cardiovascular disease . Hypertension,etc(1).pptx

Cardiovascular disease are a group of disorders of the heart and blood vessels. it includes hypertension, angina pectorise,myocardial infraction, coronary artery disease,congestive heart failure,leading to strokes,rhumatic heart disease,etc

1. Prepared By , Ms.Mokshada.R.Bhirud K.y.d.s.c.t.college of pharmacy,Sakegaon.

2. Introduction to hypertension:- Hypertension is defiend as systolic blood pressure greater than 140 mmhg and/or diastolic blood pressure greater than 90 mmhg. Primary hypertension :- It has no definite cause and should be treated by general approch & about 90%people suffer from this SBP 140- 159 mmhg,DBP- 90-99mmhg . Secondary hypertension:- It has some definite cause & about 10%people suffer from this SBP more than 160mmhg DBP more than 100mmhg Preganacy include hypertension:- Beacause of increased production of harmones and enzymes during pregnancy.

3. Classification of Hypertension BP Grading *SBP(mm Hg) *DBP(mm Hg) Normal 120- 129 and/or 80- 84 Prehypertension 130- 139 and/or 85- 89 Grade 1 Hypertension 140- 159 and/or 90- 99 Grade 2 Hypertension 160- 179 and/or 100- 109 Grade 3 Hypertension >180 and/or >110 Isolated Systolic Hypertension >140 and/or >90 Hypertensive urgency > 180and/or >110 Hypertension is defined as systolic blood pressure greater than 140 mmHg and/or diastolic blood pressure greater than 90 mmHg.

4. Etiopathogenesis of hypertension :- ( Etiopathogenesis means the cause and development of the disease or abnormal condition.) Renal Disease e.g. chronic diffuse glomerulnrphritis,pyelonephritis,polycystic kidney,etc. Endocrine Disease e.g. cushing’s syndromes,pheochromocytoma, primary hyperaldosteronism, Vascular lesions e.g. renel artery disease,contraction of arorta,etc. Hypertension is an asymptomatic condition. If untreated, it can lead to target organ damage such as, coronary artery disease, left vrntricular hypertrophy, strok, peripheral vascular diseases, renal disease, etc

5. Clinical manifestations of hypertension(Symptoms):- Often asymptomatic(silent killer). fatigue, headache, epistasis, vomiting, giddiness, breathlessness, and palpitations. Strok, acute myocardial infraction due to vascular disease. Bruits over carotid. Spells of sweating, tachycardia indicates pheochromocytoma. Neck swelling indicates thyroid disorder. Chest pain. Tiredness. Vision changes. Block in Artery Muscle Damage Heart Attack

6. Non- Pharmacological Manegement :- Physical activity. Dietary Sodium Restricton. Weight Reduction. Avoid Smoking. Avoid alcohol consumption. Stress Management. Yoga. DASH Diet(Dietary Approaches to Stop Hypertansion.

7. Pharmacological Manegment :- Pharmacological treatment means management of hypertension with drugs. Diuretics: (e.g. Hydrochlorothaizide,Furosemide). β- blockers (e.g. Atenolol). CCB- Calcium Channel blockers (e.g. Amlodipine). α- blockers: (e.g.Prazosin). ACE- Angiotensin converting enzyme inhibitor (e.g.Captopril,Ramipril,Enalapril).

8. Angina Pectoris Angina means pain and Pectis means chest “It is a pain syndrome accurs due to adverse induction in oxygen supply and oxygen demand(Iscemic Heart Disease).” Types of Angina Pectoris:- There are three types of Angina Pectoris . Stable Angina. Unstable Angina. Variant/Vsospastic Angina .

9. Stable angina generally occurs with physical exertion,but can be improved after rest. Ustable angina Unstable angina Unstable angina generally accurs at rest.is a dangerous condition emergency treatment,and is often a sing that a heart attack could accur soon. Variant angina Variant angina is a rare from that is caused by a spam in a coronary artery.

10. Causes:- Angina is the result of myocardial ischemia caused by n imbalance between myocardial oxygen supply and oxygen demand. O2 demand(Physical activity ) O2 Supply (blood flow obstruction) Symptoms:- Chest pain. Pain radiant to the neck ,jaw,teeth,back or epigastric region. Breathlessness. Fatigue. Reduced cardiac output. Indigation . Heartburn. Sweating. Nausea. 10. Shortness of breath.

11. Diagnosis:- Physical examination. ECG examination. Resting ECG. Exercise ECG. Coronary angiography. Radionuclicde Imaging. Chest X-ray. MRI. Complete blood count. Lipid profie. Pharmacological Manegment:- Tab.Aspirin 75 mg once daily (antiplatet drug). Tab.Clopidogrel 75 mg per day (antiplatet drug). Tab. Atorvastatin 40 mg per day (antihyperlipidemic drug. Nitrates- Sublingual Glyceryl trinitrate 300-500 mg t.i.d Β-blockers:Tab Metoprolol 50-200 mg/day(orally in divided dose). CC-blockers:Tab.Amlodipine 5-10 mg once a day. Stable Angina ◙ Risk Factors: Smoking Obesity Dyslipidemia Hypertension Diabetes

12. Unstable Angina Sublingually Nitroglycerin 300-600 mg stat (immediately). It can be repeated after 5 min . Max 3 doses can be given. Aspirin initial dose of 325 mg followed by 150 mg /day life long. Clopidogrel initial dose of 300 mg followed bt 75 mg/day for 2 years. Tab Atorvastatin 40 mg/day life long. Enoxaparin- Anticoagulant drugs. Non- Pharmacological Manegment:- Stable Angina Daily Exercise. Stop smoking. Avoid alcohol. Dietry modification. Avoid any activity known to precipitate angina attack. Weight reduction in obese patient

13. Unstable Angina Comlete bed rest. Coronary angiography. Regular medical check- up. Psychotherapy to relieve nervousness.

14. Hyperlipidemia defines an elevated level of lipids. like cholesterol and triglycerides. in your blood. Classification of Hyperlipidemia :- Hypercolesterolemia : increased serum level of total cholesterol (TC),low density lipoproteins (LDL), and low density lipoproteins cholesterol(LDL- C). Hypertriglyceridemia: Increased serum level of low density lipoproteins (VLDL) and triglycerides (TG). Combined hyperlipidemia : Increased TC,LDL,VLDL,LDL- C, and TG.

15. Cholesterol, Triglycerides and Phospholipids are transported in the bloodstream as complexes of lipids and proteins known as Lipoproteins. Elevated total and Low Density Lipoprotein (LDL) cholesterol and reduced high- density lipoprotein (HDL) cholesterol are associated with the development of Coronary Heart Disease (CHD). During the early stages of Hyperlipidemia, Blood monocytes and platelets attach to a vessel wall at the sites of endothelial damage. The release of the mediators such as platelet- derived growth factors leads to a proliferation of smooth cells in the intimal and medial lining of the vessel, collagen synthesis, cholesterol uptake and the beginning of the Hyperlipidaemic plaque. Plaque ruptures are resulting in the acute syndromes of unstable Angina, Myocardial Infarction and sudden cardiac death.

16. Diabetes Mellitus Hypothyrodim. Renal disease. High carbohydrate diet. Alcohol consumption. Hepatic disease. Obesity. Cholestatic liver disease. Cushing disease. Lipoprotin Lipase mutation

17. Peripheral arterial disease Coronary heart disease . Cholesterol embolizati on syndromes Carotid artery stenosis. Stroke. Myocardial infraction.

18. (i) HMG-CoA reductase inhibitors (Statins): e.g. Lovastatin, Simvastatin, Pravastatin, Atorva- statins, Rosuvastatins. (ii) Bile acid sequestrants (Resins): e.g. Cholestyramine, Colestipol, Colesevelam. (iii) Activate lipoprotein lipase (Fibric acid derivatives): e.g. Clofibrate, Gemfibrozil, Benzafibrate and Fenofibrate . ( iv) Inhibit lipolysis and triglyceride synthesis: e.g. Nicotinic acid. (v) Others: e.g. Ezetimibe, Gugulipid. Mechanism of Action of Drugs: HMG- CoA Reductase Inhibitors : Statins inhibit 3- hydroxy- 3-methylglutaryl coenzyme A (HMG- CoA) reductase enzyme (b) Bile acid sequestrants Colestipol, Colesevelam): Cholestyramine,Resins.

19. (c) Human monoclonal antibody: e.g., evinacumab. Inclisiran: It is a small- interfering RNA (siRNA) that inhibits hepatic PCSK9 thereby increasing the number of LDL- receptors on the hepatocytes. Microsomal Triglyceride Transfer Protein (MTP) Inhibitor: e.g., lomitapide (f) Lipoprotein lipase activators (PPARa activators, Fibrates): e.g., Gemfibrozil, Bezafibrate, Fenofibrate, Pemafibrate. (g) Lipolysis and triglyceride synthesis inhibitor: e.g., Niacin.

20. Non pharmacological Managemaent :- . Motivate all patients to make lifestyle modification . 1 . . . . Increase physical activity. Weight loss. Smoking cessation. Moderate alcohol intake. 2 3 4 5

21. Congestive heart failure is a chronic progressive condition in witch the heart cannot enough blood to meet the metabolic needs of the body because of pathological changes in the myocardium Causes:- Cardiac pathogenesis:- e.g. coronary artery disease,tachyarrhythmia, Hypertension. Infections:- e.g. Rhumatic fever, sexually transmitted disease,pneumonia. Endocrine disorders:- e.g. Diabetes, dyslipidemia,hypo/hyperthyroidism. Nutritionaldisorders:- e.g. Deficiency of thiamine, selenium, iron, calcium, L- carnitine. Toxins:- e.g. Alcohol,Cocaine,Cannabis. Drugs:- e.g. Beta-blockers, Severe anaemia. Obesity.

22. Fluid retention 1 Nocturia 2 Slow weight gain 3 Tachycardia, various arrhythmias 4 Cachexia 5 Elevated jugular venous pressure 6 Dyspnoea at rest oron exertion

23. ECG Ecocardiogram. Cardiac biomarkers Chest X- ray. Chest imaging Coronary angiogram

24. Types of Congestive Heart Failuare ( i ) Left-sided Heart Failure: ● This condition, the left ventrical of the heart is not able to blood the oroperly,fluid backup in the lungs. Causing shortness of the breath. ●this condition,a person has shortness of breath and coughing caused by the fluid built up in the lungs. When organ and muscle do not receive enough oxygen they can not function properly. (ii) Right-sided Heart Failure: ● This condition, the lower right chamber of the heart can not pump enough blood to the lungs it get returns from the body veins. (iii) Systolic Heart Failure: ● Systolic Heart Failure also called as heart Failure with reduced ejections fraction. ● In this condition, the heart muscles are unable to contract, to pump out oxygenated blood. ● The left ventricle cant contract fastly indicating a pumping problem

25. Heart Heart Disease Impaired Filling Increased Work Load Intrinsic Pump Failure Compensotory Action Fluid and Water Retenatation Sympathetic Activation Increased Blood Volume Increased force of contraction Improved pumping action Stretching of Ventricular figres Improved C ardiac Output Temporary Relief Fluid Vasoconstriction Increased Work Load Heart Failure Pathogenesis

26. Non-Pharmacological Treatment:- 1. Dietary sodium and fluid restriction. 2. Regular physical activity. 3. Avoid Smoking. 4. Avoid Alcolol and Tobacco. 5.Life style Changes . 6. Weight Loss. 7. Invasive device therapy,heart transplant, mechanical circulatory support.

27. Pharmacological Treatment:- √ Diuretics :- e.g. 1. Frusemide. 2. Hydrochlorthiazide. √ Beta Blockers :- e.g. 1. Metoprolol. 2. Bisoprolol. 3. Carvedilol. √ ACE Inhibitors :- e.g. 1. Hydralazine 2. Captopril 3. Nitrate. 4. Enalapril. √ Vasodilators/ ACE Inhibitors :- e.g. 1.Hydralazine. 2. Nitroprusside. √ Digoxin :- Digoxin,Doubtamine , Dopaming Amrinone , has positive inotropic effect an increase in the force of myocardial contraction