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Examen

PCCN Review Study Questions and Rationale

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05-02-2024
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2023/2024

Hypervolemia Causes Excessive fluid intake, retention of NA and water. Caused by stress response, steroid therapy, heart failure, liver failure, nephrotic syndrome, acute or chronic renal failure Hypervolemia presentation and treatments Tachycardia, high blood pressure, high filling pressures, weight gain, JVD, tachypnea, dyspnea, lethargy, disorientation, indications of pulmonary or cerebral edema, low hgb, low serum osmolality, decreasing bun with normal creatinine Managmenet: Monitor I&O, Decrease excess volume, Dialysis, fluid restriction, diuretics, prevent complications Acute renal failure Sudden severe impairment or cessation of kidney function: characterized by accumulation of nitrogenous wastes and fluid and electrolyte imbalances Pre-renal Failure Renal failure above the level of the kidney Decreased intravascular volume, poor cardiac function with resultant decreased renal artery perfusion, renal artery stenosis (place renal stent). Most common in progressive care patient. Urine Na <20 BUN/CR >20:1 Fluid + Lasix- will have urine Post-renal failure Below the level of the kidney. Disrupted urine flow such as mechanical obstruction, functional obstruction: neurogenic bladder, diabetic neuropathy, tumor Cortical renal failure intra-renal damage to renal tissue: glomerulonephritis Medullary renal failure Acute tubular necrosis: Caused by nephrotoxic drugs, prolonged ischemic injury, any causes of pre renal failure that is prolonged, diabetes, hypotension. Most common in ICU patient Urine Na+ >40-100 BUN/CR 10:1 Fluid and Lasix----no urine output Stages of Acute renal failure 1 Onset: period of time from precipitating event to beginning of oliguria/anuria Duration: Hours to days BUN/Creatinine normal or slightly increased Stages of Acute renal failure 2 Oliguric-Anuric Phase: Urine output is less than 400 mL/24 hours Duration:1-2 Weeks BUN/Creatinine elevated METABOLIC ACIDOSIS: water gain with DILUTIONAL HYPONATREMIA, HYPERKALEMIA, HYPERPHOSPHATEMIA, HYPOCALCEMIA, HYPERMAGNESEMIA, and AZOTEMIA Stages of Acute renal failure 3 Diuretic Phase: Urine output is greater 400 mL/24 hours Duration:1-2 weeks Urine output may increase to 3-4 Liters/24 hours Continues metabolic abnormalities with elevated potassium Stages of Acute renal failure 4 Recovery phase: period of time between onset and when the lab values stabilize Duration: 3-12 months Metabolic processes gradually resolve Treatment of Acute renal failure Support renal perfusion and improve GFR Volume Inotropes- Dopamine Diuretics Maintain fluid and electrolytes Diminish accumulation of nitrogenous wastes Avoid nephrotoxic agents, nurtrition, vanco/abt levels, prevent infection, Epogen for treating anemia Symptoms of Chronic renal failure Fatigue, anemia, frequent hiccups, general ill feeling, itching, weight loss, n/v, HA, confusion, decreased sensation in hands, easy bruising, decreased or increased urine output. Diagnosis: UA, creatinine, creatinine clearance, potassium, metabolic acidosis, CT scan, MRI, Ultrasound, renal biopsy. Abnormal Ca+, phosphate, parathyroid hormone, Vit D metabolism, End-stage renal disease treatment Fluid restrictions, diet control, blood pressure control, diabetes control, vitamin d supplements, drug monitoring, dialysis, control blood sugar, blood pressure Renal PEARLS Seizures are seen with hyperphosphatemia S/S of hypophophatemia: weakness, reciprocal hypercalcemia causes apathy and confusion creatinine is the best indicator of renal function creatinine is inversely proportional to GFR Low serum sodium causes aldosterone releases Cirrhosis of the liver liver cells are destroyed and replaced with fibrous tissue which results impaired liver function. Distortion, twisting, and constriction of central sections cause impedence of portal blood flow and portal hypertension occurs Portal hypertension Causes esophageal varices and splenomegaly-thrombocytopenia, vitamin k deficiency, inability to produce adequate amount of bile, impaired carb, fat, protein metabolism, inability to store vitamins and manufacture clotting factors, inability to detoxify toxins or remove bacteria. Ammonia production-breaks down protein into ammonia, then liver converts ammonia into urea and is eliminated by the kidney

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PCCN
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PCCN

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Subido en
5 de febrero de 2024
Número de páginas
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Escrito en
2023/2024
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