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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
cell swelling
water intoxication
26
clinical marker for tonicity
serum [Na+]
27
when tonicity (higher Na+ concentration) is increased, what maintains water balance
thirst vasopressin (ADH)
28
what does an increase in tonicity (conc. of Na+) mean in terms of total body water
decrease in total body H2O
29
decrease in total body H2O; increase in [Na+]; causes what that leads to thirst response
OVLT cell shrinking; TRPV1,2,4 sensing; PON; thirst
30
decrease in total body H2O; increase [Na+]; causes what that leads to increase in ADH (response)
SFO/OVLT cell shrinking; TRPV1,2,4 sensing; increase in ADH
31
water intake (behavioral response)
thirst
32
water reabsorption by
vasopressin release (ADH)
33
at what euvolemic, plasma osmolality will thirst and vasopressin release happen and why
285; to protect osmolality from increasing
34
2 determinants for osmoregulation by water (net water balance)
thirst (water intake) ADH (renal water clearance)
35
clinical result of increased total body H2O (3)
1. hyponatremia 2. hypotonicity 3. water intoxication
36
clinical result of decreased total body H2O (3)
1. hypernatremia 2. hypertonicity 3. dehydration
37
2 determinants for ECF regulation by Na+
Na+ intake renal fraction Na+ excretion
38
3 ways for Na+ intake
taste habit baroreception
39
4 ways for renal fractional Na+ excretion
Na+ reabsorption tubuloglomerular feedback macula densa ANP, BNP
40
clinical result of too much total body Na+
edema
41
clinical result of decrease in total body Na+
dehydration
42
all diuretics will affect what
ECF regulation and osmoregulation
43
major player for ADH production
PVN (paraventricular nucleus)
44
excites anterior glands to secrete ADH
parvocellular nucleus
45
second site for ADH production
SON
46
nucleus that goes with SON for ADH secretion
magnocellular nucleus
47
2 regions that induce ADH secretion
SFO and OVLT
48
is there gas exchange at the glomerulus
no
49
2 main transporters of Thick Ascending limb
NKCC2 ROMK
50
2 main transporters for early DCT
NCC NCX
51
late distal tubule and collecting duct main transporters
ENaC ROMK MR HSD2 (cortisol) aquaporins
52
low GFR (reabsorbs at PCT and wont make it to DCT) and kidney failure: what drug
TORSEMIDE
53
aquaporin channel at PCT and thin descending limb
AQP1
54
aquaporin channel at collecting duct
AQP2
55
medullary [Na+] increases with each cycle
counter current multiplier
56
O2 exchanged b/t loops of henle (vasa recta)
counter current exchange
57
blocks SGLT2 in PCT
-GLIFOZINS
58
blocks carbonic anhydrase at PCT
ACETAZOLAMIDE (-ZOLAMIDES)
59
osmodiuretic that acts on PCT, thin descending limb, and collecting duct
MANNITOL
60
acts on NKCC2 in thick ascending limb
Furosemide
61
acts on NCC in early DCT
HCTZ
62
V2 antagonists acts on connecting tubules
-VAPTANS (CONIVAPTAN)
63
targets ENaC in late distal tubule and collecting duct
Amiloride
64
targets MR in collecting duct
Eplerenone
65
at PCT, Na+ comes in and H+ goes out through counter transporter and binds what in lumen
HCO3-
66
carbonic anhydrase converts H2CO3 to what that is taken into tubule
CO2 and H2O
67
what puts HCO3- into blood at PCT
Na+/HCO3- cotransporter
68
effects of ACETAZOLAMIDE
blocks CA; HCO3- stays in urine
69
B1B2 blocker that decreases aqueous humor (used to treat glaucoma) (HCO3- and water out)
ACETAZOLAMIDE
70
used to treat high altitude sickness by pulling HCO3- and water out
ACETAZOLAMIDE
71
used to treat glaucoma and mountain sickness (reduces formation of aqueous humor and CSF)
-ZOLAMIDES
72
SE of -ZOLAMIDES
metabolic acidosis (due to loss of HCO3-)
73
can happen due to alkalization of urine
renal stones
74
what causes paracellular transport of Ca2+ and Mg2+
+10 voltage of lumen when K+ comes through ROMK (from NKCC2 activation)
75
decreases loop diuretic function
NSAIDs
76
SE's include: hypokalemic metabolic alkalosis, kidney stones, ototoxicity
loop diuretics
77
blocks NCC and puts Ca2+ into blood; (Na+ and Cl- into lumen)
thiazide diuretics
78
binds PTH1R and increases Ca2+ rebasorption
PTH
79
treatment for patient w/ HTN and osteoporosis
thiazides (Chlorthalidone)
80
SE's include: hypokalemic metabolic alkalosis hypercalcemia hyponatremia hyperuricemia
Thiazides
81
contraindicated in gout
thiazides
82
K+ sparing diuretics that block ENaC
Amiloride Triamterene
83
K+ sparing diuretics that block mineralocorticoid receptor
spironolactone eplerenone
84
this transporter in principal cell of late DCT/CD brings Na+ in and K+ out through ROMK
ENaC
85
this transporter can lead to hypokalemia
ENaC's affect on ROMK
86
during hypovolemia (due to vomiting), what will increase
RAAS (aldosterone) increases ENaC receptors
87
increase Na+ excretion and increases K+ reabsorption
K+ sparing diuretics
88
diuretic of choice in hepatic cirrhosis (edema)
SPIRONOLACTONE EPLERENONE
89
used in primary hyperaldosteronism
MR antagonists K+ sparing drugs
90
osmotic diuretic used in acute renal failure
MANNITOL
91
increases osmolality of ECF (do to decrease in water) shifts water back into ECF
mannitol in dialysis disequilibrium syndrome
92
contraindicated in active intracranial bleeding
osmotic diuretics
93
can cause edema in different places
osmotic diuretics
94
blood glucose increases, water flows in, fall in [Na+]
translocational hyponatremia
95
hyponatremia w/out change in plasma osmolality
pseudohyponatremia
96
water absorption blocked; indicated in euvolemic and hypervolemic hyponatremia
V2-antagonists (-VAPTANS)
97
antidiuretic used in diabetes insipidus, primary nocturnal enuresis, vWD disease
desmopressin (V2 agonist)
98
promotes diuresis and dilates afferent arterioles (increasing GFR)
prostaglandins
99
adenosine when it binds A1R
vasoconstriction
100
adenosine when it binds A2R
vasodilator
101
double increase in total body weight single increase in total body Na+
hypervolemia (edema)
102
DDx of hypervolemia
hyponatremia
103
to treat hypervolemia
diuretic

URN Biweekly 1 (21 decks)

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