Renal

Front 1

clearance formula

Back 1

C = UV / P

if C < GFR then there is net tubular reabsorption
if C > GFR, then there is net tubular secretion
if C = GFR than there is no secretion or reabsorption

Front 2

components of glomerular filtration barrier

Back 2

fenestrated capillary endo (size barrier)
fused basement membrane w/heparan sulfate (negative charge barrier)
epithelial layer of podocyte foot processes

Front 3

GFR formula

Back 3

inulin can be used to calculate GFR b/c is freely filtered and neither reabsorbed nor secreted

GFR = UV/P of inulin

also = Kf (Pgc-Pbs) - (Pi gc - Pi bs)

pi bs normally = 0

Front 4

ERPF formula

Back 4

can be estimated using PAH (b/c is filtered and secreted in proximal tubule)

ERPF = UV/P PAH

RBF = RPF / (1-Hct)

Front 5

filtration fraction

Back 5

FF = GFR/ RPF

** angiotenin II constricts efferent arteriole=>
low RPF, high GFR, so FF increases
(so an ACE-I leads to decreased FF)

high plasma protein = low FF
and vice versa
constricted ureter = low FF

Front 6

free water clearance

Back 6

C water = V- C osm

V = urine flow rate
C osm = UV/P osm

Front 7

NSAIDs can cause acute renal failure how?

Back 7

in high vasoconstrictive states... by inhibiting the renal production of prostaglandins
(prostaglandins vasodilate afferent arteriole to increase GFR)

Front 8

winter's formula

Back 8

Pco2 = 1.5 (HCO3) + 8 +/- 2

(use to determine compensation for metabolic acidosis)

Front 9

compensation for metabolic alkalosis

Back 9

PCO2 should increase by 0.7 for every 1 increase in bicarb

Front 10

toxicity of loop diuretics

Back 10

OH DANG!

ototoxicity, hypokalemia, dehydration, allergy [sulfa], nephritis [interstitial], gout

Front 11

ethacrynic acid

Back 11

same action as furosemide

but is NOT a sulfa drug

Front 12

toxicity of thiazides

Back 12

hyperGLUC

glycemia, lipidemia, uricemia, calcemia

also sulfa allergy, hyponatremia, hypokalemic metabolic alkalosis

Front 13

effects of diuretics on pH

Back 13

acidosis: CAIs, K sparing

alkalosis: loops, thiazides

Front 14

potter's syndrome

Back 14

= bilateral renal agenesis
when ureteric bud doesnt form from the mesonephric duct
limb, facial deformaties
oligohydraminose*
pulmonary hypoplasia
not compatible with life

Front 15

Fanconi's syndrome

Back 15

hereditary or acquired dysfxn of the proximal renal tubules
glycosuria, hyperphosphaturia, aminoaciduria, acidosis

Front 16

____ autoregulates RBF

Back 16

the renal vasculature

keeps RBF constant even when arterial pressure varies from 100-200 mmHg

*RBF = 25% of cardiac output

Front 17

types of RTA

Back 17

(normal anion gap)
type 1 [distal]: failure to excrete titratable acid, NH4
type 2: renal loss of HCO3
type 4: hypoaldosteronism (poor excretion of NH4 and hyperkalemia)

Front 18

prerenal ARF

Back 18

hypovolemia
low CO
increased systemic vasc resistance
drugs (COX inhibitors and ACE-Is)

Front 19

renal ARF

Back 19

renovesicular obstruction
glomerulonephritis
HUS, TTP, DIC, SLE, ATN, scleroderma

Front 20

postrenal ARF

Back 20

bilateral ureteric obstruction
prostatic hyperplasia
bladder neck obstruction
stricture

Front 21

WAGR syndrome

Back 21

wilm's tumor [WT-1 on chrom 11p]
aniridia [absence of the iris]
genital anomalies
mental retardation

Front 22

treatment of SIADH

Back 22

lithium or demeclocycline

block the effects of ADH (prevents excessive water retention)

Front 23

central DI treatment

Back 23

desmopression (ADH analogue)

**not useful in nephrogenic ADH, when kidneys don't respond to ADH

Front 24

kidney vasculature most susceptible to damage from a sickle crisis

Back 24

vasa recta
->due to the very high osmo of the renal medulla
->ischemia can cause patchy papillary necrosis, proteinuria, and cortical scarring

Front 25

membranous glomerulonephritis

Back 25

PAS positive electron dense deposits distributed along epithelial side of the capillary basement membrane

Front 26

nodular glomerularsclerosis [Kimmelstiel Winston disease]

Back 26

ass'd with DM
ovoid hyaline masses in the periphery of the glomerulous

also see widespread capillary basement membrane thickening and diffuse glomerulosclerosis

Front 27

renal hemodynamics in pregnancy

Back 27

increased GFR, increased circulating plasma volume

'normal' creatinine can be less than 1.0

Front 28

there is a specific association between _________ [renal disease] and HIV

Back 28

FSGS
seen with IVDU/HIV
does not respond to steroids, poor Px
also see hyalinization with focal deposits of IgM and C3

Front 29

P-osm equation

Back 29

(total body osm - urine osm)/
(total body water - urine vol)

TBW = (body wt) x 0.6 (0.5 in F)
total body osm = (intial P osm x total body osm)

Front 30

median umbilical ligament

Back 30

adult derivative of the urachus
->derivative of the allantoic duct
->normally the duct fuses
->but if it remains patent, a young patient can have urine discharge from umbilicus

Front 31

effectiveness of diuretics is dependant on the pts creatinine clearance

Back 31

loops: work down to 10 mL/min

thiazides and potassium sparing: work down to 40 mL/min

Front 32

only site in the kidney where epithelial cells have a 'brush border'

Back 32

PCT

(allows enhancement of ability reabsorb plasma constituents)

Front 33

derived from the ureteric bud

Back 33

collecting system and renal pelvis

(other parts like loop of Henle, bowman's capsule, glomerular tuft: are from metanephric mesoderm)

Front 34

segment of kidney with lowest osmolarity

Back 34

early distal tubule

is usually <150 [called the diluting segment]

Front 35

benign nephrosclerosis

Back 35

finely granular surface
multifocal loss of glomeruli in the superficial cortex

**malignant hypertension will cause a mottled, hemorrhagic appearance

Front 36

ureter is anterior to which anatomic level

Back 36

bifurcation of the common iliac artery

Front 37

retroperitoneal fibrosis

Back 37

causes progressive compression of ureters and subsequent hydronephrosis

Front 38

loop diuretics cause this type of alkalosis

Back 38

contraction metabolic alkalosis