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URN Biweekly 1 > Diuretics- Al Mehdi > Flashcards

Diuretics- Al Mehdi Flashcards

1
Q

Acetazolamide
Brinzolamide
(-ZOLAMIDES)

A

carbonic anhydrase inhibitors (diuretics)

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2
Q

Furosemide
Torsemide
Bumetanide
Ethacrynic acid

A

loop diuretics (target NKCC2 in TAL)

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3
Q

loop diuretic to use for patient allergic to sulfur

A

Ethacrynic acid

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4
Q

Chlorthalidone
HCTZ
Metolazone
Indapamide

A

thiazide/thiazide-like drugs (target NCC in early DCT)

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5
Q

Spironolactone
Eplerenone
Amiloride
Triamterene

A

K+ sparing diuretics (target ENaC and MR)

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6
Q

mannitol
glycerol

A

osmotic diuretics

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7
Q

Conivaptan
Tolvaptan
(-VAPTAN)

A

V2 antagonists

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8
Q

-VAPTANs used for what 2 disorders

A

cardiogenic edema
syndrome of inappropriate ADH secretion

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9
Q

_____ treated with MR antagonists (spironolactone and eplerenone)

A

HEPATIC EDEMA (Cirrhosis)

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10
Q

used to treat cerebral edema and glaucoma

A

osmotic diuretic (MANNITOL)

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11
Q

used to treat glaucoma and high altitude sickness

A

-ZOLAMIDES (CA inhibitors)

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12
Q

used for cardiogenic edema, hepatic edema, nephrogenic edema, syndrome of inappropriate ADH secretion, hypercalcemia

A

loop diuretics (furosemide)

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13
Q

used for HTN, nephrolithiasis, diabetes insipidus, osteoporosis

A

thiazides (HCTZ, Chlorthalidone, metolazone)

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14
Q

used to treat hypokalemia

A

K+ sparing diuretics

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15
Q

Amiloride
Triamterene

A

K+ sparing diuretics ENaC blockers

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16
Q

Spironolactone
Eplerenone

A

K+ sparing diuretics MR antagonists

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17
Q

treats hypokalemia, hyperaldosteronism, hepatic edema

A

K+ sparing diuretics MR antagonists (spironolactone and eplerenone)

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18
Q

used to treat primary nocturnal enuresis, diabetes insipidus

A

ANTIDIURETICS (desmopressin–V2 agonists)

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19
Q

what controls ECF volume

A

plasma Na+ concentration

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20
Q

136-145 mmol/L

A

normal plasma Na+ concentration

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21
Q

regulated by water balance

A

tonicity (osmotic pressure)

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22
Q

normal osmolality

A

275-295 mosm/kg

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23
Q

tonicity is maintained by water balance to prevent:

A

dehydration
water intoxication

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24
Q

cell shrinkage

A

dehydration

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25
Q

cell swelling

A

water intoxication

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26
Q

clinical marker for tonicity

A

serum [Na+]

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27
Q

when tonicity (higher Na+ concentration) is increased, what maintains water balance

A

thirst
vasopressin (ADH)

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28
Q

what does an increase in tonicity (conc. of Na+) mean in terms of total body water

A

decrease in total body H2O

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29
Q

decrease in total body H2O; increase in [Na+]; causes what that leads to thirst response

A

OVLT cell shrinking; TRPV1,2,4 sensing; PON; thirst

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30
Q

decrease in total body H2O; increase [Na+]; causes what that leads to increase in ADH (response)

A

SFO/OVLT cell shrinking; TRPV1,2,4 sensing; increase in ADH

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31
Q

water intake (behavioral response)

A

thirst

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32
Q

water reabsorption by

A

vasopressin release (ADH)

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33
Q

at what euvolemic, plasma osmolality will thirst and vasopressin release happen and why

A

285; to protect osmolality from increasing

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34
Q

2 determinants for osmoregulation by water (net water balance)

A

thirst (water intake)
ADH (renal water clearance)

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35
Q

clinical result of increased total body H2O (3)

A
  1. hyponatremia
  2. hypotonicity
  3. water intoxication
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36
Q

clinical result of decreased total body H2O (3)

A
  1. hypernatremia
  2. hypertonicity
  3. dehydration
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37
Q

2 determinants for ECF regulation by Na+

A

Na+ intake
renal fraction Na+ excretion

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38
Q

3 ways for Na+ intake

A

taste
habit
baroreception

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39
Q

4 ways for renal fractional Na+ excretion

A

Na+ reabsorption
tubuloglomerular feedback
macula densa
ANP, BNP

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40
Q

clinical result of too much total body Na+

A

edema

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41
Q

clinical result of decrease in total body Na+

A

dehydration

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42
Q

all diuretics will affect what

A

ECF regulation and osmoregulation

43
Q

major player for ADH production

A

PVN (paraventricular nucleus)

44
Q

excites anterior glands to secrete ADH

A

parvocellular nucleus

45
Q

second site for ADH production

A

SON

46
Q

nucleus that goes with SON for ADH secretion

A

magnocellular nucleus

47
Q

2 regions that induce ADH secretion

A

SFO and OVLT

48
Q

is there gas exchange at the glomerulus

A

no

49
Q

2 main transporters of Thick Ascending limb

A

NKCC2
ROMK

50
Q

2 main transporters for early DCT

A

NCC
NCX

51
Q

late distal tubule and collecting duct main transporters

A

ENaC
ROMK
MR
HSD2 (cortisol)
aquaporins

52
Q

low GFR (reabsorbs at PCT and wont make it to DCT) and kidney failure: what drug

A

TORSEMIDE

53
Q

aquaporin channel at PCT and thin descending limb

A

AQP1

54
Q

aquaporin channel at collecting duct

A

AQP2

55
Q

medullary [Na+] increases with each cycle

A

counter current multiplier

56
Q

O2 exchanged b/t loops of henle (vasa recta)

A

counter current exchange

57
Q

blocks SGLT2 in PCT

A

-GLIFOZINS

58
Q

blocks carbonic anhydrase at PCT

A

ACETAZOLAMIDE
(-ZOLAMIDES)

59
Q

osmodiuretic that acts on PCT, thin descending limb, and collecting duct

A

MANNITOL

60
Q

acts on NKCC2 in thick ascending limb

A

Furosemide

61
Q

acts on NCC in early DCT

A

HCTZ

62
Q

V2 antagonists acts on connecting tubules

A

-VAPTANS (CONIVAPTAN)

63
Q

targets ENaC in late distal tubule and collecting duct

A

Amiloride

64
Q

targets MR in collecting duct

A

Eplerenone

65
Q

at PCT, Na+ comes in and H+ goes out through counter transporter and binds what in lumen

A

HCO3-

66
Q

carbonic anhydrase converts H2CO3 to what that is taken into tubule

A

CO2 and H2O

67
Q

what puts HCO3- into blood at PCT

A

Na+/HCO3- cotransporter

68
Q

effects of ACETAZOLAMIDE

A

blocks CA; HCO3- stays in urine

69
Q

B1B2 blocker that decreases aqueous humor (used to treat glaucoma) (HCO3- and water out)

A

ACETAZOLAMIDE

70
Q

used to treat high altitude sickness by pulling HCO3- and water out

A

ACETAZOLAMIDE

71
Q

used to treat glaucoma and mountain sickness (reduces formation of aqueous humor and CSF)

A

-ZOLAMIDES

72
Q

SE of -ZOLAMIDES

A

metabolic acidosis (due to loss of HCO3-)

73
Q

can happen due to alkalization of urine

A

renal stones

74
Q

what causes paracellular transport of Ca2+ and Mg2+

A

+10 voltage of lumen when K+ comes through ROMK (from NKCC2 activation)

75
Q

decreases loop diuretic function

A

NSAIDs

76
Q

SE’s include: hypokalemic metabolic alkalosis, kidney stones, ototoxicity

A

loop diuretics

77
Q

blocks NCC and puts Ca2+ into blood; (Na+ and Cl- into lumen)

A

thiazide diuretics

78
Q

binds PTH1R and increases Ca2+ rebasorption

A

PTH

79
Q

treatment for patient w/ HTN and osteoporosis

A

thiazides (Chlorthalidone)

80
Q

SE’s include:
hypokalemic metabolic alkalosis
hypercalcemia
hyponatremia
hyperuricemia

A

Thiazides

81
Q

contraindicated in gout

A

thiazides

82
Q

K+ sparing diuretics that block ENaC

A

Amiloride
Triamterene

83
Q

K+ sparing diuretics that block mineralocorticoid receptor

A

spironolactone
eplerenone

84
Q

this transporter in principal cell of late DCT/CD brings Na+ in and K+ out through ROMK

A

ENaC

85
Q

this transporter can lead to hypokalemia

A

ENaC’s affect on ROMK

86
Q

during hypovolemia (due to vomiting), what will increase

A

RAAS (aldosterone) increases ENaC receptors

87
Q

increase Na+ excretion and increases K+ reabsorption

A

K+ sparing diuretics

88
Q

diuretic of choice in hepatic cirrhosis (edema)

A

SPIRONOLACTONE
EPLERENONE

89
Q

used in primary hyperaldosteronism

A

MR antagonists K+ sparing drugs

90
Q

osmotic diuretic used in acute renal failure

A

MANNITOL

91
Q

increases osmolality of ECF (do to decrease in water) shifts water back into ECF

A

mannitol in dialysis disequilibrium syndrome

92
Q

contraindicated in active intracranial bleeding

A

osmotic diuretics

93
Q

can cause edema in different places

A

osmotic diuretics

94
Q

blood glucose increases, water flows in, fall in [Na+]

A

translocational hyponatremia

95
Q

hyponatremia w/out change in plasma osmolality

A

pseudohyponatremia

96
Q

water absorption blocked; indicated in euvolemic and hypervolemic hyponatremia

A

V2-antagonists (-VAPTANS)

97
Q

antidiuretic used in diabetes insipidus, primary nocturnal enuresis, vWD disease

A

desmopressin (V2 agonist)

98
Q

promotes diuresis and dilates afferent arterioles (increasing GFR)

A

prostaglandins

99
Q

adenosine when it binds A1R

A

vasoconstriction

100
Q

adenosine when it binds A2R

A

vasodilator

101
Q

double increase in total body weight
single increase in total body Na+

A

hypervolemia (edema)

102
Q

DDx of hypervolemia

A

hyponatremia

103
Q

to treat hypervolemia

A

diuretic

URN Biweekly 1 (21 decks)

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