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Medicinal 3 > Anti Anginal > Flashcards

Anti Anginal Flashcards

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1
Q

What are the male manifestations of angina

A

Stabbing, pressure like, squeezing like and the pain radiated to the neck, shoulder and back

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2
Q

What are the female manifestions of angina?

A

Indigestion, Vomiting, Nasuea, Stomach pain/cramps

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3
Q

Describe the mammilian heart?

A

Double pump
Right side -> low pressure system delivering de-oxygenated blood to the lungs (Preload pressure)
Left side -> high pressure system delivering oxygenated blood to the body (Afterload pressure)

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4
Q

The walls of the right ventricle are much _____ than the left. why?

A

Thinner
Because the work load is lower for the right side of the heart.

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5
Q

Differentiate between the ventricle and atria

A

the venticular muslce -> stiff and takes time to fill with venous blood during diastole.
atria -> thin, flexible, buffers the incoming venous supply, their initial contraction at the beginning of each cardiac cycle fills the ventricles efficiently in a short space of time

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6
Q

How much blood is pumped through the heart per minute, and what is it dependent on?

A

5 liters / minute.
Dependent on:
1. HR
2. SV
3. Preload
4. Afterload

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7
Q

What is Starling’s Law?

A

Ventricular contraction is proportional to muscle fiber stretch.
Aortic output pressure rises as the venous filling pressure is increased.
Increase venous return -> increase cardiac output - up to a point.

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8
Q

Does the cardiac muscle require any nervous stimulation to contract?

A

No

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9
Q

How is each beat initiated?

A

Each beat is initiated by depolarisation of pacemaker cells in the sino-atrial (SA) node -> triggers neighboring atrial cells by direct electrical contracts and a wave of depolarisation spreads out over the atria -> exciting the atrio-ventricular (AV) node (AV is carried to ventricles by specialised bundles of conducting tissue -bundle of HIS-

Contraction of the atria -> ventricles -> forces extra blood into the ventricles and eliciting the starling response

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10
Q

The conducting tissues are derived from..?

A

modified cardiac muscle cells (the Purkinje fibers)

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11
Q

The conducting bundles divide repeatedly through

A

the myocardium to coordinated electrical and contractile activity across the heart

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12
Q

Although each cardiac muscle cell is in electrical contact with most of its neighbors, the message normally arrives first via the _________?

A

Purkinje system

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13
Q

What is angina

A

a type of chest pain caused by reduced blood flow to the heart

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14
Q

Angina is a symptom of?

A

coronary artery disease

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15
Q

Types of aniga?

A
  1. variant angina
  2. chronic stable angina
  3. unstable angina
    all of the forms are associated with a reduction in the oxygen supple/demand ration
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16
Q

Variant angina results from

A

coronary vasospam -> temporarily reduces coronary blood flow -> ischemia (supply ischemia) -> decreasing o2 supply/demand ratio

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17
Q

What could cause variant angina? and what wouldn’t cause it?

A

Variant angina could be a cause of mental stress

it IS NOT caused by atherosclerosis or physical activity

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18
Q

Could variant angina occur at rest?

A

Yes
emotional stress + dysfunctional coronary vascular endothelium (low Nitric oxide and prostacyclin) can precipitate vasospastic angina

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19
Q

What causes chronic stable angina?

A

chronic narrowing of the coronary arteries due to atherosclerosis

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20
Q

What will happen if the coronary artery is narrowed beyond a critical value (critical stenosis) in chronic stable angina

A

the myocardial tissue perfused by the artery will NOT recieve adequate blood flow -> ischemic and hypoxic tissues
particularly during times of increased oxygen demand (physical exertion)
decrease supply/demand ratio

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21
Q

Chronic stable angina is also known as

A

demand ischemia

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22
Q

True / False
The pain in chronic stable angina is usually associated with predictable threshold of physical activity

A

True

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23
Q

T/F: Large meals or emotional stress can also precipitate pain

A

True

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24
Q

What is unstable angina?

A

caused by transient formation and dissolution of a blood clot (thrombosis) within a coronary artery
here we have atherosclerosis but we haven’t reached complete closure. however, in the process, a clot forms and this clot is built on the closure area and causes it to close even more.

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25
The clots in unstable angina is often a response of?
plaque rupture in atherosclerotic coronary arteriess the clot may also form because diseased coronary artery endothelium is unable to produce nitric oxide and prostacylcin that inhibit platelet aggregation and clot formation
26
T/F: clot formation in unstable angina leads to reduction in the oxygen supply/demand ration (supply ischemia)
True
27
What happens if the clot completely occludes the coronary artery for a sufficent period of time in unstable angina?
the myocardium supplied by the vessel may become infarcted (acute myocardial infarction) and becomes irreversible.
28
What are the antianginal drugs by class
1. organic nitrates 2. calcium channel blockers (nondihydropyridine and dihydropyridine) 3. b-blockers
29
Mention organic nitrates drugs
Amyl nitrile nitroglycerine isosorbide dinitrate isosorbide mononitrate
30
mention calcium channel blockers (non dihydropyridine)
Verapamil diltiazem
31
Mention CCBs dihydropyridine
Nifedipine nicardipine amlodipine
32
mention B-blockers
Propranolol atenolol metoprolol nadolol pindolol
33
T/F: Nitric oxide is a molecule produced in many cells in the body and has several important actions
True
34
Where is Nitric oxide produced in the CVS
Vascular endothelial cells
35
What are the functions of Nitric oxide in the CVS
1. Relaxing vascular smooth muscle (vasodilation) 2. inhibiting platelet aggregation (anti-thrombotic) 3. inhibiting leukocyte-endothelial interactions (anti-inflammatory)
36
What will the decrease in Nitric oxide result in
vasoconstriction thrombosis inflammation
37
What are nitrodilators?
Drugs that mimic the actions of endogenous NO by releasing NO or forming NO within tissues
38
Where do Nitrodilators work
these drugs act directly on the vasculat smooth muscle -> relaxation -> endothelial independent vasodilators
39
T/F : organic nitrates directly release NO
False, they dont directly release NO
40
What is the MAO of organic nitrates
their nitrate group interact with enz. and intracellular sulfhydr1. RELAXING VAl groups -> reduce the nitrate groups to NO or to S-nitrosothiol which is then reduced to NO
41
What does nitric oxide activate?
1. NO activates smooth muscle soluble guanylyl cyclase (GC) to form cGMP. Increased cGMP-> inhibits calcium entry to the cells -> decreasing intracellular calcium concentrations -> causing smooth muscle relaxation 2. NO activates K+ Channels -> hyperpolarization and relaxation 3. NO -> cGMP -> cGMP dependant protein kinase -> activated myosin light chain phosphatase -> relaxation
42
What are the short acting organic nitrates? and when are they used?
For emergency 1. Nitroglycerin sublingual (0.15-1.2 mg 10-30min) 2. Isosorbide dinitrate sublingual (2.5-5mg 10-60 min) 3. Amyl nitrite inhalant (0.18-0.3 MI 3-5 min)
43
How does isosorbide dinitrate (isoket) work
it will bind on enzymes found in the veseels, these enzymes have a sulfahydryl (-SH) group. with the nitro group it will give nitroso intermediate and then Nitric oxide will be released
44
Theraputic uses of isosorbide dinitrate (isoket)
decrease the spasm of coronary arteries -> relax vein so it decrease preload oral / sublingual
45
T/F isosorbide dinitrate is very weak because it is gaseous?
True its a gas which gives it a quick onset and a 5 min duration
46
How is isosorbide dinitrate (gas) prepared?
by adsorption on a binder (like starch)
47
What type of intramolecular interaction will you find in isosorbide dinitrate (isoket)
Hydrophobic interaction
48
Is isosorbide dinitrate or mononitrate faster?
Dinitrate is faster mononitrate has a 1 hour DOA
49
T/F: isosorbide mononitrate and isosorbide dinitrate have the same MOA
True
50
What is the brand name of isosorbide mononitrate
Elantan
51
What are the brand names of nitroglycerin?
Nitroderm TTS-10 Nitroderm TTS-5
52
What are the available dosage forms of nitroglycerin
Oral Sublingual (2min) transdermal
53
What is the MOA of nitroglycerin
production of NO
54
T/F: nitroglycerin is gas, rapid onset, short duration
true
55
What kind of intermolecular interaction will you find in nitroglycerin
hydrophobic
56
What is the MOA of acebutolol
selective B1 antagonist with intrinsic agonist activity at high dose
57
What are the theraputic uses of acebutolol
INCREASE ratio of supple.demand because they are vasodilators less effective for angina than other b-blockers. used also for hypertension
58
What is the brand name of acebutolol
Sectral
59
What is the MOA of atenolol (Blokium tab)
Selective B1 Antagonist
60
What is the MOA of propanolol (Indicardin tab)
Non selective B antagonist
61
What are common Side effects of CCBs?
Fatigue because ca+2 us umportant for contraction of muscles and constipatin -> it effects the intestines
62
What is the MOA of CCBs
binds to L-TYPE Calcium channels located on vascular smooth muscles, cardiac myocytes, and cardiac nodal tissue (SA, AV nodes)
63
Calcium channels are responsible for regulating the _______ of calcium into cells
influx
64
Calcium influx stimulation in smooth muscles, cardiac myocytes, and nodes?
Smooth muscle -> contraction Cardiac myocytes -> contraction nodes -> pacemaker currents and phase 0 of Action potentials
65
What happens when you block calcium channels
1. Vasodilation 2. decrease myocardial force generation (neg intropy, dec contractility) 3. decreased HR 4. decreased conduction velocity (neg dromotropy) especialls at AV node
66
Dihydropyridines end with suffix ....?
pine
67
Theraputic indications of CCBs
HTN 1. vascular smooth muscle relaxation -> dec systemic vascular resistance -> lowers arterial bp 2. reduce HR and Contractility -> lowers CO -> lowers arterial pressure Angina 1. Vasodilator and cardiodepressant actions 2. reduces ventricular afterload (wall stress) -> lowering oxygen demand 3. dilate coronary arteries 4. prevent/reverse coronary vasospamsm (variant angina) -> inc oxygen supply Arrhythmia 1. class IV antiarrhythmics 2. suppress firing of aberrant pacemaker sites 2. decrease conduction velocity 3. prolong repolarization (AV node) 4. block reentry mechanism -> supraventricular tachycardia
68
T/F: CCBs primarily affect arterial resistance vessels with only minimal effects on venous capacitance vessels
True
69
What are the SE of dihydropyridine CCBs
flushing , headache, severe hypotension, peripheral edema, reflex tachycardia
70
T/F: dihydropyridines are less deseriable choices for stable angina than diltiazem, verapamin or BBs
True because the baroreceptor reflex activation of sympatheic nerves lack direct negative cardiac effects
71
T/F: long acting dihydropyridines (ER niedipine, amlodipine) have been shown to be safer antihypertensive drugs?
True because of reduced reflex responses makes them more suitable for angina than short acting dihydropyridines
72
T/F Long acting dihydropyridines are more suitable for angina than short acting dihydropyridines
True
73
What is the MOA of amlodipine
Greater affinity for Ca channels of vascular system than the hearts
74
Theraputic uses of amlodipine
HTN intrinsic natriuretic effect no need for diuretics
75
Side effects of Amlodipine
Constipation oedema fatigue
76
Is amlodipine a prodrug
No because the ester is active
77
What is the MOA of diltiazem (cardizebam)
affect both vessels and heart non dihydropyridine
78
Does diltiazem have SAR?
no sar
79
T/F: Felodipine and amlodipine have the same SAR?
Yes but felodipine has shorter half life
80
Where does nicardipine work
cardiac tissue and peripherally
81
Where does nifedipine work
cardiac tissue and peripherally
82
What was verapamil originally
an anti-malarial drug but it had resistance
83
T/F: verapamil is a lead compound
True
84
where does verapamil work?
both vessels and heart (L-type calcium channels)
85
T/F: Verapamil has organic cyano which inhibits CYP450 -> Drug drug interactions
True
86
Reducing O2 demand can be done using ...?
Beta blockers
87
Reducing peripheral vascular resistance can be done using..?
Vasodilators
88
What is the MOA of nitro vasodilators
Start or provoke the production of NO
89
T/F; NO is a 2nd messenger
True NO increases cGMP -> relaxation
90
Is Nitrous oxide the laughing gas
Yes
91
What intermolecular bonds can you find in Isosorbide mononitrate?
Hydrophobic interaction Hydrogen bonding (due to OH)
92
What antianginal drugs are ER drugs
Nitroglycerin 2 min Isosorbide dinitrate 5 min Isosorbide mononitrate 1 hr
93
What are the first line treatment for malaria
Quinones
94
Is amlodipine a Hydrogen bond donor?
Yes
95
Why is amlodipine not a prodrug even though it contains an ester?
because prodrugs should be metabolized in order to become active, amlodipine is already active before and after metabolism so it is NOT a prodrug
96
Why is felodipine has a shorter half life than amlodipine
No peripheral amine in felodipine
97

Medicinal 3 (6 decks)

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