tc4 Flashcards
(65 cards)
what 3 substances can cause overestimation of GFR by serum creatinine levels?
ketoacids
cimetidine
trimethoprim
these competitively inhibit tubular Cr secretion
what 4 meds can cause prerenal aki by decreasing renal blood flow
NSAIDs
ACEI
ARBs
cyclosporine
is urine Na and bun/cr ratio high or low in prerenal AKI? why?
Na is low (<20). ratio is high aka >20:1. both bc RAAS
is urine Na and bun/cr ratio high or low in ischemic ATN? why?
Urine Na is high >40. ratio is normal. both bc damaged tubules are unable to reabsorb properly.
3 general mechanisms that contrast induces AKI
- constrict afferent arteriole and vasa recta -> lower GFR and blood flow to blood vessels
- high osmolality so kidney has to work harder -> raise O2 demand of kidney
- increase ROS, decrease antioxidants -> oxidative stress/damage
what do you give to patients before contrast to reduce risk of ATN AKI?
N-acetylcystine (antioxidant properties, promotes renal vasodilation) and isotonic saline (dehydration/low ECF is a risk factor)
in pigment nephropathy, filtered myoglobin precipitates with _____. causing tubular obstruction. what is the treatment for this?
precipitates with Tamm-Horsfall protein
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treat by alkalinizing urine. it decreases precipitation
rhabdomyolysis is what causes pigment nephropathy (the myoglobin and hemoglobin come out into blood from muscles). but what are causes of rhabdomyolysis that aren’t obvious? (2)
- hmg coa reductase inhibitor aka statins
2. alcohol and drugs (like cocaine)
whats that thing that you have coke/tea colored urine and strip test is positive for blood. but if you do microscopy there’s no red blood cells?
pigment nephropathy. it’s bc of the myoglobin/hemoglobin.
Serum creatinine peaks within how many days of contrast induced AKI? returns to normal by when?
peaks in 5 days. normal in 7-10 days
what can cause AKI without oliguria
aminoglycosides nephrotoxicity. it’s bc afferent arteriole constriction is not a major player in this pathophysiology so GFR isn’t as decreased as in other AKIs. but AGs do constrict mesangial cells which causes mild decrease in GFR
2 main mechanisms of AG nephrotoxicity
- constrict mesangial cells -> mildly lower GFR
- principal cells take up AGs very concentrated. reduces ability to concentrate urine -> urine osmolalitly 300-350 (same as in glomerulus/plasma basically)
what casts do you see or not see in PRERENAL AKI?
ONLY see hyaline casts! which are NORMAL. made of Tamm Horsfall proteins (which precipitate with myoglobin in pigment nephropathy btw)
what casts in urine for ischemic ATN?
muddy brown granular casts and tubular cell casts
what things and casts in urine for glomerulonephritis?
proteinuria, RBCs, and RBC casts
serum phosphate is regulated by renal reabsorption or secretion?
reabsorbtion
serum K+ is regulated by renal reabsorption or secretion?
secretiooonnnn. can increase secretion if hyperkalemia.
kidney dz patient on ACEI or ARB or K+ sparing diuretic is bad news -> hyperkalemia
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heart failure or liver failure pt on NSAID or ACEI or ARBs is bad news -> acute kidney injury
.
these are some important “pt has underlying condition and you put them on this drug and bad things happen” examples
moving on
synthesis of what amino acid by intact nephrons maintains elevated NH4+ urinary excretion in compensated CKD?
glutamine synthesis. idk why
which 2 mediators cause unregulated/fixed Na excretion in CKD? pg 432
NPs and PGE2
.
so if Na excretion > intake, pt will have orthostatic hypotension (hypovolemic state). if intake >excretion, pt will have edema and hypertension (hypervolemic state)
.
THIS IS NOT WHAT CAUSES HYPER OR HYPONATREMIA BC REMEMBER THAT’S A WATER BALANCE ISSUE, NOT NA+ even tho its all related what the heck
why does CKD continue to progress even if you remove initial insult/offender?
high SNGFR of intact nephrons = intraglomerular hypertension. this leads to hyperfiltration injury -> proteins deposited in mesangium and tubules (also NH4+, which activates alternative complement pathway, furthering inflammation and injury) -> glomerular sclerosis and tubular fibrosis = irreversible changes. GG.
bts this makes kidneys shrink so small shrunken kidneys are end stage CKD kidneys even tho in the beginning you have hypertrophic intact nephrons
in CKD you get LVH. which 2 things predisposes you to eccentric LVH? which one for concentric LVH?
eccentric: chronic anemia and volume overload (which you can both get from CKD)
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concentric: CKD related Hypertension. obvis, from CKD.
.
its a never ending cycle gah
bad things hyper PTH does.
- arterio/atherosclerosis
- neuro calcium overload -> polyneuropathy and encephalopathy
- bone bone disorders (osteitis fibrosa cystica)
guy has CKD, comes in with FEVER and PRECORDIAL CHEST PAIN that’s worse with breathing and laying down. what is it??
uremic pericarditis. +- pericardial friction rub +- cardiac tamponade (will then have pulsus and electrical alternans where QRS goes up and down, inverted, right way up again, back and forth)