7/21/16 Flashcards
nephrotic syndromes associated with NSAIDs
minimal change disease and membranous nephropathy
tx for severe, symptomatic SIADH vs chronic SIADH
severe symptomatic: tolvaptan, conivaptan (ADH receptor antagonists)
chronic: demeclocycline (blocks action of ADH at collecting duct)
what happens if hyponatremia is corrected too quickly? hypernatremia?
hyponatremia corrected too quickly = central pontine myelinolysis/osmotic demyelinizaiton
hypernatremia corrected too quickly = cerebral edema
do ACE inhibitors cause hyper- or hypokalemia?
hyperkalemia (aldosterone decrease)
does acidosis cause hypo- or hyperkalemia and why?
acidosis causes hyperkalemia because cells will pick up hydrogen ions and release potassium ions in exchange
what three cardiovascular drugs cause hyperkalemia and how?
DIGOXIN and BETA BLOCKERS inhibit the sodium/potassium ATPase that normally brings potassium into the cells.
HEPARIN causes increased tissue release
tx for hyperkalemia causing EKG changes
calcium chloride or calcium gluconate (protects the heart, does not lower the potassium level), then sodium bicarbonate (alkalosis drives potassium into cells) and glucose with insulin
what should you consider when hypokalemia is not improving with normal supplementation?
hypomagnesemia can lead to increased urinary loss of potassium. there are magnesium-dependent potassium channels; when magnesium is low, they open and spill potassium into the urine. if magnesium is replaced, it will close up these channels and stop urinary loss.
two most important causes of metabolic acidosis with normal anion gap
renal tubular acidosis and diarrhea (normal anion gap because chloride levels rise. also referred to as hyperchloremic metabolic acidosis. anion gap increases with ingested substances or organic acids that are anionic and drive down the chloride level)
pathogenesis of distal (type I) RTA
distal tubule is responsible for generating new bicarbonate. drugs like amphotericin and autoimmune diseases damage the distal tubule. if new bicarbonate cannot be generated at the distal tubule, then acid cannot be excreted into the tubule. end result is ALKALINE URINE, which causes increased formation of calcium oxalate KIDNEY STONES.
pathogenesis of proximal (type II) RTA
normally 85-90% of filtered bicarbonate is reabsorbed at the proximal tubule. damage to the proximal tubules decreases the ability of the kidney to reabsorb bicarbonate. the end result is bicarbonate loss in the urine (ALKALINE URINE) until bicarbonate becomes so depleted that distal tubule absorbs the rest and no more bicarbonate is left to get into urine (ACIDIC URINE)
tx for proximal (type II) RTA
thiazide diuretics cause volume depletion. volume depletion will enhance bicarbonate reabsorption.
pathogenesis of type IV RTA
occurs most often in diabetes. decreased amount or effect of aldosterone at the kidney tubule, which leads to loss of sodium and retention of potassium and hydrogen ions. end result is a HIGH URINE SODIUM despite a sodium-depleted diet and NORMAL URINE PH.
most important distinction between type IV vs type I and type II RTA
type IV RTA causes HYPERKALEMIA whereas type I and type II have HYPOKALEMIA (potassium is lost in the urine)
tx for type IV RTA
fludrocortisone (steroid with the highest mineralocorticoid or “aldosteronelike” effect
what is the best way to distinguish between diarrhea and RTA when someone has non-anion gap metabolic acidosis?
urine anion gap (sodium minus chloride). positive in RTA (less chloride in urine because less acid in urine), negative in diarrhea (kidneys are still able to excrete acid and therefore chloride. diarrhea causes metabolic acidosis so kidneys try to compensate by excreting more acid)
what are the signs of ethylene glycol overdose? tx?
found in antifreeze (de-icing for windshields). anion gap metabolic acidosis, oxalic acid cystals on UA. tx is fomepizole
sx and tx of methanol overdose
sx: inflamed retina, anion gap metabolic acidosis
tx: fomepizole
tx of salicylate overdose
aspirin overdose (anion gap metabolic acidosis) is treated with urine alkalinization
3 major causes of metabolic alkalosis
vomiting, loop/thiazide diuretics, increased aldosterone
relationship between Crohn disease and kidney stones
Crohn disease causes kidney stones because of increased oxalate absorption
what are is the tx for kidney stones 5-7mm? 7mm-2cm?
5-7mm: nifedipine and tamsulosin to help them pass
7mm-2cm: lithotripsy
relationship between metabolic acidosis and calcium
chronic metabolic acidosis leaches calcium out of bones and they become soft (osteomalacia). it also increases stone formation by increasing calcium in circulation and decreasing citrate (citrate normally binds calcium, making it unavailable for stone formation)
best initial therapy for HTN in pts with coronary artery disease
beta blockers, ACE, ARB
best initial therapy for HTN in pts with depression or asthma
avoid beta-blockers
when should you suspect retroperitoneal fibrosis as the cause of postrenal failure?
history of methysergide (migraine prophylaxis), bromocriptine (dopamine agonist used in Parkinson’s, hyperprolactinemia, NMS), methyldopa, or hydralazine use
tx for AKI caused by myoglobinuria/rhabdomyolysis
hydration and diuretics
what medications commonly cause renal insufficiency or failure?
chronic NSAID use (acute tubular necrosis or papillary necrosis), cyclosporine, aminoglycosides, and methicillin
young man with hemoptysis, dyspnea, and renal failure. what is the dx and tx?
goodpasture’s syndrome, steroids and cyclophosphamide
two important associated sx of polycystic kidney disease
berry aneurysms in circle of Willis and cysts in liver
what happens to the levels of phosphate in chronic kidney disease?
hyperphosphatemia. phosphate is normally excreted through kidneys. high PTH (due to low calcium due to low activated vitamin D) causes phosphate release from bones, but THE BODY IS UNABLE TO EXCRETE IT!
abx for uncomplicated pyelonephritis
IV ceftriaxone or fluoroquinolone
similarities between HUS and TTP
both are caused by deficiency of metalloproteinase ADAMTS 13 activity (normally cleaves vWF, so loss causes increased platelet adhesions to sites of endothelial injury). both have normal PT and PTT, intravascular hemoylsis, thrombocytopenia, and renal insufficiency.
unique features of TTP that distinguish it from HUS
caused by antibody-mediated inactivation of ADAMTS 13 (in HUS, Shiga toxin binds and inactivates the same enzyme), seen in young adults (not children), associated with HIV, cancer, and drugs (cyclosporine, ticlopidine, clopidogrel), causes neurological sx and fever, treated with plasmapheresis
tx for SIADH if water restriction fails
demeclocycline (induces nephrogenic diabetes insipidus [as in, decreased sensitivity to ADH in tubules])
how do you calculate the sodium correction in pts with hyperglycemia?
once glucose is above 200 mg/dL, add 1.6 mEq/L to reported sodium level for each rise of 100 mg/dL in glucose (hyperglycemia causes FALSE HYPONATREMIA)
EKG findings of hypokalemia
flattening of T wave, presence of U waves, premature atrial and ventricular complexes, and ventricular and atrial tachyarrhythmias
what electrolyte imbalance causes tetany?
hypocalcemia
how do you calculate the calcium correction in pts with hypoproteinemia?
for every 1 g/dL decrease in albumin below 4 g/dL, correct the calcium by adding 0.8 mg/dL to the given calcium value (hypoproteinemia causes a FALSE HYPOCALCEMIA)
short fingers, short stature, mental retardation, hypocalcemia with normal levels of PTH
pseudohypoparathyroidism (end-organ unresponsiveness to PTH)
how does acute pancreatitis affect calcium levels?
hypocalcemia. severe pancreatic damage decreases lipase production/release leading to fat malabsorption in the gut. calcium binds with fat in the bowel (saponification), leading to calcium malabsorption. low calcium is associated with the worst prognosis in pancreatitis (not amylase or lipase levels)
describes what happens when a hyperventilating pt develops perioral and extremity tingling
alkalosis drives calcium into cells, so hyperventilation causes elimination of too much CO2 leading to respiratory alkalosis, which causes calcium to go into cells and leads to hypocalcemia sx
in what clinical scenario is hypomagnesemia usually seen?
alcoholism. magnesium is wasted through the kidneys
what are the sx of hypermagnesemia that you should look out for when treating preeclampsia?
loss of deep tendon reflexes first, followed by hypotension, followed by respiratory failure
maintenance fluids for adult pts who are not eating
half normal saline with 5% dextrose with potassium chloride
medications that can cause acute pancreatitis
diuretics, antiseizure drugs (valproic acid), abx (metronidazole)
what are the important renal effects seen in CHF?
activation of RAAS and production of angiotensin II causes net decrease in renal blood flow and preferential vasoconstriction of EFFERENT renal arterioles (to maintain GFR)
what are the diagnostic criteria for aspirin exacerbated respiratory disease (AERD)?
- asthma
- chronic rhinosinusitis with nasal polyposis (leading to anosmia and recurrent nasal discharge/congestion)
- bronchospasm or nasal confestion following the ingestion of aspirin or NSAIDs
what should you consider in a diabetic pt who develops community-acquired PNA and prerenal azotemia?
STOP METFORMIN!! metformin can cause LACTIC ACIDOSIS in acute kidney injury and sepsis and should be withheld until renal function improves!
what is a contraindication to the use of succinylcholine for rapid-sequence intubation?
hyperkalemia
normal JVP (in cm above sternal angle)
less than 3 cm above sternal angle
what is the only shock that causes high mixed venous oxygen saturation?
septic shock
what is the only shock that causes increased cardiac index?
septic shock
what happens to preload and afterload in cardiogenic shock?
both are increased
what dx should be suspected in an otherwise healthy pt who develops sudden onset congestive heart failure a few weeks after URI?
dilated cardiomyopathy secondary to acute viral myocarditis (typically via Coxsackie B)
what are 3 organisms that can cause prolonged (longer that 2 weeks) traveler’s diarrhea?
more likely parasitic, esp Cryptosporidium, Cystoisospora, Giardia
what organism associated with travel can cause bloody diarrhea and pseudoappendicitis?
campylobacter
what dx should be suspected in a diabetic who complains of sudden monocular vision loss with ophthalmoscope findings of loss of fundus details, floating debris and dark red glow?
vitreous hemorrhage (most common cause is diabetic retinopathy)
what dx should be suspected in a pt with a history of hypertension who complains of sudden monocular vision loss with ophthalmoscope findings of disk swelling, venous dilation and tortuosity, retinal hemorrhage, and cotton wool spots?
central retinal vein occlusion
sx of digoxin toxicity, what can precipitate it
nausea, vomiting, decreased appetite, confusion, weakness, visual sx of blind spots, blurry vision with changes in color, or blindness. inciting events: viral illness or excessive diuretic use can lead to volume depletion or renal injury that acutely elevates digoxin level. hypokalemia caused by loop diuretics can also increase susceptibility.
medication for cancer-related anorexia/cachexia syndrome
progesterone analogs (megestrol acetate and medroxyprogesterone acetate)
