58 Questions
What is the primary function of 3-Hydroxy-methylglutaryl coenzyme A (3-HMG CoA) reductase in the regulation of cholesterol synthesis?
Controlling the rate of cholesterol synthesis in the liver
What is the primary mechanism by which the liver takes up LDL?
Receptor-mediated endocytosis
What is the role of cholesterol in animal membranes?
It provides structural integrity and fluidity to the membrane
What is the fate of cholesterol and other lipids in excess of those needed by the liver?
They are exported as VLDL and converted to LDL
What is the origin of the term 'cholesterol'?
It is a combination of the Greek words for 'bile' and 'alcohol'
What is the primary mechanism by which nitrates lead to vasodilation in the treatment of angina?
Release of nitric oxide (NO) and subsequent binding to sGC
What is the key difference between stable and unstable angina in terms of chest pain?
Stable angina occurs on exertion, while unstable angina occurs at rest
What is the primary effect of β-blockers on the heart in the treatment of angina?
Negative inotropic effect, decreasing the force of heartbeat
What is the primary mechanism of action of Ca2+ channel blockers in the treatment of angina?
Inhibition of Ca2+ influx into smooth muscle cells
What is the primary effect of glyceryl trinitrate on coronary arteries in the treatment of angina?
Increase in blood flow and decrease in oxygen demand
What is the key similarity between unstable angina and myocardial infarction (MI) in terms of pathology?
Platelet and fibrin thrombus with ruptured atheroma
What is the primary risk factor for atherosclerosis?
High cholesterol
Which enzyme is inhibited by statins?
HMG CoA reductase
What is the name of the gene responsible for familial hypercholesterolemia?
LDL-R
What is the normal range for total cholesterol?
≤ 5mMol/L
What is the cause of angina in coronary heart disease?
Narrowing/blocking of coronary arteries
What is the purpose of statins in the treatment of cardiovascular disease?
To reduce lipid levels
What is the primary mechanism of action of dabigatran?
Synthetic serine protease inhibitor
What is the primary reason for avoiding warfarin in the first few months of pregnancy?
Teratogenic effects
What is the primary benefit of using bivalirudin in percutaneous coronary artery surgery?
Combined use with aspirin and clopidogrel
What is the primary mechanism by which liver disease affects warfarin therapy?
Impaired synthesis of clotting factors
What is the primary reason for monitoring prothrombin time (PT) in patients taking warfarin?
To adjust the dose of warfarin
What is the primary effect of high metabolic rate on warfarin therapy?
Increased degradation of clotting factors
What is the mechanism of action of aspirin in the context of antiplatelet therapy?
Irreversible inhibition of COX-1
Which of the following antibiotics can decrease vitamin K availability?
Broad spectrum antibiotics and sulphonamides
What is the effect of dipyridamole on platelet aggregation?
Inhibition of TXA2 synthesis
Which of the following drugs can bind to warfarin in the gut and reduce its absorption?
Colestyramine
What is the indication for using abciximab?
High risk patients undergoing coronary angioplasty
Which of the following drugs can be used as a single agent in patients intolerant to aspirin?
Clopidogrel
Cholesterol is synthesised from Acetyl-CoA in the mitochondria.
False
LDL is formed from VLDL in the liver.
False
HDL is responsible for transporting cholesterol from the liver to peripheral tissues.
False
Chylomicrons are involved in transporting dietary fats from the intestine to the liver.
True
Bile salts are synthesised from cholesterol in the liver.
True
Inhibition of myosin light chain kinase leads to decreased vasodilatation
False
Atherosclerosis is a sudden symptomatic manifestation.
False
Platelet-activating factor is involved in the coagulation cascade
True
Genetic risk factors include HMG CoA reductase polymorphism and LDL-R gene polymorphism.
True
Nifedipine is a β-blocker
False
Unstable angina is characterized by chest pain on exertion
False
Statins are used to increase LDL receptors.
False
A healthy total cholesterol level is ≤ 6 mmol/L.
False
Atenolol is a Ca2+ channel blocker
False
Angina is a symptom of atherosclerosis.
True
Glyceryl trinitrate increases the work done by the heart
False
Vasodilatation and pain are caused by the release of K+ and H+ ions.
False
Warfarin is a direct inhibitor of Factor Xa
False
Bivalirudin is an oral anticoagulant used in patients with type 2 HIT
False
Lepirudin is used in patients with type 2 diabetes
False
Dabigatran is a vitamin K antagonist
False
Rivaroxaban is used in conjunction with aspirin and clopidogrel in percutaneous coronary artery surgery
False
Thrombin is essential for the production of protein C and S.
False
Warfarin can be used safely in the first few months of pregnancy
False
Hirudins are indirect thrombin inhibitors, relying on ATIII activation.
False
Fondaparinux is an example of a low-molecular-weight heparin (LMWH).
True
Heparin is a single substance, not a family of glycosaminoglycans.
False
Gut flora can synthesise vitamin K in humans.
True
Enoxaparin is a type of novel anticoagulant.
False
Study Notes
Hypercholesterolaemia
- Cholesterol is a steroid component of animal membranes and a precursor of steroid hormones, sex hormones, Vit D, and bile salt.
- Cholesterol is synthesised from Acetyl-CoA in the ER, and its synthesis is regulated in the liver by changes in 3-Hydroxy-methylglutaryl coenzyme A (3-HMG CoA) reductase.
- Cholesterol is transported in complex with proteins (lipoproteins) – HDL, IDL, LDL, VLDL, and chylomicrons.
- The liver takes up LDL by receptor-mediated endocytosis.
Angina/Coronary Artery Disease
- Angina is a symptom of coronary heart disease, characterized by chest pain due to increased oxygen demand.
- Stable angina is predictable, whereas unstable angina occurs with less and less exertion or at rest.
- Unstable angina is caused by a platelet and fibrin thrombus with ruptured atheroma, but not complete occlusion.
Treatment for Angina
- Nitrates relax smooth muscle, releasing nitric oxide (NO), which binds to soluble guanylyl cyclase (sGC) and produces cGMP, activating protein kinase G (PKG).
- PKG inhibits myosin light chain kinase (MLCK), leading to vasodilation.
- Β-blockers have a negative inotropic effect, decreasing the force of the heartbeat and heart rate.
- Ca2+ channel blockers inhibit Ca2+ influx, leading to vasodilation.
Thrombosis
- Thrombosis is a complex process involving the coagulation cascade and platelet activation.
- Platelet-activating factor (PAF) and thromboxane A2 (TXA2) are key players in thrombosis.
Statins
- Statins are lipid-lowering drugs that inhibit HMG CoA reductase in the liver and intestine.
- Statins increase the expression of LDL receptors, leading to increased clearance of LDL from the bloodstream.
- Healthy lipid levels are: total cholesterol ≤ 5mMol/L, non-HDL ≤ 4mMol/L, LDL ≤ 3mMol/L, TC/HDL ratio ≤ 6.
Antiplatelet Drugs
- Aspirin inhibits platelet thromboxane synthesis, irreversibly inhibiting COX-1.
- Aspirin is efficacious in thrombotic stroke evolution and acute myocardial infarction.
- Dipyridamole inhibits platelet aggregation, and its effects are additive to aspirin's.
- ADP receptor (purine P2YX1/12) antagonists, such as clopidogrel, prasugrel, and ticagrelor, can be used in combination with aspirin or as a single agent in patients intolerant to aspirin.
- Glycoprotein IIB/IIIA receptor antagonists, such as abciximab, tirofiban, and eptifibatide, inhibit all platelet activation pathways.
Test your knowledge of hypercholesterolaemia, cholesterol, and statins in pharmacology. This quiz covers key facts about cholesterol, its synthesis, and its role in the body.
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