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95 Cards in this Set
- Front
- Back
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plasma volume is measured by _
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radiolabeled albumin
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extracellular volume is measured by _
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inulin
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renal clearance equation
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Cx = Ux V / Px
Cx = clearance of substance x Ux = urine [ ] of x V = urine flow rate Px = plasma [ ] of x |
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_ can be used to calculate GFR
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inulin
creatinine |
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creatinine clearance is an approximate measure of GFR
but only approximate b/c |
it slightly overestimates GFR because creatinine is moderately secreted
("slightly overestimates" but even moreso in advanced kidney disease) |
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effective renal plasma flow
ERPF can be estimated using _ why? |
clearance of PAH
because PAH is both filtered and secreted (thus, all the PAH that enters the kidney is excreted) |
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RBF =
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RPF / (1-Hct)
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EFPF does not perfectly represent RPF
(effective renal plasma flow vs. renal plasma flow) |
ERPF underestimates true RPF by ~ 10%
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filtration fraction
FF = |
GFR / RPF
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filtered load means _
filtered load = |
total amount of a substance filtered per unit time
e.g. mg/min GFR x plasma concentration |
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flow of blood in the kidney
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renal
interlobar interlobular afferent glomerulus efferent vasa recta interlobular interlobar renal |
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at plasma glucose of _
glucosuria begins at _ all transporters are fully saturated |
160-200 mg/dL
350 mg/dL |
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Tm means
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maximal rate of transport of a substance
e.g. glucose |
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hartnup's disease can be caused in the kidney by
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deficiency of
neutral amino acid (tryptophan) transporter [it's a sodium-dependent amino acid resorption transporter in the proximal tubule] |
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the 3 D's of pellagra
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dementia
dermatitis diarrhea |
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hartnup's disease can cause
--> |
pellagra
(vitamin B3 deficiency) |
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niacin is vitamin _
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B3
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vitamin B3 is
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niacin
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which part of nephron contains brush border?
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early proximal tubule
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early proximal tubule
reabsorbs _ |
all: glucose and AAs
most: --bicarb --sodium --chloride --water isotonic absorption |
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early proximal tubule secretes
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ammonia
which acts as a buffer for secreted H+ |
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how does early proximal tubule reabsorb glucose?
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Na+ / glucose cotransport
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how does early proximal tubule reabsorb bicarbonate?
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secretes H+ in exchange for Na+ reabsorption
H+ joins HCO3- = H2CO3 carbonic anhydrase on the luminal side of the cell splits it H2O + CO2; CO2 crosses back into the cell CA in the cell makes H2CO3 yielding bicarb and H+ the bicarb is reabsorbed |
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hypertonic / hypotonic absorption at 4 different parts of the nephron
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early proximal tubule:
--isotonic absorption TAL --makes urine less concentrated Thin descending --makes urine hypertonic Early distal --makes urine hypotonic |
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two hormones that act on the early proximal tubule
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PTH
--inhibits Na+ / phosphate cotransport AT II --stimulates Na+/H+ exchange |
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AT II acts on _ of the nephron
causing ... |
stimulates Na+/H+ exchange
^ Na+ and H2O reabsorption (permitting contraction alkalosis) |
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proximal tubule re: chloride
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has a Cl- / base exchanger
which reabsorbs Cl- |
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thick ascending loop
hypertonic vs. hypotonic |
impermeable to H2O
makes urine less concentrated |
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thick ascending loop does reabsorption of...
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Na+ K+ 2Cl- pump
K+ leak into lumen causes + electrochemical potential there, which induces the paracellular reabsorption of Mg++ and Ca++ |
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thin descending loop
does... |
passively reabsorbs water
by medullary hypertonicity (impermeable to sodium) concentrating segment. makes lumen hypertonic. |
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_ is called the concentrating segment
_ is called the diluting segment |
thin descending loop
early distal convoluted tubule |
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early distal convoluted tubule
what pumps and channels? |
Na+ Cl- pump on luminal side
Na+ / Ca++ exchanger on interstitial/blood side that reabsorbs Ca++ Ca++ channel on luminal side |
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parathyroid hormone has its effects on the kidney how?
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proximal tubule:
v Na+/phosphate cotransport distal convoluted tubule: ^ Ca++/Na+ exchanger (on interstitial/blood side) --> Ca++ channel on luminal side to absorb Ca++ |
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early distal tubule is aka
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diluting segment
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aldosterone leads to _ (physical)
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insertion of Na+ channel on luminal side
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ADH acts at _ receptors -->
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V2 receptors
aquaporin H2O channels on luminal side |
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_ makes angiotensinogen
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liver
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3 stimuli for renin release
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v BP at JG cells
v Na+ at MD cells ^ sympathetic tone |
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AT II blocks an overreaction to its pressor effects...
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affects baroceptors
limits reflex bradycardia which would normally accompany its pressor effects |
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ANP effects (4)
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relaxes smooth muscle via cGMP, causing
^ GFR v renin ^ Na + filtration with no compensatory Na+ reabsorption in distal nephron |
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ADH primarily regulates _
but also responds to _ |
osmolarity
low blood volume which takes precidence over osmolarity |
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aldosterone primarily regulates_
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blood volume
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in low volume states, what hormone acts to protect blood volume?
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both ADH and aldosterone
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ACE is found in the lung and
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the kidney
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AT II effects (6)
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vasoconstriction
constricts efferent arteriole stimulates --aldosterone --ADH ^ proximal tubule Na+/H+ exchange ^ hypothalamus: thirst |
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AT II effects at the proximal tubule
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^ Na+/H+ exchange
--> H2O reabsorption can permit contraction alkalosis |
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how does sympathetic stimulation mediate renin secretion?
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beta1
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erythropoietin from the kidney...
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released from endothelial cells of peritubular capillaries
in response to hypoxia |
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NSAIDs can cause _ problem for kidney
how? |
acute renal failure
inhibiting renal production of prostaglandins (which vasodilate afferent arteriole to maintain GFR) |
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PTH stimulates vitamin D activation
how exactly? |
+ 1-alpha hydroxylase
at proximal tubule cells |
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net effect of ANP at the kidneys
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Na+ loss
volume loss |
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PTH is secreted in response to (3)
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low calcium
high phosphate low 1,25 vit D |
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mechanism
AT II vs. ANP |
^ GFR and ^ FF
with compensatory Na+ reabsorption in proximal and distal nephron ----------------------------- ^ GFR and Na+ filtration with no compensatory Na+ reabsorption in distal nephron |
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AT II
vs. ANP net effect: |
Na+ loss
volume loss -------------------- preservation of renal function in low-volume state Na+ reabsorption to v additional volume loss |
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ADH is secreted in response to
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^ plasma osmolarity
v blood volume |
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aldosterone is secreted in response to what physiological stimuli
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v blood volume
^ plasma [K+] |
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potassium shifts out of cell, causing hyperkalemia in response to (6)
mechanisms? |
v Na+/K+ ATPase:
--insulin deficiency --beta blockers --digitalis acidosis, severe exercise (^ K+ / H+ exchanger) hyperosmolarity cell lysis |
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potassium shifts into the cell
causing hypokalemia causes? (4) mechanisms? |
^ Na+ K+ ATPase:
--insulin --beta agonists alkalosis (^ K+ H+ exchanger) hypo-osmolarity |
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low Na+
sxs |
disorientation
stupor coma |
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high Na+
sxs |
irritability
delirium coma |
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low Cl-
causes |
2^
--metabolic alkalosis --hypokalemia --hypovolemia ^ aldosterone |
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low K+
sxs |
U waves on EKG
flattened T waves arrhythmias paralysis |
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paralysis is a symptom of
_ kalemia |
hypokalemia
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low Ca++
sxs |
tetany
neuromuscular irritability |
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low Mg++
sxs |
neuromuscular irritability
arrhythmias |
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high phosphate
sxs |
renal stones
metastatic calcifications |
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high Mg++
sxs |
delirium
v DTRs cardiopulmonary arrest |
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high Ca++
sxs |
delirium
renal stones abdominal pain not necessarily calciuria |
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high K+
sxs |
peaked T waves
wide QRS arrhythmias |
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henderson hasselbalch eq
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pH = pKa
+ log [HCO3-]/0.03 P CO2 |
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winter's formula
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PCO2 = 1.5 * HCO3- + 8
+/- 2 |
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winter's formula is used to
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quantify
respiratory compensation in response to metabolic acidosis |
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respiratory acidosis =
what labs? |
pH < 7.4
P CO2 > 40 mm Hg |
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metabolic acidosis with
hyperventilation compensation labs |
pH < 7.4
P CO2 < 40 mm Hg |
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anion gap =
(formula) |
Na+ - (Cl - + HCO3-)
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normal blood level of sodium
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136-145
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normal plasma bicarb
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22-28
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normal plasma Cl-
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95-105
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normal plasma K+
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3.5 - 5.0
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anion gap should equal
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12 +/- 2
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^ anion gap metabolic acidosis conditions
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MUDPILES
methanol (and formic acid) uremia diabetic ketoacidosis paraldehyde, phenformin iron tablets, INH lactic acidosis ethylene glycol (& oxalic acid) salicylates |
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normal anion gap conditions include
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diarrhea
glue sniffing renal tubular acidosis hyperchloremia |
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labs for
respiratory alkalosis |
pH > 7.4
P CO2 < 40 mmHg |
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respiratory alkalosis conditions include
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respiratory alkalosis
--hyperventilation e.g. early high-altitude exposure --aspirin ingestion (early) |
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labs for
respiratory alkalosis |
pH > 7.4
p CO2 > 40 mmHg |
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respiratory alkalosis includes
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hyperventilation e.g. early high-altitude exposure
aspirin ingestion (early) |
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metabolic alkalosis
with hypoventilation compensation causes? |
diuretic use
vomiting antacid use hyperaldosteronism |
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metabolic alkalosis with hypoventilation compensation
labs |
pH > 7.4
P CO2 > 40 mmHg |
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renal tubular acidosis types
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type 1 ("distal")
type 2 ("proximal") type 4 ("hyperkalemic") |
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distal renal tubular acidosis
where/what |
defect in collecting tubule's ability to excrete H+
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proximal renal tubular acidosis
where/what |
defect in proximal tubule HCO3- reabsorption
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distal renal tubular acidosis
associations |
associated with hypokalemia &
risk for calcium-containing kidney stones |
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proximal renal tubular acidosis
associations |
hypokalemia
hypophosphatemic rickets |
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hyperkalemic renal tubular acidosis
cause |
hypoaldosterone or lack of collecting tubule response to aldosterone
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hyperkalemic renal tubular acidosis
associations |
hyperkalemia
inhibition of ammonium excretion in proximal tubule leads to v urine pH due to v buffering capacity |
