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nephro > AKI > Flashcards

AKI Flashcards

1
Q

biochemical changes in AKI

A

hyperkalemia
hyocacemia
hyponatremia

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2
Q

how to treat hyperkalemia

A

Treat with – insulin (and dextrose), calcium gluconate, salbutamol, dialasis

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3
Q

nephrotoxic drugs

A

n saids, aminoglycosided

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4
Q

indications for dialysis (there’s more)

A

hyperkalmeia
metabolic acidosis
uremic complications
drug overdoes - BLAST ME

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5
Q

TX OF acidosis

A

bicarbonate

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6
Q

tx of uraemia

A

dialysis

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7
Q

tx of pulmonary edema

A

respiratory support + furosemide to flush out

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8
Q

most common cause of AKI

A

pre- renal azotemia

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9
Q

what is pre- renal azotem divided into and examples

A

fluid responsive

fluid non responsive - HF, sepsis sometimes may not respond

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10
Q

what is pre- renal azotemia

A

rerenal azotemia refers to elevations in BUN and creatinine levels resulting from problems in the systemic circulation that decrease flow to the kidneys

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11
Q

when would we do a renal biopsy

A

when we exclude pre- renal and post renal and we suspect that there is a specific therapy we can do, e.g antibodies globular bm disease, vasculitit s, HUS

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12
Q

most common and serious complication of

AKI

A

infection either due to decreased defences or due to iatrigenic, catheters, ventilation support

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13
Q

signs of hyperkalemia

A

tall tented t waves, prolonged pR interval, short qt interval

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14
Q

normal urine output

A

up to 2000 ml a day

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15
Q

polyuria

A

> 3 L or 2 -double check

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16
Q

stages of AKI

A
  1. AKI - 2-3 days
  2. oligouric/anuric - 7 days - 10 days
  3. polyuria - 5/10 days
  4. recovery - 6-12 months
17
Q

causes of pre- renal

A 
sever vommitng/diarrhea
diabetes insipidus 
post partum hemmorgae 
hemmorgaic shock 
anaphylazis- widespread vasodilation 
hepatorenal syndrome (causes renal vasoconstriction)
drugs such as nSAIDS, calcineurin inhibitors , ACE (cause vasoconstriction) 
third spacing (pancreatitis)
hear failure , liver failure (edema)
18
Q

renal causes

A

pyelonephritis, hydronephrios,tubulointerstial injury,- caused by drugs glomerular injury, hUS

19
Q

OBSTRUCTIVE CAUSES

A 
can be intrinsic or extrinsic 
stones
bladder stenosis - marins disease 
posterior urtheral valve- 
strictures 
malignancy 
anitcholenergic agents 
neurogenic bladder

The most common cause for postrenal azotemia in men is prostatic conditions and in women gynecologic tumors, postoperative or post radiotherapy fibrosis.

20
Q

what happens if pre- renal hypoprefusion persist

A

Severe and prolonged hypoperfusion may result in tissue ischemia leading to acute tubular necrosis.

21
Q

how do we divide pre-renal azotemia

A

volume responsive and non volume responsive (cardiac, sepsis, cirrhosis)

22
Q

Compensatory mechanisms to preserve glomerular perfusion.

A

sympathetic feverous system - especially noradernelaine

RAAS-angiotensin which causes constriction of efferent preserving GFR .but in severe volume depletion it leads to afferent arteriolar constriction that reduces renal plasma flow and GFR.

23
Q

what can ace inhibitors worsen

A

in cases of heart failure of renal stenosis , where already the kidney is at risk, they further worsen the perfusion to kidneys

24
Q

risk factors for contrast induced neuropathy

and preventive methods

A

diabetic nephropathy
CKD
already having a hypo perfused state -
heart failure

relating tot he procedure

  1. using high osmolal agents (so to reduce the risk use low ones)
  2. large amount of contrast media

preventative - give them fluids before to increase the intravascular volume , stop Andy nephrotic drugs b4 hand which wouldd already impede blood flow

25
Q

pathiphys of contrast induced neuropathy

A

enal vasoconstriction leading to medullary hypoxia

toxic injury of tubular cells through direct cytotoxicity

26
Q

acute tubular necrosis

A

most common cells susceptible to AKI, especially proximal, usual cause ichecmia sepsis, lead to constriction of afferent

27
Q

causes of acute tubular injury

A

exogenous:
- antibiotics-
- chemotherapy
- calcineurin inhibitors
- snake venom
- radiocontrast media

Endo:
hemogloninuria
myoglobinuria 
uric acid
light chains
28
Q

intaluminal cast formation is associated with

A

endogenous - hemoglobinuria when you have intravascular hemolysis

29
Q

what needs to happen in order for post renal injury to be apparent

A

bilateral obstruction

or unilateral obstruction in one functioning kidney

30
Q

in AKI how can we dx between acute and chronic

A

measuring CREaTiniINE concentration over time - which is why if we don’t have previous, then we look for chronic signs of kidney dysfunction such as hyperparathyroidism,and small echogenic kidneys on us (but not always)

anemia not really helpful as often present in both

31
Q

which chronic diseases are characterised by increase in kidney size

A

diabetes
amyloidosis
HIV
PCKD

32
Q

in acute tubular necrosis what will the specific gravity of urine be

A

isothenuria at around 1.010

nephro (11 decks)

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