AKI (see DM) Flashcards
what are the 3 types of AKI
- pre renal
- renal
- post renal
what is the most common type of AKI
pre renal
what are the physiological responses seen in pre-renal AKI (4)
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
when is renal replacement therapy (dialysis) indicated in AKI
AEIOU
A - Acidosis
E - Electrolyte abnormalities
I - Ingested toxins
O - fluid Overload
U - Uraemia
how can acute tubular necrosis result in AKI (3)
- Initiation: acute decrease in renal perfusion causing a reduced GFR
- Maintenance: GFR remains low for days or weeks
- Recovery: GFR recovers, regeneration of tubulointerstitial cells, polyuric phase may occur
why are tubular cells susceptible to necrosis
- limited blood supply
- high metabolic demand
aozetemia vs ueremia
azotemia - high levels of nitrogen in the blood (both urea and creatnine)
uremia - high urea levels in the blood
examples of uremia symptoms (11)
- nausea & vomiting
- fatigue
- anorexia + weight loss
- dysgeusia (bad taste in the mouth)
- chest pain + palpitations
- SOB
- muscle cramps
- restless legs
- pruritus
- easy bleeding
- mental status changes
hypovolemic causes of pre-renal AKI (5)
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
2 types of pre renal AKI
hypovolaemic and hypervolaemic
examples of causes of hypervolaemic pre renal AKI (3)
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
what is the most common cause of intrarenal AKI
acute tubular necrosis
what can cause acute tubular necrosis (5) !!
- renal ischaemia (e.g. due to pre renal AKI)
- nephrotoxins
- glomerulonephritis
- acute interstitial nephritis
- renal artery stenosis/other vascular cause
examples of endogenous
nephrotoxins (4)
- myoglobin from damaged muscles (like in rhabdomyolysis)
- haemoglobin (massive haemolysis)
- myeloma (light chains)
- uric acid (tumour lysis syndrome)
examples of exogenous nephrotoxins (6)
- aminoglycosides antibiotics
- methotrexate
- heavy metals
- ethylene glycol
- radiocontrast dye (although it pt needs it, contrast should be used as AKI can be corrected)
- chemotheraputic agents (cisplatin)