Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
|
In acute Tubular Necrosis (ATN), do patients get increased or decreased release of renin and why?
|
decreased!
Necrotic tubules cannot maintain ion balance and dump Sodium and electrolytes into the tubular lumen. The macula densa senses higher concentrations of NaCl and thus releases less renin from the juxtaglomerular cells in the walls of the afferent arteriole. |
|
|
In tubular necrosis, does the body increase or decrease the GFR and what's the mechanism?
|
DECREASE!
Too much NaCl delivery to the macula densa decreases angiotensin II constriction of the efferent arteriole, increases release of vasodilatory prostaglandin and NO mediators and decreases vasoconstricting adenosine agents |
|
|
Does ATN cause obstruction? If so, how?
|
YES
epithelial cells are deaquamated and form casts that obstruct the tubule lumen |
|
|
What kind of casts are seen in the urine of ATN patients? What is the cast made of? Where do these thingies come from?
|
muddy brown casts composed of Tamm-Horsfall protein - a glycoprotein made in the DCT and thick ascneding limb of henle
|
|
|
What's the difference in tubular necrosis between ischemia and toxic substances?
How is it similar? |
Ischemic tubular necrosis shows patchy areas of necrosis in the ascending thick limb and DCT.
Toxic ATN shows a more uniform necrosis |
|
|
People poisoned with ethylene glycol tend to form what?
|
calcium oxalate crystals
|
|
|
3 phases of ATN
1) initiation 2) maintenance 3) recovery what defines them? |
1) initiation - 36 hours defined by a slight drop in urine output and slight azotemia
2) maintenance - HYPERKALEMIA caused by Na+/K+ flipping onto the apical membrane do to cellular damage. There's a metabolic acidosis due to the hyperkalemia. Obstruction can occur and azotemia progresses 3) recovery - tubules are repaired and the Na+/K+ ATPase pump flips back over and HYPOKALEMIA |
|
|
What's one of the best indicators for ATN?
- what conditions give a really crappy prognosis? |
if there's no oliguria - that's a good sign
severe burns, sepsis, and multiple organ failure patients have < 50% chance to survive |
|
|
most common cause of pyelonephritis?
Other big players? |
E coli
Proteus, Klebsiella, and enterobacter (or is it coccus?) |
|
|
What kind of inflammation is seen in acute pyelonephritis?
|
suppurative i.e. neutrophilic infiltrate
- in chronic you'll get a mononuclear infiltrate |
|
|
What pathogen is an emergent cause of pyelonephritis in allografts?
|
ADENOVIRUS!
|
|
|
5 risks for pyelonephritis
|
1) preexisting renal lesion
2) catheterization 3) pregnancy (from obstruction) 4) diabetes mellitus 5) immunosuppression |
|
|
what two interstitial diseases affect the calyces?
|
analgesic nephropathy and chronic pyelonephritis
|
|
|
this disease appears as "thyroidization" of the renal parenchyma
|
xanthogranulomatous pyelonephritis
|
|
|
this disease is characterized by large yellowish orange nodules that can easily be confused with renal cell carcinoma
|
xanthogranulomatous pyelonephritis
|
|
|
abuse of analgesics leads to what kind of cancer?
|
urothelial cell carcinoma of the renal pelvis
|
|
|
what chemical is present in herbs that gives Chinese Herb nephropathy?
What kind of disease process is this? |
aristocholic acid
its an interstitial nephritis that leads to interstitial fibrosis |
|
|
Uric acid nephropathy is common in what population of patients?
does a low or high urine pH precipitate crystals? - what about staghorn stones? |
leukemia patients undergoing chemo. Release of nucleic acid purines are converted to uric acid.
A low urine pH precipitates urate crystals a high urine pH precipitates magnesium ammonium sulfate |
|
|
birifringent needles found in tubular interstitium
|
chronic urate nephropathy
|
|
|
what are the 3 renal problems associated with multiple myeloma
|
1) bence jones proteinuria / castnephropathy
2) light chain deposition disease - light chains damage the glomeruli (directly toxic) 3) amyloidosis |
|
|
how can you distinguish prerenal renal failure from ATN?
|
give pt fluids and see if their condition improves over 1-2 days. If so it was prerenal!
If azotemia continues then you know you're dealing w/ acute tubular necrosis |
|
|
what BUN / creatinine ratio is present when you've got a prerenal azotemia vs. ATN?
- |
BUN/creatinine is ~20:1 when prerenal because when angiotensin is released, the BUN reabsorbtion is increased in the proximal tubule but not creatinine (recall creatinine is neither reabsorbed nor secreted for the most part like inulin)
|
|
|
How can Fractional excretion of Na be used to tell prerenal aotemia from ATN?
|
when FENa is < 1% you're dealing with something prerenal because not enough of the ardiac output is getting the the nephrons to excrete Sodium. If FENa is > 3% you know you're dumping Na+ into the urine from ATN!
|
|
|
is the urine of an ATN or prerenal patient more concentrated?
|
Probably the prerenal patient even though there is considerble overlap. ATN patients lose functionality of the medullary collecting duct cells which are responsible for aquaporin mediated reabsorption of water. prerenal patients still have can aquaporin function and thus concentrate urine more.
|
|
|
Hepatorenal syndrome
- what kills patients? - what will the BUN/creatinine ratio be like? - what's the pathogensis of hepatorenal syndrome starting from liver failure? |
- encephalopathy and variceal bleeding rather than renal failure
- normal! Creatinine concentration in the plasma will be elevated because of renal failure. However, the BUN will also be elevated because the liver that is in charge of ammonia production is cirrhotic can't produce ammonia to get rid of the nitrogen! So the ratio looks normal. Liver failure leads to a paradoxical splanchnic vasodilation (digestive tract). Hypoperfusion of the kidneys leads to even more constriction of the renal artery from angiotensin II exacerbating the ischemia. |
|
|
Why are ACE inhbitors often prescribed to patients with bilateral renal artery stenosis?
Why is this the worst idea ever? |
Because they are hypertensive!
The angiotensin II is keeping their efferent arterioles constricted so they've got some semblance of a GFR. If you remove the angiotensin with an ACE inhibitor you'll kill their GFR - though you may lower their blood pressure a little bit :) |
|
|
Why do you NEVER give a renal failure patient NSAIDs?
|
NSAIDs inhibit prostaglandins which keep the kidney arteries dilated just enough so the nephrons don't become necrotic. If you knock out prostaglandin synthesis with NSAIDS you're setting them up for kidney failure!
|
|
|
what drug is a big cause of acute tubular necrosis?
- what's the pathogenesis? - is the onset of AMG nephropathy immediate or delayed? - is the onset of NSAID or analgesic nephropathy immediate or delayed? |
Aminoglycosides (also penicillin and rifampin)
AMGs build up in tubular epithelial lysozomes and inhibit the lysozomes from breaking down other toxic chemicals. onset of AMG induced neprhropathy is DELAYED onset of NSAID or ANALGESIC nephropathy is IMMEDIATE! |
|
|
How can contrast dye induce ATN?
|
it's directly toxic to the tubules because of generation of free radicals.
|
|
|
adult polycystic kideny disease genes found on what chromosome?
|
short arm of 16
|
