Shit - Renal UWorld Flashcards
Kidney transplant prevention: drug names and MOA
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
Where is most H2O resorbed?
PCT
*no matter what condition*
Estimates of:
GFR
RPF
GFR = creatinine/inulin
RPF = PAH
CLEARANCE!
HCP: 4 s/s
Palpable purpura (buttocks and legs)
Arthralgias (large joints)
IgA neohropathy
GIT pain/bleeding (risk of intussiception)
HSV Rx renal problems:
Acyclovir/Famicyclovir/valacylovir
Ganciclovir
Foscarnet
Cidofovir
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
1st dose effect of ACE-I and risk factors
1st dose hypotension
Low Na or BV (other diuretics), low BP, renal impairments, heart failure, high renin or aldosterone levels
Hemmorhagic cytitis: causes and s/s
Caused by isophosphamide/cyclophosphamide, via metabolism to acrolein
s/s = hematuria, dysuria, frequency and urgency
Renal sign of Multiple Myelomas
Eosinophilic casts (NOT cells):
BJP overwhelm absorptive capacity –> ppt out with Tamm-Horsefall protein –> directly toxic to epi cells (atrophy) and block the lumen.
ARF with ACE-I:
Bilateral renal artery stenosis
Decompensated HF
Chronic kidney disease
Volume depletion
Diuretic causing ototoxicity
Loops (furosemide, bumetanide, torsemide)
Ototoxic drugs:
Loops. sialicylates, aminoglycosides, vancomycin, cisplatin
Hypercellularity of PSGN via:
PSGN buzzwords:
Leukocyte invation (PMN and macro) + endothelial proliferation + messangial proliferation
Buzzwords: IF = starry sky + lumpy bumpy
EM = humps
Digoxin-renal link
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
Stress Incontience: cause, s/s, etiology
Decreased sphincter control
leak with increased intra-abd pressure
weak sphincter (EUS), woman, old
Urge incontinents: cause, s/s, etiology
overactive detrussor
sudden overwhelming urge (and dont make it sometimes), frequency
frontal lobe probelm (cant control micturiction reflex)
overflow incontience: cause, s/s, etiology
cause: decreased detrussor contractility, outlet obstruction, loss of sensory
s/s full bladder that cant empty fully, constant dribbling
etiology: diabetic autonomic neuropathy
anti-PLA2-R IgG4 Abs
Idiopathic membranous nephropathy
Necessary condition for ascending pyelonephrisits
VUR!
Can be congenital, or from increased urinary retention or recurrent UTIs
Important urine buffers
NH3 → NH3+
HPO42- → H2PO4-
Kidney stone @ high pH
Ammonuim magnesium phosphate (struvite)
Ethylene glycol effect on kidneys
Metabolized to glycolic acid and oxalic acid
Glycolic acid is directly toxic to renal tubules
Oxalic acid binds Ca forming Ca-oxalate stones
Earliest manifestation if diabetic nephropathy
microalbuminuria
(via loss of negatively charged heparin sulfate via upregulation of heparinases)
Activators of RAS
Macula densa
Internal baro-R
B1 adrenergic (on JG)
Mechanism to test cause of metabolic alkalosis
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
RPF, GFR, and FF in severe hypovolemia
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]
Areas of nephron most succeptible to:
1) ischemic injury
2) nephrotoxic
ischemia = PCT and thick ascending limb
nephrotoxic = PCT
GMB collagen type
IV
Abs to a3 chain of IV = goodpastures
Mutated col IV = alports
