B4-102 CBCL: Hypertension and Treatment Flashcards

(113 cards)

1
Q

inhibit NaCl reabsorption in distal convoluted tubule

A

thiazides

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2
Q

preferred antihypertensive drugs in elderly

A
  • thiazides
  • Ca+ channel blockers
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3
Q

preferred thiazide due to long half life and proven reduction of CVD

A

chlorthalidone

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4
Q

uses for thiazides

A

* hypertension
* congestive heart failure
* nephrolithiasis
* nephrogenic diabetes insipidus

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5
Q

adverse effects: thiazides

A
  • hypokalemic metabolic acidosis
    hyponatremia
  • hypergluc
    glycemia
    lipidemia
    uricemia
    calcemia
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6
Q

potassium sparing diurectics

A

Keep your SEAT

Spironolactone
Eplerenone
Amiloride
Triamterene

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7
Q

used to counteract hypokalemia caused by loop or thiazide diuretics

A

potassium sparing diuretics

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8
Q

end in -pril

A

ACE inhibitors

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9
Q

how do ACE inhibitors lower bp?

A

reduced angiotensin and increased bradykinin cause vasodilation

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10
Q

adverse effects: ACE inhibitors

A

Captopril’s CATCHH

cough
angioedema
teratogen
creatinine (increased)
hyperkalemia
hypotension

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11
Q

first choice of treatment for hypertensive patients with
* diabetes
* chronic renal disease
* left ventricular hypertrophy

A

ACE inhibitors

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12
Q

lower BP without compromising blood supply to heart, brain, or kidneys

A

ACE inhibitors

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13
Q

do not use in combination with ARBs or direct renin inhibitor

A

ACE inhibitor

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14
Q

end in -sartan

A

angiotensin receptor antagonists

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15
Q

how do angiotensin receptor antagonists differ from ACE inhibitors?

A
  1. more specific- no bradykinin increase
  2. more complete inhibition
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16
Q

adverse effects: ARBs

A
  • hyperkalemia
  • decreased GFR
  • hypotension
  • teratogen

similar to ACE, without coughing/bradykinin induced effects

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17
Q

reduced intracellular Ca+ causing arteriolar smooth muscle relaxation

A

Ca+ channel blockers

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18
Q

do not cause reflex tachycardia

A

verapamil and diltiazem

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19
Q

verapamil
diltiazem
-dipines

A

Ca+ Channel blockers

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20
Q
  • strongest vasodilators
  • most likely to produce reflex tachycardia
A

dihyropyridines
-dipines

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21
Q

adverse effects: dihydropyridines

A

peripheral edema
flushing
dizziness

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22
Q

adverse effects: nondihydropyridines

verapamil and dilitiazem

A
  • cardiac depression
  • bradycardia
  • AV block
  • constipation
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23
Q
  • orally active
  • dose-dependent reduction of plasma renin
  • dose dependent reduction of blood pressure
A

aliskiren

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24
Q

contraindications: aliskiren

A
  • pregnancy
  • do no combine with ACE inhibitors or ARB
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25
* reduction in renal sympathetic nerve activity * may also exert direct renal activity
clonidine
26
direct renin inhibitor
aliskiren
27
drugs that block renin secretion
clonidine beta blockers
28
block intra and extra renal receptors involved in neural control of renin secretion
beta blockers
29
block adrenergic receptors at nerve endings
peripheral antagonists
30
stimulates medullary adrenergic receptors
central agonists
31
beta-1 selective blockers | 4
* atenolol * betaxolol * bisoprolol * metoprolol
32
beta-1 selective blockers | 4
* atenolol * betaxolol * bisoprolol * metoprolol
33
b1 selective and vasodilatory beta blockers | 1
nebivolol
34
non selective beta blockers | 2
* nadolol * propranolol
35
beta blockers- intrinsic sympathomimetic activity | 4
* acebutolol (b1 selective) * penbutolol (non selective) * pindolol (non selective) * carteolol (non selective)
36
beta blockers- combined a and b receptors | 2
* carvedilol (a1 antagonist, nonselective) * labetalol (a1 antagonist, nonselective)
37
beta blockers lower BP by 3 mechanisms:
1. reduce CO 2. reduce renin secretion 3. reduce sympathetic vasomotor tone
38
more effective in caucasian and young hypertensives
beta blockers
39
long term benefits on mortality and CVD when used in people with heart failure or acute MI
beta blockers
40
pose a significant risk of new-onset diabetes
beta blockers
41
can worsen symptoms of * reduced myocardial reserve * asthma * peripheral vascular neuropathy * diabetes
beta blockers
42
a1 antagonists
-zosins
43
mechanism of action: a1 antagonists
BP falls due to decreased TPR
44
centrally acting sympatholytic drugs | 3
* clonidine * methyldopa * guanfacine
45
sudden withdrawal causes hypertensive crisis, headache, tremor, abdominal pain
clonidine
46
limited to pregnancy
methyldopa
47
orally active direct vasodilators | 2
hydralazine minoxidil
48
IV direct vasodilators | 5
* **sodium nitroprusside** * diazoxide * fenoldopam * enalprilat * nicardipine
49
IV direct vasodilator used for eclampsia
hydralazine
50
when would you use IV vasodilators?
hypertensive emergencies
51
dilate arteries selectively without affecting venous smooth muscle | 3
* hydralazine * minoxidil * diazoxide
52
dilates arteries by acting as a D1 agonist
fenoldopam
53
dilates both arteries and veins
sodium nitroprusside
54
adverse effects: vasodilators
* relex tachycardia * increased renin secretion
55
may cause lupus like syndrome
hydralazine
56
causes hypertrichosis
minoxidil
57
still hypertensive with two drugs
resistant hypertension
58
recommendations for treatment in pregnancy | 4
**N**ew **M**oms **L**ove **H**ugs **n**ifedipine **m**ethyldopa **l**abetalol **h**ydralazine
59
classes for treatment of primary hypertension
* thiazide diuretics * ACE inhibitors * ARBs * dihydropyridine * Ca+ channel blockers
60
classes of treatment of hypertension with heart failure
* diuretics * ACE inhibitors * ARBs * beta blockers * aldosterone antagonists
61
classes for treatment of hypertension in diabetes mellitus
* ACE/ARBs * Ca channel blockers * thiazide diuretics * beta blockers
62
classes for treatment of hypertensions with asthma
* ARBs * Ca channel blockers * thiazides * cardioselective beta blockers
63
should be avoided in patients with hypertension and asthma
* nonselective beta blockers * ACE inhibitors
64
can mask hypoglycemia symptoms
beta blockers
65
protective against diabetic neuropathy
ACE/ARBs
66
definition of hypertension
persistent systolic BP > 130 and/or diastolic >80
67
risk factors for hypertension
* age * obesity * diabetes * sedentary * high sodium diet * excess alcohol intake * smoking * family hx
68
primary hypertension is related to
* increased CO or * increased TPR
69
secondary hypertension is related to
renal/renovascular diseases
70
severe hypertension without acute end-organ damage
hypertensive urgency
71
severe hypertension with evidence of end organ damage
hypertensive emergency
72
hypertension predisposes risk to
* CAD * LVH * HF * a fib * aortic dissection/aneurysm * stroke * retinopathy
73
life course points of intervention: genes and early life
* genetic susceptibility * prenatal exposures
74
life course points of intervention: life course contributors
* diet, exercise, sleep, stress * housing policy * environmental exposures
75
life course points of intervention: treatment
* diagnosis of hypertensions * access to treatment, follow up, adequate control * sustained control or end organ damage
76
common environmental exposures
* lead * combustion products
77
fetal and early life exposures are heavily associated with
heavy metals and organics
78
first line treatment for hypertension
* thiazides * ACE * ARB * calcium channel blockers
79
second line treatment for hypertension
* beta blockers * direct renin inhibitors * alpha blockers * centrally acting agents * vasodilators
80
examples of end organ damage by hypertension
* brain anuerysm * dementia * MI * heart failure * kidney disease * stroke * vision loss
81
should be avoided in patients with sulfa allergies
thiazides
82
social stress causes hypertension through:
* increased sympathetic tone * vasoconstriction * oxidative stress
83
can lead to significant loss of potassium and may have to be paired with a potassium sparing agent
chlorthalidone
84
could lead to hyperkalemia through decreased aldosterone levels
ACEs/ARBs
85
* beta 1 selective * used for patients with asthma
acebutolol
86
can worse diabetes and increase plasma lipids
beta blockers
87
contraindicated in pregnancy
ACEs ARBs
88
can cause reflex tachycardia
nifedipine
89
can result in bradycardia
verapamil, dilitiazem
90
first line treatment for patients with hypertension and diabetes
ACE inhibitors
91
do ACE inhibitors affect the lipid profile?
no
92
can lead to hyperglycemia and hyperlipidemia
thiazides
93
can precipitate diabetes
beta blockers
94
should not be used with ARBs or direct renin inhibitors
ACEs
95
potassium sparing agent for hypokalemia
spironolactone
96
can lead to hyperkalemia
ACEs | **cannot combine with spironolactone
97
should not be used in patients with suldonamide allergies
thiazides
98
definition of hypertension in screening and treatment guidelines
.>130 systolic **OR** >80 diastolic
99
hypertension is more common in
african american individuals
100
how is race defined in health surveys and reasearch
patient self identifies
101
DOC in elderly
thiazides or CCB
102
may worsen CVD outcomes in elderly
beta blockers
103
not as effective in elderly
ACEs ARBs
104
prevent degradation of bradykinin
ACEs
105
can lead to angioedema
ACE inhibitors
106
inhibit renin secretion
beta blockers
107
can result in dry hacking cough
ACE inhibitors
108
direct renin inhibitor
aliskiren
109
work downstream of renin secretion but do not affect its activity directly
ACEs ARBs
110
do ACEs affect blood glucose concentrations?
no
111
most common side effect is constipation
verapamil
112
may cause hypokalemia
thiazides
113
may cause hyperkalemia
ACEs ARBs