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Cardiovascular System > Clinical Pharmacology of Stable Coronary Artery Disease > Flashcards

Clinical Pharmacology of Stable Coronary Artery Disease Flashcards

1
Q

Acute Coronary Syndromes

A

MI (STEMI, NSTEMI)

Unstable Angina

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2
Q

Stable Coronary Artery Disease

A

Angina pectoris

Silent Ischaemia

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3
Q

Risk Factors (6)

A
  • Hypertension
  • Smoking
  • Hyperlipidaemia
  • Hyperglycaemia
  • Male
  • Post-menopausal females
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4
Q

• In the atherosclerosis what are most of the changes in the intimal layer a result of?

A

Accumulation of monocytes, lymphocytes, foam cells and connective tissue

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5
Q

What is the origin of foam cells

A

Smooth muscle

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6
Q

What do these accumulations in the arteries contain

A

Necrotic core

Fibrous cap

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7
Q

How cab drugs correct the imbalance of supply and demand (2)

A

Decrease myocardial oxygen demand

Increasing the supply of oxygen to ischaemic myocardium

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8
Q

How can drugs reduce the myocardial oxygen supply (3)

A

Reduce heart rate
Reduce contractility
Reduce afterload

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9
Q

The purpose of the drug treatment (5)

A
  • Relieve symptoms
  • Halt the disease process
  • Regression of the disease process
  • Prevent MI
  • Prevent death
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10
Q

Demand Ischaemia is determined by (4)

A

HR
Systolic blood pressure
Myocardial wall stress
Myocardial contractility

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11
Q

Supply Ischaemia is determined by (4)

A

Coronary artery diameter and tone
Collateral blood flow
Perfusion pressure
Heart rate (duration of diastole)

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12
Q

What is the action of beta blockers

A

Rate limiting

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13
Q

What is the use of beta blockers

A

Decrease the determinants of myocardial oxygen demand: HR, Contractility, systolic wall tension

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14
Q

What is the mechanism of beta blockers

A

Reversible antagonists of the B1 and B2 receptors

Block the sympathetic system

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15
Q

What are the contraindication for beta blockers (5)

A 
Asthma
Peripheral vascular disease
Raynauds Syndrome
Heart Failure
Bradycardia/Heart block
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16
Q

Beta Blocker adverse drug reactions (5)

A 
Tiredness/fatigue
Lethargy
Impotence
Bradycardia
Bronchospasm
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17
Q

What is the rebound phenomena

A

Sudden cessation of beta blocker therapy may precipitate myocardial infarction

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18
Q

Who is at risk of experiencing rebound phenomena

A

• Those at risk include patients with angina and men over 50 years receiving beta blockers for other reasons

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19
Q

Beta blocker + Hypotensive drugs

A

Hypotension

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20
Q

Beta Blocker + Rate limiting drug (verapamil or Diltiazem)

A

Bradycardia

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21
Q

Beta blocker + inotropic drugs (Verapamil, Diltiazem and Disopyramide)

A

Cardiac failure

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22
Q

Beta blocker + NSAIDs

A

Antagonise antihypersensitive actions

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23
Q

Beta blocker + Insulin or Oral Hypoglycaemics

A

exaggerate or mask hypoglycaemic actions

24
Q

Calcium channel action can be

A

Rate limiting

Vasodilation

25
Q

Rate limiting Calcium channel blockers use

A

Diltiazem and Verapamil reduce HR and force of contraction

26
Q

Rate limiting calcium channel blockers mechnaism

A

Prevent calcium influx into myocyte and smooth muscle lining by blocking L-type calcium channels

27
Q

Contraindications of Rate limiting calcium channel blockers

A

Post MI

Unstable angina

28
Q

How does rate limiting calcium channel blockers Dihydropyridine work

A

inhibition of the smooth muscle L-type calcium current, thus decreasing intracellular calcium concentration and inducing smooth muscular relaxation

29
Q

Adverse reactions of rate limiting calcium channel blockers (4)

A

Ankle oedema
Headache
Flushing
Palpitation

30
Q

Action of non-rate limiting calcium channel blockers

A

Nifedipine or amlodipine produce reflex tachycardia

31
Q

Mechanism of non rate limiting calcium channel blockers

A

Vasodilation

reduce vascular tone and reduce afterload

32
Q

Contraindication of non rate limiting calcium channel blockers (2)

A

Never use Nifedipine immediate release can cause MI or stroke
Don’t use post MI in patients with impaired LV function

33
Q

Action of Ivabradine

A

Rate limiting

34
Q

Action of Ivabradine

A

Reduces heart rate and myocardial oxygen demand

35
Q

Mechanism of Ivabradine

A

Selective sinus node channel inhibitor

Slows the diastolic depolarisation slope of SA node

36
Q

Contraindications of Ivabradine (3)

A

Low heart rate
Allergy
Severe Hepatic disease

37
Q

Adverse reaction of Ivabradine (5)

A 
Visual disturbances
Headache, dizziness
Bradycardia
Atrial fibrillation
Heart block
38
Q

Nitrates action

A

Vasodilators

39
Q

Examples of nitrates

A

GTN
Isosorbide Mononitrate
Isosorbide Dinitrate

40
Q

Action of Nitrates

A

Reduce preload and afterload to reduce myocardial oxygen consumption

41
Q

Mechanism of Nitrates

A

Relax almost all smooth muscle by releasing NO which then stimulates the release of cGMP which produces smooth muscle relaxation

42
Q

Complications of Nitrates

A

Tolerance

Requires nitrate free period

43
Q

Adverse reactions of Nitrates

A

Headache (increase dose slowly)

Hypotension (GTN syncope)

44
Q

Use of Clopidogrel

A

Prevents atherosclerotic events in PVD

45
Q

Mechanism of Clopidogrel

A

Inhibits ADP receptor activated platelet aggregation

46
Q

Nicorandil (4)

A
  • Activate ATP sensitive potassium channels
  • Entry of potassium into cardia myocytes inhibits calcium influx and so has a negative inotropic action
  • Ischaemic pre-conditioning (cardioprotective)
  • Vasodilation of coronary epicardial arteries
47
Q

Ranolazine

A
  • Inhibits persistent or late inward sodium current in heart muscle in a variety of voltage gated sodium channels
  • Inhibition of current leads to reductions in calcium levels
  • Reduction in calcium levels leads to reduced tension in the heart all and a reduced oxygen requirement for muscles
48
Q

When would you use antiplatelet agents

A
  • Adults unable to tolerate or have a contraindication to the use of beta-blockers
  • Used in combination with beta blockers in patients that cannot be controlled with an optimal bet-blocker dose
49
Q

Examples of Cholesterol Lowering Agents

A

• Simvastatin, Pravastatin, Atorvastatin

50
Q

Action of • Simvastatin, Pravastatin, Atorvastatin

A

• HMG CoA Reductase Inhibitors

51
Q

NICE Guiidelines for tretament

A
  • Beta blocker first line for stable angina
  • Inadequate control- calcium channel blockers are used
  • Combination of the 2 can be used if symptoms are not controlled
52
Q

Patients with stable angina due to atherosclerotic disease should be on

A

Long term aspirin and statin

53
Q

Why should they be on statin even if blood cholesterol is good

A

Stabilise plaques

54
Q

All patients with angina should be considered for treatment with

A

ACEi

55
Q

Drugs for secondary prevention

A
  • Aspirin 75mg daily (low dose to take into account risk of bleeding and comorbidities)
  • ACEI for people with stable angina and diabetes
  • Statin treatment
  • Treatment for high blood pressure
56
Q

1st line treatment

A

fast acting nitrates

Beta blocker/CCB

57
Q

2nd line (5)

A 
Ivabradine
Long acting nitrates
Nocorandil
Ranolazine
Trimetazadine

Cardiovascular System (42 decks)

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