Shit - Renal UWorld Flashcards

1
Q

Kidney transplant prevention: drug names and MOA

A

Cyclosporin and tacrolimus

Block calcineurin → prevent dephosphorylation of NFAT → NFAT cant go to nucleus to increase IL-2 TC → T-cells dont proliferate and differnentiate, preventing graft attack

Cyclosporin: binds cyclophillin, which blocks calcineurin

Tacrolimus: binds FKBP, which blocks calcineurin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is most H2O resorbed?

A

PCT

*no matter what condition*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Estimates of:

GFR

RPF

A

GFR = creatinine/inulin

RPF = PAH

CLEARANCE!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

HCP: 4 s/s

A

Palpable purpura (buttocks and legs)

Arthralgias (large joints)

IgA neohropathy

GIT pain/bleeding (risk of intussiception)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

HSV Rx renal problems:

Acyclovir/Famicyclovir/valacylovir

Ganciclovir

Foscarnet

Cidofovir

A

Acyclovir/Famicyclovir/valacylovir: obstructive crystalline nephropathy (prevent with hydration) and ARF (allergy)

Ganciclovir: some renal toxicity (crystalline)

Foscarnet: Low Mg causing PTH inhibition causing hypocalcemia and hyperphosphatemia; can cause seizures

Cidofovir: nephrotoxic, decrease with probenecid and IV saline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

1st dose effect of ACE-I and risk factors

A

1st dose hypotension

Low Na or BV (other diuretics), low BP, renal impairments, heart failure, high renin or aldosterone levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hemmorhagic cytitis: causes and s/s

A

Caused by isophosphamide/cyclophosphamide, via metabolism to acrolein

s/s = hematuria, dysuria, frequency and urgency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Renal sign of Multiple Myelomas

A

Eosinophilic casts (NOT cells):

BJP overwhelm absorptive capacity –> ppt out with Tamm-Horsefall protein –> directly toxic to epi cells (atrophy) and block the lumen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ARF with ACE-I:

A

Bilateral renal artery stenosis

Decompensated HF

Chronic kidney disease

Volume depletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diuretic causing ototoxicity

A

Loops (furosemide, bumetanide, torsemide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ototoxic drugs:

A

Loops. sialicylates, aminoglycosides, vancomycin, cisplatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypercellularity of PSGN via:

PSGN buzzwords:

A

Leukocyte invation (PMN and macro) + endothelial proliferation + messangial proliferation

Buzzwords: IF = starry sky + lumpy bumpy

EM = humps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Digoxin-renal link

A

Old age decreases renal clearance, which can cause digoxin toxicity (decreased muscle mass may prevent concomitant increase in creatinine)

Toxicity:

  • Cholinergic (with blurry yellow vision)
  • arrythmyas and AV block
  • hyperkalemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stress Incontience: cause, s/s, etiology

A

Decreased sphincter control

leak with increased intra-abd pressure

weak sphincter (EUS), woman, old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Urge incontinents: cause, s/s, etiology

A

overactive detrussor

sudden overwhelming urge (and dont make it sometimes), frequency

frontal lobe probelm (cant control micturiction reflex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

overflow incontience: cause, s/s, etiology

A

cause: decreased detrussor contractility, outlet obstruction, loss of sensory

s/s full bladder that cant empty fully, constant dribbling

etiology: diabetic autonomic neuropathy

17
Q

anti-PLA2-R IgG4 Abs

A

Idiopathic membranous nephropathy

18
Q

Necessary condition for ascending pyelonephrisits

A

VUR!

Can be congenital, or from increased urinary retention or recurrent UTIs

19
Q

Important urine buffers

A

NH3 → NH3+

HPO42- → H2PO4-

20
Q

Kidney stone @ high pH

A

Ammonuim magnesium phosphate (struvite)

21
Q

Ethylene glycol effect on kidneys

A

Metabolized to glycolic acid and oxalic acid

Glycolic acid is directly toxic to renal tubules

Oxalic acid binds Ca forming Ca-oxalate stones

22
Q

Earliest manifestation if diabetic nephropathy

A

microalbuminuria

(via loss of negatively charged heparin sulfate via upregulation of heparinases)

23
Q

Activators of RAS

A

Macula densa

Internal baro-R

B1 adrenergic (on JG)

24
Q

Mechanism to test cause of metabolic alkalosis

A

Urine Cl-

Vomiting or NG suction = loss of HCl, so fix with saline and Cl-

Thiazide/Loop = loss of Na and Cl, so fix with saline and Cl-

Mineralocorticoid excess; CANNOT fix with saline because of constant mienralocorticoid activity

25
Q

RPF, GFR, and FF in severe hypovolemia

A

Decreased RPF, which causes a decreased GFR

BUT compensation from RAS causes ang-II efferent vasocontriction to try to maintain GFR

So decrease in RPF > decrease in GFR; so FF increases

[low num/very low denom = higher number]

[eff constiction without hypovolemia also causes increased FF, but GFR is increased while RPF is only slightly decreased]

26
Q

Areas of nephron most succeptible to:

1) ischemic injury
2) nephrotoxic

A

ischemia = PCT and thick ascending limb

nephrotoxic = PCT

27
Q

GMB collagen type

A

IV

Abs to a3 chain of IV = goodpastures

Mutated col IV = alports