This document discusses angina pectoris, including its causes, types, management, and treatment. It begins by defining angina pectoris as sudden, severe chest pain caused by an imbalance between oxygen supply and demand in the heart muscle. It classifies the different types of angina and discusses the mechanisms and uses of various drug classes in treating angina, including nitrates, calcium channel blockers, beta-blockers, and potassium channel openers. Surgical therapies like balloon angioplasty and coronary bypass are also mentioned. The document provides an overview of angina pectoris aimed at reviewing its management.

1. ““ANGINA PECTORIS”ANGINA PECTORIS”
PRESENTED BY,PRESENTED BY,
SONALI DIWATE B.SONALI DIWATE B.
M.PHARMM.PHARM
(PHARMACOLOGY)(PHARMACOLOGY)
GUIDED BY,GUIDED BY,
PROF.CHANSETTI R.PROF.CHANSETTI R.
PE Society’s
Modern college of pharmacy (for ladies),
Moshi, Pune.

2. TO REVIEW AND STUDY THE MANAGEMENT OFTO REVIEW AND STUDY THE MANAGEMENT OF
ANGINA PECTORIS.ANGINA PECTORIS.
AIMAIM

3. Angina pectoris
Sudden,severe,pressing chest pain starting
substernal &radiate to left arm.
Due to imbalance between myocardium
oxygen requirement and oxygen supply.
Risk factors :
Age,sex,obesity.smoking,diabetes.

4. Classification of angina
1. Exertional angina,
Stable,Atherosclerotic,Classic,
Due to obstruction of coronaries by atheroma.
2. Variant, Vasospastic angina
due to Spasm of coronaries.
3- Unstable angina.
Due to spasm and partial obstruction of
coronaries.

5. Nitrates & Nitrites
Preparations :
1- Short acting:
Start within few minutes and total duration of
action 15-30 minutes.
A) Nitroglycerine (Glyceryl trinitrate)
Used as sublingual tablets.
B) Isosorbide dinitrate
As sublingual spray.
C) Amyl nitrite
Inhalation

6. Long acting
Nitroglycerine, Isosorbide dinitrate,
Isosorbide mononitrate,Erythrityl –
Tetranitrate.
 Action of all start withen hours and continue for
hours .
They are given :
Orally,Ointment,Buccal,Transdermal
patch,Parenteral.

7. Absorption
Well absorbed according to the route:
GIT for the long acting
short acting Sublingual

Transdermal for long acting
 inhaLation

8. Metabolism
Through first pass hepatic metabolism .
Short acting have a low oral bioavailability (10-
20%),so not given orally to avoid first pass
metabolism.
Nitroglycerine metabolites( two dinitro And
two mononitro forms).
The dinitro forms are active metabolites
and have significant vasodilator effect.

9. Metabolism
Isosorbide dinitrate metabolite (5-
mononitrate) is an active metabolite used
clinically.
Excretion
As metabolites through kidney.

10. Mechanism of action
Glutathione S-transferase
Nitroglycerine ————————→ No.
guanylyl cyclase and NO activates increase c
GMP
c GMP dephosphorelate myosin light chain
(Myosin-LC-po4) to myosin- LC
Causing muscle relaxation.

11. Pharmacological actions
Nitrates relax all types of smooth muscles
vascular or non vascular .
Relax both arteries and veins but more
effective on veins.
They have no direct effect on cardiac or
skeletal muscles.
NO released stimulate guanylyl cyclase
In platelets causing increase cGMP that
decrease platelet aggregation.

12. Clinical uses
Short acting for acute attacks
Long acting for prophylactic.
Treatment of all types of angina .

13. 1- Angina of effort
A) Decrease venous return
B) Decrease ABP
Both A&B decrease myocardial oxygen
requirement.

14. 2-Variant angina
Relax smooth muscle of epicardial coronary
artery and relief coronary spasm.

15. 3-Unstable angina
 Decrease myocardial oxygen
requirement.
 Relief coronary spasm.
Decrease platelet aggregation.

16. Adverse effects
Orthostatic hypotension
Throbbing headache
Tachycardia
Facial or cutaneous flushing
Tolerance (Tachyphylaxis)
Salt and water retention
Carcinogenicity
Methaemoglobinemia only with nitrities

17. Contraindication
Nitrates are contraindicated in increase
intracranial pressure.
Nitrates can be used safely in increase of
intraocular pressure (Glucoma).

18. Calcium channel blockers
1- They block calcium entry in myocardium
causing ;
A) decrease myocardium
contractility & myocardium
oxygen requirement.
B) decrease heart rate causing decrease in
myocardium oxygen requirement.

19. 2-Block calcium entry in vascular smooth
muscles (arterioles) causing a)decrease in
peripheral resistance( after load)------
decrease in oxygen requirement.
• b)Relief of coronary spasm.

20. Clinical uses
In all types of angina but very effective in
variant angina .
Used mainly in prophylactic therapy.

21. β-Adrenoreceptor blocking drugs
They are not vasodilators
They are used in treatment of angina :
They decrease both heart rate & myocardial
contractility that decrease in myocardial
oxygen requirement at rest & in exercise so
improve exercise tolerance.

22. Clinical uses
 They are effective in the prophylactic
treatment of classic & unstable angina.
They are not used in variant angina.
They are effective in treatment of silent or
ambulatory angina (no pain ).
Decrease mortality of patients with recent
myocardial infarction.

23. Potassium channel openers
(Nicorandil )
Activation of potassium channels.
Nitric oxide release.
Arterio & venodilators.
Used as prophylactic therapy .
May cause : Headache,flushing,dizziness.

24. Drug treatment of angina
1- Acute attack :
Short acting nitrates or nitritis.
2- Prophylactic therapy ;
Long –acting nitrates.
Calcium channel blockers.
β- adrenoceptors blockers.
Potassium channel openers.

25. Combination therapy
Nitrates and β-adrenoceptors blockers.
Calcium channel blockers and β-
adrenoceptor blockers .? ?
Calcium channel blockers and nitrates.
Calcium channel blockers, β-adrenoceptor
blockers, nitrates.

26. Surgical therapy
Ballon
Coronary by pass.