YIELD STUDY GUIDE WITH PHYSIOLOGY,
PATHOLOGY AND ACID-BASE REVIEW
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Updated 2026 Questions and Answers
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Rationales Included
,renal clearance + GFR CL = UV/P
in mL/min
NL ~ 100 mL/min
creatinine moderately overestimates GFR
(some secretion)
inulin accurately measures GFR
in pregnancy and early diabetic nephropathy -->
INCR in Cr CL
in elderly and acute/chronic renal dz -->
DECR in Cr CL
effective renal plasma flow (ERPF) CL = UV/P
use PAH as proxy
ERPF can be estimated using PAH CLEARANCE bc it is both FILTERED and
actively SECRETED (CARRIER MEDIATED TRANSPORT) in the proximal tubule +
ALL PAH entering the kidney is EXCRETED
--> typically underestimates renal plasma flow by 10%
RBF = RPF/(1 - Hct)
filtration fraction + load FF = GFR/RPF
NL ~ 20%
filtered load = GFR x plasma concentration
modulators of afferent + efferent arteriole ...
effect of plasma protein concentration on GFR, FF incr [plasma] = decr GFR, decr FF
decr [plasma] = incr GFR, incr FF
reabsorption + secretion calcs excretion rate = U x V
filtered load = GFR x [plasma]
reabsorption = filtered - excreted
secretion = excreted - filtered
,glucose clearance AT NORMAL PLASMA CONCENTRATIONS GLUCOSE IS COMPLETELY
REABSORBED IN PROXIMAL TUBULE BY
Na/glucose COTRANSPORT
DIABETES (~>160) --> GLUCOSURIA
all transporters fully saturated at 350
AA clearance Na mediated transport in PROXIMAL TUBLE
COMPETITIVE INHIBITION between AAs
--> PROTEINURIA when overloaded
HARTNUPs DZ = NEUTRAL AA TRANSPORTER DEFICIENCY - TRYPTOPHAN
TRANSPORTER in kidney
--> CANT RESORB NEUTRAL AA's - TRYPTOPHAN
--> CANT MAKE 5HT, MELATONIN, NIACIN/NAD+
TRYPTOPHAN DEFICIENCY --> PELLAGRA
membrane channels in proximal tubule Early proximal tubule - contains brush border
Reabsorbs all glucose and AA and most of the bicarbonate, Na, Cl, and water
ISOTONIC absorption
Secretes NH3, buffer for secreted H+
PTH - inhibits Na+/PO4 cotransport --> PO4 excretes
ATII - stimulates Na/H+ exchange --> Na + H2O reabsorption (CONTRACTION
ALKALOSIS).
membrane channels in thin descending limb passive resorption of H2O via countercurrent multiplier in medulla
concentrates urine in medulla
membrane channels in thick ascending limb actively reabsorbs Na+, K+, and C I- and indirectly induces2the paracellular
reabsorption of M i+ and Ca +. Impenneable to H20. Makes urine less
concentrated as it ascends.
, membrane channels in distal convoluted tubule Earlydistal convoluted tubule-actively reabsorbs Na+CI.
Diluting segment --> Makes urine hypotonic
PTH incr Ca/Na exchange --> incr Ca resorption
membrane channels in the collecting tubule reabsorb Na in exchange for secreting K and H+ (regulated by aldosterone)
Aldosterone/ENAC - leads to insertion of Na+channel on luminal side
ADH/V2Rs - insertion of aquaporin H20 channels on luminal side
total body Na ~ total body water
high TB Na = volume overload, HTN, edema, cirrhosis, HF, nephrotic
low TB Na = dehydration, hypotn,
hypernatremia = low TBW
hyponatremia = high TBW
hypovolemic - dehydration (NVD) + electrolyte loss
euvolemic - SIADH
hypervolemic - high TB Na
tubular fluid/plasma concentrations of various substances Cl reabsorption occurs at a slower rate than Na in the proximal 1/3 of the proximal
tubule and then matches the rate of Na reabsorption more distally. Thus, its
relative concentration incr before it plateaus
Na reabsorption drives H20 reabsorption, so it nearly matches osm