week 11 patho Flashcards
(50 cards)
what are some v basic characteristics of AKI
abrupt decline in kidney function, with elevated serum creatinine and reduction in urine output
how high will creatinine be with an AKI
1.5 times their baseline
what are the three main patient groups at risk for developing an AKI
patients with infections
patients with low BP (because kidneys aren’t being perfused)
patients exposed to nephrotoxins
how does sepsis cause an AKI
widespread vasodilation will lower BP, which decreases perfusion to the kidneys, also antibiotics used to treat sepsis are bad for the kidneys
what are the three types of AKI
1) pre renal
2) intra renal (intrinsic)
3) post renal
what are three causes of pre renal AKI
hypovolemia: decreased perfusion to kidneys
altered peripheral vascular resistance: ex. sepsis, anaphylaxis
cardiac disorders which ultimately lower CO and BP
bacically all have to do with decrease in glomerular filtration and BP
what are 5 causes of intra renal AKI
prolonged ischemia
nephrotoxic drugs
organic solvents like ethylene glycol
acute hemolysis or rhabdomyolysis
acute glomerulonephritis (inflammation of glomerulus)
how does acute hemolysis and rhabdomyolysis cause intra renal AKI
breakdown of these produces a substance called He which is nephrotoxic
what are the main nephrotoxic drugs
ahminoglycosides! anything that ends with -mycin
tobramycin
streptomycin
what are some examples of post renal factors of AKI
Kidney stones
enlarged prostate
urethra scarring
basically anything that affects urine leaving the kidneys and going down the urinary tract (gets all clogged up)
what is azotemia
less waste excreted in the kidneys
what happens inside the nephron during a pre renal AKI
- decreased blood flow disrupts balance of pressure in glomerulus
- glomerular hydrostatic pressure is lost as it drops
- decrease in overall GFR
- kidney activates raas to compensate, not enough to maintain GFR so you get oliguria and azotemia
what do casts in urine indicate
it means cells are dying which indicates intratubular damage
what is happening in the nephron during an intrarenal AKI
- lack of blood flow injures tubules
- causes inflammation, swelling, and loss of fx
- when epithelial cells die, they sluff off and get clogged in renal tubules
- this obstructs movement of filtrate and increases intratubular pressure
what is happening in the nephron during a post renal AKI
physical obstruction of outflow of urine leads to increased pressure in glomerulus and overall decreased GFR
what is an early intervention for a pre renal injury AKI
normalising BP
what is an early intervention for a post renal AKI
removing obstruction
what happens if you don’t intervene for a pre renal or post renal AKI
you get an intra renal injury
what are the three phases of an intra renal AKI
initiation, maintenance, recovery
what happens during initiation phase of infrarenal AKI
what sx do you see
increased Cr and BUN, decreased urine output
what happens during maintenance phase of an intrarenal AKI
- urine output
- body fluid
- acid/base balance
- electrolytes
-you see a drop of urine output by 10-14 days
-you see fluid retention which includes hypertension, edema, and weight gain
-you see metabolic acidosis
and electrolyte imbalance (low Na, high K, low Ca, high PO4)
- you see anemia
what do you see in the recovery phase of an intra renal AKI
Diuretic phase, hyponatremia and hypokalaemia,
how long does the kidney typically take to stabilise after an intrarenal AKI
12 months
what are the top 3 priorities a nurse would have when caring for a patient in the maintenance phase of ATN
1) fluid balance, make sure they aren’t hypovolemic
2) monitor acidosis
3) monitor EKG d/t high potassium
