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ICC3 > acute kidney injury > Flashcards

acute kidney injury Flashcards

1
Q

what is AKI ?

A

a rapid deterioration of kidney function , which is a clinical consequence and not a diagnosis and is usually reversible
falling urine output
rising serum urea and creatinine

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2
Q

what do the causes of AKI fall into ?

A

pre renal causes ( reduced kidney perfusion )
renal causes or intrinsic causes
post renal causes

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3
Q

what are some of the pre renal causes of AKI ?

A

hypovolemia
hypotension
reduced kidney blood flow
severe oedema

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4
Q

which patients are at higher risk of developing pre renal AKI ?

A

older patients
atherosclerotic patients
diabetics
patients with pre existing kidney disease

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5
Q

what are the causes of hypovolemia ?

A

shock

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6
Q

what are the causes of reduced kidney blood flow ?

A

NSAIDs
ACE inhibitors
angiotensin II receptor blockers
abdominal aortic aneurysm

ace inhibitors

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7
Q

what effect do ace inhibitors have on the kidneys?

A

they inhibit efferent vasoconstriction

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8
Q

what effect do NSAIDs have on the kidneys ?

A

NSAIDs inhibit prostaglandins which in turn allow for afferent vasodilatation

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9
Q

what are the causes of renal AKI ?

A 
glomerular disease which can either be :
inflammatory or thrombotic 
tubular injury 
interstitial injury 
vascular injury
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10
Q

what are the causes of post-renal AKI ?

A

intrinsic and extrinsic

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11
Q

what are the intrinsic causes of post renal AKI ?

A

stone
blood clot
papillary necrosis

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12
Q

what are the extrinsic causes of post renal AKI ?

A

prostatic hypertrophy/malignancy
pelvic malignancy
retroperitoneal fibrosis

retroperitoneal fibrosis

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13
Q

what does acute tubular necrosis happen as a result off ?

A

any pre renal cause of AKI that reaches a point where autoregulation is no longer working - this will most probably lead to ischemic ATN

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14
Q

what are the four phases of AKI ?

A

onset phase
oliguric phase
diuretic phase
recovery phase

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15
Q

when does the diuretic phase of AKI happen ?

A

when the cause of the AKI is corrected

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16
Q

what is the clinical picture of each of the causes of AKI ?

A
  1. pre-renal causes - evidence of dehydration and hypovolemia , low BP and a rapid pulse
  2. post renal causes - evidence of renal colics with acute onset anuria and hematuria
  3. renal cause - history of nephrotoxic drugs intake, sepsis
17
Q

what are the lab findings commonly found with hypovolemia ?

A

high levels of ADH , increased secretion from the pituitary gland
disproportionate rise in the plasma urea:creatinine ratio

disproportionate rise in plasma urea: creatinine ratio

18
Q

how would we differentiate between AKI and CKD using US ?

A

CKD shows a shrunken kidney
except in patients with diabetes- who have normal sized kidneys even in disease

19
Q

what investigation clues could indicate glomerulonephritis ?

A

hematuria
proteinuria
RBC casts

20
Q

in what cases may we find eosinophilia ?

A

acute interstitial nephritis
cholesterol embolism
vasculitis

21
Q

what does thrombocytopenia suggest ?

A

thrombotic microangiopathy

22
Q

what is the management for AKI ?

A

conservative management

23
Q

what is the management for hyperkalemia ?

A

urgently obtain a 12 lead ECG

  • – if k> 7mmol give 10ml of 10% calcium gluconate IV and monitor every 10 minutes
  • – if k>6.5mmol 10 units of actarapid in 100 ml of 20% dextrose over 15 minutes
  • – if 6-6.5 mmol give calcium resonium 15g along with laxatives
24
Q

what is the management for acidosis ?

A

consider giving 300-600 ml of isotonic sodium bicarbonate if venous bicarbonate is <22 mmol

25
Q

what is the management for pulmonary oedema ?

A

give high flow oxygen
if haemodynamically stablee give furosemide

if haemodynamically stable give furosemide

26
Q

if pulmonary oedema is very severe what is the best step in management ?

A

haemodialysis

haemofiltration

27
Q

what are the indications of dialysis in AKI ?

A

1- persistent hyperkalemia
metabolic acidosis
volume overload (pulmonary oedema) that are not responding to treatment
2- uremic manifestations
3- fear of volume overload
4- toxin induced AKI

28
Q

what is the mechanism of autoregulation of blood flow in the kidney ?

A

in cases of reduced blood flow to the kidney :
afferent vasoconstriction occurs by prostaglandins
efferent vasodilation occurs by action of angiotensin II

29
Q

what is the clinical application off the autoregulation mechanism ?

A

NSAIDs inhibit prostaglandins which in turn inhibit vasodilation of the afferent arteriole

ACE inhibitors or ARBs inhibit angiotensin II which in turn inhibits the vasoconstrictive effect on the efferent arteriole

both mechanisms may be overcome by hypovolemia

kol dah under the umbrella off pre renal AKI

30
Q

what is the cut off value in which autoregulation cannot be maintained ?

A

70 mmHg

31
Q

what is oliguria ?

A

urine output less than 400 ml

32
Q

what is theRIFLE criteria

A

risk
injury
failure
loss
end stage
uses an increase in serum creatinine or a decrease in urine output

33
Q

which stage ar RRT patient considered to be at according to the AKIN criteria ?

A

stage 3

34
Q

what are the LUTS ?

A

hesitancy
frequency
nocturia
palpable bladder
complete anuria

35
Q

what do different measures of urea:creatinine ratio indicate ?

A

BUN:C of more than 20:1
or
U:C of more than 40:1 is indicative of pre-renal causes off AKI

ratios more than those indicate renal causes - renal tubular acidosis

36
Q

What are the indications for a renal biopsy?

A

1: unexplained urine abnormalities
2: persistent ATN for more than 4 weeks
3: unclear etiology
4: suspicion of systemic disease

37
Q

What are the characteristic findings in the urine analysis of drug-induced nephritis?

A

proteinuria
eosinophilia

38
Q

bilateral crepitatiions in a patient with AKI ?

A

pulmonary oedema due to volume overload

39
Q

what is the calcium homeostasis like in CKD ?

A

hypocalcemia
hyperparathyroidism

ICC3 (66 decks)

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