exam questions
Cards (13)
- Explain why high blood pressure can increase the risk of developing cardiovascular disease (3)- High blood pressure causes damage to endothelium walls of arteries- This can trigger an inflammatory response causing WBC to accumulate in the area along with cholesterol and lipids causing an atheroma- Platelets can harden this atheroma causing a plaque, narrowing the lumen of the artery
- Explain how the diet of a person could affect the development of CVD (4)- Higher salt intake increases blood pressure which increases damage to endothelium walls of arteries causing an inflammatory response- High saturated fat intake/cholesterol (LDLs) increases likelihood of an atheroma forming as cholesterol and white blood cells clump together- Additionally, high alcohol consumption increases blood pressure increasing risk of damage to the endothelium
- Describe the role of LDLs in the development of atherosclerosis (3)- LDLs carry cholesterol in the blood- Cholesterol is deposited to form atheroma’s- In the endothelium of an artery
- Explain how atherosclerosis can result in damage to heart muscles (3)- Atherosclerosis in the coronary artery causes the lumen to narrow- This decreased blood flow through the artery to the heart- Thus, heart muscle not receiving enough oxygenated blood/blood flow/oxygen for the cells to aerobically respire- more anaerobic respiration= build-up of lactic acid
- Describe the role of thrombin in blood clotting (3)- Active Thrombin is an enzyme which catalyses the conversion of soluble fibrinogen to insoluble fibrin- A mesh of fibrin traps platelets/red blood cells to form a clot
- Explain how a blood clot could form in a blood vessel (4)- Damage to the endothelium wall exposes collagen fibres which would attract platelets- Platelets release thromboplastin(protein) aids the conversion of inactive prothrombin(protein) into thrombin(enzyme)- aided by clotting factors, calcium ions and vitamin K- Thrombin catalyses the conversion of soluble fibrinogen to insoluble fibrin- Fibrin forms a network/mesh of fibres which trap red blood cells and platelets to form a blood clo
- Describe how very high blood pressure could result in atherosclerosis (3)- High blood pressure causes damage to the endothelium of the artery- This triggers an inflammatory response, causing WBC to accumulate- Cholesterol and lipids join WBC forming a fatty deposit/atheroma- Atheroma can lead to plaque formation if joined by platelets
- Explain how atherosclerosis in one part of an artery could increase the likelihood of it developing in another part of the same artery (2)- Plaques/atherosclerosis narrow the lumen- Increasing blood pressure further
- Explain the benefits of plant statins to human health (2)- Lower blood cholesterol- Reducing the risk of cvd e.g., atherosclerosis (forms atheroma’s)
- Explain the role of platelet inhibitory drugs (e.g., aspirin) on patient with CVD (2)- Prevents platelets becoming activated- Prevents the formation of blood clot leading to e.g., a stroke or heart attack
- Explain the role of antihypertensives e.g., beta blockers on patient with cvd (2)- They reduce patient’s blood pressure- Less risk of damage to the endothelium wall triggering an inflammatory response- Reduced risk of atheroma
- Explain the role of antihypertensive drugs in reducing the risk of atherosclerosis (4)- They reduce blood pressure so less damage to the endothelium wall- Thus, no inflammatory response and less WBC accumulating- No cholesterol and lipids joining with WBC to form atheroma’s/fatty acid deposits- Less plaques forming- And lumen not getting narrowed
- Explain how anticoagulants can help reduce the effects of CVD (2)- Prevent the formation of a blood clot- They reduce the stickiness of platelets/reduce their effectiveness- Clotting factors are inhibited eg fibrinogen- Thus, risk of blood vessels becoming blocked is reduced