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29 Cards in this Set
- Front
- Back
acute renal failure
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Is A clinical syndrome characterized by a rapid loss of renal function with progressive azotemia
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progressive azotemia
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an accumulation of nitrogenous waste products such as urea nitrogen and creatinine in the blood
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uremia
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s a term used to loosely describe the illness accompanying kidney failure (also called renal failure), in particular the nitrogenous waste products associated with the failure of this organ.
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oliguric
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excretion of an abnormally small volume of urine, often as the result of a kidney disorder ...Oliguric: patients who excrete less than 500 milliliters per day (< 16 oz/day)
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nonoliguric
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In nonoliguric patients, the urine is of poor quality (i.e., contains little waste) because the blood is not well filtered, despite the fact that an adequate volume of urine is excreted....Nonoliguric: patients who excrete more than 500 milliliters per day (> 16 oz/day)
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Causes of Prerenal Azotemia (4)
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1. absolute extracellular fluid volume depletion
2. decreased effective arterial circulating volume 3. primary renal hemodynamic alterations 4. bilateral renal vascular obstruction |
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Causes of Postrenal Azotemia (Urinary Tract Obstruction) (4)
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1. urethral obstruction; urethral valves; urethral strictures
2. bladder outflow obstruction: prostatic hypertrophy, carcinoma 3. bilateral ureteral obstruction 4. neurogenic bladder |
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Causes of Intrarenal (intrinsic) ARF
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1. postischemic
2. nephrotoxic |
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what can cause absolute ECF depletion
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-hemorrhage from major surgery trauma/postpartum
-excessive diuresis -severe GI losses: v/d -3rd space losses: burns peritonitis; pancreatitis |
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causes for decreased effective aterial circulating volume
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- reduced cardiac output: mycardial infarction; dysrhythmias; CHF; cardiac tamponade; pulmonary embolism
-peripheral vasodilation; sepsis; anaphylaxis; drugs; anesthesia. HTN, nitrates -Hypoalbuminemia: nephrotic syndrome; liver failure (cirrhosis) |
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causes for primary renal hemodynamic alterations (4)
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a.Prostaglandin synthesis inhibitors: aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs)
b.Vasodilation of efferent arteriole: angiotensin-converting enzyme (ACE) inhibitors (e.g., captopril) c.Vasoconstrictor drugs: alpha-adrenergic agents (e.g., norepinephrine); angiotensin II d.Hepatorenal syndrome |
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Cause for Bilateral renal vascular obstruction
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a.Renal artery stenosis, emboli, thrombosis
b.Bilateral renal vein thrombosis |
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Bilateral ureteral obstruction (unilateral if one functional kidney)
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a.Intraureteral: calculi, blood clots, sloughed papillae
b.Extraureteral (compression): retroperitoneal fibrosis; neoplasm of bladder, prostate, or cervix; accidental surgical ligation or injury |
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Causes for tubular necrosis
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a.Postischemic.
Shock, sepsis, open-heart surgery, aortic surgery (all causes of severe prerenal azotemia) b.Nephrotoxic (1)Exogenous nephrotoxins (a)Antibiotics: aminoglycosides, amphotericin B (b)Iodinated contrast media (especially in diabetics) (c)Heavy metals: cisplatin, bichloride of mercury, arsenic (d)Cyclosporin; tacrolimus(e)Solvents: carbon tetrachloride, ethylene glycol, methanol |
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Endogenous Nephrotoxic
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Intratubular pigments: hemoglobin; myoglobin(b)Intratubular proteins: multiple myeloma(c)Intratubular crystals: uric acid
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(intrarenal ARF) Primary renal glomerular or vascular disease
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Intratubular pigments: hemoglobin; myoglobin(b)Intratubular proteins: multiple myeloma(c)Intratubular crystals: uric acid
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(intrarenal ARF) Acute tubulointerstital nephritis
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a.Allergic: beta-lactams (penicillins, cephalosporins); sulfonamides
b.Infection (e.g., acute pyelonephritis) |
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Initiating phase of Acute tubular necrosis
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This begins at the time of the insult and continues until the signs and symptoms become apparent. It can last hours to days.
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Oliguric phase of Acute Tubular Necrosis
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Urinary changes
Fluid volume excess Metabolic acidosis Sodium balance Potassium excess Hematologic disorders Calcium deficit and phosphate excess Waste product accumulation Neurologic disorders |
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what causes fluid volume excess?
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When urinary output decreases, fluid retention occurs. The severity of the symptoms depends on the extent of the fluid overload. The neck veins may become distended with a bounding pulse. Edema and hypertension may develop. Fluid overload can eventually lead to heart failure (HF), pulmonary edema, and pericardial and pleural effusions.
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What causes Metabolic Acidosis? ATN
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Ammonia
Bicarbonate |
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What happens with the sodium balance? ATN
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Damaged tubules cannot conserve sodium. Consequently, the urinary excretion of sodium may increase, resulting in normal or below-normal levels of serum sodium
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Why does potassium levels increase? (3) ATN
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The serum potassium levels increase because the normal ability of the kidneys to excrete 80% to 90% of the body's potassium is impaired
If the ARF is caused by massive tissue trauma, the damaged cells release additional potassium into the extracellular fluid. Bleeding and blood transfusions cause cellular destruction, releasing more potassium into the extracellular fluid Acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of the cells into the extracellular fluid. |
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What type of hematologic disorders occur with ATN? (3)
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Anemia occurs because renal failure results in impaired erythropoietin production.
The anemia may be compounded by platelet abnormalities that can lead to bleeding from multiple sources (i.e., intestines, brain). WBCs are also altered, causing immunodeficiency. |
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What waste product accumulates? ATN
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BUN
CREATINE |
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Calcium deficit and phosphate excess?????? with ATN
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activation of Vit D in the kidneys
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Neurological dosorders with ATN
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Neurologic changes can occur as the nitrogenous waste products accumulate in the brain and other nervous tissue.
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Diagnostic studies
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History
Urinalysis Renal ultrasound CT & MRI |
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Acute Renal Failure
Therapies to Treat Elevated Potassium Levels |
Regular Insulin Administration IV
Sodium Bicarbonate Calcium Gluconate IV Dialysis Sodium Polystyrene Sulfonate (Kayexalate) Dietary Restriction |