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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)
A2A 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
Organization
of the
NervousSystem
System
Figure 11.1
Sympathetic and Parasympathetic Divisions of the
Autonomic Nervous System
Figure 11.12 (1 of 2)
Sympathetic and Parasympathetic Divisions of the
Autonomic Nervous System
Figure 11.12 (2 of 2)
Hormonal Control of Blood Pressure
Table 19.2
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