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Bloc D - Renal > Jan18 M1-Acute Kidney Injury > Flashcards

Jan18 M1-Acute Kidney Injury Flashcards

1
Q

3 types of AKI

A

pre-renal, renal, post-renal

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2
Q

pre-renal AKI def

A

low BP, blood loss, hemodynamic prob (volume, pressure, fluid)

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3
Q

renal AKI def

A

disease of parenchyma (glomeruli, mesengium, tubules)

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4
Q

post-renal AKI def

A

obstruction (problem with urine outflow. stones, BPH, tumor)

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5
Q

causes of pre-renal AKI

A

relative drop in circulating volume (RAS, NSAIDs, CHF, cirrhosis/ascites, sepsis (vasodilation)) or effective drop in volume (GI loss, bleeding, etc.)

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6
Q

renal causes of AKI (5 main)

A
  • acute GN (nephritic: APIGN, SLE, etc.)
  • RPGN/crescentic
  • ATN (post-infectious or toxic)
  • AIN (drug-induced)
  • Intratubular obstruction
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7
Q

post-renal causes of AKI

A
  • prostatic disease

- pelvic or retroperitoneal malignancy

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8
Q

AKI definition

A

EITHER
1. plasma Cr +50 or + 50% or 50% drop GFR IN A MONTH
OR
2. oliguria (less 30cc/hour or less 200cc/8 hours)

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9
Q

anuria and oliguria def

A 
anuria = less 50cc/day
oliguria = less 500cc/day
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10
Q

how to calculate one’s minimal urine output

A

daily solute load in mosm/1200 mosmkg-1 (which is the max U conc)

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11
Q

ATN as cause vs as consequence of AKI

A

ATN can cause a renal AKI

ATN can be a consequence of a pre-renal AKI bc of ischemia and damage to the tubules

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12
Q

why ATN occurs

A

O2 level already low in medulla + high metabolism in the tubules (*PCT and TAL) so vulnerable to low flow

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13
Q

can ATN heal? why?

A

yes. tubules are epithelial cells, like skin, so they can repair

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14
Q

4 most common causes of AKI in the hospital

A

ATN, pre-renal, acute on chronic (already vulnerable bc low GFR), obstruction (urinary tract)

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15
Q

how to dx ATN vs pre-renal cause of AKI (clinically with no labs)

A

pre-renal: Cr and UO improved with fluid

ATN: takes days to months to repair (tubular damage)

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16
Q

labs to differentiate ATN vs pre-renal

A

ATN: urine sediment has muddy brown casts (dead tubular cells)
pre-renal: no muddy brown casts

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17
Q

can you get pre-renal failure from RAS alone?

A

no. need to add a clear cut time where the BP drop or gave ACEi

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18
Q

ATN vs pre-renal AKI: how U lytes can help** (must remember!!)**

A

pre-renal: U Na less 25 mM

ATN: U Na more 40 mM

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19
Q

best test to diff pre-renal vs ATN

A

FENa (fractional excretion of Na)

20
Q

FENa value for pre-renal vs ATN AKI

A

less 1% = pre-renal
1-2% = can be any
more 2% = ATN

21
Q

FENa formula

A

(UNa x PCr)/(PNa x UCr) x 100

22
Q

other tests to check pre-renal vs ATN

A

serum urea to Cr: above 20 favors ATN (no urea reabso)
U osms: above 500 favors pre-renal (bc holding on to water)
gravity: more 1.020 is pre-renal (bc holding on to wateR)

23
Q

treatment + what if no improvement in ATN

A

NS until euvolemia (check ctly volume status

Cr still rising in CHF + worsening = dialysis

24
Q

how to control BP in unilateral vs bilateral RAS

A

unilateral: give ACEi (one kidney drops GFR, other increases)
bilateral: can’t give ACEi bc both kidneys drop their GFR

25
Q

why are the patients hypertensive when they have RAS

A

RAAS activated. low flow to the kidney

26
Q

NSAIDs can cause AKI in what specific patients and why

A

-pt with ongoing CKD

block PGs which dilate the AA

27
Q

alternative to NSAIDs in CKD patients

A

ASA or tylenol

28
Q

8 renal causes of AKI

A
  • myeloma
  • rhabdomyolysis
  • TTP
  • HUS
  • AIN
  • aminoglycoside toxicity
  • contrast nephropathy
  • RPGN
29
Q

pathophgy (1 thing) in multiple myeloma (to the kidneys)

A

IgG produced by plasma cells can precipitate in the tubule and obstruct it

30
Q

test to check for multiple myeloma

A

serum free light chains

31
Q

rhabdomyolysis pathophgy to the kidneys

A

myoglobin is toxic to the PCT

pigment cast toxic to the distal tubule

32
Q

how to check for rhabdo

A

+ for blood on dipstick but no urine on microscopy

33
Q

TTP: thrombotic thrombocytopenic purpura. pathophgy to the kidneys

A

microclots form and go to the kidney, embolize the glomerulus and renal capillaries

34
Q

why TTP is part of hemolytic anemias

A

if RBCs go through a microclot’s mesh, they are broken down

35
Q

how to check for TTP (related to its cause)

A

ADAMTS13 molecule presence. if absent, is TTP. bc this molecule is supposed to break down endoth-platelet-vWF clots

36
Q

HUS: hemolytic uremic syndrome pathophgy

A

damage to renal endothelium causing microembolic in the glomerulus

37
Q

HUS associated with what

A

bad e.coli (toxin in it)

38
Q

AIN def and cause (3 typical)

A

allergic rx of the kidney typically caused by antibiotics, PPIs and NSAIDs

39
Q

AIN pathophgy

A

WBCs aggregate and block the blood flow to the kidney

40
Q

aminoglycoside toxicity pathophgy

A

toxicity of certain antibiotics (..mycin) to PCT: tubular toxicity

41
Q

AIN vs aminoglycoside toxicity and can you take the drug again?

A

AIN: allergy, can’t take it again

aminoglycoside toxicity: dose was too high, can take it again. not an allergy

42
Q

contrast nephropathy pathophgy

A

causes intense renal vasoconstriction

43
Q

why RPGN and crescents cause a problem

A

crescent compresses on glomerular capillaries

44
Q

urine colour in RPGN

A

red or brown

45
Q

3 types of RPGN

A
  • anti-GBM
  • immune complex (APIGN, lupus, IgA nephropathy)
  • pauci-immune
46
Q

pathophgy of pauci-immune RPGN

A

microscopic vascular disease where endothelium is damaged and mesengium and podocytes too

47
Q

why US is the test of choice to verify for an obstruction OF THE URINARY TRACT

A

check for hydronephrosis

Bloc D - Renal (32 decks)

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