NEET MDS Lessons
Pharmacology
Beta - Adrenergic Blocking Agents
Mechanisms of Action
- Initial decrease in cardiac output, followed by reduction in peripheral vascular resistance.
- Other actions include decrease plasma renin activity, resetting of baroreceptors, release of vasodilator prostaglandins, and blockade of prejunctional beta-receptors.
Advantages
- Documented reduction in cardiovascular morbidity and mortality.
- Cardioprotection: primary and secondary prevention against coronary artery events (i.e. ischemia, infarction, arrhythmias, death).
- Relatively not expensive.
Considerations
- Beta blockers are used with caution in patients with bronchospasm.
- Contraindicated in more than grade I AV, heart block.
- Do not discontinue abruptly.
Side Effects
- Bronchospasm and obstructive airway disease.
- Bradycardia
- Metabolic effects (raise triglyerides levels and decrease HDL cholesterol; may worsen insulin sensitivity and cause glucose intolerance). Increased incidence of diabetes mellitus.
- Coldness of extremities.
- Fatigue.
- Mask symptoms of hypoglycemia.
- Impotence.
Indications
- First line treatment for hypertension as an alternative to diuretics.
- Hypertension associated with coronary artery disease.
- Hyperkinetic circulation and high cardiac output hypertension (e.g., young hypertensives).
- Hypertension associated with supraventricular tachycardia, migraine, essential tremors, or hypertrophic cardiomyopathy.
Beta adrenergic blocker Drugs
Atenolol 25-100
Metoprolol 50-200
Bisoprolol 2.5-10
Prostaglandines:
Every cell in the body is capable of synthesizing one or more types of PGS. The four major group of PGs are E, F, A, and B.
Pharmacological actions:
stimulation of cyclicAMP production and calcium use by various cells
CVS
PGE2 acts as vasodilator; it is more potent hypotensive than Ach and histamine
Uterous
PGE2 and PGF2α Contract human uterus
Bronchial muscle
PGF2α and thromboxan A2 cause bronchial muscle contraction.
PGE2 & PGI2 cause bronchial muscle dilatation
GIT: PGE2 and PGF2α cause colic and watery diarrhoea
Platelets
Thromboxan A2 is potent induce of platelets aggregation
Kidney
PGE2 and PGI2 increase water, Na ion and K ion excretion (act as diuresis) that cause renal vasodilatation and inhibit
tubular reabsorption
USE
PGI2: Epoprostenol (inhibits platelets aggregation)
PGE1: Alprostadil (used to maintain the potency of arterioles in neonates with congenital heart defects).
PGE2: Dinoproste (used as pessaries to induce labor)
Synthetic analogue of PGE1: Misoprostol (inhibit the secretion of HCl).