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Markers used to measure TBW?
tritiated water
D20
antipyrene
Markers used to measure ECF?
sulfate
inulin
mannitol
markers used to measure plasma?
RISA
evan's blue
measuring interstitial fluid?
ISF = ECF - plasma
measuring ICF
ICF = TBW - ECF
Volume of body compartment calculation
Volume = Amt injected - Amt excreted / concentration
infusion of isotonic NaCl

aka. iso-osmotic volume expansion
- ECF volume increases
- no change in osmolarity
- no change in ICF volume
- plasma protein/ Hct decrease
- arterial BP increases
diarrhea

aka. isoosmotic volume contraction
- ECF volume decreases
- no change in osmolarity
- no change in ICF volume
- plasma protein/Hct increase
- arterial BP decreases
excessive NaCl intake

aka. hyperosmotic volume expansion
- ECF osmolarity increases
- volume shifts from ICF to ECF
- ECF volume increases
- ICF volume decreases
- plasma protein/Hct decrease
sweating in a desert - loss of water

aka. hyperosmotic volume contraction
- ECF osmolarity increases
- water shifts from ICF to ECF until osmolarity has equilibriated
- ICF volume increases
- plasma protein conc. increases
- Hct remains the same
syndrome of inappropriate ADH

aka. hypoosomotic volume expansion
- water retention = decreased ECF osmolarity, increased ECF volume
- water shifts from ECF to ICF --> ICF volume increases, osmolarity decreases
- plasma protein decreases
- hct unchanged
adrenocortical insufficiency - loss of NaCl

aka. hypoosmotic volume contraction
- osmolarity of ECF decreases
- volume of ECF decreases, shifts to ICF
-ICF osmolarity decreases, volume increases
- plasma protein conc. increases
- Hct increases
clearance
- definition (1)
- equation (2)
1 = amount of plasma cleared of a substance per unit time
2 - C = UV/P
renal blood flow (RBF)
- (1) % of CO
- proportional to pressure diff. between (2) and (3)
- inversely proportional to resistance of (4)
1 = 25$
2 = renal artery and renal vein
4 = renal vasculature
angiotensin II preferentially constricts (1) arteriole causing an (2) in GFR
1 = efferent arteriole
2 = increaes
vasodilation of renal arterioles causes an (1) in RBF and is caused by: (2), (3), (4) and (5)
1 = increase
2 = PGE2, PGI2
3 = bradykinin
4 = NO
5 = dopamine
autoregulation of RBF
maintains a constant range of arterial pressure between 80 -200 mmHg; mainly affects the afferent arteriole
myogenic mechanism of autoregulation of RBF
renal afferent arterioles contract in response to stretch
tubuloglomerular feedback
increased renal arterial pressure leads to increased delivery of fluid to macula densa; macula densa causes constriction of nearby afferent arteriole
para-aminohippuric acid (PAH) is used to measure (1); PAH is both (2) and (3) by renal tubules
1 = effective renal plasma flow
2 = filtered
3 = secreted
Formula for RPF
RPF = C pah = U(pah)V(pah) / Ppah
Formula for RBF
RPF / (1 - Hct)
What substance can you use to measure GFR? Why?
inulin
-bc it is filtered but it is NOT secreted or reabsorbed
blood urea nitrogen and serum creatinine (1) when GFR (2)
1 = increase
2 = decreases
formula for filtration fraction

normal value for filtration fraction
filtration fraction = GFR / RPF

normal = 0.20
increase in filtration fraction produces an (1) in protein conc. of peritubular capillary blood, which causes (2)
1 = increased
2 = increased reabsorption in proximal tubule
glomerular barrier
- components (1)
- lined with? (2)
1 = capillary endothelium
basement membrane
filtration slits of podocytes

2 = anionic glycoproteins (prevent proteins from passing through)
glomerular capillary hydrostatic pressure
- increased by dilation of (1) and constriction of (2)
1 = afferent arteriole
2 = efferent arteriole
bowman's space hydrostatic pressure
- increased by constriction of (1)
1 = ureters
glomerular capillary oncotic pressure
- increases along (1) due to increased (2)
1 = length of glomerular capillary bed
2 = increased protein conc.
constriction of afferent arteriole:
- (1) GFR
- (2) RPF
- (3) filtration fraction
1 = decreases
2 = decreases
3 = no change
constriction of efferent arteriole:
- (1) GFR
- (2) RPF
- (3) filtration fraction
1 = increases
2 = decreases RPF
3 = increases
increased plasma protein causes:
- (1) GFR
- (2) RPF
- (3) filtration fraction
1 = decreased
2 = no change on RPF
3 = decreased FF
ureteral stone causes:
- (1) GFR
- (2) RPF
- (3) filtration fraction
1 = decreased GFR
2 = no change RPF
3 = decreased FF
formula for filtered load
filtered load = GFR x plasma conc.
excretion rate
excretion rate = V x urine conc.
reabsorption rate
reabsorption rate = filtered load - excretion rate
secretion rate
secretion rate = excretion rate - filtered load
where is glucose reabsorbed in nephron? what kind of transporter?
proximal tubula

Na+ glucose cotransport
Tm for a carrier (1)

Tm of glucose = (2)
1 =reabsorptive rate at which carriers are saturated
2 = 350 mg/dL
threshold (1)

threshold of glucose (2)
1 = plasma conc. at which substance first appears in urine
2 = 250 mg/dL
splay
region between threshold and Tm
--> represents excretion of glucose in urine before saturation of reabsorption (Tm) is full achieved

for glucose = between 250 and 350
where does secretion of PAH occur?
proximal tubule
which form of weak acid can back diffuse from urine to blood?
HA - lipid soluble, uncharged
which form of weak base can back-diffuse from urine to blood?
B form - uncharged, lipid soluble
TF/ P ratio = 1.0
no reabsorption of substance (or reabsorption exactly proportional to water)
where does TF/P = 1,0?
Bowman's space
if TF/ P is less than 1.0
reabsorption of substance has been greater than reabsorption of water

--> conc. in tubular fluid is less than plasma
if TF/P is greater than 1.0
either reabsorption has been less than water OR there has been secretion of substance
Na+ reabsorption in PCT
- percent?
- along with?
1 = 67%
2 = H20 - isosmotic
Na+ reabsorption in early PCT
- transporters? (2)
1 = Na+ cotransport with glucose, amino acids, phosphate and lactate
2 = Na+ and H+ exchanger
Na+ reabsorption in late PCT
Na+ reabsorbed with Cl-
carbonic anhydrase inhibitors
ex. acetazolaminde
- diuretics
- act on early PT
- inhibit reabsorption of filtered HCO3-
ECF volume contraction (1) reabsorption; ECF volume expansion (2) proximal tubular reabsorption
1 = increases reabsorption
2 = decreases reabsorption
Na+ reabsorption in Thick Ascending Loop of Henle
- percent? (1)
- transporter? (2)
1 = 25%
2 = Na+ K+ 2Cl- transporter
loop diuretics inhibit?
Na+/K+/2Cl- cotransporter in TAL

ex. furosemide
ethacrynic acid
bumetanide
What part of nephron is impermeable to water?
thick ascending limb of loop of henle
Na+ reabsorption in distal tubule and collecting duct
- percent? (1)
- transporters? (2)
1 = 8%
2 - Na+ Cl- co transport
thiazide diuretics inhibit?
Na+ Cl- cotransporter in distal tubule/collecting duct
principal cells of late distal tubule/CD
- reabsorb? (1)
- secrete? (2)
- function increased by what hormone? (3)
1 = Na+ and H20
2 = secrete K+
3 = aldosterone
ADH acts on (1) cells in (2) nephron segment to increase (3)
1 = principal cells
2 = late DT and CD
3 = water permeability
K+ sparing diuretics
ex. (1)
- function? (2)
1 = spironolactone, triamterene, amiloride
2 = decrease K+ secretion in principal cells of late DT and CD
alpha-intercalated cells
- location? (1)
- function? (2)
1 = late DT and CD
2 = secreted H+ and reabsorb K+ by an H+/K+ ATPase
Causes of Hyperkalemia?
insulin deficiency
B-adrenergic antagonists
acidosis
hyperosmolarity
inhibitors of Na+/K+ pump
exercise
cell lysis
Causes of Hypokalemia?
insulin
B-adrenergic agonists
alkalosis
hypoosmolarity
K+ reabsorption
- PCT (1)
- TAL of henle (2)
- a-intercalated cells (3)
1 = 67%
2 = 20% (Na+ K+ 2Cl- cotransporter)
3 = H+K+ ATPase
Causes of Hypokalemia?
insulin
B-adrenergic agonists
alkalosis
hypoosmolarity
K+ secretion occurs in (1) and is mediated by what transporter? (2)
1 = principal cells of distal tubule
2 = passively secreted down electrochemical gradient
K+ reabsorption
- PCT (1)
- TAL of henle (2)
- a-intercalated cells (3)
1 = 67%
2 = 20% (Na+ K+ 2Cl- cotransporter)
3 = H+K+ ATPase
Causes of Increased Distal K+ secretion? (6)
high K+ diet
hyperaldosteronism
alkalosis
thiazide diuretics
loop diuretics
luminal anions
K+ secretion occurs in (1) and is mediated by what transporter? (2)
1 = principal cells of distal tubule
2 = passively secreted down electrochemical gradient
Causes of Decreased Distal K+ secretion? (4)
low K+ diet
acidosis
hypoaldosteronism
K+ sparing diuretics
Causes of Increased Distal K+ secretion? (6)
high K+ diet
hyperaldosteronism
alkalosis
thiazide diuretics
loop diuretics
luminal anions
Causes of Decreased Distal K+ secretion? (4)
low K+ diet
acidosis
hypoaldosteronism
K+ sparing diuretics
Where and what percent is urea absorbed?
50% of urea is reabsorbed in the proximal tubule
ADH increases the permeability to urea in (1)
inner medullary collecting ducts
low urine flow rate, (1) urea reabsorption and (2) urea excretion; high urine flow rate, (3) urea reabsorption and (4) urea excretion
1 = greater
2 = decreased
3 = decreased
4 = increased
where is phosphate reabsorbed? (1)
- how much of it is reabsorbed? (2)
- transporter? (3)
1 = proximal tubule
2 = 85%
3 = Na+ phosphate cotransport
What hormone inhibits phosphate reabsorption?
PTH
- causes phosphaturia and increased urinary cAMP
Which diuretics increase Ca2+ excretion (1) and which decrease Ca2+ excretion (2)?
1 = loop diuretics (furosemide)
2 = thiazide diuretics
Mg2+ and Ca2+ compete for reabsorption in the (1)
1 = thick ascending limb
presence of ADH (1) the size of corticopapillary osmotic gradient by stimulating reabsorption of (2) in (3)
1 = increases
2 = NaCl
3 = thick ascending limb
presence of ADH (1) the size of corticopapillary osmotic gradient by stimulating reabsorption of (2) in (3)
1 = increases
2 = NaCl
3 = thick ascending limb
osmolarity of final urine = (1)
1200 mOsm/L
osmolarity of final urine = (1)
1200 mOsm/L
What area of nephron does urine get concentrated? (1)
- due to presence of (2) and (3)
1 = collecting ducts
2 = ADH which increases H20 permeability AND corticopapillary gradient
What area of nephron does urine get concentrated? (1)
- due to presence of (2) and (3)
1 = collecting ducts
2 = ADH which increases H20 permeability AND corticopapillary gradient
corticopapillary osmotic gradient is (1) without ADH
decreased
corticopapillary osmotic gradient is (1) without ADH
decreased
free water clearance
estimates the ability to concentrate or dilute urine
free water clearance
estimates the ability to concentrate or dilute urine
Positive C H20 (free water clearance)
- low ADH (no ADH)
- urine is hypoosmotic to plasma
- high water intake, central diabetes insipidus, nephrogenic diabetes insipidus
Negative C H20 (free water clearance)
high ADH
- urine is hyperosmotic to plasma
- water deprivation or SIADH
Ch20 = ZERO
produced with loop diuretics
-> inhibit both dilution in TAL and production of corticopapillary osmotic gradient which prevents concentration in CD
volatile acid
CO2
--> produced by aerobic metabolism of cells
non volatile acid
aka. fixed acids
- sulfuric acid
- phosphoric acid
- ketoacids
- lactic acid
- salicylic acid
major extracellular buffer
HCO3-
minor extracellular buffer
phosphate
most important urinary buffer
phosphate
intracellular buffers (2)
organic phosphates
proteins
major intracellular buffer
hemoglobin (deoxy is better than oxy)
Where does reabsorption of filtered HCO3- occur?
proximal tubule
increases in filtered load for HCO3- result in (1) rates of HCO3- reabsorption until person develops (2) and then HCO3- is (3)
1 = increased
2 = metabolic alkalosis
3 = excreted
increased PCO2 = (1) HCO3- reabsorption

- basis for renal compensation of (2)
1 = increased
2 = respiratory acidosis
ECF volume expansion = (1) HCO3- reabsorption
ECF volume contraction = (2) HCO3- reabsorption
1 = decreased
2 = increased
angiotensin II stimulates (1) and thus (2) HCO3- reabsorption which contributes to (3) seen with ECF volume contraction
1 = Na+ H+ exchange
2 = increases
3 = contraction alkalosis
aldosterone increases (1) on PT luminal mb which increases (2) of H+ and reabsorption of (3)
1 = H+ ATPase
2 = secretion
3 = reabsorption of HCO3-
amount of H+ excreted as NH4+ depends on (1) and (2)
1 = amount of NH3 synthesized by renal cells
2 = urine pH
hyperkalemia (1) NH3 synthesis resulting in (2) H+ excretion as NH4+
1 = inhibits
2 = decreased
metabolic acidosis
- increase in arterial (1)
- decrease in arterial (2) (buffer)
- respiratory compensation is (3)
1 = H+ conc.
2 = HCO3- conc.
3 = hyperventilation
compensation of metabolic acidosis
- increased excretion of (1)
- increased reabsorption of (2)
- adaptive increase in (3)
1 = H+ as titratable acid and NH4+
2 = HCO3-
3 = NH3 synthesis
serum anion gap
[Na+] - ( [Cl-] + [HCO3-] )

represents unmeasured anions in serum including phosphate, citrate, sulfate and protein
normal value of serum anion gap
12mEq/L
serum anion gap is (1) if the conc. of an unmeasured anion is (2) to replace HCO3-
1 = increased
2 = increased
serum anion gap is (1) if the conc. of Cl- is (2) to replace HCO3-
1 = normal
2 = increased

aka. hyperchloremic metabolic acidosis
metabolic alkalosis
- decrease in arterial (1)
- increase in arterial (2)
- respiratory compensation with (3)
1 = H+ conc.
2 = HCO3- conc.
3 = hypoventilation
What happens when metabolic alkalosis is accompanied by ECF volume contraction?
reabsorption of HCO3- increases, worsening the metabolic alkalosis (contraction alkalosis)
respiratory acidosis
- caused by (1)
- increased arterial (2)
- increased arterial (3) and (4)
1 = decrease in respiratory rate and retention of CO2
2 = PCO2
3 = H+ and HCO3-
compensation for respiratory acidosis
- respiratory comp (1)?
- renal comp (2)
1 = no respiratory compensation
2 = increased excretion of H+ and increased reabsorption of HCO3-
respiratory alkalosis
- caused by (1)
- decreased arterial (2)
- decreased arterial (3) and (4)
1 = increase in respiratory rate and loss of CO2
2 = PCO2
3 = H+ and HCO3-
compensation for respiratory alkalosis
- respiratory comp?
- renal comp?
1 = no respiratory compensation
2 = decreased excretion of H+ and decreased reabsorption of HCO3-