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;
47 Cards in this Set
- Front
- Back
Acute kidney injury classification |
1) oliguric (<400cc/24 hrs) worse prognosis can give them fluid challenge to convert from oliguric --> non-oliguric 2) non-oliguric (>400cc/24 hrs) |
|
Prerenal vs intrarenal |
BUN/creatinine ratio pre-renal: >20 urine Na will be very low intra-renal: 10 urine Na can be high (indicates tubular injury) |
|
Glomerulonephritis |
has RBCs in urine can be described as dysmorphic RBCs or erythrocyte casts order following Abs: dsDNA, ANA, antistreptolysin O, HIV serology, complement level, cryoglobulins, p-ANCA (microscopic PAN), c-ANCA (Wegener's), anti-GBM |
|
Chronic kidney issues on u/s |
will find small kidneys normal size kidneys on u/s indicate an acute process |
|
Reasons for dialysis |
refractory hyperkalemia profound metabolic acidosis AMS refractory fluid overload uremic pericarditis (BUN consistently >100) |
|
Acute tubular necrosis |
minimal proteinuria with muddy brown casts can be due to drugs (eg NSAIDs) cannot hold onto Na so urine Na will be high |
|
Acute interstitial nephritis |
allergic reaction eosinophilia, eosinophiluria w/ or w/o rash may or may not have eosinophils but must have WBC casts in urine hx of prior catheterization p/w AKI --> chol emboli & look for violaceous reticular rash or livedo reticularis should do urine cx to r/o pyelo bc of WBC in urine |
|
Enlarged kidneys on u/s |
obstructive uropathy diabetes amyloidosis HIV nephropathy polycystic kidney disease |
|
Hyperphosphatemia and hypocalcemia |
can be seen in pts with CKD tx hyperphosphatemia with calcium acetate, calcium carbonate, or sevelamer hypocalcemia bc of vitamin D def (low 1,25 Vit D) |
|
Lowering K+ |
sodium polystyrene sulfonate (Kexellate) also lowers K+ insulin (with glucose or HCO) will transport K+ intracellular thereby reducing serum K+ --> most rapid way of lowering K+ very high K+ with EKG changes --> CaCl or Ca gluconate IV with insulin |
|
Essential HTN |
need 3 independent visits with BP >140/90 or 1 reading of >160/100 single high reading does not warrant medication 6 months of diet, exercise, reduced etoh then if no improvement --> medication (diuretic first then add ACEI, ARB, or CCB) |
|
BP goals |
<140/90 if >160/100 --> start with 2 meds (diuretic + ACEI) if >140/90 and diabetes --> start with 2 meds |
|
b-blocker side effects |
depression memory loss impotence fatigue may mask Sxs of hypoglycemia in diabetics Raynaud phenomenon & can worsen PVD |
|
ACE inhibitors |
first choice for: DM CHF previous MI chronic renal failure with proteinuria use in any pt with nephrotic syndrome contraindicated in: hyperkalemia pregnancy b/l renal artery stenosis |
|
Hypertensive urgency vs emergency |
urgency: >180/120 with NO end organ damage (aSx) cont home meds if not on meds, observe, reduce with ACEI in office, then d/c with 2 meds emergency: >180/120 with end organ damage (eg SOB, chest pain, encephalopathy, retinopathy, AKI) admit, IV b-blocker, CCB, diuretics, or nitroglycerin |
|
Left ventricular hypertrophy on EKG |
S wave in V1 & R wave in V5 >35mm |
|
W/u of suspected renal artery stenosis |
duplex u/s of renal artery Magnetic resonance angiography renal artery arteriography (gold standard) |
|
Tx of renal artery stenosis |
balloon angioplasty repeat angioplasty if first fails surgical repair if angioplasty not possible or effective tx with ACEI if angioplasty doesnt work & surgery is not an option ONLY in unilateral renal artery stenosis |
|
Causes of renal artery stenosis |
fibromuscular dysplasia young woman <30 atherosclerotic dz older male |
|
Serum osmolality vs urine osmolality |
major osmoles in serum are glucose and Na increase in urine osmolality in euvolemic & hyponatremic pt --> too much ADH ADH --> increases urine osmolality if no reason for high ADH (dehydration, bleed, liver failure, etc) --> high urine osmolality (>100) indicates SIADH |
|
Causes of hyponatremia |
hypovolemic: addison dz GI losses burns diuretic use with free water intake euvolemic: SIADH psychogenic polydipsia hypothyroid hypervolemic: CHF nephrotic syndrome cirrhosis |
|
Causes of SIADH |
pulmonary small cell carcinoma CNS neoplasm medications SSRI |
|
Tx of SIADH |
mild (Na >120): restrict water severe (Na <120): give saline and diuretic emergent level (Na <110) or severe sxs (coma or seizures): hypertonic saline if Na rises too fast --> central pontine myelinolysis if Na is lowered rapidly --> cerebral edema |
|
Kidney stone |
tx with hydration until it passes if >5cm or hydration doesnt work, need to remove with intervention bc cant pass it (eg shock wave lithotripsy) renal u/s is almost 100% sensitive for stones in kidney (but not if in ureter) but best imaging test is abd CT after stone passes, need to fig out why stone formed most common is Ca stones and less common uric acid --> serum Ca and uric acid + 24hr urine Ca, oxalate, citrate, uric acid, Mg, Phos |
|
Kidney stone composition |
Ca oxalate - 70% Ca phosphate - 10% Struvite - 10-15% (occurs in setting of repeated UTI with Proteus) Uric acid - 5-10% Cysteine - 1% recurrences in 50-80% alkaline urine predisposes to calcium stones acidic urine predisposes to uric acid stones |
|
Chronic metabolic alkalosis |
weakness fatigue muscle cramps diminished reflexes hypokalemia anyone with metabolic alkalosis will have high aldosterone |
|
Mg, K, Ca |
all go together and hypomagnesaemia leads to hypokalemia and hypocalcemia should correct hypomagnesaemia first bc it acts as co-factor for other 2 |
|
Aldosterone |
decreases K and H+ in blood Conn syndrome --> tumor secretes aldo Bartter syndrome --> inability of loop of Henle to reabsorb KCl leading to secondary hyperaldo |
|
Metabolic alkalosis and urine Cl |
urine Cl <20 --> GI loss, prior diuretic, adenoma urine Cl >20 --> check BP normal BP --> Bartter or Gitelman syndrome, hypokalemia, hypomag, active diuretic use high BP --> check plasma renin and aldo level |
|
Periorbital edema |
indicates either nephrotic syndrome or cirrhosis |
|
Oval fat bodies in urine |
means pt has nephrotic syndrome |
|
Nephrotic syndrome |
edema proteinuria (>3.5g/24 hr) hypoalbuminemia hyperlipidemia lipiduria most common cause in adults is FSGS most common cause of nephrotic range proteinuria is DM also assoc with SLE, HIV, and amyloid |
|
Nephrotic syndrome w/u |
albumin BUN/creatine lipid profile protein:creatine ratio UA HgA1c if all c/w nephrotic syndrome --> renal bx with EM |
|
DDx for nephrotic syndrome |
1) minimal change dz assoc with Hodgkins 2) membranous nephropathy assoc with breast cancer & B-cell lymphomas have increased thrombotic risk 3) FSGS assoc with HIV & African Americans 4) membranoproliferative assoc with Hep C |
|
Tx of nephrotic syndrome |
low risk - ACEI high risk - immunosuppressors w/ or w/o steroids dialysis and/or transplant maybe indicated with advanced dz DO NOT GIVE STEROIDS ALONE |
|
Painless hematuria w/u |
thinking nephritic syndrome UA BUN/creatine HIV testing serology for C3, C4, ANA, ANCA, anti-GBM urine protein/creatine ratio cholesterol renal u/s and/or CT scan |
|
DDx of glomerulonephritis |
IgA nephropathy post-infectious GN rapidly progressive GN systemic dz that can cause: goodpasture wegener's SLE dx via a renal bx |
|
Frothy urine |
implies proteinuria |
|
Renal Tubular Acidosis Type 1 (distal) |
inability to excrete acid at distal tubule resulting in alkaline urine urinary loss of K+ due to failure of H/K ATPase results in hypokalemia, hyperchloremic metabolic acidosis assoc with autoimmune dz (eg SLE, Siogren) can cause kidney stones (Ca stones) bc of alkaline urine tx with HCO- |
|
Renal Tubular Acidosis Type 2 (proximal) |
inability to reabsorb HCO- in prox tubule body loses HCO- in urine until supply is so depleted that distal tubule can absorb the rest initially urine pH is basic then becomes acidic normally p/w hypokalemia and serum HCO- 18-20 common cause is MM tx with high dose HCO- and thiazide diuretics and K+ |
|
Renal Tubular Acidosis Type 4 (distal) |
hypoaldosterone like state results in decreased K+ excretion results in normal anion gap metabolic acidosis with hyperkalemia (only RTA that has hyperkalemia) affects distal tubule tx with fludrocortisone |
|
DDx for normal anion gap metabolic acidosis |
RTAs diarrhea acetazolamide (carbonic anhydrase inhibitors) |
|
Diarrhea vs distal RTA |
calculate urinary anion gap: urine Na + urine K - urine Cl diarrhea is negative RTA is positive or 0 |
|
DDx for AMS with no focal neurologic findings |
drugs infections metabolic |
|
AMS initial w/u |
dextrose/thiamine/naloxone CBC BMP UA CXR ABG EKG blood etoh level |
|
Ethylene glycol vs methanol AGMA |
ethylene glycol: forms oxalate crystals in urine ataxia, confusion, hallucinations, coma methanol: causes blindness tx both w/fomepizole OR ethyl alcohol |
|
UV fluorescence and ethylene glycol |
if u take pt urine & shine UV light, will see green fluorescent substance |