AKI Flashcards
biochemical changes in AKI
hyperkalemia
hyocacemia
hyponatremia
how to treat hyperkalemia
Treat with – insulin (and dextrose), calcium gluconate, salbutamol, dialasis
nephrotoxic drugs
n saids, aminoglycosided
indications for dialysis (there’s more)
hyperkalmeia
metabolic acidosis
uremic complications
drug overdoes - BLAST ME
TX OF acidosis
bicarbonate
tx of uraemia
dialysis
tx of pulmonary edema
respiratory support + furosemide to flush out
most common cause of AKI
pre- renal azotemia
what is pre- renal azotem divided into and examples
fluid responsive
fluid non responsive - HF, sepsis sometimes may not respond
what is pre- renal azotemia
rerenal azotemia refers to elevations in BUN and creatinine levels resulting from problems in the systemic circulation that decrease flow to the kidneys
when would we do a renal biopsy
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
most common and serious complication of
AKI
infection either due to decreased defences or due to iatrigenic, catheters, ventilation support
signs of hyperkalemia
tall tented t waves, prolonged pR interval, short qt interval
normal urine output
up to 2000 ml a day
polyuria
> 3 L or 2 -double check
stages of AKI
- AKI - 2-3 days
- oligouric/anuric - 7 days - 10 days
- polyuria - 5/10 days
- recovery - 6-12 months
causes of pre- renal
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)
renal causes
pyelonephritis, hydronephrios,tubulointerstial injury,- caused by drugs glomerular injury, hUS
OBSTRUCTIVE CAUSES
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.
what happens if pre- renal hypoprefusion persist
Severe and prolonged hypoperfusion may result in tissue ischemia leading to acute tubular necrosis.
how do we divide pre-renal azotemia
volume responsive and non volume responsive (cardiac, sepsis, cirrhosis)
Compensatory mechanisms to preserve glomerular perfusion.
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.
what can ace inhibitors worsen
in cases of heart failure of renal stenosis , where already the kidney is at risk, they further worsen the perfusion to kidneys
risk factors for contrast induced neuropathy
and preventive methods
diabetic nephropathy
CKD
already having a hypo perfused state -
heart failure
relating tot he procedure
- using high osmolal agents (so to reduce the risk use low ones)
- 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
pathiphys of contrast induced neuropathy
enal vasoconstriction leading to medullary hypoxia
toxic injury of tubular cells through direct cytotoxicity
acute tubular necrosis
most common cells susceptible to AKI, especially proximal, usual cause ichecmia sepsis, lead to constriction of afferent
causes of acute tubular injury
exogenous:
- antibiotics-
- chemotherapy
- calcineurin inhibitors
- snake venom
- radiocontrast media
Endo: hemogloninuria myoglobinuria uric acid light chains
intaluminal cast formation is associated with
endogenous - hemoglobinuria when you have intravascular hemolysis
what needs to happen in order for post renal injury to be apparent
bilateral obstruction
or unilateral obstruction in one functioning kidney
in AKI how can we dx between acute and chronic
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
which chronic diseases are characterised by increase in kidney size
diabetes
amyloidosis
HIV
PCKD
in acute tubular necrosis what will the specific gravity of urine be
isothenuria at around 1.010
