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Renal Final > Changes in Flow > Flashcards

Changes in Flow Flashcards

1
Q

three phases of unilateral ureteral obstruction

A

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)

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2
Q

two phases of bilateral ureteral obstruction

A

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

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3
Q

sodium reabsorption changesi n unilateral ureteral obstruction

A

inability to reabsorb Na throughout the nephron leads to salt wasting

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4
Q

volume changes in bilateral ureteral obstruction

A

volume expansion

ANP blocks effects of renin –> decreased angiotensin OO therefore net result in diuresis and natriuresis

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5
Q

how does the urinary concentration change in obstruction?

A

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

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6
Q

tubular dsyfuction changes potassium concentration in which direction

A

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

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7
Q

RTA type that occurs in tubular dysfunction d/t low-flow luminal states

A

RTA type I

generalized tubular defect

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8
Q

change in RBF, GFR, medullary blood flow and vasodilator concentrations of prostaglandin and nitric oxide in acute bilateral ureteral obstruction

A

increased RBF
decreased GFR
decreased medullary blood flow
increased concentration of vasodilators prostaglandin and nitric oxide

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9
Q

acute bilateral ureteral obstruction effects on tubules

A

increased ureteral and tubule pressures

increased reabosroption of Na, urea and water

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10
Q

change in RBF, GFR, vasoconstrictor porstaglandins and RAAS system in chronic bilateral ureteral obstruction

A

decreased RBF
double decreased GFR
increased vasoconstrictor prostaglandins
icnreased RAAS stimulation

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11
Q

chronic bilateral ureteral obstruction effects on tubules

A

decreased medullary osmolarity
decreased concentrating ability
parenchymal atrophy
decreased transport functions for Na. K. H

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12
Q

clinical features of chronic bilateral ureteral obstruction

A 
azotemia
hypertension
avp-insensitive polyuria
natriuresis
hyperkalemic
hyperchloremic acidosis
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13
Q

after release of bilateral ureteral obstruction, what change can be expected in the GFR

A

slow rise in GFR

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14
Q

after release of bilateral ureteral obstruction, what change can be expected in the tubules

A

postobstructive diuresis
decreased tubule pressure
increase solute load per nephron
natriuretic factors present

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15
Q

patient presentation for urinary tract obstruction

A

azotemia
HYPERkalemia
metabolic acidosis

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16
Q

congenital causes for mechanical urinary tract obstruction

A

UJP narrowing or obstruction
uretovesical junction narrowing or obstruction and reflux
ureterocele
retrocaval ureter

17
Q

congenital causes for mechanical bladder outlet obstruction

A

bladder neck bostruction

ureterocele

18
Q

congenital causes for mechanical blockage of the urethra

A 
posterior urethral valves
anterior urethral valves
stricture
meatal stenosis 
phimosis
19
Q

aqcuired intrinsic defects in ureters leading to mechanical obstruction

A 
calculi
inflammation
infection
trauma
sloughed papillae
tumor
blood clots
20
Q

acquired intrinsic defects in bladder outlet leading to mechanical obstruction

A 
BPH
cancer of prostate
cancer of bladder
calculi
diabetic neuropathy
spinal cord disease
anticholinergic drugs and alpha adrenergic antagonists
21
Q

acquired intrinsic defects in the urethra leading to mechanical obstruction

A 
stricture
tumor
calculi
trauma
phimosis
22
Q

acquired extrinsic defects in ureter leading to mechanical obstruction

A 
pregnant uterus
retroperitoneal fibrosis
AA
uterine leiomyomata 
carcionoma of the uterus, prostate, bladder, colon, rectum
lymphoma
PID, endometriosis 
accidental surgical ligation
23
Q

acquired extrinsic defcts in bladder outletleading to mechanical obstruction

A

carcinoma of cervix, colon

trauma

24
Q

while acute urinary obstruction is often assocaited with obvious clinical symptoms, chronic obstruction

A

may be insidious or clinically silent

25
Q

most common inherited anomaly of the GU tract

A

vesicoureteral reflux

26
Q

vesicoureteral reflux is clinically important becuase it presents with

A

frequent UTI or pyelonephritis

more common in males

27
Q

clinical presentation of BPH

A 
slow stream
increase urgency
dribbling after finishing
incomplete emptying 
nocturia 
eventualy pressure in the bladder will icnrease such that urine is forced into the ureters, causing hydronephrosis
28
Q

cycle of BPH obstruction

A

incomplete emptying –>
stretch of bladder wall and muscle –>
ineffective bladder contraction –>
incomplete emptying

29
Q

ultrasound evalutation of post-void residual urine can be easily performed after instructing the patient to void when bladder feels full and using USG to estimate volume left in the bladder
what residual volume indicates incomplete emptying

A

100mL

30
Q

neurogenic bladder causes include:

A

spinal cord trauma
spinal myelomeningocele
less commonly: spinal stenosis and herniated discs

31
Q

why is it important to tmonitor patients iwth a neurogenic bladder

A

> 40cm H2O increase risk of hydronephrisis and subsequent decrease in GFR
want to monitor for hydronpehrosis to subvert before irreversible injury occurs

32
Q

preferred radiography for diagnosis of renal lithiasis

A

CT
not all stones are radiographic however
tx is to remove the stone

33
Q

pregnant patient presents with mild hydronephrosis in the first trimester on routine fetal USG but otherwise patient is asymptomatic: what do you do

A

monitor until it becomes symptomatic

if it does relieve the obstruction with a stent

34
Q

pathophys of postobstructive diruesis following BUO

A

combination of fluid overload, urea accumulation, electrolyte imbalance
results from donwregulatino of Na transporters during obstruction
ANP released in reponse to cardiac preolaod during obstruction

35
Q

tx for postobstructive diuresis

A

fluid replacement and careful monitoring of urine and serum osmolality as well as serum electrolytes

Renal Final (6 decks)

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