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27 Cards in this Set
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- Back
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diabetic nephropathy
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kidney disease associated with DM. principle cause of chronic renal failure. damages renal glomeruli & results in destruction of functional nephrons via progressive scar tissue, mediated in part by inflammatory response.
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advanced glycosylation end products (AGEs)
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produced when glucose forms irreversible cross-links w/ kidney & plasma proteins. stimulate secretion of GFs from glomerular cells, which promote glomerular basement membrane thickening.
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microalbuminuria -> overt proteinuria in 10-15 yrs. by that time, # of functional nephrons decreased so kidneys cannot excrete adequate amts of waste products (ESRD).
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proteinuria defined as the secretion of more than 300mg albumin/day.
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end stage renal disease (ESRD)
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renal failure has worsened to point that kidney function is less than 10% of normal. must be treated by dialysis or transplant, otherwise death.
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ACE inhibitors slows or halts progression of proteinuria and ESRD. prevent formation of angiotensin II >> arterial bp and glomerular capillary pressure remain w/in their normal values.
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ACE inhibitors + angiotensin receptor blockers (ARBs) = angiotensin II molecules cannot bind to their receptors >> proteinuria decreases up to 45%.
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diuretics:
* cspoxa |
carbonic anhydrase inhibitors, sodium ion reabsorption inhibitors, potassium-sparing diuretics, osmotic diuretics, xanthines, alcohol.
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carbonic anhydrase inhibitors
reduces rate of H+ secretion and reabsorption of HCO3- |
useful in treating glaucoma and altitude sickness
*effect lost w/ long term use |
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sodium ion reabsorption inhibitors
promote loss of Na+, Cl-, and water. |
thiazide types for people w/ hypertension; others: bumetanide, furosemide, & ethacrynic acid specifically inhibit transport in ascending loop of henle >> chf, cirrhosis, & renal disease. *may increase excretion of K+
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potassium-sparing diuretics
commonly used in combo w/ Na+, Cl- symport inhibitors |
act on dcts & collecting ducts to reduce exchange between Na+ and K+. some drugs act by competitive inhibition of aldosterone, others inhibit the symporters for Na+ in apical membranes of cell in dcts and collecting ducts. both = Na+ excretion and K+ retention.
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osmotic diuretics
*urea, mannitol, glycerine |
work by elevating osmotic concentration of filtrate >> reducing amt of water moving by osmosis out of nephron. not commonly used but effective for cerebral edema & edema in ARF.
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xanthines
*caffeine and related substances |
increase renal blood flow & rate of glomerular filtrate formation, also influence nephron by decreasing Na+ & Cl- reabsorption
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alcohol acts as a diuretic but not clinically used for that purpose
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inhibits ADH secretion from posterior pituitary >> increased urine volume
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kidney stones: hard objects usually found in pelvis of kidney. ~2-3mm in diameter w/ either smooth or jagged surface
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65% calcium oxylate mixed w/ calcium phosphate; 15% magnesium ammonium phosphate; 10% uric acid or cystine; ~2.5% of each stone is mucoprotein.
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staghorn stone
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large branching kidney stone formed in renal pelvis
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symptoms associated w/ kidney stones occur when stone passes into ureter >> referred pain down back, side, and groin area.
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ureter contracts around stone >> irritated epithelium & hematuria. in addition they can block ureter >> ulceration & increased probability of bacterial infections
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cause of kidney stones obscure; predisposing conditions: concentrated urine & abnormally high calcium concentration in urine (cause of calcium concentration usually unknown)
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magnesium ammonium phosphate stones often found in people w/ recurrent kidney infections; uric acid stones -in people w/ gout
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lithotripsy pulverizes kidney stones w/ ultrasound or lasers.
replaced most traditional surgical procedures |
severe stones must be removed surgically. 1% of all autopsies reveal stones, many occur w/out symptoms.
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automatic bladder- micturition reflex exists but no conscious control over its onset or duration.
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spinal cord damaged above sacral region >> no micturition reflex exists for a time but if bladder is emptied frequently, mic reflex eventually becomes adequate to cause emptying. after time the mic reflex can integrate w/in spinal cord to operate.
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noncontracting bladder- mic reflex cannot occur >> bladder fills to capacity, & urine is forced in a slow dribble thru external urinary sphincter.
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damage to sacral region of spinal cord or to nerves that carry APs between spinal cord & bladder can result in failure of bladder to contract.
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hyperexcitable bladder- w/out inhibition, sacral centers are hyperexcitable; even a small amt of urine in bladder can elicit an uncontrollable mic reflex
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in elderly people or patients w/ damage to the brainstem or spinal cord, loss of inhibitory APs to sacral region of spinal cord can occur.
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glomerular nephritis- results from inflammation of filtration membrane w/in renal corpuscle.
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characterized by increased permeability of filtration membrane & accumulation of numerous wbcs in the area >> high concentration of plasma proteins enters filtrate, along w/ many wbcs & greater than normal urine volume w/ increase in plasma proteins in urine.
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acute glomerular nephritis- often occurs 1-3 wks after severe bacterial infection, such as strep throat or scarlet fever.
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antigen-antibody complexes associated w/ the disease become deposited in the filtration membrane and cause inflammation. acute inflammation normally subsides after several days.
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chronic glomerular nephritis- longterm & usually progressive, filtration membrane thickens & is replaced by connective tissue.
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early stages resembles acute form, in advanced stages many renal corps have been replaced by fibrous connective tissue, & kidney ceases to function.
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pyelonephritis- inflammation of renal pelvis, medulla, & cortex. affects medulla more than cortex--kidney's ability to concentrate urine is dramatically affected.
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often begins as bacterial infection of renal pelvis extending into kidney (ex. E coli). may destroy nephrons & renal corps.
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acute renal failure- kidney damage is extensive & leads to accumulation of urea in blood & to acidosis.
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arf can result from agn or it can be caused from damage or blockage of renal tubules. Hg ions or C tetrachloride cause necrosis of nephron epithelium. also severe ischemia assoc w/ circ shock from symp vasoconstiction of renal blood vessels.
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chronic renal failure- remaining functional nephrons cannot adequately compensate.
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causes: cgn, trauma to kidneys, absence of kidney tissue d/t congenital abnormalities, or tumors. UT obstruction by kidney stones, damage from pyelonephritis, sever arteriosclerosis of renal arteries also cause degeneration of the kidney.
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crf: the gfr is dramatically reduced, & kidney is unable to excrete excess products incl. electrolytes and metabolic wastes >> water retention & edema.
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K+ levels in extracellular fluids elevated & acidosis occurs because dcts and collecting ducts cannot excrete sufficient amts of K+ & H+. >> mental confusion, coma death when severe.
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