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20 Cards in this Set
- Front
- Back
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Pre-renal causes of ARF?
Intrarenal causes? Post-renal cause? Pre-renal failure: _______ glomerular perfusion, leading to drops in _______ (3) |
decreased blood supply to kidney
blood vessels, tubule changes output obstruction decreased glomerular perfusion --> drop in hydrostatic pressure, GFR, urinary excretion |
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____% of normal flow is adequate to sustain metabolism of normal tissues.
Some common pre-renal causes? |
20-25%
volume depletion - hemorrhage, dehydration, GI fluid loss, burns cardiac failure hypotension from vasodilation (shock) renal artery blockage - embolus, stenosis |
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_____ forms when renal perfusion pressure is low, causes _________ constriction, _____ GFR, ______ interstitial pressure.
What drugs given to combat hypertension from renin/ang II? |
Ang II - efferent arteriole constriction, increased GFR, decreased interstitial pressure
ACEI's |
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GN usually caused by a ______ infection.
pathology? |
Strep
Ab-Ag complexes deposited in glom basement membrane --> attracts WBC's --> inflammation, blockage, less affected glomeruli filter more, allow proteins to pass |
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Intra-renal failure: Two causes of tubular necrosis?
Post-renal causes of renal failure? |
Ichemia from extreme hypotension --> cell necrosis blocks tubules
Toxins - cells slough off post renal - blockage, stones |
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ARF --> retention of: (4)
ARF untreated can lead to chronic renal disease, which is loss of _________. |
azotemia - uric acid, urea, Cr
H2O metabolic wastes (NH4+) electrolytes - K+ loss of functional gloms, remaining gloms overwork --> necrosis |
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1. How does arteriosclerosis cause CKD?
2. Chronic GN usually caused by: 3. damage to interstitial tissue from infection: 4. usually damages what part of kidney? |
1. renal artery stenosis/plaque --> less perfusion, more renin --> HTN --> constriction of afferent arteriole --> decreased renal perfusion, GFR
2. SLE 3. pyelonephritis - 4. medulla, concentrating ability |
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Nephrotic syndrome:
Leaky glom leaks _____ into filtered fluid, due to loss of ___________. More proteins in urine lead to decreased ______, ____ of fluid into Bowman's capsule, and peripheral ______. |
protein leakage due to loss of basement membrane negativity
decreased GCOP, incresaed loss of fluid into Bowman's capsule --> peripheral edema |
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inability to concentrate urine, and mechanism:
CKD usually leads to a decrease in ______ HCO3- |
isothenuria - loss of fxnal nephrons - remaining nephrons work harder, lose countercurrent mechanism in LOH
CKD - decrease in plasma HCO3- |
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Renal failure effects:
_____ due to retained electrolytes _____ due to retained acids ______ due to loss of erythropoietin _______ due to lack of Vitamin D activation, increased Ca binding by HPO4- |
edema - electrolytes
acidosis - acids anemia - erythropoietin osteomalacia - loss of Vitamin D, Ca binding |
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Tubular disorders can often lead to ______ and ______ in urine.
Renal tubule disorders can lead to nephrogenic DI due to failure of kidneys to respond to _____. |
glucose, AA's
ADH |
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Match the following by the tubular disorder discription...
a. when all amino transport mechanisms are limited b. when cystine reabsorption is limited c. caused by failure to reabsorb phosphate ions in face of low plasma levels |
a. aminoaciduria
b. cystinuria c. renal hypophosphatemia |
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What causes physiologically Renal tubular acidosis?
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inability to secrete hydrogen
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caused by failure of kidneys to respond to ADH
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nephrotic diabetes insipidus
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Name the classes (big buckets) of diuretics...
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1. Osmotic diuretics
2. Loop diuretics 3. Thiazide diuretics 4. Carbonic anhydrase inhibitors 5. Aldosterone antagonists 6. Sodium channel blockers |
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What does the osmotic diuretic (mannitol) affect?
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increases osmolarity in the tubes, which increases urine flow mostly effecting proximal convoluted tubules
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Where does the loop diuretics (furosemide, bumetanide) effect?
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Inhibit the Na,K,Cl co-transport of thick ascending loop of Henle
- abolishs hypertonicity of medulla, preventing concentration of urine which increases Ca excretion. - Remember Loops Lose Ca |
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Where and what does the thiazide diuretics (hydrochlorothiazide, chlorthalidone) effect?
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inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron and decreasing Ca excretion
- Hyper GLUC (glycemia, lipidemia, uricemia, calcemia) |
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Describe the carbonic anhydrase inhibitors (acetazolamide) area of affecting the diuretics...
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Inhibit H+ secretion and HCO3- reabsorption (reduces Na+ reabsorption), remember
ACIDazolamide causes ACIDosis |
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Aldosterone antagonists (spironolactone, eplerenone) aka K+ sparing diuretics
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– Decreases Na+ reabsorption in collecting tubules
- remember the K+ STAys (Spironolactone, Triamterene, Amiloride, eplerenone spirolactone is a competitive aldosterone receptor antagonist in the cortical collecting tubule. |
