Exam 2 - CRF

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Exam 2 - CRF
2011-09-26 22:54:11
Chronic Renal Failure

Exam 2 - Chronic Renal Failure
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  1. Chronic Renal Failure
    • -Progressive irrerersible loss of kidney function
    • -Involves prescence of kidney damage or GFR <60 mL/min for 3 months or longer. (Normal GFR ~125 mL/min)
    • -5 stages of CKD which are dependent on GFR
  2. 5 Stages of Kidney Failure
    Table 47-6
    Stage 1 - Kidney damage with normal or increased GFR (GFR >=90)

    Stage 2 - Kidney damage with mild decrease in GFR (GFR = 60-89)

    Stage 3 - Moderate decrease in GFR (GFR = 30-59)

    Stage 4 - Severe decrease in GFR (GFR = 15-29)

    Stage 5 - End stage renaal disease. Kidney failure. (GFR less than 15) Dialysis needed
  3. Healthy People
    Prevention and Detection of CKD
    • -Early detection and treatment are the primary methods for reducing CKD
    • -Monitor BP to detect elevations so treatment can be started early
    • -Ensure proper diagnosis and treatment of DM as it is the leading cause of CKD
    • -Treat HTN appropriately and aggressively as it is the second leading cause of CKD
  4. Cultural and Ethnic Disparities
    Chronic Kidney Disease
    • -CKD has a disproportionate impact on minority populations, especially African Americans (AA) and Native Americans (NA)
    • -A hx of HTN and DM is also more common in AA & NA.
    • -The rate of CKD is 6 x higher among NA's with DM than other ethnic groups w/ DM.
    • -The risk of CKD as a complication of HTN is significantly increased in AAs.
    • -AA live longer and have better outcomes on chronic dialysis than whites.
  5. Clinical Manifestations of Chronic Uremia
    • -Denial
    • -Anxiety
    • -Depression
    • -Psychosis
  6. Clinical Manifestations of Chronic Uremia
    • HTN: Most common CV abnormality. Is aggravated by Na retention and increased ECF volume.
    • -HF
    • -Atherosclerotic heart disease
    • -Pericarditis: manifested by friction rub, chest pain & low-grade fever.
    • -Myocardiopathy
    • -Pericardial effusion
    • -Left ventricular hypertrophy: R/T long standing HTN, ECF volume overload and amenia.
    • -Cardiac dysrhythmias: R/T hyperkalemia, hypocalcemia, and decreased coronary artery perfusion
  7. Clinical Manifestations of Chronic Uremia
    • -Anorexia, N/V: caused by irritation of the GI tract by waste products which contributes to weight loss and malnutrition
    • -Uremic ulcer/Peptic Ulcer: caused by an increase ammonia produced by bacterial breakdown of urea.
    • -GI bleeding: R/T mucosal irritation coupled with platlet defect.
    • -Stomatitis: commonly with exudates and ulcerations, a metalic taste in the mouth and uremic fetor (a urinous odor of breath)
    • -Gastritis
    • -Constipation: R/T to ingestion of iron salts and/or calcium-containing phosphate binders
    • -Diarrhea: R/T hyperkalemia and altered calcium metabolism.
  8. Clinical Manifestations of Chronic Uremia
    • -Hyperparathyroidism
    • -Thyroid abnormalities: Many patients with CKD exhibit hypothyroidism. Test may yield low to low-normal levels of triiodothyronine (T3) and thyroxine (T4)
    • -Amenorrhea
    • -Infertility
    • -Sexual Dysfunction
    • -Azoospermia
  9. Clinical Manifestations of Chronic Uremia
    • -Altered CHO metabolism: caused by impaired glucose use resulting from cellular insensitivity to the normal action of insulin
    • -Hyperlipidemia: Altered lipid metabolism is R/T decreased levels of enzyme lipoprotein lipase.
    • -Change in insulin excretion: patients with DM who become uremic may require less insulin b/c the insulin reamins in circulation longer
    • -Elevated triglycerides: Hyperinsulinemia stimualtes hepatic production of triglycerides. The seum level of triglycerides does not usually decrease fter dialysis b/c glucose is absorbs from the dialysis fluid causing insulin to be secreted stimulating the liver to produce triglycerides.
    • -Nutritional deficiencies
    • -Gout
  10. Clinical Manifestations of Chronic Uremia
    • -Anemia: Decreased production of erythropoietin therefore decreased production of RBCs. Other contributing factors: decreased RBC lifespan, increased hemolysis of RBCs, frequent blood samplings and bleeding from the GI tract.
    • -Bleeding: defect in platlet function due to alterations in the coagulation system. Generally corrected with HD or PD.
    • -Infection: Changes in leukocyte function and altered immune response. Decreased inflammatory response decreasing WBC accumulation at the site of injury.
    • -Increased incidence of cancer: lung, breast, uterus, colon, prostate, and skin malignancies most common
  11. Clinical Manifestations of Chronic Uremia
    • -Fatigue/confusion/lethargy/apathy/irritability: R/T depression of the CNS
    • -HA
    • -Sleep disturbances
    • -Muscular irritability: muscle twitching, jerking, asterixis (hand flapping tremor), and nocturnal leg cramps.
    • -Seizures/Coma: R/T rapidly increasing BUN & hypersensitive encephalopathy.
  12. Clinical Manifestations of Chronic Uremia
    -Hypersensitive retinopathy
  13. Clinical Manifestations of Chronic Uremia
    • -Uremic lung: AKA Uremic pnueonitis is typically found in CKD as interstial edema on an x-ray.
    • -Pulmonary edema
    • -Uremic pleuritis
    • -Dyspnea: R/T to fluid overload, pulmonary edema, uremic pleuritis and plueral effusion.
    • -Pnuemonia: Predisposition for respiratory infections R/T decreased macrophage activity.
    • -Depressed cough reflex
    • -Kussmaul breathing: to compensate for metabolic acidosis
  14. Clinical Manifestations of Chronic Uremia
    • -Pallor: Skin appears pale as a result of anemia
    • -Pigmentation changes: most noticible change is a yellow-gray discoloration of the skin
    • -Pruritus: Commonly results from dry skin & calcium-phosphate deposition in the skin and sensory neuropathy.
    • -Ecchymosis: R/T platelet abnormalities
    • -Excoriations
    • -CaPO4 deposition
    • -Uremic frost: A rare condition in which urea crystallizes on the skin and is usually only seen when BUN levels are extremely high.
    • -Dry, scaly skin: R/T to decreased oil ans sweat gland activity.
  15. Clinical Manifestations of Chronic Uremia
    -Peripheral Neuropathy-
    • -Paresthesias: mainly in the legs & feet described as a burning sensation
    • -Motor weakness: may lead to bilateral foot drop, muscular weakness and atrophy and loss of DTRs
    • -Restless leg syndrome
  16. Clinical Manifestations of Chronic Renal Failure
    • -Same as Oliguric Phase in ARF
    • -Specific gravity is fixed at 1.010
    • -Polyuria/nocturia due to inability to concentrate urine turns into oliguria/anuria as CKD worsens.
    • -If patient is still producing urine, proteinuria, casts pyuria and hematuria could be present depending on the cause of the KD.
  17. Clinical Manifestations of Chronic Uremia
    -Electrolyte and Acid-Base Balances-
    • -Potassium: Fatal dysrhythmias can occur when K level is 7-8 mEq/L
    • -Sodium: Sodium excretion is impaired and may be normal to low due to dilutional hyponatremia.
    • -Calcium & Phosphate
    • -Magnesium: primary excreted by the kidneys. Hypermagnesmia is rare but is manefested by an absence of reflexes, decreased mental status, cardia dysrhythmias, hypotension and resp. failure.
    • -Metabolic acidosis: Impaired ability of the kidneys to excrete the acid load. In RF, the plasma bicarb is usually 16 to 20 mEq/L instead of the normal 22-26 mEq/L.
  18. Clinical Manifestations of Chronic Uremia
    -Musculoskeletal System-
    • -Renal osteodystrophy: a syndrome of skeletal changes in CKD that is a result of alterations in calcium and phosphate metabolism.
    • -Two types of renal osteodystrophy: osteomalacia and ostetis fibrosa cystica
    • -Osteomalacia: A condition of demineralization that results from slow bone turnover and defective mineralization of newly formed bone.
    • -Osteitis fibrosa cystica: A condition that results from decalcification of the bone and replacement of bone tissue with fibrous tissue.
  19. Conservative Therapy - CKD
    • Diagnostic
    • -Hx & Physical exam
    • -Identification of reversible renal disease
    • -Renal ulrasound
    • -Renal Scan
    • -BUN, serum creatinine, and creatinine clearance levels
    • -Serum electrolytes
    • -Protein-to-creatinine ratio in first am voided specimen
    • -UA and urine culture
    • -Hematocrit and hemoglobin levels
  20. Conservative Therapy - CKD
    • Collaborative Therapy
    • -Correction of ECF volume fluid volume overload or deficit
    • -Nutritional therapy
    • -Erythropoietin therapy
    • -Calcium supplementation, phosphate binders or both
    • -Anti HTN therapy
    • -Measures to lower K
    • -Adjustment of drug dosages to degree of renal function
  21. Conservative Therapy - CKD
    -Detect and treat any potentially reversible causes of RF

    • Goals
    • -Preserve kidney function
    • -Treat clinical manifestations
    • -Prevent complications
    • -Provide for patient's comfort
    • -Correct fluid volume imbalances
  22. Conservative Therapy for CKD
    • HTN
    • -BP < 130/80
    • -Weightloss
    • -Exercise
    • -Avoid alcohol
    • -Quit smoking
    • -Diet changes
    • -Medication: Diuretics & B-Blockers are reccomended initial therapy for non diabetics. ACE inhibitors and ARBs are used with diabetics however they must be used with caution in ESRD b/c they can further decrease GFR and increase K levels.
  23. Conservative Therapy for CKD
    -Renal osteodystrophy-
    • Renal osteodystrophy
    • -Limit daily phosphate to less than 1000mg/day
    • -Administer phosphate binders such as calcium carbonate (Tums) and calcium acetate (PhosLo). These bind phosphate with the stool so it is excreted. Take meds with meals. Constipation is often a side effect.
    • -Suplement Vitamin D to assist with hypocalcemia. It is important that phosphate levels are lowered before administration of Vit D b/c they may contribute to soft tissue calcification if both calcium and phosphate are elevated.
    • -Control hyperparathyroidism: calcemic agents are a new class of drugs to help control PTH secretion by increasing the sesitivity of the parathyroid to serum calcium levels
  24. Conservative Therapy for CKD
    • Anemia
    • The most important cause of anemia is decreased production of erythropoietin due to a decrease in the number of functioning renal tubular cells.
    • Meds to keep Hgb w/in a normal range (12-18 g/100 mL)
    • -Epoetin alfa (Epogen/Procrit) (IV/SQ)
    • -Darbepoeitin alfa (Aranesp)
    • -Side effects: HTN

    • Iron Supplements
    • -Do not take iron and calcium phosphate binders within 2 hours of each other

    • Folic Acid
    • -Is generally supplemented 1 mg daily b/c it is needed for RBC formation and is removed by dialysis.

    • Blood Transfusions PRN
    • -These should be avoided in treating anemia unless the patient experiences an acite blood loss or has symptomatic anemia (dyspnea, excess fatigue, tachycardia, palpitations, chest pain). Undesirable effects are the suppression of erythropoiesis and the possibility of iron overload (unit of blood ~ 250 mg iron)
  25. Kidneys and Drugs
    • -Digitalis: excreted primarily by the kidneys and RF can increase drug toxicity. Dialysis does not affect dig levels but it does affect K levels. Hypokalemia can potentiate the effects of digitalis.
    • -Antobiotics: Aminoglycosides, penicillin in high doses, and tetracyclines are potentially nephrotoxic and require dose adjustment. Vancomycin & gentamycin must be decreased b/c they rely on the kidneys for excretion.
    • -Pain Medications: Meperidine (Demerol) should never be given to a patient with CKD b/c the liver metabolizes it to normeperidine which is dependent on the kidneys for excretion. Seizures can result. Doses of other pain meds must be used with caution
    • -NSAIDS: Patients with CKD should avoid these drugs b/c they block the synthesis of renal prostaglandins that promote vasodilation. This can decrease renal perfusion. Acetaminophen can be substituted.
  26. Patient Education - CKD
    • Diet
    • -Protein restriction
    • -Low phosphorous
    • -Amino acids suplementation
    • -Sufficient calories from fat and CHO
    • -Water restriction: generally 600 mL plus an aamount equal to the previous days urine output
    • -Na restriction to 2-4 g/day
    • -K restriction to 2-4g/day
    • -Phospahte restriction to 1000 mg/day
  27. Patient Education - CKD
    Table 47-10
    • 1. Explain dietary (protein, K, Na, phosphate) and fluid restrictions
    • 2. Encourage discussion of difficulties in modifying diet and fluid intake
    • 3. Explain S/S of electrolyte imbalance, especially in high K
    • 4. Teach alternate ways of reducing thirst such as sucking on ice chips, lemon or hard candy
    • 5. Explain the rationale for prescribed drugs and common side effects.
    • -Phosphate binders (including calcium supplements used as phospahte barriers) should be taken with meals.
    • -Calcium supplements prescribed to treat hypocalcemia directly should be taken on an empty stomach (but not at the same time as iron supplements)
    • -Iron supplements should be taken between meals
    • 6. Explain the importance of reporting any of the following:
    • -Weight gain greater than 4 lb (2kg)
    • -Increasing BP
    • -SOB
    • -Edema
    • -Increasing fatigue or weakness
    • -Confusion or lethargy
    • 7. Encourage patient and family to share concerns about lifestyle changes, living with chronic illness, and decisions aboout type of dialysis or transplantation
  28. Nursing Diagnosis - CKD
    Excess fluid volume
    Excess fluid volume R/T inability of the kidneys to excrete fluid ad excessive fluid intake AMB edema, HTN, bounding pulse, weight gain, SOB, pulmonary edema

    • Interventions
    • -Monitor resp. pattern for symptoms of resp. difficulty
    • -Weigh patient daily and monitor trends
    • -Provide appropriate diet to help control edema and HTN
    • -Instruct pt. and/or family on measures instituted to treat the hypervolemia (daily weights, fluid restrictions) to help monitor and control fluid overload and related HTN
  29. Nursing Diagnosis - CKD
    Risk for Injury
    Risk for Injury R/T alterations in bone structure due to decreased calcium absorption, retention of phosphate and altered vitamin D metabolism

    • Interventions
    • -Monitor trends in serum levels of calcium to provide early intervention if needed
    • -Monitor for electrolyte imbalances associated with hypocalcemia to determine degree of bone demineralization and potential risk for fracture
    • -Administer appropriate prescribed calcium salt (calcium carbonate, calcium gluconate, aclcium chloride)
    • -Provide adequate intake of vitamin D to facilitate GI absorption of calcium to prevent and/or treat the bone demineralization
  30. Nursing Diagnosis - CKD
    Imbalanced Nutrition Less than body Requirements
    Imbalanced Nutrition Less than body Requirements R/T restricted intake of nutrients (especially protein), N/V, anorexia, and stomatitis AMB loss of appetite and weight

    • Interventions
    • -Monitor for N/V to intervene PRN
    • -Monitor trends in weighth loss and gain to detect changes in status
    • -Monitor albumin, total protein, Hgb, Hct levels as indicators of nutritional status and response to treatments.
    • -Monitor caloric and nutrient intake to detect changes.
    • -Provide oral care before meals to prevent stomatitis, remove bad taste, and increase pt appetite
  31. Nursing Diagnosis - CKD
    Risk for Infection
    Risk for infection R/T suppressed immune system, access sites and malnutrition seconary to dialysis and uremia

    • Interventions
    • -Monitor for systemic and localized S/S of infection (pain on urination, hematuria, cloudy urine, chills, fever) to ensure early identification & treatment
    • -Screen all visitors for comminicable disease
    • -Limit # of visitors to decrease risk of infection
    • -Ensure aseptic handling of all lines
    • -Wash hands