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GIR Test 4 > B5-041 Renal Physiology IV > Flashcards

B5-041 Renal Physiology IV Flashcards

1
Q

what receptor does ADH bind to to cause vasocontriction?

A

V1

triggers Ca2+ release –> actin-myosin coupling –> vasoconstriction

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2
Q

do V1 or V2 receptors have a higher affinity for ADH?

A

V2 has higher affinity

thats why osmolarity causes big changes in ADH and pressure only small

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3
Q

small cell lung carcinoma and lung infections can cause

A

SIADH

secretes peptides similar to ADH, too much ADH

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4
Q

central Diabetes insipidus causes water diuresis because

A

hypothalmus does not secrete ADH

decreased water absorption, urine dilution

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5
Q

nephrogenic diabetes insipidus causes water diuresis due to

A

mutation in V2 (lithium ingestion)

decreased water reabsorption, urine dilution

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6
Q

diabetes mellitus causes […] diuresis

solute or water

A

solute

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7
Q

how does a normal individual react to a water restriction test?

A

osmolarity increases, volume decreases

primary polydipsia would be similar

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8
Q

how does an individual with central diabetes insipidus react to a water restriction test?

A
  • very little change in volume/osmolarity until ADH is added
  • then, osmolarity will go up and volume wil go down
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9
Q

how does an individual with nephrogenic diabetes insipidus react to a water restriction test?

A

kidneys do not respond to ADH

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10
Q

treatment for diabetes insipidus

A

ADH analog
(desmopressin)

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11
Q

treatment of SIADH

A

treat underlying cause or inhibit V2 receptors

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12
Q

4 main effector pathways regulating salt and water excretion

A
  1. ADH
  2. natriuretic peptides
  3. RAAS
  4. sympathetic nervous system
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13
Q

stimulus for release of ANP

A

increased heart volume

released from atria

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14
Q

stiumulus for release of BNP

A

increased heart volume

released from ventricle

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15
Q

stimulus for release of CNP

A

increased intravascular volume

released from brain

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16
Q

stimulus for release of urodilatin

A

increased volume and Na+ load

released from kidney

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17
Q

describe the mechanism of action of natriuretic peptides

A
  • bind to NPR on vascular smooth muscle cells
  • diminish calcium
  • cause vasodilation
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18
Q

inhibits ENac in the collecting duct causing less sodium reabsorption

more dilute urine

A

urodilatin

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19
Q

how does sympathetic nervous activity regulate GFR?

A

produces vasoconstriction

constrict vessels –> less volume in afferent arteriole –> low GFR

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20
Q

sensors that regulate ECF volume

2

A

baroreceptors
volume receptors

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21
Q

sensors that regulate ECF osmolarity

A

hypothalmic osmoreceptors

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22
Q

effector pathways for regulation of ECF volume

4

A
  • ADH
  • ANP
  • RAAS
  • SNS
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23
Q

effector pathways that regulate ECF osmolarity

2

A
  • ADH
  • thirst
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24
Q

all transport in the proximal tubules is associated with

A

Na+

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25
Q

the proximal tubule gets rid of bicarb through

A

bicarb-sodium transporter in basolateral membrane

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26
Q

what cells in the distal and collecting tubules regulate pH?

A

a intercalated

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27
Q

how do cells a intercalated cells get rid of H+?

A

H+ active transporters on the apical side of cells

require ATP

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28
Q

for every proton that comes out, one […] comes in

A

bicarbonate

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29
Q

what cells are very important for getting rid of H+ and protect from acidosis?

A

a intercalated cells

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30
Q

what cells are very important for getting rid of bicarbonate and protecting from alkalosis?

A

b intercalated cells

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31
Q

transporter on apical side of b intercalated cells

A

HCO3/Cl- exchanger

basolateral in a- intercalated cells

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32
Q

transporter on basolateral side of b-intercalated cells

A

active H+ transport pump

apical in a-intercalated cells

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33
Q

what part of the tubule reabsorbs 80% of bicarb through Na/HCO3 transporter in the basolateral membrane?

A

proximal tubule

34
Q

how does the kidney buffer urine?

A
  • combine H+ with HPO4 to make phosphoric acid
  • combine H+ with HCO3 to make carbonic acid

urine acidification

35
Q

how does the kidney produce ammonium?

A
  • glutamine –> glutamate = a-ketoglutarate + NH3
  • NH3 combines with H+ to make ammonium (NH4)
36
Q

how to calculate urine anion gap

A

(Na + K) - Cl

should be a negative number

37
Q

urine anion gap is an indicator of the ability of the kidney to

A
  • produce ammonium
  • get rid of protons
38
Q

if the UAG is negative, what does this mean?

urine anion gap

A

normal
kidneys are producing ammonium and eliminating H+ appropriately

39
Q

equation for plasma anion gap

A

Na - (Cl + HCO3)

40
Q

normal anion gap

A

8-16

41
Q

what does a normal anion gap indicate?

A

kidneys are eliminated excess fixed acids

42
Q

plasma anion gap […] as pH is reduced

A

increases

43
Q

what cells work to compensate for alkalosis?

A

b- intercalated cells

44
Q

if PCO2 rises, proton secretion becomes dominant and the kidney excretes […]

A

acid

raises blood pH

45
Q

if HCO3 in plasma rise, HCO3 filtration increases and the kidney excretes […]

A

alkali

reducing blood pH

46
Q

how does the kidney respond to respiratory acidosis?

A
  1. excretes protons in the proximal and distal portions of the nephron
  2. reabsorbs bicarb (bicarb raised in plasma)
  3. pH normalizes
47
Q

how will the kidneys respond to respiratory alkalosis?

A

excrete bicarb (through saturation and b- intercalated cells)

48
Q

causes of metabolic acidosis with normal PAG

A
  • bicarb loss (diarrhea, proximal renal tubular acidosis)
  • decreased acid secretion/bicarb consumption (distal renal tubular acidosis, aldosterone deficiency)
49
Q

causes of metabolic acidosis with high PAG

A
  • high acid input (keto acidosis, lactic acidosis, salicylate, methanol, ethylene glycol)
  • low acid input (renal failure)
50
Q
  • decreased distal acidification
  • low plasma bicarb
  • normal PAG
  • low serum K
  • urine pH > 5.5
A

type I
distal RTA

51
Q
  • decreased bicarbonate reabsorption
  • very low plasma bicarb
  • normal PAG
  • low serum K+
  • normal/low urine pH
A

type II
proximal RTA

52
Q
  • decreased aldosterone
  • low plasma bicarb
  • normal PAG
  • high serum K+
  • normal/low urine pH
A

type IV
distal hyperkalemic RTA

53
Q

with more aldosterone, you have more […] secretion

A

hydrogen

54
Q

if you have hyperaldosteronism, will cause

A

alkalosis

55
Q

if you have high aldosterone, the patient will become

A

alkalotic

56
Q

in a patient who is hypoventilating due to chronic lung disease, the kidneys will respond by

A

increasing net secretion of acid

H2PO4, CO3H2, NH4+

57
Q

in a patient who is hypoventilating, the PCO2 will

A

increase

58
Q

an increase in PCO2 will activate […] in the kidney

A

mechanism involved in acid secretion

59
Q

PCO2 is an important regulator of the activity of […] in intercalated cells

A

H-ATPase

60
Q

actively secretes protons into the tubular lumen

A

H-ATPase

61
Q

for each proton excreted, one […] is reabsorbed

A

bicarbonate

62
Q

when excretion of NH4+ is adequate, the UAG is

A

negative

63
Q

patients with type I distal renal tubular acidosis have an inability to secrete

A

protons

reduces amount of NH4+, UAG positive

64
Q

what 2 molecules are low in urine in RTA?

A

bicarb
ammonium

65
Q

bicarb reabsorption in the proximal tubule is tightly coupled to

A

secretion of protons by Na-H exchanger

66
Q

a positive urine anion gap indicates

A

inappropriate excretion of ammonium

67
Q

secreted by JG cells in response to decreased renal perfusion pressure

A

renin

68
Q

increases renal sympathetic discharge (B1 effect) and decreases NaCl delivery to macula densa cells

A

renin

69
Q

catalyzes conversion of angiotensin I to angiotensin II

A

ACE

70
Q

produced by vascular endothelial cells in the lung

A

ACE

71
Q

helps maintain blood pressure and blood volume

A

angiotensin II

72
Q

affects baroreceptor function; limits reflex bradycardia which would normally accompany its pressor effects

A

angiotensin II

73
Q

released from atria and ventricles in response to increased volume

A

ANP, BNP

74
Q
  • inhibits RAAS system
  • relaxes vascular smooth muscle via cGMP to increase GFR and decrease renin
  • dilates afferent arteriole
A

ANP, BNP

75
Q

primarily regulates serum osmolality

A

ADH

76
Q

stimulates reabsorption of water in collecting ducts

A

ADH

77
Q

stimulates reabsorption of urea in collecting ducts to maximize corticopapillary osmotic gradient

A

ADH

78
Q

primarily regulates ECF volume and Na+ content

A

aldosterone

79
Q
  • release is increased in hypovolumic states
  • responds to hyperkalemia by increasing K+ excretion
A

aldosterone

80
Q

how to beta blockers inhibit renin release?

A

inhibit B1 receptors in JG cells causing decreased renin release

GIR Test 4 (18 decks)

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