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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

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2
Q

Myocardial oxygen demand determinants

A

Heart rate
Contractility
Intramyocardial wall tension

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3
Q

Angina pectoris

A

Chest pain caused by accumulation of metabolites caused by myocardial infarction

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4
Q

Three kinds of angina pectoris

A

Stable
Unstable
Variant

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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

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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

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7
Q

Variant angina

A

Uncommon

Coronary artery spasm due mostly to atheromatous disease

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8
Q

Variant angina therapy

A

Vasodilators - organic nitrates, calcium antagonists

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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

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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

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11
Q

Class of drugs used in angina

A 
Organic nitrates 
Calcium channel blockers
B blockers 
Ranolazine
Ivabradine
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12
Q

Action of drugs in ischemic disease

A

Decrease myocardial oxygen requirements

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13
Q

Nitrates and nitrites drugs

A 
Nitroglycerin 
isosorbide dinitrate
Isosorbide mononitrates
Amyl nitrates
Nicorandil
Nitropusside
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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

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15
Q

What enzyme is responsible for bio activation of nitroglycerin

A

Glutathione s transferase

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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)

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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

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18
Q

Nicorandil action

A

Reduce preload and afterload

Arterial and venodilAtor

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19
Q

Nicorandil adverse effects

A

Flushing dizziness headache

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20
Q

Where Or nitrates inactivated in the body

A

In the liver buy organic nitrate reductase

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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

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22
Q

Route of administration of nitrates

A

Oral
transdermal
Buccal absorption
sublingual

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23
Q

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

A

Because they are highly volatile liquids

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24
Q

Route of administration of nitrites

A

Inhalational

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25
Active metabolites of isosorbide dinitrate
Isosorbide mononitrate
26
Excretion of isosorbide mono nitrate
By kidney in the form of glucuronide derivatives
27
Calcium channel blocker’s groups
Phenylalkylamines Dihydropyridines Benzothiazepines
28
Phenylalkylamines drug name
Verapamil ( cardioselective , neg chronotropic initropic effect)
29
Dihydropyridines drugs name
``` Nifedipine Amlodipine felodipine Isradipine Nicardipine ``` Smooth muscle selective Potent vasodilators
30
Benzothiazepines
Diltiazem ( intermediate selective)
31
Dominant type of calcium channel in cardiac and smooth muscle
Voltage gated L-type calcium channel With alpha1 alpha2 Beta Gamma Delta
32
Calcium channel blocker Mechanism of action
``` Bind calcium channel Prevents opening due to depolarization Decrease transmembrane calcium current leads to lasting relaxation Reduced contractility in cardiac muscle ```
33
Why does verapamil have limited vasodilation
Because also act on potassium channels In vascular smooth muscle
34
Ostium channel blocker’s effects on smooth muscle
Relaxed smooth muscle ( bronchiolar vascular G.I. Uterine) Decreased blood pressure Decreased peripheral vascular resistance Decreased coronary artery spasm (good in variant angina)
35
Effect of calcium channel blocker’s on cardiac muscle
Decreased impulse generation in the sinostrial node Decreased conduction in the atrioventricular node’s Reduce the cardiac contractility Sometimes cardiac output decreases
36
Effet of CCB Skeletal muscul
Not really affected because not same calcium channel
37
CCB used in stroke
Verapamil (intra arterial route) and | Nicardipine (IV)
38
Cccan CCB reduce cerebral damage after thromboembolic stroke ?
Yes
39
dihydropyridine toxic effect
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
CCBs action
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
Clinical uses of CCBs
Angina hypertension supraventricular tachyarrhythmias Hypertrophic cardio myopathy migraine Raynauds phenomenon Nifedipine in pre term labor
42
When should you use nifedipine
When there’s AV conduction abdormakities because nifedipine does not decrease its conduction
43
Consequence of combination of verapamil or diltiazem with B blockers
AV block
44
Why can’t you use CCBs in heart failure
Worsen failure because of negative inotropic effect (except Amlodipine in heart failure due to non ischemic left ventricular systolic dysfunction)
45
dihydropyridines in low BP patients
Will worsen low BP so should use verapamil and diltiazem
46
Which CCB should you use if patient also has atrial tachycardia, flutter , fibrillatikn
Verapamil and diltiazem because of antiarrythmic effect
47
Which CCB can increase digoxin level when administering digitalis
Verapamil
48
Advantage of B blockers in managing angina
Decrease heart rate Decrease blood pressure Decrease contractility So decrease myocardial oxygen requirement
49
B blockers used in
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
Why is a nitrates use associated with beta blockers
Nitrates counterbalance the increase in end diastolic volume and increase ejection time caused by beta blocker
51
Contra indications of beta blockers
``` Asthma severe bradycardia AV blockade Bradycardia tachycardia syndrome severe unstable left ventricular failure ```
52
Beta blockers adverse effects
``` Fatigue impaired exercise deliverance insomnia Unpleasant dreams worsening of claudication erectile dysfunction ```
53
Ranolazine
Newer antianginal drug that reduce sodium currents( sodium current normally facilitates calcium entry via sodium calcium exchanger) Reduce cardiac contractility and work
54
Trimetazidine (metabolic modifier ranolazine ) of action
Fatty acid oxidation inhibitors Which decreases oxygen requirement that exist due increase fatty acid oxidation in ischemic myocardium
55
Allopurinol (metabolic modifier ranolazine ) of action
Inhibit xanthines oxidase which reduces oxidative stress and endothelial dysfunction
56
Ivabradine
Bradycardic drug selective for Na channel blocker Reduce cardiac rate by inhibiting hyperpolarization activated Na channel in SA node Reduces angina attacks
57
Fasudil action
Inhibitor of smooth muscle Rho kinase ( rho kinase inhibit vascular relaxation) Reduce coronary vasospasm
58
Most common cause of angina
Atherosclerotic disease of the coronaries
59
Factors affecting first line therapy of CAD
``` Changing risk factors such as : Smoking Hypertension Hyperlipidemia Obesity Clinical depression ``` Anti platelet drugs
60
Therapy to prevent MI and death
Antiplatelet agents - aspirin, ADP receptor blockers, clopidogrel, prasugrel Lipid lowering agents ( statins ) ACE inhibitors
61
Aggressive therapy for unstable angina and non ST segment elevation MI
Coronary stenting Anti lipid drug Heparin Antiplatelet agent Surgical revascularisation to restore coronary blood flow
62
Is surgical revascularisation and angioplasty indicated in patients with variant angina
No
63
Unstable angina therapy
Aggressive antiplatelet therapy (aspirin and clopidogrel) IV heparin Abciximab if percutaneous coronary intervention done Nitroglycerin and bblockersw Lipid lowering and ACE inhibitor
64
Concept of Treatment of claudication (peripheral artery disease )
``` Reversal of atherosclerosis Control of hyperlipidemia Hypertension Obesity Smoking cessation Diabetes ```
65
Treatment of PAD
Physical therapy Exercise Antiplatelet drug (aspirin , clopidogrel) Pentoxifylline ( reduce viscosity of blood ) Cilostazol (PDE3 inhibitor - antiplatelet and vasodilation effect ) Percutaneous angioplasty with stenting
66
Myocardial infarction cardiac event
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
Cause of MI
Coronary artery blocker by thrombus
68
Gold standard biochemical marker of MI
Troponin
69
types of MI
Anatomically -> transmural or subendocardial Diagnostically -> ST elevation and non ST elevation is
70
Risk of MI
``` Age Gender FHx Smoking Diabetes Hypertension Hyperlipidemia Obesity Physical activity ```
71
Where does MI starts
Endocardium
72
Severity of MI depends on
Level of occlusion Length of time of occlusion Presence or not of collateral circulation
73
Signs of MI
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
Assessment for chest pain
PQRST assessment ``` Precipitating events Quality of pain Radiation of pain Severity of pain Timing ```
75
CDV changes in MI
``` Initially high BP and pulse Later BP drops Urine output decreases Crackling lung sound Obvious pulsation in jugular vein due to distension ```
76
Early assessment of MI at hospital
``` Vital signs Oxygen saturation IV access 12 lead ECG Brief history Physical exam Blood sample for cardiac markers , electrolyte and coagulation ```
77
MONA treatment of ischemia
Morphine Oxygen Nitroglycerin Aspirin
78
Treatment of MI
Opening of occluded artery - angioplasty more effective than thrombolytics
79
Concept of tratemrn of MI
Improve cardiac function by maintaining oxygenation Reduce cardiac work Treat pain Prevent further thrombosis
80
Drugs class used in MI treatment
Thrombolytic and antiplatelet (aspiring and clopidogrel , heparin) Oxygen Opioids with antiemetic Organic nitrates Beta blockers, ACES
81
Fibrinolytic therapy
In patient with STEMI MI Within 12h of symptoms Break down clots
82
Fibrinolytic classsa
Tissue plasminogen activator ( alteplqse, retaplase, tenecteplase) Streptokinase ( natural streptokinase, anjstreplase) Urokinase
83
Fibrinolytic contra indication
Post op Hemorrhagic stroke history Ulcer Pregnancy
84
Long term care of MI
``` Smoking cessation Lifestyle medication Aspirin beta blocker and clopidogrel indefinite Lipid lowering medication Diet modification ```
85
MONA treatment of ischemia
Morphine Oxygen Nitroglycerin Aspirin
86
Treatment of MI
Opening of occluded artery - angioplasty more effective than thrombolytics
87
Concept of tratemrn of MI
Improve cardiac function by maintaining oxygenation Reduce cardiac work Treat pain Prevent further thrombosis
88
Drugs class used in MI treatment
Thrombolytic and antiplatelet (aspiring and clopidogrel , heparin) Oxygen Opioids with antiemetic Organic nitrates Beta blockers, ACES
89
Long term care of MI
``` Smoking cessation Lifestyle medication Aspirin beta blocker and clopidogrel indefinite Lipid lowering medication Diet modification ```
90
Fibrinolytic contra indication
Post op Hemorrhagic stroke history Ulcer Pregnancy
91
Fibrinolytic classsa
Tissue plasminogen activator ( alteplqse, retaplase, tenecteplase) Streptokinase ( natural streptokinase, anjstreplase) Urokinase
92
Fibrinolytic therapy
In patient with STEMI MI Within 12h of symptoms Break down clots

Cardiovascular Module (21 decks)

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