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Complex II final exam review- chornic kidney Disease
Nursing Care- Complex Health Problems II (11-63-375)
University of Windsor
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COMPLEX II: FINAL EXAM REVIEW: CHRONIC KIENY DISEASE Chronic Kidney Disease: (CKD): - Involves progressive, irreversible loss of kidney function - Defined as kidney damage or GFR < 60 mL/min for > 3 months (N = 90-120) - GFR - volume of fluid filtered from glomerular capillaries into Bowman's capsule per unit time - eGFR – estimated GFR derived from serum creatinine; a better measure of overall kidney function than BUN or creatinine CKD statistics: - 1 in 10 Canadians has CKD (4 million people) - 11th leading cause of death in 2016 - Number of Canadians living with ESRD up 35% since 2008. - 46% of new renal failure patients are < 65 yrs - Almost 49,000 Canadians being treated for kidney failure: ü 57% are on dialysis ü 42% have a functioning transplant Stages of CKD: Based on decrease in GFR Stage 1 Kidney damage with normal GFR 125 mL/min Stages 2 – 4 Progressive damage and decreasing GFR Stage 5: Kidney failure; end-stage renal disease (ESRD GFR <15 mL/min Generally requires dialysis or transplant Chronic Kidney Disease: - Leading causes of kidney failure: o Diabetes (38%) o Renal vascular disease (15%) o Hypertension - Up to 80% of GFR may be lost with few overt changes in body function - Can survive without RRT until almost 90% of nephrons are lost Clinical Manifestations: Clinical Manifestations: - Result of retained substances - Affect every body system - Manifestations vary among people Uremia - Constellation of S/S resulting from waste build-up and fluid excess - Often occurs with GFR < 10 mL/min/1 Clinical Manifestations: electrolyte imbalance: - K+ excess – as per ARF - Na+ - normal or low. - Impaired Na excretion → water retention ( & possible dilutional hyponatremia) → edema, HTN, CHF - Mg – usually not problematic unless ingesting it (milk of magnesia, antacids with Mg) - Ca 2+ & PO4 alterations - ↓ Ca 2+ (see ARF) stimulates PTH → Ca 2+ & PO4 liberated from bone → hyperphosphatemia Added: We don’t want to give patients with kidney problems milk of magnesia we need to give them a different type of laxative. If we see an order for anything with magnesium and they are renal failure, we need to question this. Calcium levels will go down, phosphate levels go up. Stimulates PTH (calcium levels low, needs to give more thyroid hormone, which stimulates the bone, we worry about osteo problems or patho fractures) Clinical Manifestations: Acid-Base imbalance: - Metabolic acidosis o Defective acid (ammonia) excretion o Defective reabsorption/regeneration of bicarbonate Added: We need to be giving meds to correct this acidosis .. What would we give them? Sodium bicarb! We can give this by IV, or tablets. The lungs can only compensate so much, it cant blow off ALL the carbon dioxide, so some of these patients will require sodium bicarbt ablets at home. Clinical Manifestations: Hematological: Anemia due to ↓’d erythropoiesis, nutritional deficiencies, ↓’d RBC lifespan & ↑ hemolysis, frequent blood draws, GI bleeding, iron deficiency, blood loss in dialyzer Bleeding tendencies due to Defective platelets, altered coagulation Infection due to Impaired WBC and immune fxn; malnutrition, hyperglycemia, invasive procedures Added: Erythropoiesis comes from the kidneys to stimulate the bone marrow to make RBCs. This is decreased in kidney failure. Watching the patients CBC’s is important Clinical Manifestations: Cardiovascular: - CVD is a leading cause of death in CKD - HTN (r/t Na and fluid retention; increased renin production in some), elevated triglycerides - → atherosclerosis → MI, stroke - → LV hypertrophy and heart failure → pulmonary & peripheral edema - Dysrhythmias (d/t CAD, K and Ca imbalance) - Pericarditis – d/t irritation r/t uremic toxins Added: Potassium levels can significantly drop after dialysis and puts them in an arrhythmia. Need to be monitoring them when they are down in dialysis. Clinical Manifestations Respiratory: Fluid overload, pulmonary edema → dyspnea Kussmaul's respiration – in very advanced CKD Uremic pleuritis Pleural effusion Predisposition to respiratory infections Uremic pneumonitis (interstitial edema on CXR) Clinical Manifestations: GI Excessive urea results in Inflammation throughout GI tract → mucosal ulcerations, stomatitis, GI bleeding Metallic taste Uremic fetor (urinous odour of the breath) Anorexia, N/V → weight loss, malnutrition Constipation due to ingestion of iron salts, phosphate binders; fluid restrictions, inactivity Added: Breath smells like urine because they are trying to blow off the ammonia. Phosphate levels go ip so we need to put them on medications that bind up with this phosphate and remove it through the stool Personality, behaviour changes, emotional lability, depression Infertility but still can get pregnant while being on dialysis, just needs careful monitoring. Clinical Manifestations: musculoskeletal: CKD-mineral and bone disorder (CKD-MBD) A systemic disorder of mineral and bone metabolism due to CKD, manifested by one or more of: - Abnormalities of Ca, PO4, PTH, or Vit D metabolism - Abnormalities of bone turnover, mineralization, linear growth, or strength - Extra-skeletal calcification Clinical Manifestations Muskuloskeletal: CKD-MBD Renal osteodystrophy – collective term describing skeletal abnormalities due to disorders of bone turnover and mineralization. Typical symptoms: Bone pain Joint pain Bone deformation Bone fractures Poor mobility Added: Renal osteodystrophy joint pain might be the first thing they complain of. Risk for falls as well. So prominent in patients with chronic renal failure. Clinical manifestations: CKD-MBD- vascular and soft tissue calcifications - Excess phosphate binds with calcium-. Calcifications throughout Metastatic Calcifications - Blood vessels - GI tract - Skin - Eyes - Lungs Subcutaneous tissue Myocardium Muscles Added: Calcifications can get into organs as well. It’s not “cancer” it’s just metastatic in the fact that it goes all over the body, but these are calcifications not tumours. Chronic kidney Disease: Diagnostic Studies History and physical examination Laboratory tests Proteinuria – impt risk factor for progression of CKD; also earliest marker of kidney disease Urinalysis (casts, RBCs, WBCs, protein, glucose) eGFR, BUN, Creatinine, ‘lytes, Ca, PO4, PTH levels, Hgb GFR is the preferred measure; Creatinine alone is not a good indicator (elevates only after significant loss of function) Renal ultrasound, renal scan, CT scan, renal biopsy Added: Why do they have proteinuria? Protein leaks out because nephrons are being destroyed. This is a early marker (indicator) that identifies this. Why would we wanna do a renal ultrasound, CT, etc? tells us the structure of the kidneys, or if there is a reversible cause. They could have a tumour on the kidneys, or a stricture in the ureter, massive kidney stone. We want to rule out other causes that might be fixable. Collaborative Care: Goals Prevention: Detect and treat reversible causes (as per AKI) Preserve existing function; delay progression Treat clinical manifestations Prevent complications Education re disease, treatment options, prepare for RRT Prevent and treat hyperkalemia (see ARF) Non-pharmacological approaches for K > 5 Restrict high-K foods and drugs Pharmacological intervention for K > 6 Calcium gluconate or calcium chloride to ↓ risk of dysrhythmias Insulin/glucose – shifts K into cells Salbutamol – shifts K into cells Loop diuretics – to excrete K Sodium polystyrene (hours to days to work) RRT Treat Hypertension Controlling HTN can delay CKD progression Goal: Non diabetic < 140/90; Diabetic < 130/80 Exercise, weight reduction, avoid alcohol, stress management Na & fluid restriction Added: Potassium level 6 (H) than we can try these short fixes, but we might need to urgently dialyze them, because they will go into cardiac dysrhythmias We need to be careful with ACE and ARBS in chronic kidney disease because it can make it worse. if we give them a unit of packed RBC, the total volume will increase, and now they will be in fluid overload. Even patients with functioning kidneys, if we give them packed RBC we usually give them lasix as well, but we cant do that with these patients. They need to be on statins to lower their lipids. Need to avoid NSAIDS especially if they still have SOME function because we want to keep that function. If they have completely useless kidneys than they can take NSAIDS because they are going to be dialyzed anyway. When we type and cross them, they look for certain antibodies. There will always be antibodies that the body forms, the more antibodies they have, the more difficult it can be to match them with a donor if they need a transplant. Most of their cals come from carbs and fats. Need to balance this. Need to watch their sodium. Fluid restriction (output in last 24 hours and add 600) Nursing management: Assessment Individual/family history of renal disease Risk factors Diet, height, weight, weight changes Clinical manifestations of CKD Family, social, work, self image, coping, psychological Treatment preferences Nursing Diagnosis Excess fluid volume Impaired skin integrity Risk for injury Activity intolerance Imbalanced nutrition: Less than body requirements Anticipatory grieving Risk for infection Health promotion Identify and monitor individuals at risk for CKD (personal/family hx of renal disease; diabetes, HTN, repeated UTI) Regular checkup including creatine, BUN, urinalysis Report changes in urinary appearance, frequency and volume Monitor renal fxn if taking potentially nephrotoxic agents Reduce risk for progression and for CVD Manage diabetes, BP, etc. Regular checkups including creatine, Bun and Urinalysis Care for later stages of CKD Self care and self-monitoring is a major component CKD management – education!!! Daily weight, BPs Identify S/S of fluid overload and 'lyte imbalance Strict dietary adherence Medication education / meds to avoid Motivate clients to manage their disease Ambulatory and home care When conservative therapy is no longer effective, options are: HD, PD, and transplant Client/family need clear explanation of dialysis and transplantation Dialysis machines at home. Transplants is also something that we need to discuss with the patient. Evaluation Maintenance of ideal body weight Acceptance of chronic disease No infections No edema Hematocrit, hemoglobin, and serum albumin levels in acceptable range
Complex II final exam review- chornic kidney Disease
Course: Nursing Care- Complex Health Problems II (11-63-375)
University: University of Windsor
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