of the high rate of skeletal growth About 85% is located in bones and teeth, 14% in soft tissue, and less than 1% in the ECF Level decreases with age Function Phosphate is necessary to produce ATP, which provides energy for nearly all cell functions. Also is necessary in RBC cells for production of 2,3 diphosphoglycerate (2,3-DPG), which facilitates release of oxygen from hemoglobin. Maintenance of acid-base balance
enal System
Cause Clinical Manifestation
enal System
Hypophosphatemia (<2.5 Paresthesias mg/dL) Muscle weakness Refeeding after starvation Bone pain and Alcohol withdrawal tenderness Diabetic ketoacidosis Chest pain Respiratory alkalosis Confusion Decreased magnesium Cardiomyopathy Decreased potassium Respiratory failure Hyperparathyroidism Increased Vomiting susceptibility to Diarrhea infection Hyperventilation Vitamin D deficiency associated with malabsorptive disorders
Cause Hyperphosphatemia (>4.5 mg/dL) . Acute and chronic renal failure . Excessive intake of phosphorus . Vitamin D excess . Respiratory acidosis . Hypoparathyroidism . Volume depletion . Leukemia/lymphoma treated with cytotoxic agents . Increased tissue breakdown Clinical Manifestation Tetany Tachycardia Anorexia Nausea and vomiting Muscle weakness Signs and symptoms of hypocalcemia
enal System
Medical Management A. Hypophosphatemia 1. The main goal in hypophosphatemia is prevention. 2. For patients at risk, serum phosphate levels should be monitored closely and correction initiated before deficits become severe. 3. Aggressive IV phosphorus correction is usually limited to patients whose serum phosphorus levels fall below 1 mg/dL and whose GI tract is not functioning. -Possible dangers of IV phosphorus administration include hypocalcemia and metastatic calcification from hyperphosphatemia -Rate of administration should not exceed 10 mEq /hour and site should be monitored for tissue sloughing and necrosis that can occur with infiltration 4. In less acute situations, oral phosphorus replacement is adequate.
enal System
enal
Medical Management B. Hyperphosphatemia 1. Treatment is directed at the underlying disorder. 2. Administration of phosphate-binding gels System - Basogel liquid taken with meals and at bedtime - Amphogel 3. Low phosphate dietavoid dairy products and other high protein foods.
Nursing Management A. Hypophosphatemia 1. Identify and monitor patient at risk for hypophosphatemia. 2. For malnourished patients receiving TPN, gradually introduce the feeding solution to avoid rapid shift of phosphorus into the cells 3. Prevent infection because hypophosphatemia may alter the granulocytes. 4. Monitor serum phosphorus levels and document and report early signs of hypophosphatemia (apprehension, confusion, change in LOC)
enal System
Nursing Management Hyperphosphatemia 1. Monitor patient at risk for hyperphosphatemia 2. When a low-phosphorus diet is prescribed, instruct the patient to avoid phosphorus-rich foods such as: Systemcheese . Cream . Hard . Nuts . Whole grain cereals . Dried fruits and vegetables . Kidneys . Sardines . Sweet breads . Foods made with milk 3.When appropriate, instruct the patient to avoid phosphate-containing substances such as laxatives and enemas that contain phosphate 4.Teach the patient to recognize the signs of impending hypocalcemia and to monitor changes in
enal
CHLORIDE
Major anion of the ECFrepresents 70% of the bodys total negative ion content Also contained in gastric and pancreatic juices as well as in sweat Reflects a change in dilution or concentration of the ECF and does so in direct proportion to sodium 98 -106 mEq/L
enal System
Function As the principal negatively charged ion, it serves as one of the main electrolytes of the body. In addition to potassium and sodium, it assists in the conduction of electrical impulses when dissolved in bodily water. Its negative charge balances with the positive charges of sodium and potassium in order to maintain serum osmolality Combines with hydrogen ion in the stomach tom form hydrochloric acid
Cause
Hypochloremia (<96mEq/L) Addisons disease Reduced chloride intake or absorption Untreated diabetic ketoacidosis Chronic respiratory acidosis Excessive sweating Vomiting Gastric suction Diarrhea Sodium and potassium deficiency Metabolic alkalosis Loop, osmotic, or thiazide diuretic use Overuse of bicarbonate Rapid removal of sodium ascetic fluid Intravenous fluids that lack chloride (dextrose and water) Draining fistulas and ileostomies Congestive heart failure
Clinical Manifestation
Agitation Irritability Tremors Muscle cramps Hyperactive deep tendon reflexes Hypeertonicity Tetany Slow, shallow respirations Seizures Dysrhythmias Coma Labs indicate: -decrease serum chloride and sodium -increase pH and serum bicarbonate -increase total carbon dioxide content -decrease urine chloride level
enal System
Cause Clinical Manifestation
enal System
Hyperchloremia (> 108 mEq/L) Tachypnea Excessive sodium chloride infusions Lethargy with water loss Weakness Head injury (sodium retention) Deep rapid respirations Hypernatremia Decline in cognitive status Renal failure Decreased cardiac output Corticosteroid use Dyspnea Dehydration Tachycardia Severe diarrhea (loss of bicarbonate) Pitting edema Respiratory alkalosis Dysrhythmias Administration of diuretics Coma Overdose of salicylates, Labs indicate Kayexalate, acetazolamide, --increased serum chloride and phenylbutazone and ammonium chloridesodium use -decreased serum pH Hyperparathyroidism -decreased serum bicarbonate Metabolic acidosis -normal anion gap -increased urinary chloride level
Medical Management
A. Hypochloremia 1. Treatment involves correcting the underlying cause and contributing electrolyte and acid-base imbalances 2. Chloride replacement intravenously --Normal saline or half-strength saline (0.45%) solution 3. Patients receiving the following diureticsloop, osmotic, or thiazide, should be reevaluated. These medications should be discontinued or changed to another diuretic. 4. Foods high in chloride are provided. Tomato juice Salty broth Canned vegetables Processed meats and fruits 5.Avoid drinking free water (without electrolyte) which will excrete large amount of chloride. 6.Ammonium chloride, an acidifying agent, is used to treat metabolic alkalosis.
enal System
Medical Management
B. Hyperchloremia
enal
1. Correct the underlying cause and restore electrolyte, fluid, and acidbase balance. System the bicarbonate level and correct the acidosis 2. Increase -Lactated Ringers solution (conversion of lactate to bicarbonate in the liver) -Sodium bicarbonate (leads to renal excretion of chloride ions as bicarbonate 3. Diuretics are administered to eliminate chloride. 4. Sodium, fluids, and chloride are restricted.
Nursing Management A. Hypochloremia 1. Monitor intake and output, arterial blood gas values, and serum electrolyte levels, as well as the patients level of consciousness, muscle strength and movement 2. Report changes to physician promptly. 3. Teach patient about foods with high chloride content. B. Hyperchloremia 1. Monitor vital signs, arterial blood gas values, and intake and output to assess patients status and effectiveness of treatment 2. Respiratory, neurologic, and cardiac changes should be promptly reported. 3. Teach the patient to avoid foods rich in chloride (salty, processed and canned foods).
enal System
ABG Reading
Normal Values: Arterial Blood Parameter pH PaCO2 System PaO2 HCO3 Base excess or deficit
Oxygen Saturation
enal
Arterial Sample 7.35 -7.45 35-45 mmHg 80-100 mmHg 22-26 mEq/L + or -2
95% - 100%
Acid Base Disturbances and Compensation

DISORDER
Respiratory Acidosis
INITIAL EVENT
COMPENSATION
PaCO2, or Kidneys eliminate normal HCO3, pH H+ and retain HCO3 PaCO2, or normal HCO3, pH Kidneys conserve H+ and excrete HCO3
Respiratory enal System Alkalosis Metabolic Acidosis Metabolic Alkalosis
or normal PaCO2, Lungs eliminate CO2, conserve HCO3 HCO3, pH or normal PaCO2, Lungs ventilation HCO3, pH to PCO2, kidneys conserve H+ to excrete HCO3
Causes of Acid- Base Disorders

Acid-base disorder
Respiratory acidosis
Causes
Signs and Symptoms
enal System
Hypoventilatio PR, RR, BP n Mental cloudiness Neuromuscula Feeling of r disorders fullness in the Airway head obstruction Ventricular CNS fibrillation depression ICP Papilledema Dilated conjunctival blood vessel Hyperkalemia Tachypnea Cyanosis

Acid-base disorder
Respiratory alkalosis
Causes
Signs and Symptoms
enal System
Hyperventilation Lightheadedness Sepsis Inability to Pregnancy concentrate Mechanical Numbness and ventilation tingling Fever Tinnitus Loss of consciousness

Acid-base disorder
Metabolic acidosis
Causes
Diabetic ketoacidosis Renal failure Methanol/aspirin overdose Renal tubular acidosis Diarrhea Chronic alcoholism
Signs and Symptoms

Headache Confusion Drowsiness RR and depth Nausea Vomiting Cardiac output BP Cold and clammy skin Dysrhythmias Shock
enal System

Acid-base disorder
Metabolic alkalosis
Causes
vomiting diuretics alkali ingestion
Signs and Symptoms

Tingling of fingers and toes Dizziness Hypertonic muscles Symptoms of hypocalcemia RR Atrial tachycardia Hypokalemia Dysrhythmia Paralytic ileus
enal System

Acid-base disorder
Metabolic alkalosis
Causes
vomiting diuretics alkali ingestion
Signs and Symptoms

Tingling of fingers and toes Dizziness Hypertonic muscles Symptoms of hypocalcemia RR Atrial tachycardia Hypokalemia Dysrhythmia Paralytic ileus
enal System
Acid- Base Disorders

Acid-Base Imbalances Management Type of Imbalance
Respiratory Acidosis
Management
Improving ventilation Bronchodilators Antibiotics for infection Thrombolytics and anticoagulants (pulmonary emboli) Pulmonary hygiene Mechanical ventilation Semi-Fowlers position Treatment of the underlying cause Breathe into a paper bag Sedative
enal System
Respiratory Alkalosis
Acid- Base Disorders

Acid-Base Imbalances Management Type of Imbalance
Metabolic Acidosis
Management
enal System
Treatment is correcting the underlying defect. Eliminating source of chloride Bicarbonate Alkalizing agents Hemodialysis Peritoneal dialysis Treatment of underlying disorder Chloride supply Sodium chloride fluids KCl H2-receptor antagonists (Cimitidine) Carbonic anhydrase inhibitors
Metabolic Alkalosis
Interpretation of Laboratory Values

pH Respiratory Acidosis Uncompensated Normal Partially compensated - Compensated Respiratory Alkalosis - Uncompensated Normal - Partially compensated - Compensated 7.35 PCO2 HCO3
enal System
Move toward normal but still Normal
7.45
Interpretation of Laboratory Values

pH
Metabolic Acidosis
PCO2
Normal
HCO3
enal System
Uncompensated Partially compensated - Compensated
7.35
Metabolic Alkalosis
Uncompensated Partially compensated - Compensated
7.45 Normal Move toward normal but still Normal
Examples: pH= 7.51, PCO2= 22, HCO3= 16 partially compensated respiratory alkalosis - pH= 7.30, PCO2= 31, HCO3= 12 - pH= 7.15, PCO2= 88, HCO3= 22
partially compensated metabolic acidosis enal System uncompensated metabolic acidosis - pH= 7.20, PCO2= 35, HCO3= 11 uncompensated metabolic acidosis - pH= 7.42, PCO2= 50, HCO3= 40 compensated metabolic alkalosis`
enal System

Renal

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Renal System

Functions of the Renal System

Classification of Renal Disorders

Causes of Urinary Tract Obstruction

Causes of Urinary Tract Obstruction

Composition of Renal Stones

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Sodium or potassium phosphate Thiazide diuretics enal System

Ascorbic acid (to acidify urine)

Summary of Diet Principles in Renal Stone Disease

Acid-Ash and Alkaline-Ash Food Groups `

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Transurethral Resection Prostatectomy

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Acute Renal Failure

enal System Epidemiology

Acute Renal Failure

Phases of Acute Renal Failure

OLIGURIC PHASE Increased BUN, Inability to creatinine excrete metabolic wastes

Inability to regulate electrolytes

Hyperkalemia Hyponatremia Acidosis

Phases of Acute Renal Failure

Acute Renal Failure

Phases of Acute Renal Failure

Chronic Renal Failure

Chronic Renal Failure

Arteriovenous peritoneum fistula Subclavian/femoral vein catheterization SystemArteriovenous graft

36 hours exit site infection peritonitis hernias pulmonary complications

complication dysequilibrium s syndrome hypotension bleeding sepsis

enal System Function

Acid Base Disturbances and Compensation

Respiratory enal System Alkalosis Metabolic Acidosis Metabolic Alkalosis

Causes of Acid- Base Disorders

Signs and Symptoms

Causes of Acid- Base Disorders

Signs and Symptoms

Causes of Acid- Base Disorders

Signs and Symptoms

Causes of Acid- Base Disorders

Signs and Symptoms

Causes of Acid- Base Disorders

Signs and Symptoms

Acid- Base Disorders

Acid- Base Disorders

Interpretation of Laboratory Values

Move toward normal but still Normal

Move toward normal but still Normal

Interpretation of Laboratory Values

Uncompensated Partially compensated - Compensated

Move toward normal but still Normal

Uncompensated Partially compensated - Compensated

7.45 Normal Move toward normal but still Normal

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