Antianginal, Reg Of Bp (1st Class) Flashcards

0
Q

Isosorbide Mononitrate (active metabolite of dinitrate)

A
A= organic nitrate, anti-anginal 
B= free nitrate ions are released -> converted into NO which activates enzyme guanylate Cyclase -> increases I/c cGMP --> dephosphylation of myosin chain of SMC -> muscle relaxation and vasodilation& reduction of venous return -> reduction of left ventricular work and improves coronary blood flow & decreases myocardial oxygen demand 
C= angina prophylaxis due to CAD
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1
Q

Glyceryl trinitrate/nitroglycerin (acute/short acting) sublingual

A
A= organic nitrates, anti-anginal 
B= free nitrate ions are released -> converted into NO which activates enzyme guanylate Cyclase -> increases I/c cGMP --> dephosphylation of myosin chain of SMC (decreases ca2+ levels) -> muscle relaxation and vasodilation& reduction of venous return -> reduction of left ventricular work and improves coronary blood flow & decreases myocardial oxygen demand (more venous tone than arterial)
C= angina treatment, hypertensive crisis
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2
Q

Nifedipine

A
A= calcium channel blocker, 2nd generation dihydropyridine derivative, vasoselective
B= blocks voltage gated vascular alpha1 subunit of L-type calcium channels, decreases I/c levels of calcium in vascular smc, decreases contraction, cause muscle relaxation and vasodilation (reduces vascular resistance) may also facilitate the release of kidney stones
C= hypertension, angina pectoris, anti arrhythmiac, prinzmetal angina
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3
Q

Amlodipine

A
A= calcium channel blocker, 3rd generation dihydropyridine derivatives
B= blocks voltage gated vascular alpha1 subunit of L-type calcium channels, decreases I/c levels of calcium in vascular smc, decreases contraction, cause muscle relaxation and vasodilation (reduces vascular resistance)
C= hypertension, angina pectoris, anti arrhythmiac
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4
Q

Diltiazenum

A

A= calcium channel blocker, benzothiazepines (non -DHP)
B=blocks voltage gated vascular alpha1 subunit of L-type calcium channels, decreases I/c levels of calcium in vascular smc, decreases contraction, cause muscle relaxation and vasodilation (reduces vascular resistance). More selective for cardiac calcium channels
C= hypertension, angina pectoris, anti arrhythmiac (supraventricular paroxysmal tachycardia), cardio depressive properties, CAD

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5
Q

Propranolol

A
A= adrenonegative drug, non cardioselective beta blocker without ISA
B= blocks beta1and 2 receptors --> reduction in caricac ino-chronotropic-batmo-dromotropic effects as well as blood pressure and reflex orthostatic hypotension. Prevents sympathetic cardiac stimulation/ and reduce plasma renin secretions
C= angina pectoris, hypertension, tachycardia, heart failure, migraine, anti-anxiety activity (blocks serotonin receptors) acute myocardial infarction, hyperthyroidism, pheochromocytoma
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6
Q

Metoprolol tartrate

A
A= adrenonegative drug, selective beta1 antagonist without ISA 
B= blocks beta1>beta2 (cardioselective) --> reduces cardiac output (negative ino/batmo/chrono/dromotropic effects) 
C= angina pectoris, hypertension, arrhythmias, migraine, stenocardia, acute myocardial infarction, chronic heart failure!
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7
Q

Ivabradinum

A
A= cardiotonic/bradycardiac agent
B= acts by reducing HR (chronotropy) by its action on the SA node. It acts on the If ion motion which is highly expressed on the SA node. And blocking this channel reduces cardiac pacemaker activity, slows HR and thus allowing more time for blood to flow through myocardium
C= angina in patients with stable sinusrytm when beta blockers are contraindicated or not tolerated
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8
Q

Acetylsalicylic acid/aspirin? Low dosage= antiplatelet function (50-150 mg) high dosage= 500-1000 mg= anti inflammatory function

A
A= NSAID, analgesic, antipyretic, antiplatelet
B= irreversible inhibits cycloxygenases, Cox, and prostaglandins synthesis and inhibits thromboxane A2 synthesis --> antiplatelet aggregation --> reduce blood viscosity and improve blood flow (irreversible antiplatelet function)
C= inflammatory disorders, pain, fever, primary prophylaxis of MI prevention, TIA, stroke, unstable angina, CA thrombosis with MI
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9
Q

Clopidogrel

A
A= antiplatelet
B= anti thrombotic actions--> reduce platelet aggregation by inhibiting the ADP pathway of platelets--> irreversible blocks ADP receptors (specifically P2Y12 receptors are blocked by "grels" on platelets, thereby reducing glycoprotein 2b/3a -mediated aggregation (pathway of fibrinogen binding)
C= reduces ischemic events, secondary prevention of CAD, stroke, unstable angina, NSTEMI plus aspirin, thrombosis prevention in patients undergoing coronary stent placement, peripheral vascular disease
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10
Q

Trimetazidine

A
A= metabolic modulator, pFOX inhibitor
B= controls myocardial ischemia through intracellular metabolic changes. Ischemic myocardium metabolism shifts to oxidation of fatty acids --> the oxygen demand increases. Trimetazidine partially inhibits this fatty acid oxidation pathway in myocardium. In other words it helps by switching myocardial metabolism from fatty acid oxidation to glucose metabolism --> requires less oxygen
C= reduces angina frequency, tinnitus, dizziness
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11
Q

Ranolazinum

A
A= anti anginal drug, metabolic modulator
B= reduces a late sodium current (Ina) that facilitates calcium entry via the sodium/calcium exchanger port -> reduction of I/c calcium --> reduces cardiac work and contractility. Also modifies the fatty acid oxidation metabolism which may improve efficancy of cardiac oxygen utilization.  In other words it helps by switching myocardial metabolism from fatty acid oxidation to glucose metabolism --> requires less oxygen
C= angina prophylaxis, CAD
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12
Q

Atorvastatinum

A
A= statins 
B= competetive inhibitor of HMG coA reductase -> reduced cholesterol synthesis and up regulate LDL receptors on hepatocytes --> modest reduction in triglycerides
C= treatment of dyslipidemia, prevention of cardiovascular diseases and MI, antifibrotic and anti inflammatory effects on vessel wall, anti oxidant (=stabilizes the fatty plaque)
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13
Q

Fenofibratum

A
A= lipid lowering drug, fibric acid derivative
B= PPARalpha agonist, decrease VLDL and LDL levels, increase lipoprotein lipase activity (tous breaks down lipoprotein), increase HDL levels
C= hypertriglycerinemia, low HDL, prevention of cardiovascular disease, CAD and MI
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14
Q

Ezetimibum

A
A= lipid lowering drug, cholesterol absorption inhibitor
B= blocks sterol transporter NPCILI in intestine brush border, inhibits re absorption of cholesterol (decreasing exogenous levels of cholesterol) decreases LDL and phytosterols levels
C= elevated LDL, phytosterolemia, CAD
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15
Q

Nicotinic acid/Laropiprantum 1000mg by dose results in release of prostaglandins (= vitamin B3)

A
A= cholesterol reducer, vasodilator and spasmolytic
B= reduction of blood cholesterol levels in combination with niacin. Vit B3 acts as coenzymes participating in lipid metabolism--> reducing primarily triglycerides, inhibits free fatty acids of adipocytes
C= hypercholesterolemia, improves blood supply in extremities, CAD, MI prophylaxis
16
Q

Naftidrofurylum

A
A= vasodilator
B= vasodilator and thrombocyte aggregation inhibitor due to 5HT serotonin receptor antagonism
C= controls peripheral and cerebral vascular disorders, spasmolytics, idiopathic hearing loss, tinnitus
17
Q

Diosminum/hesperidium

A
A= vasoconstrictor, vasoprotector, bioflavonoid
B= prolongs vasoconstrictor effects of NE on vein walls, increases venous tone, reducing venous capacitance, distensibility and stasis. Acts as vitamine p, vasoprotector increases metabolism of bv wall --> decreases permeability of bv wall
C= chronic venous insufficiency, hemorrhoidal diseases, varicose veins
18
Q

Pentoxyphyllinum

A
A= xanthine derivative
B= competetive nonselective phosphodiesterase inhibitor, raising I/c cAMP, decreases ca2+ levels, improves flexibility of erythrocytes, activate PKA, inhibits leuktriens and TNF synthesis --> reduces inflammation and innate immunity
C= peripheral vascular diseases
19
Q

Nicergolinum

A
A= adrerenonegative drug, non selective alpha antagonist, ergot alkaloid derivative 
B= blocks both alpha1 and alpha2 receptors --> decreases peripheral resistance and constrictions of blood vessels --> vasodilation--> improves blood flow
C= improves blood flow in cerebral blood disorders (e.g atherosclerosis and thrombosis) and also migraines of vascular origin, transient ischemia, senile dementia, endarteritis obliterans, Raynaud's disease and hypertensive crisis, trophic ulcers (peripheral vascular disorders!, diabetes).