Pharmacology of angina Flashcards
(24 cards)
What is angina pectoris?
Chest pain that occurs when the heart muscle doesn’t get supplied with adequate oxygen
due to coronary heart disease
Symptoms?
Cramping
Chest constriction
Referred pain of jaw, shoulders neck and arms
Associated with shortness of breath, sweating, nausea, and increased heart rate
What compounds does the locally affected myocardium release
Potassium
lactate (which builds up)
Adenosine
Bradykinin
Prostaglandins
Classifications of angina pectoris?
Stable angina:
-Attributed to myocardial infarction
-Coronary artery disease
Unstable angina:
-Due to complication from stable angina
Prinzmetal angina:
-Usually due to a spasm in the coronary arteries
-Tends to happen in cycles
-Cocaine was the leading cause of coronary vasospasms
Microvascular angina:
-Patients have angina symptoms but no evidence of coronary heart artery disease
-Normal/near normal coronary angiogram
What causes pain in angina?
Ischaemia
Myocardium releases compounds
Activates myocardial pain receptors
Signal is sent via sensory neurons
What is the aetiology of unstable anginas ?
Clot formation occludes artery (plaque rupture)
Critical reduction in blood flow so that oxygen supply is inadequate even at rest
SEVERE PAIN
What are the characteristics of Prinzmetal angina (inversa/atypical/variant)
Usually occurs while resting and during the night or early morning hours
Rare (1 in 100 cases)
What is the aetiology of microvascular angina
Impaired coronary circulation leads to reduced coronary perfusion causing pain
Due to abnormal vasodilation or increased vasoconstriction
Demand ischaemia/Supply ischaemia
Demand = Stable angina
Supply = Prinzmetal + Unstable angina
Prophylactic treatments?
- Lipid lowering drugs
- Anti-coagulants
- Fibrinolytic
- Anti-platelet
From excitation to contraction
heart muscle
Increase in cytoplasmic Ca+(from sarcoplasmic reticulum)
Ca+ binds to troponin
ca+ troponon causing tropomyosin to move exposing binding sites on actin
Cross bridge cycle
Contraction by pulling actin along myosin
Smooth muscle contraction?
Increase in cytoplasmic Ca+
(most from interstitial fluid)
Ca+ binds to calmodulin
Ca+ calmodulin complex leads to phosphorylation of myosin
Cross bridge cycle
Contraction by pulling actin along myosin
Nitrates?
Decrease intraventricular pressure - decreases cardiac preload
Arterial dilation - decrease TPR - reduces afterload
Lowers oxygen demand by decreasing work of heart
Mechanism of action of Nitrates?
Mimics effects of endigenous NO
NO to Protein kinase G
PKG reduces smooth muscle tone
Beta blockers
Examples - atenolol , bisoprolol
Inhibits pacemaker current - decreases heart rate
Reduces force of cardiac contraction
Beta blockers mode of action
Reduces sympathetic activity of noreadrenaline and adrenaline on beta 1 adrenoreceptors in heart
3 types of Ca+ channel blocker
Vascular
Cardiac
Both
Ca+ channel mode of action
Reduces Ca+ entry into cardiomyocytes - reduces contractility
Coronary vasodilation - more coronary blood flow
Prophylactic drugs for angine examples
Aspirin - inhibits COX, decreases thromboxane
Clopidogrel - inhibits ADP receptor on platelets - reduces aggregation
Statins - HMG Co-A reductase inhibitor - reduces cholesterol levels
What is the fine line symptom control?
Nitrates
Beta blockers
Second line of control
Calcium channel blocker
What are angina treatment strategies
- to increase perfusion
- reduce metabolic demand
- prevention
Drugs for prinzmetal angina?
calcium channel blockers
Drugs for other angina (not prinzmetal)
Beta blockers
Nitrates
