Lecture 16

Question 1

CVD

Answer 1

4 mil aussies this year, 1 in 4 deaths. $5B per year. Rate of death decreases. High prevalence in Indigenous populations

Question 2

Ischemia

Answer 2

O2 supply-demand imbalance due to occlusion in coronary or cerebral arteries, decreases provision of O2 or anaemia, increases O2 demand. Impact determined by length of attack. In brain, called transient ischemic attack, in heart called myocardial stunning. Short and reversible injury (apoptosis). If it’s long = infarction which is no longer reversible as cells are necrosis.

Question 3

Atherosclerosis + thrombosis

Answer 3

Vulnerable plaque causes clotting cascade

Question 4

Embolism

Answer 4

Material dislodge from large vessels and lodges in small vessel. If it arises from periphery, it travels to the RA to RV leading to pulmonary embolism. If it arises from LA, in response to atrial fibrillation, can travel to viscera leading to stroke or HA.

Question 5

Consequences of ischemia

Answer 5

Heart and brain have high energy requirements therefore need nutrients and O2. During ischemic attack, increase aerobic metabolism which promotes increase lactate = acidosis. Also, Na is drawn into cell = increase passive transport of H2O = cytotoxic oedema. Mismatch in Ca2+ handling = ROS generation. Heart stops contracting and neuronal transmission stops. If blood flow not restored cardiomyocytes replaced with fibrous scar tissue and neuroplasticity generates neural networks.

Question 6

MI and stroke risk factor

Answer 6

Smoking, alcohol, systemuc hypertension, atherosclerosis, obesity, sedentary lifestyle, disbetes, dislipidaemia, age, race, male sex and clotting disorders

Question 7

Ischemic stroke

Answer 7

arterial blockage due to thrombosis or embolism, usually in internal carotid or middle cerebral artery ~85% strokes

Question 8

Hemorrhagic stroke

Answer 8

arterial break. aneurysm ~15% strokes