AKI (see DM) Flashcards

1
Q

what are the 3 types of AKI

A
  1. pre renal
  2. renal
  3. post renal
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2
Q

what is the most common type of AKI

A

pre renal

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3
Q

what are the physiological responses seen in pre-renal AKI (4)

A

lower perfusion pressure = enhanced sodium and water re-absorption
1. Baroreceptors in the carotid artery and aortic arch respond to lower blood pressure with sympathetic stimulation
2. vasoconstriction of the glomerular efferent arteriole and dilation of the afferent arteriole -> maintainence of glomerular filtration within a relatively narrow range
3. Decreasing perfusion promotes activation of RAAS -> Angiotensin II, a potent vasoconstrictor, stimulates aldosterone release, promoting sodium and water reabsorption at the collecting duct
4. Low blood volume is also a stimulus to the hypothalamus promoting ADH release and increased tubular water re-absorption, concentrating the urine

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4
Q

when is renal replacement therapy (dialysis) indicated in AKI

A

AEIOU
A - Acidosis
E - Electrolyte abnormalities
I - Ingested toxins
O - fluid Overload
U - Uraemia

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5
Q

how can acute tubular necrosis result in AKI (3)

A
  1. Initiation: acute decrease in renal perfusion causing a reduced GFR
  2. Maintenance: GFR remains low for days or weeks
  3. Recovery: GFR recovers, regeneration of tubulointerstitial cells, polyuric phase may occur
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6
Q

why are tubular cells susceptible to necrosis

A
  1. limited blood supply
  2. high metabolic demand
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7
Q

aozetemia vs ueremia

A

azotemia - high levels of nitrogen in the blood (both urea and creatnine)
uremia - high urea levels in the blood

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8
Q

examples of uremia symptoms (11)

A
  1. nausea & vomiting
  2. fatigue
  3. anorexia + weight loss
  4. dysgeusia (bad taste in the mouth)
  5. chest pain + palpitations
  6. SOB
  7. muscle cramps
  8. restless legs
  9. pruritus
  10. easy bleeding
  11. mental status changes
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9
Q

hypovolemic causes of pre-renal AKI (5)

A

decreased renal blood flow due to:
1. acute hemorrhage
2. gastrointestinal losses (e.g. D&V)
3. renal losses- diuretics or osmotic diuresis in hyperglycemia
4. dermal losses- burns
5. sequestration of fluid (third-spacing) - e.g. acute pancreatitis or sepsis

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10
Q

2 types of pre renal AKI

A

hypovolaemic and hypervolaemic

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11
Q

examples of causes of hypervolaemic pre renal AKI (3)

A

low effective circulating volume
1. cardiorenal syndrome -> severe systolic heart failure leading to low Cardiac output
2. hepatorenal syndrome -> hypoalbuminemia from decompensated liver disease
3. drugs e.g. NSAIDs, ACE-inhibitors, ARBs, cyclosporine and iodinated contrast

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12
Q

what is the most common cause of intrarenal AKI

A

acute tubular necrosis

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13
Q

what can cause acute tubular necrosis (5) !!

A
  1. renal ischaemia (e.g. due to pre renal AKI)
  2. nephrotoxins
  3. glomerulonephritis
  4. acute interstitial nephritis
  5. renal artery stenosis/other vascular cause
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14
Q

examples of endogenous
nephrotoxins (4)

A
  1. myoglobin from damaged muscles (like in rhabdomyolysis)
  2. haemoglobin (massive haemolysis)
  3. myeloma (light chains)
  4. uric acid (tumour lysis syndrome)
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15
Q

examples of exogenous nephrotoxins (6)

A
  1. aminoglycosides antibiotics
  2. methotrexate
  3. heavy metals
  4. ethylene glycol
  5. radiocontrast dye (although it pt needs it, contrast should be used as AKI can be corrected)
  6. chemotheraputic agents (cisplatin)
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16
Q

what is acute interstitial nephritis

A

a type I or type IV hypersensitivity reaction, and is typically a response to a medication like NSAIDs, penicillin, and diuretics, such as thiazide diuretics, like chlorothiazide -> Early symptoms include fever and

17
Q

causes of post renal AKI (4)

A

obstruction to the outflow of urine from the kidneys
1. benign prostate hyperplasia
2. prostatic cancer
3. intra-abdominal tumors that compress the ureter
4. kidney stones (get stuck in the ureter or in the urethra) -> renal function is usually preserved if only one ureter is obstructed (unilateral obstruction), but if bilateral obstruction occurs, this can cause AKI

18
Q

what is BUN

A

blood urea nitrogen

19
Q

what does an high BUN:creatnine ratio indicate

A

kidney damage -> urea/nitrates not being filtered out properly

20
Q

what is the BUN to creatinine ratio in pre-renal AKI

A

usually 20:1 (high)

21
Q

what system is activated in pre renal AKI

A

RAAS - in order to try and increase renal perfusion

22
Q

what is the urine osmolality in pre renal AKI

A

> 500 mOsm/kg (aka concetrated urine) -> sodium and water are retained

23
Q

what is the urine osmolality in interstitial renal AKI

A

<500 mOsm/kg

24
Q

what is the urine osmolality in post renal AKI

A

<500 mOsm/kg if tubular damage, otherwise >500

25
Q

what is the BUN to creatinine ratio in post-renal AKI

A

less than 20:1 if tubules damaged, otherwise > 20:1

26
Q

what is AKI

A

a sudden decline in renal function over hours or days (<3 months), diagnosis based on creatnine levels and urine output

27
Q

what must be done after starting a pt on ACEi/ARBs

A

repeat bloods (U&Es) for 7 days after starting incase of AKI

28
Q

what is the classification used in AKI

A

kidney disease: improving global outcomes

29
Q

what are the stages of AKI

A

stage 1 - serum Cr >1.5x ref range; UO <0.5mL/kg/hr for 6 consecutive hours

stage 2 - sreum creatnine 2-2.9 x ref range; UO < 0.5mL/kg/hr for 12hrs

stage 3 - serums Cr x3 red range or on RRT; UO <0.3mL/kg/hr for >24hrs or anuria

30
Q

what are the 3 protective mechanisms of the renal system

A
  1. myogenic reflex
  2. tubuloglomerular feedback
  3. renin-angiotensin system
31
Q

risk factors for AKI (5)

A
  1. elderly
  2. arteriosclerosis
  3. pre exisiting renal condition
  4. CVD
  5. ACEi/ARB/NSAID etc. use
32
Q

2 types of post renal AKI

A
  1. intrinsic (stone, blood clot, bladder tumour etc.)
  2. extrinsic (prostate, pelvic etc.)
33
Q

indications for urgent dialysis (5)

A
  1. hyperkalemia resistant to treatment
  2. resistant pulmonary oedema
  3. uraemic (encephalopathy, pericarditis)
  4. acidosis
  5. drug overdose

AEIOU - acidosis, electrolyte imbalance, intoxications, overload (oedema), uremia