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
Hypokalemia promotes ---- exchange in | the distal nephron
Hypokalemia promotes H/K exchange in | the distal nephron
26
Potassium-Sparing Diuretics prevent
hypokalemic alkalosis
27
DCT Transport water
impermeable to water, does not respond to ADH
28
DCT Transport Na and Cl cross by ---
cotransport
29
DCT Transport Reabsorbs about % of filtered NaCl
5%
30
DCT Transport Thiazide diuretics bind to the
Cl- site on NaCl cotransporter
31
Thiazide Diuretics pH
alkalosis
32
Thiazide Diuretics K
hypokalemia
33
Thiazide Diuretics Na
hyponatremia
34
Thiazide Diuretics Ca
potential hypercalcemia
35
Thiazide Diuretics Mg
potential decrease with prolonged use
36
Thiazide Diuretics major use
Diuretic especially for hypertension
37
Thiazide Diuretics cause --- loss leading to
Na loss leading to water loss
38
Potassium-Sparing Diuretics pH
acidosis
39
Potassium-Sparing Diuretics Na
decrease reabsorption
40
Potassium-Sparing Diuretics H
increase excretion
41
Potassium-Sparing Diuretics K
hyperkalemia
42
Thiazides Toxicities and Interactions: -Na+ and volume depletion activates --- and can cause ----
RAAS; dehydration
43
Thiazides Toxicities and Interactions: Metabolic --- and ---
Metabolic alkalosis and hypokalemia
44
Thiazides Toxicities and Interactions Hypo
HYPO—kalemia, natremia, magnesemia
45
Thiazides Toxicities and Interactions Hyper
uricemia, glycemia, calcemia
46
Thiazides Toxicities and Interactions can cause --- by causing hypokalemia
digoxin toxicity
47
K competes with --- for binding to Na/K-ATPase
K competes with | digoxin for binding to Na/K-ATPase
48
TAL Transport % Na reabsorbed
25%
49
TAL Transport NaCl reabsorption occurs by
NKCC2
50
Thick ascending limb water permeability
not permeable
51
Thick ascending limb Lumen is positively charged making it a key site for
key site for | Ca++ and Mg++ resorption
52
luminal membrane is hyperpolarized
K+ leaving
53
basal membrane is depolarized
Cl- leaving
54
luminal membrane is depolarized
Na+ entering
55
basal membrane is hyperpolarized
K+ leaving
56
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
positive
57
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
negative
58
Loop Diuretics urine effects
increase in Na+, K+, Mg2+, Ca2+, and urine flow rate
59
Loop Diuretics ph
alkalosis
60
Loop Diuretics K
hypokalemia
61
Loop Diuretics Mg
Hypomagnesemia
62
Loop Diuretics Ca
hypocalcemia - rare
63
Loop Diuretics bock --- increasing renal blood flow
Flow sensing mechanism TGF
64
most effective Diuretic
Loop Diuretic
65
Loop Diuretic inhibit --- which abolishes ---
NKCC2; luminal positivity
66
Bartters Syndrome: Defective --- or ---
NKCC2 or ROMK - | hypoklaemia, metabolic alkalosis and hyperaldosteronism
67
Loop Diuretics Toxicities and Interactions hypo
HYPO—kalemia, magnesemia
68
Loop Diuretics Toxicities and Interactions hyper
HYPER—uricemia
69
Loop Diuretics can cause --- and ---
Metabolic alkalosis and dehydration
70
Loop Diuretics can cause --- toxicity
digoxin
71
Loop Diuretics can cause --- which is reversibly
ototoxicity
72
PCT Transport
NHE3
73
NHE3 is stimulated by
SNS and angiotensin II
74
Proximal Tubule water
freely permeable
75
Hyperglycemia causes
osmotic diuresis
76
Glucose
holds water in urine
77
Carbonic Anhydrase Inhibitors Major Use
Limited usefulness as diuretic | Treatment of glaucoma—topical dorzolamide
78
Carbonic Anhydrase Inhibitors pH
decrease bicarb leading to acidosis
79
Carbonic Anhydrase Inhibitors Cl
hyperchloremia
80
Carbonic Anhydrase Inhibitors K
hypokalemia