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BMS 615 Cardiovascular > Test2: Wk7: 4 Bridge to pharmacology - renal transport mechanism - Puri > Flashcards

Test2: Wk7: 4 Bridge to pharmacology - renal transport mechanism - Puri Flashcards

1
Q

Na transport along the nephron: thin loops only use — transport

A

passive

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2
Q

Na transport along the nephron: PCT 3 transporters

A

NHE
SGLT2
Na-AA-Cotransporter
66%

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3
Q

Na transport along the nephron TAL 2 transporters

A

NKCC2
ROMK
25%

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4
Q

Na transport along the nephron DCT 2 transporters

A

Na-Cl cotransport
Epi Ca Channels
5%

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5
Q

Na transport along the nephron CT 3 transporters

A

Epi Na Channels
ROMK
H-ATPase/ K-H exchanger
3%`

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6
Q

Na transport along the nephron: — can absorb 100% of Na

A

TAL

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7
Q

Na transport along the nephron: — is the only site of active reabsorptions of Ca

A

DCT

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8
Q

% Na filtered appears in urine

A

~1%

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9
Q

Cortical Collecting Tubule: Na+ resorption by

A

ENaC

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10
Q

Cortical Collecting Tubule: Na+ resorption creates

A

luminal negativity

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11
Q

luminal negativity leads to

A

K+ secretion

H+ secretion

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12
Q

3.Antidiuretic hormone (ADH) inserts — channels in the luminal membrane

A

H2O

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13
Q

— sensitive to amiloride

A

ENaC

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14
Q

𝜶-intercalated cells in the Cortical Collecting Tubule/Duct Primary Transporter

A

H-ATPase

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15
Q

𝜶-intercalated cells in the Cortical Collecting Tubule/Duct Secondary Transporter

A

HK- antiport

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16
Q

Aldosterone has three effects

A

Directly stimulate H-ATPase

  • ↑Na-K-ATPase, which ↑Na gradient to enter the cell
  • ↑ENaC activity and number—↑Luminal negativity—More H+ can be secreted
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17
Q

Na+ resorption in CT is key to — and —

excretion → activated by —

A

Na+ resorption in CT is key to K+ and H+

excretion → activated by aldosterone

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18
Q

Aldosterone — Na+ and K+ channel activity and

the activity of the Na/K-ATPase

A

Aldosterone ↑ Na+ and K+ channel activity and

the activity of the Na/K-ATPase

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19
Q

Na+ resorption creates luminal

A

negativity

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20
Q

3.Luminal negativity “draws” out

A

K

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21
Q

aldosterone “exchanges” — for —-

in the lumen of the distal nephron

A

Na for K

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22
Q

Luminal negativity also facilities H+ secretion

by

A

H-ATPase

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23
Q

when is aldosterone activated

A

when circulating blood volume is decreased

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24
Q

increased luminal flow increases K secretion resulting in

A

increased urine flow and increased K excretion

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25
Q

Hypokalemia promotes —- exchange in

the distal nephron

A

Hypokalemia promotes H/K exchange in

the distal nephron

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26
Q

Potassium-Sparing Diuretics prevent

A

hypokalemic alkalosis

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27
Q

DCT Transport water

A

impermeable to water, does not respond to ADH

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28
Q

DCT Transport Na and Cl cross by —

A

cotransport

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29
Q

DCT Transport Reabsorbs about % of filtered NaCl

A

5%

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30
Q

DCT Transport Thiazide diuretics bind to the

A

Cl- site on NaCl cotransporter

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31
Q

Thiazide Diuretics pH

A

alkalosis

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32
Q

Thiazide Diuretics K

A

hypokalemia

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33
Q

Thiazide Diuretics Na

A

hyponatremia

34
Q

Thiazide Diuretics Ca

A

potential hypercalcemia

35
Q

Thiazide Diuretics Mg

A

potential decrease with prolonged use

36
Q

Thiazide Diuretics major use

A

Diuretic especially for hypertension

37
Q

Thiazide Diuretics cause — loss leading to

A

Na loss leading to water loss

38
Q

Potassium-Sparing Diuretics pH

A

acidosis

39
Q

Potassium-Sparing Diuretics Na

A

decrease reabsorption

40
Q

Potassium-Sparing Diuretics H

A

increase excretion

41
Q

Potassium-Sparing Diuretics K

A

hyperkalemia

42
Q

Thiazides Toxicities and Interactions: -Na+ and volume depletion activates — and can cause —-

A

RAAS; dehydration

43
Q

Thiazides Toxicities and Interactions: Metabolic — and —

A

Metabolic alkalosis and hypokalemia

44
Q

Thiazides Toxicities and Interactions Hypo

A

HYPO—kalemia, natremia, magnesemia

45
Q

Thiazides Toxicities and Interactions Hyper

A

uricemia, glycemia, calcemia

46
Q

Thiazides Toxicities and Interactions can cause — by causing hypokalemia

A

digoxin toxicity

47
Q

K competes with — for binding to Na/K-ATPase

A

K competes with

digoxin for binding to Na/K-ATPase

48
Q

TAL Transport % Na reabsorbed

A

25%

49
Q

TAL Transport NaCl reabsorption occurs by

A

NKCC2

50
Q

Thick ascending limb water permeability

A

not permeable

51
Q

Thick ascending limb Lumen is positively charged making it a key site for

A

key site for

Ca++ and Mg++ resorption

52
Q

luminal membrane is hyperpolarized

A

K+ leaving

53
Q

basal membrane is depolarized

A

Cl- leaving

54
Q

luminal membrane is depolarized

A

Na+ entering

55
Q

basal membrane is hyperpolarized

A

K+ leaving

56
Q

If the luminal membrane is hyperpolarized (K+ leaving) and/or the basal membrane is depolarized (Cl- leaving) the potential difference between the lumen and the interstitium is lumen

A

positive

57
Q

If the luminal membrane is depolarized (Na+ entering)
and/or the basal membrane is hyperpolarized (K+
leaving) the potential difference between the lumen
and the interstitium is lumen

A

negative

58
Q

Loop Diuretics urine effects

A

increase in Na+, K+, Mg2+, Ca2+, and urine flow rate

59
Q

Loop Diuretics ph

A

alkalosis

60
Q

Loop Diuretics K

A

hypokalemia

61
Q

Loop Diuretics Mg

A

Hypomagnesemia

62
Q

Loop Diuretics Ca

A

hypocalcemia - rare

63
Q

Loop Diuretics bock — increasing renal blood flow

A

Flow sensing mechanism TGF

64
Q

most effective Diuretic

A

Loop Diuretic

65
Q

Loop Diuretic inhibit — which abolishes —

A

NKCC2; luminal positivity

66
Q

Bartters Syndrome: Defective — or —

A

NKCC2 or ROMK -

hypoklaemia, metabolic alkalosis and hyperaldosteronism

67
Q

Loop Diuretics Toxicities and Interactions hypo

A

HYPO—kalemia, magnesemia

68
Q

Loop Diuretics Toxicities and Interactions hyper

A

HYPER—uricemia

69
Q

Loop Diuretics can cause — and —

A

Metabolic alkalosis and dehydration

70
Q

Loop Diuretics can cause — toxicity

A

digoxin

71
Q

Loop Diuretics can cause — which is reversibly

A

ototoxicity

72
Q

PCT Transport

A

NHE3

73
Q

NHE3 is stimulated by

A

SNS and angiotensin II

74
Q

Proximal Tubule water

A

freely permeable

75
Q

Hyperglycemia causes

A

osmotic diuresis

76
Q

Glucose

A

holds water in urine

77
Q

Carbonic Anhydrase Inhibitors Major Use

A

Limited usefulness as diuretic

Treatment of glaucoma—topical dorzolamide

78
Q

Carbonic Anhydrase Inhibitors pH

A

decrease bicarb leading to acidosis

79
Q

Carbonic Anhydrase Inhibitors Cl

A

hyperchloremia

80
Q

Carbonic Anhydrase Inhibitors K

A

hypokalemia

BMS 615 Cardiovascular (49 decks)

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