Changes in Flow Flashcards
(35 cards)
three phases of unilateral ureteral obstruction
initial phase - urine back-flow increase intra-luminal hydrostatic pressure - offset by simultaneous increase in glomerular capillary pressure at the afferent to maintain GFR - activates RAAS –>
Second phase - decrease glomerular blood flow d/t afferent arteriole vasoconstriction
third phase - decreased luminal hydrostatic pressure AND renal blood flow –> 50% drop in GFR (one kidney out)
two phases of bilateral ureteral obstruction
initial phase - urine back flow increases intraluminal hydrostatic pressure, increase in glomerular capillary pressure induced by afferent arteriolar vasodilation to maintain GFR - activates RAAS
second phase - decrease glomerular blood flow d/t afferent arteriole vasoconstriction, persistent efferent and partial afferent arteriole vasoconstriction maintains GFR
sodium reabsorption changesi n unilateral ureteral obstruction
inability to reabsorb Na throughout the nephron leads to salt wasting
volume changes in bilateral ureteral obstruction
volume expansion
ANP blocks effects of renin –> decreased angiotensin OO therefore net result in diuresis and natriuresis
how does the urinary concentration change in obstruction?
inability to absorb Na in the ascending limb and dilute the filtrate in the DCT leads to excretion of solute
defective urea recycling : transporter defect reduces concentrating effect and allows urea to be excreted
tubular dsyfuction changes potassium concentration in which direction
leads to hyperkalemia
low-flow luminal states lead to high urinary k+ concentrations in the collecting duct result in a loss of the graident between cell and lumen
RTA type that occurs in tubular dysfunction d/t low-flow luminal states
RTA type I
generalized tubular defect
change in RBF, GFR, medullary blood flow and vasodilator concentrations of prostaglandin and nitric oxide in acute bilateral ureteral obstruction
increased RBF
decreased GFR
decreased medullary blood flow
increased concentration of vasodilators prostaglandin and nitric oxide
acute bilateral ureteral obstruction effects on tubules
increased ureteral and tubule pressures
increased reabosroption of Na, urea and water
change in RBF, GFR, vasoconstrictor porstaglandins and RAAS system in chronic bilateral ureteral obstruction
decreased RBF
double decreased GFR
increased vasoconstrictor prostaglandins
icnreased RAAS stimulation
chronic bilateral ureteral obstruction effects on tubules
decreased medullary osmolarity
decreased concentrating ability
parenchymal atrophy
decreased transport functions for Na. K. H
clinical features of chronic bilateral ureteral obstruction
azotemia hypertension avp-insensitive polyuria natriuresis hyperkalemic hyperchloremic acidosis
after release of bilateral ureteral obstruction, what change can be expected in the GFR
slow rise in GFR
after release of bilateral ureteral obstruction, what change can be expected in the tubules
postobstructive diuresis
decreased tubule pressure
increase solute load per nephron
natriuretic factors present
patient presentation for urinary tract obstruction
azotemia
HYPERkalemia
metabolic acidosis
congenital causes for mechanical urinary tract obstruction
UJP narrowing or obstruction
uretovesical junction narrowing or obstruction and reflux
ureterocele
retrocaval ureter
congenital causes for mechanical bladder outlet obstruction
bladder neck bostruction
ureterocele
congenital causes for mechanical blockage of the urethra
posterior urethral valves anterior urethral valves stricture meatal stenosis phimosis
aqcuired intrinsic defects in ureters leading to mechanical obstruction
calculi inflammation infection trauma sloughed papillae tumor blood clots
acquired intrinsic defects in bladder outlet leading to mechanical obstruction
BPH cancer of prostate cancer of bladder calculi diabetic neuropathy spinal cord disease anticholinergic drugs and alpha adrenergic antagonists
acquired intrinsic defects in the urethra leading to mechanical obstruction
stricture tumor calculi trauma phimosis
acquired extrinsic defects in ureter leading to mechanical obstruction
pregnant uterus retroperitoneal fibrosis AA uterine leiomyomata carcionoma of the uterus, prostate, bladder, colon, rectum lymphoma PID, endometriosis accidental surgical ligation
acquired extrinsic defcts in bladder outletleading to mechanical obstruction
carcinoma of cervix, colon
trauma
while acute urinary obstruction is often assocaited with obvious clinical symptoms, chronic obstruction
may be insidious or clinically silent
