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renal > antihypertensives > Flashcards

antihypertensives Flashcards

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1
Q

hypertension systolic and diastolic

A

> 130/80

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2
Q

six types of diuretics

A 
carbonic anhydrase inhibitors
loop
thiazides
potassium sparing
vaptans
osmotic
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3
Q

acetazolamide is a

A

carbonic anhydrase inhibitor

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4
Q

carbonic anhydrase inhibitors MOA

A

inhibition of carbonic anhydrase in PCT leads to Na and HCO3 diuresis

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5
Q

indications for carbonic anhydrase inhibitors

A

acute glaucoma
altitude sickness
metabolic alkalosis
alkalinizes urine

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6
Q

carbonic anhydrase inhibitors adverse effects

A

sulfa allergies
hypokalemia
kidney stones
metabolic acidosis due to HCO3 loss

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7
Q

thiazides MOA

A

blocks NaCl cotransporter in distal tubule leading to increased sodium and water excretion

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8
Q

thiazides adverse effects

A

increase glucose, lipids, calcium, uric acid
hypOnatremia, hypokalemia
sulfa allergies

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9
Q

thiazide indications

A

HTN
peripheral edema
nephrogenic diabetes insipidus

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10
Q

furosemide is a

A

loop diuretic

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11
Q

loop diuretics MOA

A

inhibit NKCC2 symporter on TAL of LOH leading to dilute urine
(no reabsorption of Na, K Cl)

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12
Q

loop diuretics adverse effects

A

decreased electrolytes
ototoxicity
hypotension
sulfa allergy

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13
Q

loop diuretics indication

A

HTN
edema
hypercalcemia
hypermagnesemia

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14
Q

can be used for hypercalcemia

A

loop diuretics reduce reabsorption

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15
Q

K sparing agents MOA

A

aldosterone receptor antagonist in collecting duct increases Na and water excretion while concerning K and H

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16
Q

aldosterone antagonist K sparing diuretics indications

A

weak alone, use with thiazide/loop

hypokalemia
primary hyperaldosteronism
HTN
edema/ascites
CHF
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17
Q

Aldosterone antagonist K sparing diuretics adverse effects

A

hyperkalemia
gynecomastia
ED
Metabolic acidosis

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18
Q

ENaC K sparing diuretics adverse effects

A

kidney stones
hyperkalemia
metabolic acidosis

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19
Q

ENaC K sparing diuretics MOA

A

directly inhibit epithelial Na channel in collecting duct to increase NaCl and water loss

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20
Q

ENaC K sparing diuretics indications

A

HTN

CHF

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21
Q

ENaC blockers

A

triamterene

amiloride

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22
Q

vasopressin antagonists

A

tolvaptan

conivaptan

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23
Q

vasopressin antagonists’ MOA

A

block vasopressin type 2 receptor (V2) to prevent aquaporin insertion and decrease water reabsorption

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24
Q

Vasopressin antagonists’ adverse effects

A

hepatotoxicity
hypernatremia
thirst
(it is not really used)

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25
vasopressin antagonists indication
hyponatremia (but they correct this too quickly)
26
mannitol is a(n)
osmotic agent
27
osmotic agents MOA
mannitol is a non-metabolized sugar which increases osmotic pressure of glomerular filtrate draws more water into tubule to decrease reabsorption and increase diuresis
28
mannitol indications
elevated intracranial or intra-ocular pressure urogenital irrigation (not as an antiHTN)
29
mannitol adverse effects
hypotension hypovolemia pulmonary edema vesicant >5% concentration
30
CCBs general MOA
bind to and block L-type calcium channels in smooth muscle cells leading to vasodilation and a drop in BP
31
DHP rx
amlodipine nifedipine nicardipine clevidipine
32
DHPs primarily act on
vascular smooth muscles | amlodipine: arteries
33
Non DHP CCBs
verapamil | diltiazem
34
Non DHP CCBs act on
the heart | verapamil ventricles
35
what happens when the calcium channel is blocked?
Calcium cannot be released and the muscle cannot contract . | Ca is usually the signal for contraction
36
preferred DHP in pregnancy
nicardipine
37
Non DHPs _____ peripheral dilation, ______ HR, and ________ contractility
increase decrease decrease
38
DHPs _____ peripheral dilation
increase
39
adverse effects of Non-DHPs
bradycardia heart block gingival hyperplasia constipation
40
adverse effects of DHPs
headache peripheral edema flushing reflex tachycardia
41
indications for DHP CCBs
HTN angina Raynauds
42
indications for Non-DHP CCBs
HTN SVT angina cardiomyopathy
43
contraindications for DHP CCBs
hypertrophic obstructive cardiomyopathy stenotic valve defects hypotension ACS
44
contraindications for Non-DHP CCBs
``` ACS hypotension bradycardia conduction disorders DO NOT USE WITH beta blockers ```
45
do not use ______ with Non-DHPs because it will lead to _____
Beta blockers | severe bradycardia, AV block, decreased contractility
46
5 classes of antihypertensives
``` Diuretics RAAS inhibitors CCBs Adrenergic Agents Direct-Acting Vasodilators (Drugs Really Can Alter Diastole) ```
47
RAAS inhibitors classes
Angiotensin-converting enzyme inhibitors (ACEis) | Angiotensin receptor blockers (ARBs)
48
ACEi names end in ____
"pril"
49
ARBs names end in
"sartan"
50
ACEi MOA
blocks angiotensin converting enzyme in RAAS which does not allow angiotensin I to be converted to angiotensin II. decreased angiotensin II decreased aldosterone vasodilation
51
ACEis lead to a decrease in _____ and _____, which leads to ______
angiotensin II aldosterone vasodilation (lower BP)
52
ACEi indications
``` HTN HFrEF previous MI CKD diabetic nephropathy ```
53
2 drug classes that are nephroprotective
ACEIs and ARBs
54
ARBs MOA
block angiotensin II from binding to AT1 receptor which blocks the action of angiotensin II vasodilation and lower BP
55
ACEis and ARBs both _____ after load and _____ BP
decrease | lower
56
angiotensin II causes
vasoconstriction (that is why is is targeted to treat HTN)
57
aliskiren is a
direct renin inhibitor
58
ACEi adverse effects
cough angioedema hypotension hyperkalemia
59
ARBs adverse effects
angioedema hyperkalemia decreased GFR
60
direct renin inhibitor MOA
selectively blocks renin from activating RAAS which stops the whole process upstream so that vasoconstriction is decreased decreased BP
61
direct renin inhibitors adverse effects
diarrhea hyperkalemia teratogenicity
62
direct renin inhibitors contraindications
pregnancy if taking ACEs and ARBs (hyperkalemia) DM
63
ACEI/ARBs contraindications
pregnancy aortic stenosis renal artery stenosis
64
do not combine ____ and ACEI/ARBs
direct renin inhibitors
65
initial HTN treatment for a diabetic patient
ACEIs or ARBs
66
increase in bradykinin concentration can lead to
dry cough | bradykinin mediated angioedema
67
bradykinin is increased with use of what rx
ACEi
68
bradykinin
inflammatory marker that leads to vasodilation
69
chronotropic
affects HR
70
inotropic
affects contractility
71
alpha 1 blockers
doxazosin prazosin terazoin
72
a1 blockers MOA
block a1 receptor on vascular smooth muscle to cause vasodilation
73
a1 blockers adverse effects
orthostatic hypotension dizziness nausea
74
prazosin indication
HTN
75
terazosin/doxazosin indication
BPH | HTN
76
A2 agonists
methyldopa | clonidine
77
a2 agonists MOA
agonize A2 receptors to decrease vasoconstriction and lower BP
78
direct vasodilators
hydralazine | minoxidil
79
direct vasodilators MOA
direct relaxation of vascular smooth muscles to increase vasodilation and lower BP
80
direct vasodilators adverse effects
rebound tachycardia

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