B4-050 Treatment of Angina Flashcards
(89 cards)
1
Q
angina occurs when the oxygen need
A
exceeds the supply
2
Q
immediate relief of angina
A
organic nitrates
3
Q
angina prophylaxis
A
calcium channel blockers
beta blockers
4
Q
angina is typically relieved with
A
rest and/or nitroglycerin
5
Q
typical location of angina
A
retrosternal
radiating to left/both arms
6
Q
classic or variant angina?
atheromatous obstruction of large coronaries, especially with exercise
A
classic
7
Q
classic or variant angina?
may require CABG or angioplasty if uncontrolled
A
classic
8
Q
classic or variant angina?
spasm or constrication in atherosclerotic coronary vessels
A
variant
9
Q
classic or variant angina?
relieved by nitrates and ca channel blockers
A
variant
10
Q
oxygen demand is determined by
A
- contractility
- heart rate
- wall stress
11
Q
main energy source in heart
A
fatty acid oxidation
12
Q
drugs that can shift myocardial metabolism toward glycolysis and reduce oxygen demand without affecting hemodynamics
A
- trimetazidine
- pFOX inhibitors
13
Q
oxygen supply depends on
A
- O2 delivery
- O2 extraction
14
Q
agents decreasing O2 demand
A
- beta blockers
- verapamil/dilitiazem
15
Q
agents that increase o2 supply
A
- dehydropyridines
- statins
- anti-thrombotics
16
Q
drugs that can relax vascular smooth muscle work by
A
- decreasing intracellular Ca (CCB)
- preventing depolarization (nicorandil)
- increasing cGMP (NO)
17
Q
3 drug groups used to treat angina
A
- organic nitrates
- CCBs
- beta blockers
18
Q
organic nitrates, CCBs, beta blockers
decrease myocardial oxygen demand by decreasing:
A
- HR
- ventricular volume
- blood pressure
- contractility
19
Q
- reduces intracellular Ca+ concentration, reducing cardiac contractility and work
- recently approved
A
ranolazine
20
Q
partially inhibits fatty acid oxidation
A
trimetazidine
21
Q
- inhibits xanthine oxidase
- prolongs exercise time in patients with angina
A
allopurinol
22
Q
direct bradycardic agent inhibiting the hyperpolarization activated Na+ channel in the SA node
A
ivabradine
23
Q
- rho-kinase inhibitor
- reduces coronary vasospasm in experimental animals
A
fasudil
24
Q
short acting nitrates
3
A
- amyl nitrate, inhaled
- nitroglycerin, sublingual
- isosorbide dinitrate
25
how are different vessel types affected by NO?
* large veins are markedly dilated
* arterioles and precapillary spinchters are dilated less
26
can potentiate action of NO in angina, causing severe hypotension and MI
sildenafil
27
can be used to treat cyanide poisoning
NO
28
# effect and result: beneficial nitrate effects
decreased BP and vasodilation
reduced myocardial O2 demand
29
# effect and result: beneficial nitrate effects
reduced ventricular diastolic pressure
improved subendocardial perfusion
30
# effect and result: beneficial nitrate effects
dilation of epicardial arteries
redistribution of coronary flow to ischemic area
31
# effect and result: beneficial nitrate effects
increased collateral flow
improved perfusion to ischemic areas
32
# effect and result: harmful nitrate effects
reflex increases in HR and contractility
increased myocardial O2 demand
33
# effect and result: harmful nitrate effects
reflex tachycardia
reduced perfusion due to shorter diastole
34
oral nitrates are rapidly metabolized by
hepatic reductase
35
What two nitrates should be given sublingual for rapid absorption and to avoid hepatic destruction?
* nitroglycerin
* isosorbide dinitrate
36
what nitrate, if given IV, dilates both arteries and veins equally?
sodium nitroprusside
37
fastest acting nitrate preparations
amyl nitrate, inhaled
sodium nitroprusside, IV
nitroglycerin, sublingual
38
acute nitrate toxicity can cause
* orthostatic hypertension
* tachycardia
* throbbing headaches
39
frequent exposure to nitrates can cause
tolerance
| Monday disease
40
CCBs are orally active drugs that block
L type Ca channels
41
Ca channels are opened by
stimulation of B receptors
42
CCBs affects [...] more than [...]
| blood vessels
arteries; veins
43
* dihydropyridine
* binding site 1A
* vascular selectivity
nifedipine
44
* benzothiapine
* binding site 1B
* selective for both vascular and myocardium
diltiazem
45
* phenylalkylamine
* binding site 1C
* selective for myocardial tissue
verapamil
46
CCB that is the strongest vasodilator, causes reflex tachycardia
nifedipine
47
CCB with strongest cardiac affects, causes myocardial depression, decreases HR
verapamil
48
short acting CCBs should be avoided in patients with
hypertension
49
beneficial effects of dihydropyridines
* coronary vasodilation (increased O2 supply)
* systemic arteriole vasodilation (decreased afterload)
50
harmful effects of dyhydropyridines
severe hypotension -> reflex tachy -> increased cardiac workload -> increased risk of MI
51
beneficial effects of verapamil and diltiazem
* reduced SA automaticity and AV conduction
* decreased myocardial contractility and bradycardia --> decreased cardiac work load
52
harmful effects of verapamil and diltiazem
cardiac depression, resulting in cardiac arrest, AV block, or CHF
53
may enhance digoxin toxicity
verapamil/diltiazem
54
should not be used in patients with ventricular dysfunction or SA/AV node disturbances
verapamil/diltiazem
55
* inhibit insulin secretion
* interfere with platelet aggregation
* relatively minor side affects
CCBs
56
extremely useful for the mangement of angina associated with effort
beta blockers
57
do not dilate coronary arteries
beta blockers
58
beneficial effects of beta blockers
* decreased sympathetic activity (decreased cardiac work)
* direct vasodilation
* bradycardia (increased perfusion time)
59
may induce or worsen CHF in patients with acute MI or decompensated HF
beta blockers
60
potentially harmful in variant angina
beta blockers
61
may increase plasma triglycerides and decrease HDL causing atherosclerosis
beta blockers
62
most common cause of angina pectoris
atherosclerotic disease of the coronaries
63
first line therapy: angina
* modify risk factors
* antiplatelets
64
what drugs are more effective for variant angina?
nitrates and CCBs
65
most effective drug combinations for angina
* b-blockers and CCBs or,
* 2 CCBs
66
potentially harmful effects of CCBs or beta blockers can be prevented by
nitrates
| and vice versa
67
relfex tachycardia can be minimized by combining nitrates with
CCBs or beta blockers
68
result in pronounced dilation of large vessels, reduce preload
nitrates
69
reduce afterload and/or cardiac function
CCBs
70
reduce vasocontriction and cardiac function
beta blockers
71
increase risk for new onset diabetes
beta blockers
72
acute nitrate toxicity
* headaches
* orthostatic hypertension
* tachycardia
73
potentiate the action of nitrates and lead to MI
PDE-5 inhibitor
| sildenafil
74
cause decreased oxygen demand
verapamil/dilitiazem
| suppress AV and SA nodes
75
decrease preload via venodilation
nitrates
76
* decrease afterload by arteriodilation
* decrease TPR
dihydropyridine and nitrates
77
increase oxygen supply by redistributing blood flow
nitrates
78
increase oxygen supply by coronary vasodilation
dihydropyridines
79
reduce sympathetic activity on the heart
beta 1 blockers
80
decrease peripheral resistance by reducing angiotensin 2
ACE/ARBs
81
slow down heart rate by depressing SA and AV node
verapamil
82
short acting nitrate used for acute anginal attacks
sublingual nitroglycerin
83
short acting nitrate for chronic treatment of angina
oral isosorbide mononitrate
84
used to treat hypertension and heart failure but can precipitate angina due to reflex cardiac stimulation
hydralazine
85
result in tolerance or marked reduction of effect upon repeated exposure
nitroglycerin
86
to reduce nitroglycerin tolerance,
use lowest effective dose with nitrate free intervals of 10-12 hrs daily
87
preferentially acts as a vasodilator leading to reflex tachy
nefedipine
88
work as vasodilators without causing relfex tachycardia
a1 blockers
| zosins
89
suppress SA/AV nodes leading to bradycardia
verapamil/diltiazem
