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Renal 3/31 -4/2 > Renal- UWORLD > Flashcards

Renal- UWORLD Flashcards

1
Q

76- Q 10. chronic renal failure with sign of renal osteodystropy. What is level of phosphate

A

high

  • Keep it simple. Due to renal dysfunction in chronic renal failure, phosphate is not being excreted at PCT.
    I initially thought phosphate level will be down because PTH is high in renal osteodystropy.
    But what is action of PTH? It BLOCKS phosphate reabsorption at PCT.
    With renal dysfunction, however. amount of FILTERED phosphate is low in the beginning due to low GFR. So elevated PTH will not really exert its function.
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2
Q

76- Q 30. Bethanechol

  • what drug class
  • what renal condition can it be used?
  • what GI condition can it be used?
A
  • M3 agonist
  • urinary incontinence due to low bladder tone
  • ileus (hypomobility of gut)
  • sketchy: Beth with cola holds bladder hose and there is gut cement pouring right next to her
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3
Q

76- Q 31. Within true pelvis, ureter passes anteriorly to which artery?

A

internal iliac

  • ureter passes anteriorly both internal and external iliac, but external iliac does not pass true pelvis
    True pelvis refers to inside of big cavity within pelvic bones
  • ureter anatomy: water (ureter) under bridge (artery)
    under- above- under

under: gonadal artery
above: internal/external iliac ( this is exception of water under bridge)
under: uterine artery

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4
Q

77- Q 2. chronic transplant rejection

  • onset?
  • biopsy finding?
A
  • months to years

vascular pathology: fibrous intimal thickening
-> ischemic damage -> shrunken kidney

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5
Q

77- Q 10. How is high dietary calcium intake associated with calcium oxalate kidney stone?

A

decreases the risk of calcium oxalate stone
: high calcium in the gut -> more calcium oxalate precipitation in the gut, which will then subsequently removed via feces.

  • This is kinda opposite mechanism in which Crohn’s disease increases calcium oxalate stone formation
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6
Q

77- Q 19. Diuretics are used for symptomatic relief of HF. Which diuretics has the most significant effect of symptomatic relief? why?

A

loop diuretics

Salt is absorbed in much more quantity in TAL than DCT

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7
Q

77- Q 22. What is the change of level of H2PO4- in metabolic acidosis? explain physiology

A

HPO4 —> H2PO4 in collecting duct

In metabolic acidosis, more H+ is excreted into urine at collecting duct (as a renal compensation). Thus, more H2PO4- will be detected in urine

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8
Q

77- Q 26. (Hematology question) Defense mechanism of eosinophils against parasites?

A

IgE coating on eosinophil

  • > degranulation of eosinophil and subsequent release of major basic protein (MBP, cytotoxic to parasites. Also called as helminthotoxin)
  • Thus it is antibody-dependent (IgE) cytotoxcitiy
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9
Q

77- Q 34. Involuntary urine loss, difficulty in initiating and maintaining urination.

  • diagnosis?
  • two underlying pathophysiology
  • treatment
A
  • overflow urinary incontinence
  • two possible etiologies
    1. loss of detrusor tone
    2. outflow obstruction
  • muscarinic agonist (bethanechol)
  • catherization to drain urine
  • alpha blockers (for BPH)
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10
Q

77- Q36. Explain how urea curve is look like in relative concentration along PCT. Explain why

  • X axis: distance along PCT
  • Y axis: [tubular fluid]/[plasma]
A

Urea is not actively reabsorbed at PCT.

So it increases initially (as water is getting reabsorbed, tubular concentration gets higher), but platau later along PCT (as water is no longer getting actively reabsorbed)

  • Some of Urea are reabsorbed at CT by ADH. This reabsorbed urea is useful for MAINTAINING CONCENTRATION GRADIENT AT MEDULLA

But most of urea is ultimately excreted via urine as it is toxic metabolite

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11
Q

77-Q 39. What two renal pathologies are associated with NSAID?

A
  • interstitial nephritis
  • paipillary necrosis
  • I thought NSAID also can cause ischemic injury due to inhibition of prostaglandin (thus afferent arteriole constriction), but this effect is not significant enough to give ischemic injury. Hypotension or massive hemorrhage can cause ischemic injury
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12
Q

77- Q 40. Vesicoureteral reflux vs. posterior urethral valve

  • pathophysiology
  • affected gender
A

Vesicoureteral reflux

  • obstruction at vesicoURETERal valve
  • both male and females are affected

Posterior URETHRAL valve
- embryogenic malformation in junction where wolffian duct is inserted -> blockage of urine outlet in urethra

  • only male is affected ( it is wolffian duct issue)
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13
Q

78- Q 7. Aldesleukin

  • MOA
  • indications (2)
A

IL-2 analogue
-> NK cell activation -> kill cancer cells

indications: RCC, metastatic melanoma

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14
Q

78- Q 22. Two electrolyte imbalance caused by Forscanet?

A

hypomagenesemia

hypocalcemia

  • sketchy: M magnet and milk are spilled on ground
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15
Q

78- Q 23. ADPKD vs. ARPKD: compare how each progresses

A

ADPKD: microscopic cysts may present (or even not present) in newborn, cysts progresses and renal failure progresses over 10-20 yrs

ARPKD: macroscopic cysts in newborn or first yr of life

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16
Q

78- Q 34. antibody to phospholipase A2 receptor on podocytes. what disease is this?

A

membranous nephropathy

17
Q

78- Q 38. Describe histologic finding of acute pyleonephritis due to ureter obstruction

A

neutrophilic infiltration in INTERSTITIUM of kidney

18
Q

79- Q 2. oxalate crystals in urine. what intoxication should I think about?

A

ethylene glycol
: ethylene glycol is metabolized to oxalate, also increasing chance of calcium oxalate kidney stone formation

  • ethylene glycol also can cause anion gap metabolic acidosis
  • It is E of MUDPILES
19
Q

79- Q 12. Side effects of EPO treatment for anemia in hemodialysis for end stage renal disease?

A
  • thromboembolic effect: hyperviscosity

- hypertension: mechanism unknown, potentially because EPO stimulates its receptor on endothelial cell

20
Q

79- Q 13. What is renal presentation of HUS (hemolytic uremic syndrome)?

A

Acute kidney injury: hematuria and oliguria

21
Q

79- Q 19. Side effect of lithium on kidney?

A

nephrogenic DI
: can be reversed with amilolide

  • sketchy: almond seller is pushing away kid with lithium balloon
22
Q

79- Q 21. What is histologic feature of RCC? what is it composed of?

A

clear cytoplasm, which is accumulated with glycogen and lipid

23
Q 
# 107- Q 28. MOA of ARBs (-sartan)?
 Effect on level of
- Renin
- AngI
- AngII
- Aldo
- Bradykinin
A

ANGII receptor blocker (not aldo blocker! aldo blocker is spironlactone!)

  • Renin, AngI, AngII: increased
  • Aldo: DECREASED!
  • aldo is synthesized by action of AngII on adrenal cortex
  • no change in Bradykinin (vs. ACEI, which increased bradykinin, leading to angioedema)

Renal 3/31 -4/2 (6 decks)

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