Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular Module > Pharmaco Ischemic Heart Disease > Flashcards

Pharmaco Ischemic Heart Disease Flashcards

1
Q

Main cause of ischemic heart disease

A

Atherosclerotic plaque Resulting in in balance between oxygen supply and demand leading to myocardial ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Myocardial oxygen demand determinants

A

Heart rate
Contractility
Intramyocardial wall tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Angina pectoris

A

Chest pain caused by accumulation of metabolites caused by myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Three kinds of angina pectoris

A

Stable
Unstable
Variant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Stable angina

A

Predictable Chest pain on exertion due to increased demand on the heart due to fixed narrowing of coronary vessels by atheroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How to treat stable angina

A

Reduce cardiac work ( organic nitrates, beta blockers, calcium antagonists)

Treat Underlying atheromatous disease including a statin

Prophylaxis against thrombosis with an anti platelet drug , usually aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Variant angina

A

Uncommon

Coronary artery spasm due mostly to atheromatous disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Variant angina therapy

A

Vasodilators - organic nitrates, calcium antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Unstable angina

A

Pain that occurs with less and less exertion , culminating in pain at rest platelet fibrin thrombus associated with ruptured atheromatous plaque , without complete obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Treatment of unstable angina

A

Anti platelet drugs - aspirin , ADP antagonists - reduce MI

Heparin and platelet glycoprotein receptor antagonist

Organic nitrate - relieve ischemic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Class of drugs used in angina

A 
Organic nitrates 
Calcium channel blockers
B blockers 
Ranolazine
Ivabradine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Action of drugs in ischemic disease

A

Decrease myocardial oxygen requirements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Nitrates and nitrites drugs

A 
Nitroglycerin 
isosorbide dinitrate
Isosorbide mononitrates
Amyl nitrates
Nicorandil
Nitropusside
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Month of action of nitrates nitrates

A

Increase of NO level
NO Activates heme group of guanylyl Cyclase
Guanylyl cyclase convert GTP to cGMP
CGMP act on myosin to form myosinLC which induce relaxation of vascular smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What enzyme is responsible for bio activation of nitroglycerin

A

Glutathione s transferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effects of nitroglycerin

A

Relaxation of veins
increased venous capacitance ( Can lead to syncope)
decreased Ventricular preload ( good in heart failure)
Reduced pulmonary vascular pressure
decreased heart size
Cardiac output decreased
Orthostatic hypotension
Decreased platelet aggregation (good in unstable angina)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

nitrates nitrates adverse effects

A

Orthostatic hypotension
tachycardia
throbbing headache

Patches of transdermal nitroglycerin should not be used with external defibrillator because risk of ignition

Tolerance
carcinogenicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Nicorandil action

A

Reduce preload and afterload

Arterial and venodilAtor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Nicorandil adverse effects

A

Flushing dizziness headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where Or nitrates inactivated in the body

A

In the liver buy organic nitrate reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why is sublingual roots of administration for nitrates preferred

A

Because they do not have first bus metabolism so that therapeutic blood level is achieved rapidly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Route of administration of nitrates

A

Oral
transdermal
Buccal absorption
sublingual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why are nitrites packaged in fragile glass ampules with a protective cloth

A

Because they are highly volatile liquids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Route of administration of nitrites

A

Inhalational

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Active metabolites of isosorbide dinitrate

A

Isosorbide mononitrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Excretion of isosorbide mono nitrate

A

By kidney in the form of glucuronide derivatives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Calcium channel blocker’s groups

A

Phenylalkylamines

Dihydropyridines

Benzothiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Phenylalkylamines drug name

A

Verapamil ( cardioselective , neg chronotropic initropic effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Dihydropyridines drugs name

A 
Nifedipine 
Amlodipine
 felodipine
Isradipine
Nicardipine

Smooth muscle selective
Potent vasodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Benzothiazepines

A

Diltiazem ( intermediate selective)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Dominant type of calcium channel in cardiac and smooth muscle

A

Voltage gated L-type calcium channel With alpha1 alpha2 Beta Gamma Delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Calcium channel blocker Mechanism of action

A 
Bind calcium channel
Prevents opening due to depolarization
Decrease transmembrane calcium current 
leads to lasting relaxation 
Reduced contractility in cardiac muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why does verapamil have limited vasodilation

A

Because also act on potassium channels In vascular smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Ostium channel blocker’s effects on smooth muscle

A

Relaxed smooth muscle ( bronchiolar vascular G.I. Uterine)

Decreased blood pressure

Decreased peripheral vascular resistance

Decreased coronary artery spasm (good in variant angina)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Effect of calcium channel blocker’s on cardiac muscle

A

Decreased impulse generation in the sinostrial node
Decreased conduction in the atrioventricular node’s
Reduce the cardiac contractility
Sometimes cardiac output decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Effet of CCB Skeletal muscul

A

Not really affected because not same calcium channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

CCB used in stroke

A

Verapamil (intra arterial route) and

Nicardipine (IV)

38
Q

Cccan CCB reduce cerebral damage after thromboembolic stroke ?

A

Yes

39
Q

dihydropyridine toxic effect

A

Risk of cardiac event if patient has HT
Nifedipine increase risk of MI if patient has hypertension

Cardiodepressant effect if B blocker administered

Flushing 
Diziness 
Constipation 
Nausea
Peripheral edema
40
Q

CCBs action

A

Decrease myocardial contract I’ll force decrease myocardial oxygen requirements
decrease arterial And intraventricular pressure

Left ventricular wall stress declines -> reduces my cardiologist requirements

Decreased HR -> Less oxygen requirements ( verapamil, diltiazem)

Prevent focal coronary artery spasm in variant angina

SA and AV nodes affected ( verapamil mostly and then diltiazem) -> supraventricular reentry tachycardia

Pfff

41
Q

Clinical uses of CCBs

A

Angina hypertension supraventricular tachyarrhythmias
Hypertrophic cardio myopathy migraine
Raynauds phenomenon
Nifedipine in pre term labor

42
Q

When should you use nifedipine

A

When there’s AV conduction abdormakities because nifedipine does not decrease its conduction

43
Q

Consequence of combination of verapamil or diltiazem with B blockers

A

AV block

44
Q

Why can’t you use CCBs in heart failure

A

Worsen failure because of negative inotropic effect (except Amlodipine in heart failure due to non ischemic left ventricular systolic dysfunction)

45
Q

dihydropyridines in low BP patients

A

Will worsen low BP so should use verapamil and diltiazem

46
Q

Which CCB should you use if patient also has atrial tachycardia, flutter , fibrillatikn

A

Verapamil and diltiazem because of antiarrythmic effect

47
Q

Which CCB can increase digoxin level when administering digitalis

A

Verapamil

48
Q

Advantage of B blockers in managing angina

A

Decrease heart rate
Decrease blood pressure
Decrease contractility
So decrease myocardial oxygen requirement

49
Q

B blockers used in

A

Exercise angina
Silent or ambulatory ischemia

Decrease mortality in recent myocardial infarction
prevents stroke in patients with hypertension
Better agents in stable angina than CCBs

50
Q

Why is a nitrates use associated with beta blockers

A

Nitrates counterbalance the increase in end diastolic volume and increase ejection time caused by beta blocker

51
Q

Contra indications of beta blockers

A 
Asthma 
severe bradycardia 
AV blockade 
Bradycardia tachycardia syndrome 
severe unstable left ventricular failure
52
Q

Beta blockers adverse effects

A 
Fatigue
 impaired exercise deliverance 
insomnia 
Unpleasant dreams
 worsening of claudication 
erectile dysfunction
53
Q

Ranolazine

A

Newer antianginal drug that reduce sodium currents( sodium current normally facilitates calcium entry via sodium calcium exchanger)
Reduce cardiac contractility and work

54
Q

Trimetazidine (metabolic modifier ranolazine ) of action

A

Fatty acid oxidation inhibitors

Which decreases oxygen requirement that exist due increase fatty acid oxidation in ischemic myocardium

55
Q

Allopurinol (metabolic modifier ranolazine ) of action

A

Inhibit xanthines oxidase which reduces oxidative stress and endothelial dysfunction

56
Q

Ivabradine

A

Bradycardic drug selective for Na channel blocker

Reduce cardiac rate by inhibiting hyperpolarization activated Na channel in SA node
Reduces angina attacks

57
Q

Fasudil action

A

Inhibitor of smooth muscle Rho kinase ( rho kinase inhibit vascular relaxation)
Reduce coronary vasospasm

58
Q

Most common cause of angina

A

Atherosclerotic disease of the coronaries

59
Q

Factors affecting first line therapy of CAD

A 
Changing risk factors such as : 
Smoking 
Hypertension 
Hyperlipidemia
Obesity 
Clinical depression

Anti platelet drugs

60
Q

Therapy to prevent MI and death

A

Antiplatelet agents - aspirin, ADP receptor blockers, clopidogrel, prasugrel

Lipid lowering agents ( statins )

ACE inhibitors

61
Q

Aggressive therapy for unstable angina and non ST segment elevation MI

A

Coronary stenting

Anti lipid drug

Heparin

Antiplatelet agent

Surgical revascularisation to restore coronary blood flow

62
Q

Is surgical revascularisation and angioplasty indicated in patients with variant angina

A

No

63
Q

Unstable angina therapy

A

Aggressive antiplatelet therapy (aspirin and clopidogrel)

IV heparin

Abciximab if percutaneous coronary intervention done

Nitroglycerin and bblockersw

Lipid lowering and ACE inhibitor

64
Q

Concept of Treatment of claudication (peripheral artery disease )

A 
Reversal of atherosclerosis 
Control of hyperlipidemia 
Hypertension 
Obesity 
Smoking cessation 
Diabetes
65
Q

Treatment of PAD

A

Physical therapy
Exercise
Antiplatelet drug (aspirin , clopidogrel)

Pentoxifylline ( reduce viscosity of blood )

Cilostazol (PDE3 inhibitor - antiplatelet and vasodilation effect )

Percutaneous angioplasty with stenting

66
Q

Myocardial infarction cardiac event

A

Zone of infarction - center area , dead not viable tissue , scar tissue

Zone of injury - viable tissue between ischemic and infarctus area

Zone of ischemia - outer most area , source of arryhtmkas , viable

67
Q

Cause of MI

A

Coronary artery blocker by thrombus

68
Q

Gold standard biochemical marker of MI

A

Troponin

69
Q

types of MI

A

Anatomically -> transmural or subendocardial

Diagnostically -> ST elevation and non ST elevation is

70
Q

Risk of MI

A 
Age 
Gender
FHx
Smoking 
Diabetes 
Hypertension
Hyperlipidemia 
Obesity 
Physical activity
71
Q

Where does MI starts

A

Endocardium

72
Q

Severity of MI depends on

A

Level of occlusion
Length of time of occlusion
Presence or not of collateral circulation

73
Q

Signs of MI

A

Chest pain discomfort ( heaviness , pressure , fullness, crushing sensation)

Nausea and vomiting ( reflex from severe pain)

Sympathetic nervous system stimulation (diaphoresis, vasoconstriction of peripheral blood vessels, cool sweat , temperature increases)

74
Q

Assessment for chest pain

A

PQRST assessment

Precipitating events 
Quality of pain
Radiation of pain
Severity of pain
Timing
75
Q

CDV changes in MI

A 
Initially high BP and pulse 
Later BP drops 
Urine output decreases 
Crackling lung sound
Obvious pulsation in jugular vein due to distension
76
Q

Early assessment of MI at hospital

A 
Vital signs 
Oxygen saturation
IV access
12 lead ECG 
Brief history 
Physical exam
Blood sample for cardiac markers , electrolyte and coagulation
77
Q

MONA treatment of ischemia

A

Morphine
Oxygen
Nitroglycerin
Aspirin

78
Q

Treatment of MI

A

Opening of occluded artery - angioplasty more effective than thrombolytics

79
Q

Concept of tratemrn of MI

A

Improve cardiac function by maintaining oxygenation

Reduce cardiac work

Treat pain

Prevent further thrombosis

80
Q

Drugs class used in MI treatment

A

Thrombolytic and antiplatelet (aspiring and clopidogrel , heparin)

Oxygen

Opioids with antiemetic

Organic nitrates

Beta blockers, ACES

81
Q

Fibrinolytic therapy

A

In patient with STEMI MI
Within 12h of symptoms
Break down clots

82
Q

Fibrinolytic classsa

A

Tissue plasminogen activator ( alteplqse, retaplase, tenecteplase)

Streptokinase ( natural streptokinase, anjstreplase)

Urokinase

83
Q

Fibrinolytic contra indication

A

Post op
Hemorrhagic stroke history
Ulcer
Pregnancy

84
Q

Long term care of MI

A 
Smoking cessation 
Lifestyle medication 
Aspirin beta blocker and clopidogrel indefinite
Lipid lowering medication 
Diet modification
85
Q

MONA treatment of ischemia

A

Morphine
Oxygen
Nitroglycerin
Aspirin

86
Q

Treatment of MI

A

Opening of occluded artery - angioplasty more effective than thrombolytics

87
Q

Concept of tratemrn of MI

A

Improve cardiac function by maintaining oxygenation

Reduce cardiac work

Treat pain

Prevent further thrombosis

88
Q

Drugs class used in MI treatment

A

Thrombolytic and antiplatelet (aspiring and clopidogrel , heparin)

Oxygen

Opioids with antiemetic

Organic nitrates

Beta blockers, ACES

89
Q

Long term care of MI

A 
Smoking cessation 
Lifestyle medication 
Aspirin beta blocker and clopidogrel indefinite
Lipid lowering medication 
Diet modification
90
Q

Fibrinolytic contra indication

A

Post op
Hemorrhagic stroke history
Ulcer
Pregnancy

91
Q

Fibrinolytic classsa

A

Tissue plasminogen activator ( alteplqse, retaplase, tenecteplase)

Streptokinase ( natural streptokinase, anjstreplase)

Urokinase

92
Q

Fibrinolytic therapy

A

In patient with STEMI MI
Within 12h of symptoms
Break down clots

Cardiovascular Module (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions