banannie's version from 2016-02-22 20:44

FAST ASSOCIATIONS for nephritic/nephrotic syndromes

Question Answer
wire loops on LMDPGN
full house stainingDPGN
Henoch-schonlein purpuraIgA
retinopathy/lens dislocationAlport
basket-weave appearance on EMAlport
can't see, can't pee, can't hear a buzzing beeAlport
tram trackMPGN
nephritic-nephroticMPGN, DPGN
dense depositsintramembranous MPGN
starry skyPSGN
lumpy bumpyPSGN
subepithelial humpsPSGN
linear IFRPGN goodpastures
subepithelial depositsPSGN, membranous nephropathy
subendothelial depositsMPGN, DPGN
mesangial hypercellularityIgA, MPGN
Hep Bmembranous
spike and domemembranous
hodgkins lymphomaminimal change
normal glomerulus in LMminimal change
hispanics and AAFSGS
white peoplemembranous
kidsminimal change, PSGN
sickle cellFSGS
multiple myelomaamyloidosis
kimmelstiel wilson lesionsdiabetic glomerulonephropathy (just expansion of mesangium--not hypercellularity)
defined by M protein virulence factorPSGN
X-linkedAlport syndrome
low serum C3 levelsPSGN, MPGN
how is the plasma oncotic pressure in nephrotic syndromes?low plasma oncotic pressure --> net plasma filtration into interstitium --> decreased intravascular volume --> RAAS activation --> edema
alpha 3 chain of type IV collagengood pastures (RPGN)
C-ANCAwegeners granulomatosis with polyangitis
P-ANCAmicroscopic polyangitis
upper respiratory tract infectionwegeners g with p (C anca) --> RPGN
pauci-immunegranulomatosis with polyangitis RPGN (wegeners)
solid tumorsmembranous nephropathy
thrombotic complicationsnephrotic syndrome loss of antithrombin III (hyper coagulable state)
maltese cross in the urineoval fat bodies seen under polarized light from the urine of nephrotic syndrome patients
- liver starts making more lipoproteins due to the protein loss
fibrils on EMamyloid


Question Answer
renal clearance formulaCx = UxV/Px
what is used as a proxy for GFR?creatinine clearance(inulin is most perfect tho)
what is used as a proxy for RPF?PAH clearance
general GFR formulaKf[(Pgc - Pbs) - (πgc - πbs) --> remember that πbs is normally 0 bc no protein in filtrate
normal GFR?about 100 mL/min
normal FF?about 20%
RBF formulaRPF/(1 - Hct)
eRPF formulaeRPF = Upah x V/Ppah = Cpah
what is number 1 indicator of diabetic nephropathy?albuminuria
normal clearance variations in pregnancy?glucosuria and aminoaciduria bc decreased ability of PCT to reabsorb these
AA constrictiondecreased GFR, decreased RPF, no change FF
EA constrictionincreased GFR, decreased RPF, increased FF
increased plasma protein concentrationdecreased GFR, no change RPF, decreased FF
decreased plasma protein concentrationincreased GFR, no change RPF, increased FF
ureter constrictiondecreased GFR, no change RPF, decreased FF
anion gap formulaNa - (Cl + HCO3)
winters formulafor metabolic acidosis compensation --> PCO2 = 1.5 (HCO3-) + 8 +/- 2

ACID/BASE and Inspidus

Question Answer
reasons for anion gap metabolic acidosisMethanol/metformin, Uremia, Dka, Propylene glycol, Iron, Lactic acidosis, Ethylene glycol, Salicilate
reasons for nongapped acidosisFistula, Ureterograstric conduits (colostomy), Saline administration, Endocrine (low aldo), Diarrhea (low HCO3), Carbonic Anhydrase inhibitors, Acid infusion, Renal tubular acidosis, Spironolactone
reasons for metabolic alkalosiscontraction alkalosis (Cl sensitive--Cl < 15--diruetic loss, GI loss via vomiting, Barters syndrome) and Cl insensitive--(Cl > 20--exogenous bicarb, hyperaldosteronism, renal artery stenosis, cushing little, licorice)examples of water diuresis central DI, nephrogenic DI, psychogenic polydipsia
examples of solute diuresishyperglycemia, post obstructive diuresis
serum Na+ before water deprivation in CDInormal
urine osm before water deprivation in CDIlow
serum Na+ after water deprivation in CDIhigh
urine osm after water deprivation in CDIlow
serum Na+ after desmopressin in CDInormal
urine osm after desmopressin in in CDIhigh
serum Na+ before water deprivation in NDInormal
urine osm before water deprivation in NDIlow
serum Na+ after water deprivation in NDIhigh
urine osm after water deprivation in NDIlow
serum Na+ after desmopressin in NDIhigh
urine osm after desmopressin in in NDIlow
serum Na+ before water deprivation in psychogenic polydipsialow
urine osm before water deprivation in psychogenic polydipsialow
serum Na+ after water deprivation in psychogenic polydipsianorm
urine osm after water deprivation in psychogenic polydipsiahigh
indications for acute hemodialysissevere metabolic Acidosis, severe Electrolyte disorders (hyperkalemia), drug Intoxication, refractory fluid Overload, Uremia


Question Answer
Pathogenesis of Prerenaldecreased RBF leads to decreased GFR. Sodium/Water and BUN retained by kidney in an attempt to conserve volume. Increase in BUN/Creatinine ratio. Decrease in FENa.
Pathogenesis of intrinsic renal failuredue to acute tubular necrosis or ischemia/toxins. There is a decrease in GFR. BUN reabsorption is impaired. BUN/Creatinine ratio decreases.
Pathogenesis of postrenal failuredue to outflow obstruction. Develops only with bilateral obstruction. Must relieve the obstruction.
low urine Na+ of < than 20prerenal
normal urine sedimentprerenal
feNa+ < than 1%prerenal
B:C > 20prerenal
urine osm > 500prerenal
B:C < 15intrarenal
urine Na+ > 20intrarenal
FeNa+ >1%intrarenal
urine osm is similar to plasmaintrarenal (about 290)
urine Na+ > 40postrenal
FeNa+ > 1%postrenal
urine osm < 350postrenal
Consequences of chronic renal failureMAD HUNGER (Metabolic Acidosis, Dyslipidemia, Hyperkalemia, Uremia (marked by increased BUN), Na/H20 retention, Growth retardation, Erythropoietin failure, Renal Osteodystrophy

Random high yield RENAL ASSOCIATIONS

Question Answer
Fanconi syndromeresorptive defect in PCT --> increased excretion of AA, glucose, HCO3, PO4, metabolic acidosis
Bartter syndromereabsorptive defect in thick ascending loop of henle causing hypokalemia, metabolic alkalosis, hypercalciuria (similar to furosemide use bc affects Na/K/2cl)
Gitelman syndromeresorptive defect of NaCl in DCT --> hypokalemia, hypomagnesemia metabolic alkalosis, hypocalciuria
Liddle syndromeincreased Na resorption in collecting tubules (enac channel) --> HTN, hypokalemia, met alk, decreased aldo
how to treat Liddle?amiloride
licoricesyndrome of apparent mineralocorticoid excess --> HTN, hypokal, met alk, low aldo
beta blocker effects on kidneyblock beta1 receptors of JGA --> decreased renin
NSAID effect on kidneyblock prostaglandin synthesis --> constriction of AA --> decreased GFR and RPF --> could cause acute renal failure
where does PTH work?PCT
where does AII work?EA constriction
where does ANP work?AA and DCT causing increased GFR and increased Na filtration --> Na+ loss and volume loss
where does aldo work?collecting duct alpha intercalated and principal cells
where does ADH work?collecting duct principal cells
torsades de pointeslow Mg++
prolonged QTlow Ca++
U waveshypokalemia
flattened T waveshypokalemia
wide QRShyperkalemia
peaked T waveshyperkalemia
calcium oxalate stone treatmentcitrate, thiazides, hydration
vericocelepresentation of L RCC that travels and obstructs spermatic vein off of renal vein
triad of RCChematuria, flank pain, palpable mass
RCC gene deletionchromosome 3 von hippel lindau
VHL diseaseincreased risk of hemangioblastoma of cerebellum and RCC
angiomyolipoma associationtuberus sclerosis
Beckwith-wiedemann syndromewilms tumor, macroglossia, organomegaly, hemihypertrophy
WAGR complexwilms tumor, aniridia, GU malformation, mental Retardation
Schistosomiasissquamous cell carcinoma of bladder
thyroidization of kidneychronic pyelonephritis
common cause of chronic pyelonephritisvesicoureteral reflux ( reflux from bladder up the ureters to the kidneys)
crush injurynephrotoxic acute tubular necrosis
muddy brown castsacute tubular necrosis
where does RCC originate from?PCT cells
ethylene glycolcalcium oxalate stones, nephrotoxic acute tubular necrosis
other causes of nephrotoxic acute tubular necrosisahminoglycosides (amphotericin B), radio contrast dye, antivirals (foscarnet, cidofovir), lead, crush injury (myoglobinuria), ethylene glycol, urate, hemoglobinuria, tumor lysis syndrome
sickle cell diseaseFSGN, renal papillary necrosis
causes of renal papillary necrosisSickle cell, Acute pyelonephritis, Analgesics (NSAIDS), Diabetes mellitus
portal HTN in babyARPKD
berry aneurysmsADPKD
white cell castspathognomonic for pyelonephritis
eosinophilic castschronic pyelonephritis (thyroidization of kidney)
pyuria with eosinophils and rashinterstitial nephritis
eosinophiluriadrug induced interstitial nephritis
aminoglycosidesacute tubular necrosis
abdominal and flank bruitsRenal artery stenosis
causes of renal artery stenosisatherosclerotic plaques in arterial intima of elderly, fibromuscular dysplasia of women of child bearing age
test for cysteine stonesfirst check for elevated urinary cysteine levels (aminoaciduria) but also can use sodium cyanide nitroprusside test to qualitatively screen for urinary cystine. Positive test results in a red-purple discoloration.
sodium cyanide nitroprusside testqualitative screen for urinary cystine. + is red purple discoloration


Question Answer
causes pulmonary edemamannitol
work in PCTmannitol, acetazolamide
used for glaucoma and pseudo tumor cerebraacetazolamide
causes HCO3 excretionacetazolamide
loop diuretic for someone with a sulfa allergyethacrynic acid
ototoxicityloop diuretics
decreased Ca+loops
increased Ca+thiazides
where do loops workTAL (block Na/K/2Cl)
where do thiazides workDCT
can be used to treat osteoporosisthiazides
hyperkalemiaK+ sparing diuretics (spironolactone and epleronone)
ACE inhibitor effect on GFRnormally decreases AII and decreases GFR by preventing constriction of EA (rise in renin and in bradykinin) BUT, cause dangerous decrease in GFR (increased creatinine) in bilateral renal artery stenosis
treats pulmonary edemaloops
carbonic anhydrase inhibitoracetazolamide
where do K+ sparing diuretics work?collecting duct
beta blocker effectsbock beta 1 receptors of JG apparatus --> decreased renin, decreased Angiotensin I, decreased Angiotensin II, decreased Aldosterone, no change in bradykinin
ARB effectsblock AT1 receptor and inhibit effects of Angiotenin II while also disturbing the negative feedback --> increased renin, increased Angiotensin I, increased Angiotensin II, decreased aldo, no change in bradykinin --> overall decrease in GFR
when do you avoid kayexalate?post op patients or those with GI issues--can cause intestinal necrosis

FAST ASSOCIATIONS for nephrolithiasis

Question Answer
ethylene glycolcalcium oxalate stones
radiolucenturic acid stones
vitamin C abusecalcium oxalate stones
dumbbell shapecalcium oxalate stone
envelope shapecalcium oxalate stone
coffin lidammonium magnesium phosphate stone
staghorn calculi in adultsammonium magnesium phosphate stone
staghorn calculi in kidscysteine stone
hexagonal/benzene ring shapecysteine stone
leukemia/myeloproliferative disordersuric acid stones
rhomboiduric acid stone
rosetteuric acid stone
crohns diseasecalcium oxalate stones
principal site of uric acid stone formationcollecting duct due to acidic urine pH
tumor lysis syndrome can causeuric acid stone formation
calcium levels for most folks with calcium stonesnormocalcemia, (idiopathic) hypercalciuria