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26 Cards in this Set

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prerenal failure gen
-caused before the kidney
=diminished blood supply
intrarenal failure gen
-cause is inside the kidney
-eg tissue injury, capillaries, glomerula
post-renal failure gen
-after the kidney
-eg obstrustion of ureters, bladder, urethra
acute renal failure gen
-kidneys abruptly stop working, partly or totally
-may eventually recover to normal or near normal fx
chronic renal failure gen
-kidney(s) progressively decrease overall fx caused by a progressive loss of fx nephrons
-irreversible loss of large # nephrons: loss up to 70% tolerated without clinical symptoms
causes of acute prerenal failure
decreased blood supply:
1. heart failure
2. diminished BV
3. renal artery stenosis
4. peripheral vasodilation: hypertension
5. embolism, thrombosis of renal a or v:
a. anaphylactic shock
b. anesthesis
c. sepsis, severe infections
causes of acute intrarenal failure
1. small vessel/ glomerular injury:
a. cholesterol embolism
b. malignant hypertension
c. glomerulonephritis
2. tubular necrosis:
a. ischemia
b. toxins: heavy metals, ethylene glycol, insecticides, mushrooms
3. renal interstitial injury:
a. pyelonephritis
b. allergic interstitial nephritis
prerenal acute failure with decrease in blood flow
-decrease in B flow decreases GFR= less urine output of H2O and solutes
-kidneys normally receive 20-25% cardiac output
-oliguria: reduced urine production
-anuria: cessation of urine production
- accumulation of water and solutes in body fluids
- edema, azotemia, intoxication
prerenal acute failure with severe decrease in blood flow
-cause ischemia
-B flow:
1) >20 %of normal: renal failure can usually be reversed if the cause of ischemia is corrected within hours
2) < 20% of normal:
-basal requirements of the kidney tissues cannot be met anymore
- hypoxia damages cells: tubular epithelial cells are very sensitive
causes of acute post-renal failure
-block or partial block of the lower urinary tract:
1. bilateral obstruction of the pelvises
2. bilateral obstruction of the ureters
3. obstruction of the bladder
4. obstruction of the urethra
acute intrarenal failure: glomerulonephritis
-abnormal immune reaction
-eg streptococcal sore throat or tonsilitis
1. antibodies and antigens form an insoluble complex that becomes entrapped in the glomeruli and blocks them
2. permeability of the remaining functional glomeruli increase: proteins and erythrocytes leak into the glomerular filtrate
acute intrarenal failure: tubular necrosis
=destruction of epithelial cells
1) severe renal ischemia: mainly prerenal causes
-circulatory shock, severe imbalance of renal B supply
2. toxins or medications:
-carbon tetrachlorides, heavy metals (Hb, Pb), ethylene glycol (antifreeze), insecticides, antibiotics
- if basement membrane remains intact, full recovery possible in 2 weeks
mushroom intoxication: amanita phalloides
-1st signs 8-24 hours without warning:
severe diarrhea without vomiting causes exsiccosis
- after 1-2 days, deceptive recovery for 1 day
- results in necrosis of liver and renal tubules
-death caused by liver coma rather than uraemia
post-renal accute failure: unilateral
-unilateral obstruction, causing decrease of urine flow
- pelvis, ureter
- by stones, clots, tumors
- contralateral kidney increases urine production:
1. no major change in body fluid composition
2. normal kidney function can be restored
post-renal accute failure: bilateral
-bilateral obstruction of the urinary tract
- both pelvuses, ureters, bladder, urethra
- stones, clots, tumor
-accumulaton of metabolic end products in blood= intoxication
effects of acute moderate renal failure
-retention of water, electrolytes, and metabolic wastes
-hypernatriaemia: water retention, causes hypertension and edema
-hyperkaliaemia: bradycardia, arrhythmia, heart arrest
effects of acute severe renal failure
-oligouria followed by anuria
- uraemia after 5-10 days:
1. intoxication by metabolic wastes: urea, uric acid, creatinine, organic acids, K, P, (phen)guanidine metabolites, phenol compounds
2) acidosis
3) anaemia
-exitus after 8-14 days without treatment
causes of chronic renal failure
1. metabolic disorders: diabetes mellitus, amyloidosis
2. heart failure: low BP and vasoconstriction
3. renal vascular: artheroschlerosis
4. immunologic: glomerulonephritis
5. infections: pyelonephritis, tuberculosis
6. primary tubular: nephrotoxins eg analgesics, heavy metals
7. urinary tract obstruction: renal calculi, urethral constriction
8. congenital: renal hypoplasia (absence of kidney tissue)
1st course of chronic renal failure: # of functional nephrons decreases
-various causes
- loss of up to 70% tolerated without major changes in renal fx
2nd course of chronic renal failure: polyuria
*longest phase of chronic RF:
# of nephrons lost >70%
- increased excretion of H2O and solutes
- GFR increases: rapid tubular flow=
1. reduced water resorption
2. failure of the countercurrent mechanism: no interstitial gradient = no urine concentration
3rd course of chronic renal failure: oligouria
-further decrease in the number of functional nephrons:
1. remaining nephrons fail to excrete enough water and solutes
2. metabolic waste products accumulate
4th course of chronic renal failure: anuria
-only a few or no functional nephrons remain:
1. generalized edema
2. uremia: high blood [phenols, sulfates, phosphates, K and guanidine bases]
3. accumulation of non-protein N in blood: urea, creatinine, uric acid
4. intoxication lead to death 1-2 weeks unless kidney fx restored, eg dialysis
effects of chronic renal failure on blood
-decrease of erythropoeitin secretion in kidneys:
1. stimulus of erythropoeitin on the bone marrow to produce erythrocytes decreases
2. anaemia develops
effects of chronic renal failure on bones
1. production of active vit D decreases:
Ca absorption in intestines decreases
2. decreased phosphate excretion causes increase of plasma phosphate concentration:
-phosphate binds Ca in plasma, thus reducing the ionized Ca
-low [Ca] causes secretion of parathyrine--> stim release of Ca from bones --> demineralization--> secondary hyperparathyreodism
effects of renal failure on ECF and cardiovascular system
1. moderate cases, the major effect of oliguria is water and solute retention:
- increase in ECF volume may cause hypertension and edema
- excessive retention of K affects the conductive system of the heart :arrhythmia, bradycardia, arrest in diastole
2. low perfusion (eg intrarenal stenosis or embolism) causes release of renin--> angiotensin causes hypertension
urolithiasis
-kidney stones formed by precipitation:
1. Ca oxalate, phosphate, carbonate
2. uric acid, urate (dalmations, cats)
3. phosphate of ammonium and magnesium: triple phosphate, struvite, common in tomcats
4. cystine: amino acids, common in dachshunds
5. xanthine: product of purin base metabolism