eesohbel's version from 2015-08-06 23:02

Renal embryo/anatomy/physio

Question Answer
as they ascend during fetal development horseshoe kidneys get trapped underIMA
horseshoe kidney associated withTurner, Patau, Edwards
which kidney is taken during donor transplantationleft kidney because it has a longer renal vein
ureters pass underuterine artery and ductus deferens
ureter may be damagedduring ligation of cardinal ligaments
major cation within ICFpotassium
major cation within ECFsodium
glomerular filtration barrier composed offused basement membrane (negative charge barrier), fenestrated capillary endothelium, epithelial layer consisting of podocyte foot processes
prostaglandins and affect on arterioledilate afferent arteriole
dilate afferent arterioleincrease GFR, increase RPF, FF remains constant
NSAIDSconstrict afferent arteriole
constrict afferent arterioledecreased GFR, decrease, RPF, FF remains constant
angiotensin IIconstricts efferent arteriole
constrict efferent arterioledecrease RPF, increase GFR. FF increases.
ACE inhibitorsdilate efferent arteriole
dilate efferent arterioleincrease RPF, decrease GFR. FF decreases.
ureteral constrictiondecreases GFR. . FF decreases
GFR equationkf[ (pressure in glommerular capillary-pressure in bowman's space)-(oncotic pressure in glomerular capillary)]
increase plasma protein concentrationincrease oncotic glomerular capillary pressure and decrease GFR
constriction of ureterincreases pressure in Bowman's space. decreases GFR
what glucose concentration are all transporters fully saturated375
what glucose concentration does glucosuria begin200
macula densa located DCT senses NaCl
JGA cells locatedafferent arteriole. are smooth muscle and secrete renin.

Physio continued

Question Answer
ANP and the glomerulusdilates afferent increases GFR. ANP limits sodium reabsorption in PCT and CD and inhibits renin secretion
isotonic reabsorption in nephronearly PCT
hypertonic within nephronthin descending loop of henle
hypotonic wihtin nephronthick ascending loop of henle
urine msot diluteearly DCT
Bartter syndromesimilar to giving furosemide
low aldosterone levelsliddle syndrome and syndrome of apparent mineralocorticoid excess
acidosis and potassiumshifts potassium of of cells
alkalosisshifts potassium into cells
insulinshifts potassium into cells
b beta blockersshifts potassium of of cells

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 depositMPGN, DPGN
mesangial hypercellularityIgA, MPGN
Hep Bmembranous
spike and dome. supepithelial depositsmembranous. ~nephrotic unlike PSGN and MPGN
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)
upper respiratory tract infectionwegeners g with p (C anca) --> RPGN
pauci-immune(wegeners) gpa
solid tumorsmembranous nephropathy
thrombotic complicationsnephrotic syndrome loss of antithrombin III (hyper coagulable state)
maltese cross in the urinethis is the description of oval fat bodies seen under polarized light from the urine of nephrotic syndrome patients--> bc liver starts making more lipoproteins due to the protein loss
fibrils on EMamyloid
nephrotic syndromemassive proteinuria, hypoalbuminemia, edema, hyperlipidemia, hypercoaguable state due to loss antithrombin III in urine, increased risk of infection due to loss of immunoglobulins in urine


Question Answer
how to calculate anion gapNa - (Cl+HCO3)
reasons high anion gap metabolic acidosisMUDPILES (Methanol, Uremia, DKA, Propylene glycol, Iron, Lactic Acidosis, Ethylene glycol, Salicylates)
reasons for non anion gap metabolic acidosisHARDASS (Hyperalimentation, Addison's, RTA, Diarrhea, Acetazolamide, Spironolactone, Saline)
reasons for respiratory acidosis thinkhypoventilation
reasons for respiratory alkalosishyperventilation, salicylates, restrictive lung disease
to figure out reason for metabolic alkalosischeck urine chloride!!!
how do you calculate winter's formula1.5(HCO3)+8+/- 2. this gives you the expected PaCO2
if PaCO2 lower than expectedsecondary respiratory alkalosis
if PaCO2 higher than expectedsecondary respiratory acidosis
type I RTAdifficulty in alpha intercalacted cells to secrete H+. Leads to metabolic acidosis. alkaline urine
Type 2 RTAincreased excretion of HC03. Metabolic acidosis. Acid urine.
Type IV RTAtoo little aldosterone leads to hyperkalemia. acidic urine.


Question Answer
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 and intrarenal
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

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
treat with alkalinization of urineuric acid stones

Renal cancer

Question Answer
originates from PCTrenal cell carcinoma
when RCC invades into renal veincan precipitate renal vein thrombosis
extension of left kidney RCCcan cause left sided variocele due to obstruction of left testicular vein
Wilms tumorsmooth mass does not cross midline. no calcification on x-ray.
Neuroblastomairregular mass. crosses midline. calcification on x-ray. dancing eyes
transitional cell carcinomamost common tumor of urinary tract. two pathways flat and papillary. flat is early p53 mutation begins as a high grade tumor. papillary begins as low grade and progresses.
schistosomasquamous cell carcinoma of bladder


Question Answer
what is necessary for development of acute pyelonephritisanatomic of function vesicouretal reflex. AKA retrograde flow
thyrodization of kidney can happen inchronic pyelonephritis
causes of papilary necrosisthink SAAAD (sickle cell trait, acute pyelo, analgesics, diabetes)


Question Answer
preformed antibodies against grafthyper acute
minutes to hourshyper acute
gross mottling and cyanosishyper acute
arterial fibrinoid necrosishyper acute
capillary thrombotic occlusionhyper acute
less than 6 months post transplantacute
humoral/cellular activation of naive cellsacute
C4d depositionacute (humoral)
neutrophilic infiltrateacute (humoral)
necrotizing vasculitisacute (humoral)
lymphocytic interstitial infiltrateacute cellular
endotheliitisacute cellular
monts to yearschronic
low grade immune response refractory to immunosuppressantschronic
vascular wall thickeningchronic
luminal narrowingchronic
interstitial fibrosischronic
parenchyma atrophychronic
type II HSRhyperacute rejection (antibody mediated)
type IV HSRacute or chronic (cell mediated)


Question Answer
intraabdominal pressure exceeds urethral sphincter pressurestress
loss of urethral supportstress
leaking with sneezing, coughing, laughing, liftingstress
detrusor overactivityurge
sudden overwhelming frequent need to empty bladderurge
impaired detrusor contractilityoverflow
bladder outlet obstructionoverflow
constant involuntary dribbling of urineoverflow
incomplete emptyingoverflow
treatment for urge incontinenceantimuscarinic (M3 receptor) meds --> decrease IP3 --> decrease Ca release --> relaxation
urge continencegive oxybutinin (muscaranic anatongist)
outflow incontinence (BPH)zosin, but give finasteride to shrink the prostate
someone who cannot pee after surgery or atonic bladder (urinary retention)bethanechol (muscarinic agonist)
stress incontinencegive alpha agonist