Drug treatments for cardiovascular disease 1 Flashcards

1
Q

Ischaemic heart disease

A

Narrowing of lumen of coronary arteries resulting in imbalance between supply of oxygen and myocardial demand resulting in myocardial ischaemia and chest pain

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2
Q

Regulation of cardiac workload

A

End diastolic volume regulated by sympathetic system, RAAS (contractility of venules), RAAS (Na+ and H2O retention)

Heart rate (sympathetic system/ Ca2+)

Contractility (sympathetic system/ Ca2+)

Total peripheral resistance (sympathetic system, RAAS)

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3
Q

Stable angina

A

A predictable pattern of pain during exercise that is relieved by rest

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4
Q

Side effects of nitrates

A

Postural hypotension

Reflex tachycardia

Headache

Dizziness

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5
Q

Reflex tachycardia

A

Due to activation of sympathetic nervous system

If treatment causes this, look to block effects of SNS using a beta blocker (atenolol)

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6
Q

Beta blockers

A

Decrease frequency and force contraction

Decreased cardiac output

Inhibit renin release from kidney so inhibit RAAS

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7
Q

Side effects of beta blockers

A

Bronchoconstriction

Fatigue

Contraindicated in patients with peripheral vascular disease

Bisoprolol

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8
Q

Ca2+ channel antagonists

A

Decrease frequency and force contraction (phenylalkylamines/ benzothiazepines)

Increase dilation in arterioles (dihydropyridines)

Decrease cardiac workload

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9
Q

Ivabradine

A

Blocks the pacemaker current in the nodal tissue of the heart (blocks Na+ entry)

Side effects:

  • luminous phenomena in retina
  • blurred vision
  • dizziness
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10
Q

Alternatives

A

Long acting nitrates (isosorbide mononitrate)
- decrease preload

Nicorandil
- decreases afterload

Ranolazine
- reduces work done by the heart

Trimetazidine
- rebalances energy metabolism in the cell

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11
Q

Treatment to reduce hypocholesterolaemia secondary prevention

A

Drugs designed to either inhibit uptake from GI tract or reduce production in liver

Frontline treatment are statins

  • simvastatin
  • atorvastatin
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12
Q

Statins

A

Decrease production of cholesterol in liver by inhibiting the HMG CoA enzyme

Stimulates liver cells to express LDL receptors and allows liver cells to scavenge LDL cholesterol from plasma

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13
Q

Further secondary prevention

A

Aspirin

  • antiplatelet agents
  • aspirin/ clopidogrel

ACE inhibitors

  • decrease the workload on the heart
  • ramipril

ARBs

  • decrease the workload on the heart
  • losartan
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14
Q

Mechanism of action of prasugrel

A

Rapid absorption after oral ingestion

Hydrolysis by esterases

Oxidation by cytochrome P-450

Active metabolite binds to ADP P2Y receptor

Platelet activation decreased

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15
Q

Diagnosis of myocardial infarction

A

Pain

Sweating, tachycardia, cold clammy skin

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16
Q

MI treatment

A
Pain relief (diamoprhine, u-opioid receptors)
- decreases pain, anxiety, sympathetic drive, vasodilates

Oxygen

Aspirin/ GTN

Clot busting drugs (tenecteplase, alteplase, streptokinase)
- stimulate conversion plasminogen to plasmin

17
Q

Beta blocker MI treatment

A

Decrease cardiac workload

Prevents arrhythmias

  • metoprolol
  • bisoprolol
18
Q

ACE inhibitor MI treatment

A

Decrease cardiac workload

Prevents remodelling development of heart failure

  • ramipril
19
Q

Anticoagulant MI treatment

A

In case of long term bed rest

Prevents thrombus formation

  • warfarin
20
Q

Treatment of heart failure

A

Digoxin binds to Na+/K+ ATPase and inhibits action

Increase Na+ inside heart muscle cells

Increase inhibits Na+/Ca2+ exchanger

Leads to build up of Ca2+ inside muscle cell so stronger contraction

21
Q

Treatment of dysrhythmias

A

Amiodarone

K+ channel blockers

Increases refractory period of ventricular myocytes and can terminate arrhythmias