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WEEK 4:
Acute kidney failure: why when and how:
| Question | Answer |
|---|---|
| normal GFR range | between 60 and 120ml/min/1.73^2 |
| person with GFR of 100ml/min/1.73^2 produces how much filtrate a day | 144L/day (142L reabsorbed) |
| acute kidney injury (AKI) | sudden loss of function within hours, days, or weeks and is often largely reversible once healing has occurred |
| acute kidney disease | severe recurrent or persistent acute injury and can lead to CKD |
| glomerulonephritis (GN) | when glomerular damage leads to loss of integrity of glomerular basement membrane resulting in blood and/or protein leaking into urine |
| types of glomerulonephritis (GN) | acute or chronic where some are treatable or not |
| chronic kidney disease | slow loss of function over months or years associated with scarring which is irreversible |
| untreated or untreatable GN may lead to | CKD |
| some forms of GN can cause | AKI that may be treatable or self limiting |
| definition of AKI | abrupt deterioration of renal function sudden onset, present for less than 3 months often reversible - common medical problem |
| features of acute kidney injury (AKI) | oliguria, electrolyte imbalance, and rapidly rising blood urea |
| describe oliguria | production of small amounts of urea (less than 400ml) |
| describe electrolyte imbalance | |
| describe rapidly rising blood urea | |
| causes of AKI (3) | pre-renal (reduction in renal perfusion), intrinsic kidney damage (Damage to kidney tissue resulting in sudden loss of function), and post-renal (blockage to outflow of urine) |
| explain pre-renal causation of AKI | shock experienced due to reduced perfusion of tissue which results in impaired oxygenation of tissue |
| prerenal causation of AKI causes (4) | Bleeding, Burns, Sepsis, Dehydration (hypovolaemia) Heart failure (also a type of shock cardiogenic) Sepsis Anaphylaxis |
| prerenal causation of AKI treatment | |
| things that can cause damage to kidney (but can be reversible if treated early enough) (3) | toxic drugs, autoimmune diseases, and allergies |
| nephrotoxics (toxic drugs to kidney) include | penicillins, cephalosporins, sulfonamides, thiazide diuretics, furosemide, NSAIDs and rifampicin |
| example of drugs causing direct toxicity to renal tubules (cute tubular necrosis) (3) | aminoglycosides, amphotericin, and ciclosporin |
| slide 12 | |
| post renal causes of AKI include (3) | stones, enlarged prostate gland, and pelvic cancers |
| how to determine how severe a patients AKI is | look at changes in serum creatinine or drop in urine output |
| slide 16 - table | |
| name for opposite of oliguria | |
| anuria | minimal to no urine output <100mL/day |
| acute tubular necrosis (ATN) | |
| pathophysiology of acute tubular necrosis | |
| ischaemic acute tubular necrosis (ATN) | ischaemia damages tubal cells, dead cells dont produce natural vasodilators NO/ PGI2 causing detachment of tubular cells into lumen causing obstruction |
| differences pre-renal AKI vs ATN |
Created by:
22tango
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