Gilead -Topics in Human Pathophysiology Fall 2010 Drug Safety and Public Health.

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Presentation transcript:

Gilead -Topics in Human Pathophysiology Fall 2010 Drug Safety and Public Health

Figure 8.7b

 Systole – ventricles contract, semilunar valves open to allow blood to large arteries; AV valves close to prevent backflow to the atria  Diastole – ventricles relax, semilunar valves close to prevent backflow into the ventricles, AV valves open to allow ventricles to fill

 SA node is primary pacemaker  AV node is secondary pacemaker  AV bundle carries signal to ventricles  Electrical signal stimulates muscle contraction  For the conduction system to work properly adequate blood supply is required.

 Coronary artery disease  Myocardial ischemia  Myocardial hypoxia  Myocardial infarct  Myocardial necrosis

From wikipedia

Age Male sex Heredity Smoking Diabetes mellitus Hypertension High cholesterol Obesity Lack of exercise

 Diagnosis ◦ BP monitoring ◦ Symptoms ◦ ECG ◦ Angiogram ◦ Stress Test ◦ Nuclear myocardial perfusion tests

 For myocardial perfusion imaging (MPI)  A 2A adenosine receptor agonist  Vasodilates coronary arteries as if exercising  Injected into blood stream prior to gamma camera scan  Can give a good indication of myocardial perfusion

Treatment – Coronary bypass surgery – Angioplasty – Stents – Cholesterol lowering agents – Anticoagulents – Antianginal medications

 For angina  Thought to inhibit a sodium ion channel in the cardiac muscle cells  Contraction of those cells might normally cause compression of cardiac blood vessels during diastole.  Can be taken with other anti-anginal meds  Very effective

Congestive Heart Failure Heart becomes weak Blood backs up in veins and capillaries Fluid excess in tissues Symptoms include shortness of breath, edema, difficulty breathing (especially when lying down,) difficulty exercising

Congestive Heart Failure Causes: – cardiomyopathy – hypertension – lung disease – coronary artery disease – previous MI – valve disease

Blood Vessels and Pressure Artery structure and function Control over smooth muscle Vascular Disease – Atherosclerosis – Pulmonary hypertension

Figure 8.10

Figure 8.1

Vessel Wall Structure Tunica intima – epithelium and connective tissue Tunica media – smooth muscle Tunica externa– connective tissue and epithelium

Arterial blood pressure and flow Systolic and diastolic pressure Regulatory factors – Cardiac – Sympathetic nervous system from vasomotor center of brain stimulates smooth muscle – Chemical messengers – hormones, paracrines

Components of Orthe Nervous System Figure 11.1 Organization of the Nervous System

Figure (1 of 2) Sympathetic and Parasympathetic Divisions of the Autonomic Nervous System

Figure (2 of 2) Sympathetic and Parasympathetic Divisions of the Autonomic Nervous System

Table 19.2 Hormonal Control of Blood Pressure

Pulmonary Arterial Hypertension (PAH) Pulmonary arteries become narrowed causing decreased gas exchange and difficulty breathing Causes R ventricular hypertrophy Blood will back up in veins

Pulmonary Hypertension

Common causes of PAH Genetic defect Autoimmune diseases, such as scleroderma Congestive heart failure History of blood clot in the lung HIV infection Lung or heart valve disease Obstructive sleep apnea In many cases the cause is unknown- Idiopathic pulmonary arterial hypertension

Symptoms of PAH Chest pain, usually in the front of the chest Dizziness Fainting Fatigue Leg edema Light-headedness during exercise Shortness of breath during activity Weakness

Treatment for PAH Letairis (ambrisentan) Flolan or other prostacyclins Bosentan (Tracleer) Calcium channel blockers Diuretics Sildenafil (Viagra) Supplemental oxygen Surgical correction of defects Lung transplant