PHARMACOTHERAPY OF MYOCARDIAL INFARCTION

DEFINITION,ETIOLOGY,EPEDIMIOLOGY,TYPES PATHOGENESIS ,PHARMACOLOGICAL & NON-PHARMACOLOGICAL TREATMENT

1. MI BY HEENA PARVEEN

2. MYOCARDIAL INFARCTION René Marie in France in 1896 provided a classical description of clinical coronary disease, and George Dock in the U.S. the same year reported having made the clinical diagnosis during life in a patient with an anatomical  myocardial infarction  at autopsy.

3. A diseased condition caused by reduced blood flow in a coronary artery due to Atherosclerosis & Occlusion of an Artery by an embolus or thrombus. MI/HEART ATTACK is irreversible damage of myocardial tissue caused by prolonged ischaemia & Hypoxia.

4. ETIOLOGY

5. PATHOPHYSIOLOGY

6. EPEDIMIOLOGY

7. INVESTIGATIONS & DIAGNOSIS A stress test to see how your heart responds to certain situations, such as exercise. An angiogram with coronary catheterization to look for areas of blockage in your arteries. An echocardiogram to help identify areas of your heart that aren't working properly.

8. N0N-PHARMACOLOGICAL MANAGEMENT

9. PHARMACOLOGICAL TREATMENT 1)Anti-platelet agents : Aspirin,Clopidogrel . 2) Thrombolytics : Streptokinase,Anistreplase , Reteplase,Tenecteplase , Urokinase . 3)Nitrates : Trintroglycerine . 4)ACE inhibitors : Captopril . 5)Analgesics : Morphine,Pethidine . 6)Vasodilators : Nitroprusside . 7)Beta-Blockers : Metaprolol . 8)Anti-anxiety : Diazepam , Alprazolam . 9)Anti-coagulants : Heparin,Warfarin . 10)Anti- arrhythmics : Lidocaine,Procainamide . 11) Inotropics : Dopamine,Dobutamine . 12)Miscellaneous : Atropine,Sodium bicarbonate.

10. MECHANISM OF ACTION OF ORAL ANTI-PLATELETS

11. Aspirin irreversibly inhibits COX-1 enzyme & reduces TXA2generation by both platelets & Vascular endothelium & prolong bleeding time. Aspirin acts by irreversibly acetylating a serine residue in the active site of the enzyme COX that results in reduced generation of TXA2 by platelets & Pgi2 BY Vascular endothelium---Aspirin affects balance between TXA2 & PGI2. Pharmacokinetics: Oral Route—Excellent Absorption. Vd—0.17L/kg. Distribution—Body fluids, Tissues, CSF,Placenta . Excretion--Urine

12. Pharmacological effects Analgesic effect, Anti-pyretic effect, Anti-inflammatory effect, Hyperventilation, Uricoseric effect, GI bleeding. DI: Aspirin Probenecid’s Uricoseric effect. Displaces drugs ( Warfarin , Phenytoin,Methotrexate ) from protein biding sites. Displaces Thyroxine Adverse Effcets Nausea,Emesis,Dyspepia , Diarrhoea , GI irritation, Peptic Ulcers, Oesophagitis (Due to decreased Gastroprotectve PG’s) Renal papillary necrosis, Oedema , CHF. Headache, Vertigo, Confusion, Depression, Seizures. Rashes, Urticaria , Asthma, Reye’s syndrome( brain and liver damage). C.I: Haemophilics , Childrean below 12years age, Asthmatic patients, Patients allergic to Ibuprofen/Naproxen. -

13. Analgesics Morphine –Prototype of Opioid drugs. MOA: Morphine bind with opioid receptors & results in Physiological changes in nerve tissue: Inhibition of Adenylcyclase cAMP concentration decreases Increases K+ efflux( Hyperpolarisation ) Decreases Ca+2 infux

14. Pharmacokinetics: Absorption—well in gut, Distribution—Body tissues, Metabolism—Liver, Plasma Half-life—2-3hrs, Excretion—Urine(-90%) Faeces (-10%). USES: Relieve Acute & Chronic pain, Relieve Anxiety & Apprehension in MI,Haematemesis,Threatened abortion, As a Pre- anaesthetic medication. Anti- diarrhoeal agent. Adverse Effects: Sedation,Mental clouding, Dysphora,Blurred vision, Postural Hypotension, Resp.Depression,N&V,Headache,Delirium,Tremors . In elderly (Constipation & Urinary retention). Histamine release causes Pruritis , Lips swelling, Urticaria . Tolerance Physical & Psychological dependence .

15. Nitrate Compounds

16. Pharmacological effects: Reduction of Preload & Afterload . Relaxation of Coronary arteries. Dilation of Cutaeneous & Meningeal Vessels—Facial flushing & Headache. Relaxation of Smooth muscles—Bronchi, Oesophagus , Biliary tract. Pharmacokinetics: Good lipid solubility, Greater Bioavailability –Sub-lingual route, Extesivve first-pass metabolism. Adverse effect: Facial flushing & Headache, Sweating,Palpitation,Weakness,Dizziness,Skin rashes, Drug tolerance, Drug Dependence. USES: In Angina Pectoris, In CHF, In Left Ventricular fibrillation, In Myocardial infarction, I Oesophageal spasms, Prophylaxis of Cyanide poisoning.

17. TH9 Q