Cardiology Week 6 Scq Study Guide Questions

CARDIOLOGY WEEK 6 Saq STUDY GUIDE QUESTIONS 1. Draw the mechanism of action of warfarin ( 2. Explain the structure of unfractionated vs fractionated heparin and relate this to their functions (3 marks) Answer: • fractionated heparin is made out of a pentasschride chain with a short GAG tail, but unfractionated heparin it is also made out of a pentasschride chain, but it has a longer GAG tail Because of this fractionated heparin can only inhibit factor X unfractionated because it is longer and can reach more can inhibit both factor II and X This means the fractionated heparin only inhibits factor X directly while in inhibits factor II in directly, while fractionated inhibits both X and II directly This makes unfractionated work faster more effective • • • • 3. Compare and contrast acute and subacute ineffective endocarditis Answer: • • • • - Both involve some form of infection It starts of with the endocardium and them progresses into the valves Acute: Infection of a perivously normal valve IV drug users Vegetation, cell derbis and bulky Subacute Infection of a perivously abnormal valve Poor oral health, dental surgery Involves a murmur 5. Describe four genetic mutations that lead to inherited cardiovascular diseases (6 marks) Answer: • • • • Genes controlling K+ channels -> long QT interval Genes coding for myosin and actin -> hypertrophy Genes coding for cytoskeleton -> ventricle dilation Genes coding for LDL intake -> atherosclerosis 6. Compare and contrast cardiac output during rest and exercise Answer: At rest the cardiac output is 5L. it is distributed in the following portions: • - LKMBSSH Liver and GIT: 1250 mL Kidney: 1000 mL Muscles: 1000 mL Brain: 750 mL Skeleton: 750 mL Skin: 300 mL Heart 250 mL At exercise the cardiac output is increased to 25L • - MSHGKBS Muscle:18000mL Skin:3500mL Heart:1250mL Gut and liver: 1250 mL Kidney:1000mL Brain:750mL Skeleton:500mL 7. Outline the mechanism of 2 drugs that affect the cardiac contractility, rate and rhythm. Give examples of appropriate clinical use for this drugs including risks and benefits associated with treatment. Answer: Beta blockers: • Block adrenergic beta-1 receptors on the heart -> prevent catecholamine binding -> inhibit Gs protein -> decreases AC activation -> decreased conversion of ATP into cAMP -> deceased PKA -> decreased phosphorylation of L-type Ca2+ channels and myosin heads -> negative chronotropic and inotropic effects -> decreased heart rate and contractility • • Clinical uses: useful for MIs, angina and tachycardias Side effects: they are non-selective so can bind to beta 2 receptors on the smooth muscle of the bronchus causing bronchospasm -> shortness of breath, bradycardia and hypotension Na+ channel blockers • Block voltage gated Na+ channels • Decease heart rate and contractility • Clinical uses: same as beta blockers • Side effects: bradycardia, nightmares and hypotension 2024 8. a. Explain how hyperkalaemia can lead to sinus bradycardia. b. Discuss the complications of arrhythmias. Answer: a. Hyperkalaemia -> increased concentrations of K+ in the blood and thus in the extracellular environment of the cell -> the extracellular environment of the cell will be too positive -> K+ from inside the cell will be less likely to come out -> K+ stays in the cell for longer -> the membrane potential of the pacemaker cells will increase -> this will increase the membrane potential of the pacemaker cells -> it will be harder for the Na+ channels to reach a state where they can be re-activated once again. b. When there is bradycardia, there will be a low cardiac output. This will lead to the following events: • Low organ perfusion ->low oxygen delivery -> lethargy, confusion, and syncope due to low perfusion to the brain -> altered mental status. • Blood will remain in the heart chambers as they heart rate is too slow so blood will accumulate there: - Blood will back up into the lungs -> pulmonary edema. - As blood will become stagnant for prolonged periods -> clot formation -> increase stroke and PE risk. • Decreased blood flow and perfusion to the coronary arteries -> ischemia and possibly infarction -> angina.