Pharm CVS Flashcards
(469 cards)
1
Q
SBA: What is the primary equation for calculating blood pressure?
A
Answer: Blood pressure = Cardiac output × Peripheral resistance.
2
Q
SBA: What is the role of baroreceptors in blood pressure regulation?
A
Answer: Detect changes in arterial pressure and signal the brainstem to adjust heart rate and vascular tone.
3
Q
SBA: Which part of the brain regulates cardiovascular responses to blood pressure changes?
A
Answer: Medulla and pons (cardiovascular center).
4
Q
SBA: What is the primary vasoconstrictor in the renin-angiotensin-aldosterone system (RAAS)?
A
Answer: Angiotensin II.
5
Q
SBA: What triggers the release of erythropoietin (EPO)?
A
Answer: Hypoxia in the kidneys.
6
Q
SBA: Which adrenergic receptor subtype increases heart rate and force of contraction?
A
Answer: Beta-1 adrenergic receptors.
7
Q
SBA: What is the function of atrial natriuretic peptide (ANP) in blood pressure control?
A
Answer: Promotes sodium and water excretion, reducing blood volume and pressure.
8
Q
SBA: Which hormone is released in response to hypovolemia to retain water?
A
Answer: Antidiuretic hormone (ADH, also known as vasopressin).
9
Q
SBA: What is the physiological impact of systemic vasodilation on blood pressure?
A
Answer: Decreases peripheral resistance and lowers blood pressure.
10
Q
SBA: What is the key feature differentiating primary from secondary hypertension?
A
Answer: Primary hypertension has no identifiable cause, while secondary hypertension has an underlying condition or drug-related cause.
11
Q
EMQ: Match the blood pressure regulation mechanism to its function.
A
Baroreflex: Short-term blood pressure regulation.
RAAS: Long-term blood pressure regulation.
Autoregulation: Maintains consistent perfusion at the tissue level.
12
Q
EMQ: Match the hormone to its action in blood pressure regulation.
A
Angiotensin II: Vasoconstriction and aldosterone release.
ADH: Increases water reabsorption and vasoconstriction.
ANP: Promotes sodium and water excretion.
13
Q
EMQ: Match the symptom to the blood pressure condition.
A
Severe headache and vision problems: Hypertension.
Lightheadedness and fainting: Hypotension.
Chronic fatigue and chest pain: Hypertension or low cardiac output.
14
Q
EMQ: Match the blood pressure target to the treatment strategy.
A
Decrease cardiac output: Beta-blockers.
Decrease peripheral resistance: Calcium channel blockers.
Increase blood volume: Fluid therapy or ADH.
15
Q
EMQ: Match the risk factor to the cardiovascular disease continuum.
A
Hypertension: Atherosclerosis and heart failure.
Dyslipidaemia: Coronary artery disease.
Smoking: Endothelial dysfunction and thrombosis.
16
Q
Describe the role of the RAAS in blood pressure regulation.
A
Answer: Renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II by ACE. Angiotensin II causes vasoconstriction and aldosterone release, increasing sodium and water reabsorption. (2 marks)
17
Q
What are the main triggers for baroreceptor activation?
A
Answer: Changes in arterial pressure, such as hypotension or hypertension. (2 marks)
18
Q
List three pharmacological approaches to treat hypertension and their mechanisms.
A
Answer:
Beta-blockers: Decrease heart rate and cardiac output.
ACE inhibitors: Block angiotensin II formation, reducing vasoconstriction.
Calcium channel blockers: Dilate blood vessels by inhibiting calcium influx. (3 marks)
19
Q
What is the physiological response to hypotension due to hypovolemia?
A
Answer: ADH release, vasoconstriction, and increased water retention. (2 marks)
20
Q
How does autoregulation maintain perfusion during ischemia?
A
Answer: Local metabolic factors like low oxygen and high CO2 levels cause vasodilation to restore blood flow. (1 mark)
21
Q
SBA: What blood pressure reading in a clinic suggests the need for further investigation with ABPM or HBPM?
A
Answer: Clinic BP >140/90 mmHg.
22
Q
SBA: What is the first-line pharmacological treatment for hypertension in patients under 55 years of age?
A
Answer: ACE inhibitors (e.g., Ramipril).
23
Q
SBA: Which hypertension drug class is contraindicated in asthmatic patients?
A
Answer: Beta-blockers.
24
Q
SBA: What lifestyle modification is recommended for sodium intake in hypertension management?
A
Answer: Reduce salt intake to below 6 g/day.
25
SBA: Which drug class reduces blood pressure by blocking angiotensin II receptors?
Answer: ARBs (e.g., Losartan).
26
SBA: What side effect is most commonly associated with dihydropyridine calcium channel blockers like Amlodipine?
Answer: Peripheral oedema.
27
SBA: What is the target BP for patients under 80 years with hypertension?
Answer: <140/90 mmHg.
28
SBA: Which electrolyte imbalance is a common side effect of thiazide-like diuretics?
Answer: Hypokalaemia.
29
SBA: What is the mechanism of action of spironolactone in hypertension management?
Answer: Blocks aldosterone receptors, promoting sodium excretion and potassium retention.
30
SBA: What is the significance of a >15 mmHg difference between arms when measuring BP?
Answer: Use the higher reading for future measurements and investigate for vascular disease.
31
EMQ: Match the antihypertensive drug to its side effect.
ACE inhibitors: Dry cough.
Beta-blockers: Bradycardia.
Calcium channel blockers: Flushing.
Thiazide diuretics: Hyperglycaemia.
Spironolactone: Gynaecomastia.
32
EMQ: Match the hypertension drug to its monitoring requirement.
ACE inhibitors: Renal function and potassium.
ARBs: Renal function and potassium.
Thiazide diuretics: Sodium and potassium levels.
Beta-blockers: Heart rate.
Spironolactone: Potassium levels.
33
EMQ: Match the patient group to their recommended first-line antihypertensive therapy.
Under 55 years: ACE inhibitors or ARBs.
Over 55 years or Black patients: Calcium channel blockers.
Resistant hypertension: Spironolactone or Alpha-blockers.
34
EMQ: Match the BP measurement method to its application.
Clinic BP: Initial diagnosis.
Ambulatory BP monitoring (ABPM): Confirming diagnosis.
Home BP monitoring (HBPM): Alternative to ABPM.
Manual BP measurement: Pulse irregularity.
35
EMQ: Match the lifestyle modification to its cardiovascular benefit.
Exercise: Reduces resting blood pressure.
Weight loss: Improves BP control.
Salt reduction: Lowers BP by reducing water retention.
Smoking cessation: Reduces cardiovascular risk.
36
Describe the initial steps for BP measurement.
Answer: Measure BP in a relaxed environment, both arms, and document the higher reading. If >140/90 mmHg, confirm with ABPM or HBPM. (2 marks)
37
What assessments are made alongside BP measurement?
Answer: Assess cardiovascular risk (e.g., QRISK3), target organ damage (e.g., kidneys, heart, eyes), and perform relevant blood tests. (2 marks)
38
What are the key lifestyle modifications recommended?
Answer: Reduce salt intake, increase exercise, achieve a healthy BMI, and limit alcohol consumption. (2 marks)
39
Describe the stepwise pharmacological treatment for hypertension.
Answer:
Step 1: ACE inhibitors or ARBs (under 55 years); Calcium channel blockers (over 55 years or Black patients).
Step 2: Combine ACE inhibitors/ARBs with Calcium channel blockers or Thiazide-like diuretics.
Step 3: Triple therapy with ACE inhibitors/ARBs, Calcium channel blockers, and Thiazide-like diuretics.
Step 4: Add Spironolactone or Alpha-blockers for resistant hypertension. (3 marks)
40
What is the target BP for patients under and over 80 years?
Answer: <140/90 mmHg (under 80 years) and <150/90 mmHg (over 80 years). (1 mark)
41
SBA: What is the first-line pharmacological treatment for primary prevention of CVD in patients with a QRISK3 score ≥10%?
Answer: Atorvastatin 20 mg daily.
42
SBA: What is the main treatment goal in lipid modification therapy?
Answer: Achieve a ≥40% reduction in non-HDL cholesterol levels.
43
SBA: What condition is characterized by high cholesterol levels due to a defective gene?
Answer: Familial hypercholesterolaemia.
44
SBA: Which statin intensity category is atorvastatin 80 mg classified under?
Answer: High-intensity statin.
45
SBA: What non-statin medication inhibits intestinal cholesterol absorption?
Answer: Ezetimibe.
46
SBA: What is the role of PCSK9 inhibitors in hyperlipidaemia treatment?
Answer: Increase LDL receptor recycling, enhancing LDL cholesterol clearance.
47
Answer: Increase LDL receptor recycling, enhancing LDL cholesterol clearance.
Answer: Liver function tests and lipid profile.
48
SBA: What lifestyle modification is essential in hyperlipidaemia management to reduce saturated fat intake?
Answer: Limit saturated fat to <7% of total daily energy intake.
49
SBA: What is a common side effect of statins?
Answer: Myopathy or muscle pain.
50
SBA: Which medication is contraindicated in pregnancy for hyperlipidaemia treatment?
Answer: Statins.
51
EMQ: Match the condition to its associated hyperlipidaemia risk.
Familial hypercholesterolaemia: Genetic defect in LDL receptor.
Diabetes mellitus: Increased triglycerides and LDL cholesterol.
Chronic kidney disease: Dysregulation of lipid metabolism.
52
EMQ: Match the medication to its mechanism of action.
Statins: Inhibit HMG-CoA reductase.
Ezetimibe: Inhibits cholesterol absorption in the intestine.
Bempedoic acid: Inhibits ATP citrate lyase.
53
EMQ: Match the side effect to the lipid-lowering drug.
Muscle pain: Statins.
Gout: Bempedoic acid.
Injection site reactions: Inclisiran.
54
EMQ: Match the non-pharmacological intervention to its benefit.
Smoking cessation: Reduces cardiovascular risk.
Weight loss: Improves lipid profile and BP.
Exercise: Increases HDL cholesterol.
55
EMQ: Match the hyperlipidaemia drug to its indication.
Inclisiran: High-risk patients with LDL-C ≥4.0 mmol/L.
Atorvastatin: First-line for primary and secondary prevention.
Fibrates: Severe hypertriglyceridemia.
56
Describe lifestyle modifications for hyperlipidaemia management.
Answer:
Smoking cessation.
Reduce total fat intake (<30%) and saturated fat (<7%).
Increase intake of fruits, vegetables, and oily fish.
Exercise for at least 150 minutes/week.
Limit alcohol to ≤14 units/week. (3 marks)
57
What baseline tests are required before starting statin therapy?
Answer: Non-fasting lipid profile, liver function tests, renal function, HbA1c, creatine kinase, and thyroid-stimulating hormone (if indicated). (2 marks)
58
Answer: Non-fasting lipid profile, liver function tests, renal function, HbA1c, creatine kinase, and thyroid-stimulating hormone (if indicated). (2 marks)
Answer:
First-line: Atorvastatin 20 mg (primary prevention) or 80 mg (secondary prevention).
Add ezetimibe if LDL-C reduction is insufficient.
Consider bempedoic acid or PCSK9 inhibitors (e.g., Inclisiran) for high-risk patients. (3 marks)
59
What are the contraindications and monitoring requirements for statin use?
Answer: Contraindicated in pregnancy and active liver disease. Monitor liver function and lipid profile 3 months after initiation and annually. (2 marks)
60
SBA: What is the primary route of administration for most antihypertensive drugs?
Answer: Oral.
61
SBA: Which antihypertensive drug undergoes significant first-pass metabolism, reducing its bioavailability?
Answer: Propranolol.
62
SBA: What is the key enzyme involved in the metabolism of calcium channel blockers like amlodipine?
Answer: CYP3A4.
63
SBA: Which class of antihypertensive drugs is most affected by reduced renal function?
Answer: ACE inhibitors (e.g., Ramipril).
64
SBA: Why should grapefruit juice be avoided with calcium channel blockers?
Answer: Grapefruit juice inhibits CYP3A4, increasing plasma drug levels.
65
SBA: What is the mechanism of action of ARBs?
Answer: Block angiotensin II at the AT1 receptor.
66
SBA: What type of interaction occurs when NSAIDs reduce the efficacy of ACE inhibitors?
Answer: Pharmacodynamic interaction.
67
SBA: Which antihypertensive drug is a prodrug activated in the liver?
Answer: Enalapril.
68
SBA: What is the primary organ responsible for the excretion of ARBs?
Answer: Kidneys.
69
SBA: Which antihypertensive drug has the highest risk of causing bradycardia when combined with verapamil?
Answer: Beta-blockers (e.g., Atenolol).
70
EMQ: Match the antihypertensive drug to its absorption characteristic.
Captopril: Food reduces absorption.
Amlodipine: High oral bioavailability.
Propranolol: Significant first-pass metabolism.
71
EMQ: Match the antihypertensive drug class to its metabolism.
Beta-blockers (e.g., Metoprolol): CYP2D6.
CCBs (e.g., Verapamil): CYP3A4.
ACE inhibitors (e.g., Lisinopril): Active in administered form (no liver metabolism).
72
EMQ: Match the interaction type to the example.
Pharmacokinetic: Grapefruit juice with amlodipine.
Pharmacodynamic: Thiazide diuretics with ACE inhibitors causing severe hypotension.
Drug-food: Captopril with food reducing efficacy.
73
EMQ: Match the adverse effect to the antihypertensive drug class.
Hyperkalaemia: ARBs and potassium-sparing diuretics.
Hypokalaemia: Thiazide diuretics.
Peripheral oedema: Calcium channel blockers.
74
EMQ: Match the elimination route to the drug.
Renal: Losartan.
Hepatic: Amlodipine.
Mixed (renal and hepatic): Metoprolol.
75
Describe the absorption of antihypertensive drugs.
Answer: Most are orally administered; factors like food and gastric pH can influence bioavailability (e.g., captopril). (2 marks)
76
Explain the metabolism of ACE inhibitors and beta-blockers.
Answer:
ACE inhibitors: Most are prodrugs activated in the liver, except Lisinopril.
Beta-blockers: Metabolised by CYP2D6 enzymes. (2 marks
77
What is the impact of renal function on antihypertensive drug elimination?
Answer: Drugs like ACE inhibitors and ARBs rely on renal excretion, making dosage adjustments necessary in renal impairment. (2 marks)
78
List two examples of drug-drug interactions involving antihypertensive drugs.
Answer:
NSAIDs reduce the antihypertensive effect of ACE inhibitors.
Verapamil and beta-blockers increase the risk of severe bradycardia. (2 marks)
79
Why should patient education include warnings about grapefruit juice with certain antihypertensives?
Answer: Grapefruit juice inhibits CYP3A4, increasing the plasma concentration of calcium channel blockers and raising the risk of adverse effects. (2 marks)
80
SBA: What is the primary action of ACE inhibitors in hypertension?
Answer: Reduce the conversion of angiotensin I to angiotensin II, leading to vasodilation and reduced blood pressure.
81
SBA: What common side effect is associated with ACE inhibitors and caused by bradykinin accumulation?
Answer: Dry cough.
82
SBA: What is the mechanism of action of ARBs?
Answer: Block angiotensin II at AT1 receptors, preventing vasoconstriction and aldosterone release.
83
SBA: What class of drugs inhibits L-type calcium channels to manage hypertension?
Answer: Calcium channel blockers (CCBs).
84
SBA: What adverse effect is commonly associated with dihydropyridine CCBs like amlodipine?
Answer: Peripheral oedema.
85
SBA: What diuretic class is considered first-line in hypertension management?
Answer: Thiazide-like diuretics.
86
SBA: What is the mechanism of action of spironolactone in hypertension treatment?
Answer: Antagonizes aldosterone receptors, promoting sodium excretion and potassium retention.
87
SBA: What antihypertensive drug class is contraindicated during pregnancy?
Answer: ACE inhibitors and ARBs.
88
SBA: What type of beta-blocker is propranolol classified as?
Answer: Non-selective beta-blocker.
89
SBA: Which diuretic is most effective at reducing blood pressure by blocking sodium reabsorption in the distal convoluted tubule?
Answer: Thiazide-like diuretics (e.g., indapamide).
90
EMQ: Match the antihypertensive drug class to its adverse effect.
ACE inhibitors: Dry cough
Beta-blockers: Bradycardia
Calcium channel blockers: Flushing and headache
Thiazide diuretics: Hypokalaemia
91
EMQ: Match the drug to its primary mechanism of action.
Captopril: Inhibits ACE.
Losartan: Blocks AT1 receptors.
Amlodipine: Blocks L-type calcium channels.
92
EMQ: Match the clinical scenario to the most appropriate antihypertensive drug.
Hypertension with diabetes: ACE inhibitors (renal protection).
Resistant hypertension: Spironolactone.
Elderly patients: Calcium channel blockers.
93
EMQ: Match the antihypertensive drug class to its renal effect.
Thiazides: Reduce calcium excretion.
Potassium-sparing diuretics: Increase potassium retention.
ACE inhibitors: Reduce proteinuria.
94
EMQ: Match the contraindication to the drug.
Pregnancy: ACE inhibitors.
Bradycardia: Beta-blockers.
Bilateral renal artery stenosis: ARBs.
95
Describe the mechanism of action of ACE inhibitors and ARBs.
Answer:
ACE inhibitors block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone release.
ARBs block AT1 receptors, preventing angiotensin II action. (2 marks)
96
List two common adverse effects of ACE inhibitors.
Answer: Dry cough and hyperkalaemia. (1 mark)
97
Explain the role of thiazide-like diuretics in hypertension.
nswer: Block sodium-chloride symporters in the distal convoluted tubule, reducing blood volume and lowering blood pressure. (2 marks)
98
What are the clinical considerations for prescribing beta-blockers?
Answer: Use caution in asthma, bradycardia, and in combination with calcium channel blockers (risk of severe bradycardia). (2 marks)
99
Discuss the monitoring requirements for patients on ACE inhibitors.
Answer: Regularly check renal function (serum creatinine) and potassium levels to prevent hyperkalaemia and renal impairment. (2 marks)
100
SBA: What is the primary mechanism of action of statins?
Answer: Inhibition of HMG-CoA reductase.
101
SBA: Which lipoprotein is referred to as "good cholesterol"?
Answer: High-Density Lipoprotein (HDL).
102
SBA: What is the main role of PCSK9 inhibitors in lipid management?
Answer: Increase LDL receptor recycling, reducing circulating LDL cholesterol.
103
SBA: What lipid parameter is targeted for ≥40% reduction in patients on statin therapy?
Answer: Non-HDL cholesterol.
104
SBA: What is the primary cause of familial hypercholesterolaemia?
Answer: Genetic mutations in LDL receptor or PCSK9.
105
SBA: Which lipoprotein is the main carrier of triglycerides in the bloodstream?
Answer: Very Low-Density Lipoprotein (VLDL).
106
SBA: What is the key characteristic of reverse cholesterol transport?
Answer: Movement of cholesterol from peripheral tissues back to the liver via HDL.
107
SBA: What is the main side effect of fibrates?
Answer: Myopathy, especially when combined with statins.
108
SBA: What is a contraindication for statin therapy?
Answer: Pregnancy.
109
SBA: Which lipid-lowering drug can cause flushing as a common side effect?
Answer: Niacin (nicotinic acid).
110
EMQ: Match the drug to its mechanism of action.
Statins: Inhibit HMG-CoA reductase.
PCSK9 inhibitors: Prevent LDL receptor degradation.
Ezetimibe: Inhibits cholesterol absorption in the intestine.
111
EMQ: Match the lipoprotein to its function.
LDL: Delivers cholesterol to peripheral tissues.
HDL: Mediates reverse cholesterol transport.
Chylomicrons: Transport dietary lipids from the intestine.
112
EMQ: Match the lipid-lowering drug to its adverse effect.
Statins: Myopathy.
Fibrates: Gallstones.
Niacin: Flushing.
113
EMQ: Match the lipid abnormality to the associated drug therapy.
Elevated LDL: Statins or PCSK9 inhibitors.
Elevated triglycerides: Fibrates or omega-3 fatty acids.
Mixed dyslipidaemia: Combination of statins and fibrates.
114
EMQ: Match the lipid-lowering drug to its clinical consideration.
Statins: Monitor liver function tests.
Fibrates: Avoid in severe renal impairment.
Niacin: Take aspirin to reduce flushing.
115
Explain the role of lipoproteins in lipid transport.
Answer:
Chylomicrons transport dietary triglycerides.
VLDL transports triglycerides synthesized in the liver.
LDL delivers cholesterol to peripheral tissues.
HDL mediates reverse cholesterol transport. (2 marks)
116
Describe the pathophysiology of atherosclerosis in dyslipidaemia.
Answer:
LDL oxidation in the arterial wall leads to foam cell formation.
Chronic inflammation results in plaque development and narrowing of arteries. (2 marks)
117
Outline the pharmacological management of dyslipidaemia.
Answer:
Statins: First-line therapy for LDL reduction.
PCSK9 inhibitors: Used in high-risk patients not achieving goals on statins.
Fibrates: Target elevated triglycerides.
Ezetimibe: Add-on therapy for further LDL reduction. (3 marks)
118
What lifestyle interventions support pharmacological treatment in dyslipidaemia?
Answer:
Diet low in saturated fats.
Regular physical activity.
Smoking cessation. (2 marks)
119
What are the monitoring requirements for statin therapy?
Answer:
Check lipid profile 3 months after initiation and then annually.
Monitor liver enzymes before starting and periodically. (1 mark)
120
SBA: What is the primary target of ACE inhibitors in the treatment of hypertension?
Answer: Angiotensin-Converting Enzyme (ACE).
121
SBA: What is the common side effect of ACE inhibitors due to bradykinin accumulation?
Answer: Dry cough.
122
SBA: Which functional group in captopril enhances binding to the zinc ion in ACE?
Answer: Sulfhydryl (SH) group.
123
Answer: Sulfhydryl (SH) group.
Answer: Sulfhydryl (SH) group.
124
SBA: Which ARB has a tetrazole ring to enhance metabolic stability and bioavailability?
Answer: Losartan.
125
SBA: Which drug class inhibits L-type calcium channels to manage hypertension?
Answer: Calcium channel blockers (CCBs).
126
SBA: What is the mechanism of action of HMG-CoA reductase inhibitors (statins)?
Answer: Inhibit the rate-limiting step in cholesterol biosynthesis.
127
SBA: What chemical feature allows atorvastatin to bind effectively to HMG-CoA reductase?
Answer: Open lactone ring mimicking the tetrahedral intermediate.
128
SBA: What adverse effect is commonly associated with statins?
Answer: Myopathy.
129
SBA: What is the primary site of action for thiazide-like diuretics?
Answer: Distal convoluted tubule.
130
EMQ: Match the antihypertensive drug to its mechanism of action.
ACE inhibitors: Block conversion of angiotensin I to angiotensin II.
ARBs: Block AT1 receptors.
CCBs: Block L-type calcium channels.
131
EMQ: Match the drug to its adverse effect.
Statins: Myopathy.
ACE inhibitors: Dry cough.
Thiazides: Hypokalaemia.
132
EMQ: Match the drug to its structural feature.
Losartan: Tetrazole ring.
Captopril: Sulfhydryl group.
Enalapril: Ester prodrug.
133
EMQ: Match the drug class to its therapeutic use.
ARBs: Hypertension in ACE inhibitor-intolerant patients.
Statins: Hyperlipidaemia.
Thiazides: First-line for hypertension.
134
EMQ: Match the calcium channel blocker to its subclass.
Nifedipine: 1,4-Dihydropyridine.
Verapamil: Phenylalkylamine.
Diltiazem: Benzothiazepine.
135
Describe the mechanism of action of ACE inhibitors.
Answer: Inhibit ACE, preventing conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion.
136
Explain why enalapril is preferred over enalaprilat for oral administration.
Answer: Enalapril is a prodrug with superior bioavailability due to esterification, allowing absorption in the intestine. Enalaprilat is poorly absorbed due to its zwitterionic nature. (2 marks)
137
What is the role of the tetrazole ring in ARBs like losartan?
What is the role of the tetrazole ring in ARBs like losartan?
138
List two adverse effects of calcium channel blockers and the associated subclasses.
Answer: Peripheral oedema (1,4-dihydropyridines) and bradycardia (phenylalkylamines). (2 marks)
139
How do statins achieve their lipid-lowering effects?
Answer: Inhibit HMG-CoA reductase, reducing cholesterol synthesis and increasing LDL receptor expression for enhanced clearance of LDL cholesterol. (2 marks)
140
SBA: What is the primary diagnostic marker for myocardial infarction?
Answer: Troponin.
141
SBA: What is the first-line treatment for stable angina?
Answer: Glyceryl trinitrate (GTN) for symptom relief.
142
SBA: Which drug class is used for secondary prevention post-MI to reduce lipid levels?
Answer: Statins.
143
SBA: What is the gold standard treatment for STEMI if performed within 120 minutes of medical contact?
Answer: Percutaneous coronary intervention (PCI).
144
SBA: Which medication is contraindicated in acute MI due to its ability to increase heart rate?
Answer: Ivabradine.
145
SBA: What is the typical dose of aspirin given in the initial management of ACS?
Answer: 300 mg.
146
SBA: Which beta-blocker is commonly used for secondary prevention post-MI?
Answer: Bisoprolol.
147
SBA: What is the mechanism of action of fibrinolytics in STEMI management?
Answer: Activation of plasminogen to form plasmin, which breaks down fibrin clots.
148
SBA: What is the GRACE score used for in ACS management?
Answer: Predicts the 6-month mortality risk in patients with ACS.
149
SBA: Which medication is often used as a second-line treatment for angina if beta-blockers are contraindicated?
Answer: Calcium channel blockers (e.g., amlodipine).
150
EMQ: Match the ACS condition to its typical presentation.
Stable angina: Pain on exertion, relieved by rest.
Unstable angina: Pain at rest, unresponsive to GTN.
STEMI: Persistent chest pain with ST elevation on ECG.
151
EMQ: Match the medication to its role in ACS management.
Aspirin: Antiplatelet therapy.
Enoxaparin: Anticoagulation.
Ticagrelor: P2Y12 inhibitor for dual antiplatelet therapy.
152
EMQ: Match the drug to its contraindication in ACS.
ACE inhibitors: History of angioedema.
Beta-blockers: Severe bradycardia.
Nitrates: Severe hypotension.
153
EMQ: Match the diagnostic test to its role in ACS.
ECG: Identifies ischemic changes like ST elevation.
Troponin levels: Confirms myocardial necrosis.
GRACE score: Risk stratification.
154
EMQ: Match the lifestyle advice to the outcome in ACS management.
Smoking cessation: Reduces risk of recurrent MI.
Mediterranean diet: Improves lipid profile.
Physical activity: Enhances exercise capacity and reduces mortality.
155
List the key symptoms and diagnostic tests for STEMI.
Answer:
Symptoms: Severe chest pain, radiating to jaw/arm, nausea, sweating. (1 mark)
Tests: ECG showing ST elevation; raised troponin levels. (1 mark)
156
Describe the pharmacological treatment during initial STEMI management.
Answer:
Aspirin 300 mg STAT (antiplatelet). (1 mark)
Ticagrelor or prasugrel STAT (dual antiplatelet therapy). (1 mark)
Fondaparinux or enoxaparin for anticoagulation. (1 mark)
157
Outline the reperfusion therapy options for STEMI.
Answer:
PCI within 120 minutes of contact (gold standard).
Fibrinolysis (if PCI unavailable) using alteplase or streptokinase. (2 marks)
158
What lifestyle interventions are recommended post-STEMI?
Answer:
Smoking cessation.
Mediterranean diet.
Regular physical activity (20–30 mins/day). (2 marks)
159
What is the rationale for statin therapy in STEMI patients?
Answer:
Reduces LDL cholesterol, stabilizes plaques, and decreases the risk of recurrent events. (1 mark)
160
SBA: What is the most common cause of heart failure?
Answer: Left ventricular dysfunction following myocardial infarction.
161
SBA: Which peptide is used to confirm or rule out heart failure diagnosis?
Answer: NT-proBNP.
162
SBA: What is the first-line pharmacological therapy for heart failure with reduced ejection fraction (HFrEF)?
Answer: ACE inhibitor and beta-blocker.
163
SBA: What is the typical dose range for furosemide in managing oedema in heart failure?
Answer: Up to 80 mg/day, titrated as needed.
164
SBA: Which drug class reduces mortality and hospitalisation when added to ACE inhibitors and beta-blockers in HFrEF?
Answer: Mineralocorticoid receptor antagonists (MRAs).
165
SBA: Which heart failure medication is a combination of sacubitril and valsartan?
Answer: Entresto®.
166
SBA: What is a common side effect of digoxin that requires monitoring?
Answer: Digitalis toxicity (e.g., nausea, vomiting, confusion).
167
SBA: Which functional classification system is used to assess the severity of heart failure symptoms?
Answer: New York Heart Association (NYHA) classification.
168
SBA: What lifestyle advice should be given to a stable heart failure patient regarding exercise?
Answer: Regular, supervised exercise within functional limitations.
169
SBA: What is the role of SGLT2 inhibitors in heart failure?
Answer: Reduce cardiovascular death and hospitalisation for HFrEF patients.
170
EMQ: Match the drug to its mechanism of action.
ACE inhibitors: Inhibit conversion of angiotensin I to angiotensin II.
MRAs: Antagonise aldosterone receptors.
Digoxin: Inhibit Na+/K+ ATPase to increase contractility.
171
EMQ: Match the symptom to the heart failure feature.
Fatigue: Decreased cardiac output and oxygen delivery.
Peripheral oedema: Fluid retention.
Orthopnoea: Redistribution of fluid to the lungs when lying down.
172
EMQ: Match the drug to its specialist use in HFrEF.
Ivabradine: Patients with sinus rhythm and heart rate ≥75 bpm.
Entresto®: Alternative to ACE inhibitors for NYHA Class II-IV patients.
Hydralazine: Patients of African-Caribbean descent with persistent symptoms.
173
EMQ: Match the diagnostic test to its purpose in heart failure.
NT-proBNP: Confirms/rules out diagnosis.
Echocardiography: Assesses ventricular function.
ECG: Identifies underlying causes like arrhythmias or ischemia.
174
EMQ: Match the lifestyle advice to its benefit in heart failure.
Balanced diet: Maintains healthy weight and reduces strain on the heart.
Timed diuretic use: Improves sleep by reducing nocturia.
Smoking cessation: Reduces disease progression.
175
List the key symptoms and diagnostic tools for heart failure.
Answer:
Symptoms: Fatigue, breathlessness, oedema.
Diagnostics: NT-proBNP levels, echocardiography, ECG. (2 marks)
176
Describe the first-line pharmacological management for HFrEF.
Answer:
ACE inhibitor (e.g., Ramipril).
Beta-blocker (e.g., Bisoprolol).
Add MRA (e.g., Spironolactone) if symptoms persist. (3 marks)
177
What are the specialist treatment options for HFrEF?
Answer:
Ivabradine for patients with sinus rhythm and HR ≥75 bpm.
Entresto® as a substitute for ACE inhibitors.
Digoxin for severe cases. (2 marks)
178
What lifestyle advice should be provided to heart failure patients?
Answer:
Regular exercise within limits.
Balanced diet, reduced salt intake, and weight management.
Smoking cessation and limited alcohol consumption. (2 marks)
179
How is heart failure treatment monitored?
Answer:
Monitor renal function, electrolytes, and NT-proBNP levels.
Regular assessment of symptoms and medication compliance. (1 mark)
180
SBA: What is the most common sustained arrhythmia in clinical practice?
Answer: Atrial fibrillation (AF).
181
SBA: Which scoring system is used to assess stroke risk in patients with AF?
Answer: CHA₂DS₂-VASc score.
182
SBA: Which drug is a direct thrombin inhibitor used for anticoagulation in AF?
Answer: Dabigatran.
183
SBA: What is the mechanism of action of warfarin?
Answer: Vitamin K antagonist, inhibiting the synthesis of clotting factors II, VII, IX, and X.
184
SBA: Which type of AF resolves spontaneously within 48 hours?
Answer: Paroxysmal AF.
185
SBA: What is the first-line drug class for rate control in AF?
Answer: Beta-blockers (e.g., bisoprolol).
186
SBA: Which drug is recommended for pharmacological cardioversion in AF patients with structural heart disease?
Answer: Amiodarone.
187
SBA: What is the target INR range for patients on warfarin for stroke prevention in AF?
Answer: 2.0–3.0.
188
SBA: What is a contraindication for beta-blockers in AF management?
Answer: Severe bradycardia.
189
SBA: Which anticoagulant is associated with the risk of gastrointestinal bleeding but does not require INR monitoring?
Answer: Rivaroxaban (a DOAC).
190
EMQ: Match the type of AF to its definition.
Paroxysmal AF: Episodes terminate spontaneously within 48 hours.
Persistent AF: Lasts >7 days or requires treatment for termination.
Permanent AF: Continuous and unresponsive to treatment.
191
EMQ: Match the drug to its mechanism of action.
Dabigatran: Direct thrombin inhibitor.
Rivaroxaban: Factor Xa inhibitor.
Warfarin: Vitamin K antagonist.
192
EMQ: Match the AF treatment to the associated monitoring requirement.
DOACs: Renal function monitoring annually.
Warfarin: Regular INR checks.
Amiodarone: Thyroid and liver function monitoring.
193
EMQ: Match the risk stratification score to its purpose.
CHA₂DS₂-VASc: Stroke risk.
HAS-BLED: Bleeding risk.
ORBIT: Assessing overall anticoagulation safety.
194
EMQ: Match the patient scenario to the anticoagulant recommendation.
Male with CHA₂DS₂-VASc score of 0: No anticoagulation.
Female with CHA₂DS₂-VASc score of 2: DOAC or warfarin.
Patient with CrCl <30 mL/min: Warfarin (avoid DOACs).
195
List three common symptoms of AF.
Answer: Palpitations, breathlessness (dyspnoea), and fatigue. (1 mark)
196
What tests are used to diagnose AF?
Answer: ECG (to confirm arrhythmia), blood tests (e.g., thyroid function), and echocardiography (to assess ventricular function). (2 marks)
197
Explain the CHA₂DS₂-VASc scoring system for stroke risk in AF.
Answer: Includes factors like congestive heart failure, hypertension, age ≥75 years (2 points), diabetes, stroke/TIA (2 points), vascular disease, and sex (female = 1 point). (2 marks)
198
Outline pharmacological options for rate control in AF.
Answer:
Beta-blockers (e.g., bisoprolol): First-line therapy.
Calcium channel blockers (e.g., diltiazem): If beta-blockers are contraindicated.
Digoxin: For sedentary patients with non-paroxysmal AF. (2 marks)
199
Discuss the benefits of DOACs compared to warfarin in AF management.
Answer: DOACs have a fixed dose, no routine INR monitoring, and a lower risk of intracranial bleeding. (2 marks)
200
SBA: What is the most common mechanism for pharmacokinetic drug interactions?
SBA: What is the most common mechanism for pharmacokinetic drug interactions?
201
SBA: Which drug interaction resource provides the most detailed explanation for interaction mechanisms?
Answer: Stockley’s Drug Interactions
202
SBA: What is the primary clinical concern when combining NSAIDs with DOACs?
Answer: Increased risk of gastrointestinal bleeding.
203
SBA: Which enzyme does grapefruit juice inhibit, leading to increased drug plasma levels?
Answer: CYP3A4.
204
SBA: What is the effect of inducing CYP450 enzymes on drug metabolism?
Answer: Increased metabolism, leading to reduced plasma concentrations of the drug.
205
SBA: Which food component interacts with MAOIs and can cause a hypertensive crisis?
Answer: Tyramine.
206
SBA: What is the recommendation for administering levothyroxine with calcium-containing antacids?
Answer: Separate administration by 2-4 hours.
207
SBA: Which protein plays a major role in drug transport and can be inhibited by certain drugs like amiodarone?
Answer: P-glycoprotein.
208
SBA: What is a potential interaction when warfarin is combined with cranberry juice?
Answer: Increased bleeding risk due to CYP450 inhibition.
209
SBA: What characteristic of a drug increases the likelihood of protein binding interactions?
Answer: High protein-binding (>90%).
210
EMQ: Match the drug to the common interaction mechanism.
Warfarin: CYP450 inhibition by other drugs or food (e.g., cranberry juice).
Ciprofloxacin: Chelation with calcium-containing products.
Amiodarone: P-glycoprotein inhibition.
211
EMQ: Match the patient characteristic to the increased risk of drug interactions.
Elderly: Reduced renal and hepatic function.
Children: Underdeveloped metabolism.
Polypharmacy: Higher risk of adverse drug interactions.
212
EMQ: Match the pharmacodynamic interaction to the drug pair.
DOAC + NSAIDs: Increased bleeding risk.
Beta-blockers + Verapamil: Severe bradycardia.
Antihypertensives + Diuretics: Excessive hypotension.
213
EMQ: Match the resource to its feature.
Stockley’s: Detailed explanation of interaction mechanisms.
BNF paper: Pharmacodynamic interaction tables.
SPC: Scientific data from clinical trials.
214
EMQ: Match the interaction type to its management.
CYP450 induction: Consider dose increase of affected drug.
Chelation: Separate administration by a few hours.
P-glycoprotein inhibition: Monitor drug levels and side effects.
215
Differentiate between pharmacokinetic and pharmacodynamic drug interactions.
Answer:
Pharmacokinetic: Alter ADME (absorption, distribution, metabolism, excretion). (1 mark)
Pharmacodynamic: Additive, synergistic, or antagonistic effects at the receptor or physiological level. (1 mark)
216
Explain the clinical significance of CYP450 inhibitors and inducers.
Answer:
Inhibitors: Increase plasma drug levels, increasing toxicity risk (e.g., amiodarone).
Inducers: Reduce plasma drug levels, leading to therapeutic failure (e.g., carbamazepine). (2 marks)
217
List three examples of food-drug interactions and their outcomes.
Answer:
Grapefruit juice + simvastatin: Increased statin toxicity.
Green leafy vegetables + warfarin: Reduced anticoagulant effect.
Tyramine-rich foods + MAOIs: Hypertensive crisis. (3 marks)
218
Outline management strategies for drug interactions.
Answer:
Adjust dosing (e.g., when using enzyme inducers).
Monitor therapeutic drug levels (e.g., warfarin).
Counsel patients to avoid specific food-drug interactions. (2 marks)
219
What is the pharmacist's role in minimizing drug interactions?
Answer:
Anticipate interactions using resources like BNF and Stockley’s.
Educate patients on signs of toxicity or reduced efficacy. (1 mark)
220
SBA: Which coronary artery supplies the sinoatrial (SA) node in most individuals?
Answer: Right coronary artery.
221
SBA: What is the primary pacemaker of the heart?
Answer: Sinoatrial (SA) node.
222
SBA: What ion influx is responsible for the depolarization phase in cardiac pacemaker cells?
Answer: Calcium (Ca²⁺)
223
SBA: What does the P wave on an ECG represent?
Answer: Atrial depolarization.
224
SBA: What is the normal duration of the PR interval on an ECG?
Answer: 0.12–0.20 seconds.
225
SBA: What is the most common cause of prolonged QT interval?
Answer: Hypocalcaemia.
226
SBA: Which part of the ECG corresponds to ventricular depolarization?
Answer: QRS complex.
227
SBA: What is the normal heart rate range for sinus rhythm?
SBA: What is the normal heart rate range for sinus rhythm?
228
SBA: What condition is characterized by a heart rate <60 beats per minute with regular rhythm?
Answer: Sinus bradycardia.
229
SBA: Which formula is used to calculate the corrected QT interval (QTc)?
Answer: Bazett’s formula.
230
EMQ: Match the cardiac rhythm to its ECG feature.
Sinus bradycardia: Heart rate <60 bpm, regular rhythm.
Sinus tachycardia: Heart rate >100 bpm, regular rhythm.
Atrial fibrillation: Irregular rhythm, absence of P waves.
231
EMQ: Match the ion to its effect on cardiac action potential.
Sodium (Na⁺): Rapid depolarization.
Calcium (Ca²⁺): Plateau phase in ventricular action potential.
Potassium (K⁺): Repolarization.
232
EMQ: Match the part of the ECG to its corresponding event.
P wave: Atrial depolarization.
QRS complex: Ventricular depolarization.
T wave: Ventricular repolarization.
233
EMQ: Match the condition to its ECG change.
Hypercalcaemia: Shortened QT interval.
Hypocalcaemia: Prolonged QT interval.
Myocardial infarction: ST elevation.
234
EMQ: Match the cardiac pacemaker to its intrinsic rate.
SA node: 60–100 bpm.
AV node: 40–60 bpm.
Purkinje fibers: 20–40 bpm.
235
Outline the key components of the ECG and their significance.
Answer:
P wave: Atrial depolarization.
PR interval: Time for electrical conduction from SA node to AV node (0.12–0.20 seconds).
QRS complex: Ventricular depolarization (<0.10 seconds).
ST segment: Isoelectric line; elevation indicates ischemia or infarction.
T wave: Ventricular repolarization. (2 marks)
236
Explain the role of the SA node in cardiac rhythm.
Answer: Primary pacemaker; generates impulses at 60–100 bpm. (1 mark)
237
What is the significance of QT interval prolongation?
Answer: Increased risk of ventricular arrhythmias, such as Torsades de Pointes. Causes include hypocalcaemia, medications (e.g., amiodarone), and genetic mutations. (2 marks)
238
How is heart rate calculated from an ECG strip?
Answer: Count the number of large boxes between consecutive R waves and divide 300 by this number. (1 mark)
239
List three factors that can alter the QT interval.
Answer: Plasma calcium levels (hyper/hypocalcaemia), medications (e.g., amiodarone), and genetic mutations (e.g., LQT1, LQT2). (2 marks)
240
What are the criteria for normal sinus rhythm on an ECG?
Answer:
Regular rhythm.
Heart rate of 60–100 bpm.
1 P wave for every QRS complex.
PR interval <0.20 seconds. (2 marks)
241
SBA: What is the hallmark ECG feature of atrial fibrillation?
Answer: Absence of P waves with an irregularly irregular rhythm.
242
SBA: What ion imbalance is most commonly associated with Torsades de Pointes?
Answer: Hypokalemia or hypomagnesemia.
243
SBA: Which arrhythmia presents with a sawtooth pattern on ECG?
Answer: Atrial flutter.
244
SBA: What is the ventricular rate in atrial fibrillation if not controlled?
Answer: 120–200 beats per minute.
245
SBA: What is the primary treatment for pulseless ventricular tachycardia?
Answer: Immediate CPR and defibrillation.
246
SBA: Which drug is used to manage symptomatic bradycardia?
Answer: Atropine.
247
SBA: What ECG feature differentiates ventricular tachycardia from supraventricular tachycardia?
Answer: Wide QRS complexes in ventricular tachycardia.
248
SBA: What is the most common cause of ventricular fibrillation?
Answer: Myocardial infarction.
249
SBA: What is the rate of the sinoatrial (SA) node under normal physiological conditions?
Answer: 60–100 beats per minute.
250
SBA: What arrhythmia can result in sudden cardiac death without immediate treatment?
Answer: Ventricular fibrillation.
251
EMQ: Match the arrhythmia to its ECG characteristic.
Atrial fibrillation: Irregular rhythm with no P waves.
Ventricular tachycardia: Wide QRS complexes, no P waves.
Atrial flutter: Sawtooth P wave pattern.
252
EMQ: Match the arrhythmia to its primary treatment.
Atrial fibrillation: Rate control with beta-blockers or digoxin.
Ventricular fibrillation: CPR and defibrillation.
Sinus bradycardia: Atropine.
253
EMQ: Match the arrhythmia to its cause.
trial fibrillation: Hypertension or heart failure.
Torsades de Pointes: Prolonged QT interval.
Supraventricular tachycardia: Reentrant circuit in AV node.
254
EMQ: Match the arrhythmia to its symptoms
Sinus bradycardia: Fatigue, lightheadedness.
Ventricular tachycardia: Syncope, dyspnea.
Atrial fibrillation: Palpitations, breathlessness.
255
EMQ: Match the arrhythmia to its associated risk.
Atrial fibrillation: Stroke.
Ventricular fibrillation: Sudden cardiac death.
Torsades de Pointes: Progression to ventricular fibrillation.
256
List the main mechanisms of arrhythmias.
Answer:
Disturbances in impulse formation.
Disturbances in impulse conduction.
Combination of both. (2 marks)
257
Outline the symptoms of supraventricular arrhythmias.
Answer:
Atrial fibrillation: Palpitations, breathlessness.
Atrial flutter: Chest discomfort, fatigue.
Supraventricular tachycardia: Dizziness, syncope. (2 marks)
258
What are the key differences in ECG features between ventricular and supraventricular arrhythmias?
Answer:
Ventricular: Wide QRS complexes, no P waves.
Supraventricular: Narrow QRS complexes, normal or absent P waves. (2 marks)
259
Describe the management of ventricular tachycardia.
Answer:
If pulseless: CPR and defibrillation.
If with a pulse: Antiarrhythmic drugs (e.g., amiodarone) or synchronized cardioversion. (2 marks)
260
Explain the risk of stroke in atrial fibrillation and its prevention.
Answer:
Irregular rhythm causes blood pooling in the atria, leading to thrombus formation.
Prevented with anticoagulants (e.g., warfarin or DOACs). (2 marks)
261
SBA: What is the primary mechanism of action for Class I antiarrhythmic drugs?
Answer: Sodium channel blockade.
262
SBA: Which Class I antiarrhythmic drug is contraindicated in ischemic heart disease?
Answer: Flecainide.
263
SBA: What is the primary effect of beta-blockers (Class II) on cardiac action potential?
Answer: Decrease conduction velocity through the AV node and reduce heart rate.
264
SBA: What is the effect of calcium channel blockers (Class IV) on pacemaker cells?
Answer: Decrease firing rate and conduction velocity in the SA and AV nodes.
265
SBA: Which Class III drug is used for both supraventricular and ventricular arrhythmias?
Answer: Amiodarone.
266
Answer: Decrease firing rate and conduction velocity in the SA and AV nodes.
Answer: Adenosine.
267
SBA: What is the Vaughan Williams classification based on?
Answer: Electrophysiological effects of drugs on cardiac cells.
268
SBA: Which drug class prolongs the refractory period by blocking potassium channels?
Answer: Class III.
269
SBA: What is the primary adverse effect of amiodarone due to its iodine content?
Answer: Thyroid dysfunction.
270
SBA: What is the role of magnesium sulfate in arrhythmias?
Answer: Used in Torsades de Pointes to stabilize cardiac repolarization.
271
EMQ: Match the drug to its mechanism of action.
Flecainide: Class I - Sodium channel blocker.
Propranolol: Class II - Beta-adrenergic antagonist.
Amiodarone: Class III - Potassium channel blocker.
Verapamil: Class IV - Calcium channel blocker.
272
EMQ: Match the class of drugs to their ECG effects.
Class I: Widen QRS complex.
Class III: Prolong QT interval.
Class IV: Prolong PR interval.
273
EMQ: Match the drug to its therapeutic indication.
Adenosine: Paroxysmal supraventricular tachycardia.
Amiodarone: Ventricular fibrillation.
Digoxin: Atrial fibrillation with heart failure.
274
EMQ: Match the antiarrhythmic drug to its contraindication.
Verapamil: AV block.
Flecainide: Structural heart disease.
Propranolol: Severe bradycardia.
275
EMQ: Match the phase of the cardiac action potential to the drug action.
Phase 0: Class I - Sodium channel blockers.
Phase 3: Class III - Potassium channel blockers.
Phase 4: Class IV - Calcium channel blockers.
276
List the Vaughan Williams classes and their primary mechanisms.
Answer:
Class I: Sodium channel blockers (e.g., flecainide).
Class II: Beta-adrenergic blockers (e.g., propranolol).
Class III: Potassium channel blockers (e.g., amiodarone).
Class IV: Calcium channel blockers (e.g., verapamil). (2 marks)
277
Provide two examples of arrhythmias treated by each class.
Answer:
Class I: Ventricular tachycardia, paroxysmal supraventricular tachycardia.
Class II: Atrial fibrillation, atrial flutter.
Class III: Ventricular fibrillation, atrial fibrillation.
Class IV: Supraventricular tachycardia, atrial flutter. (4 marks)
278
What is the mechanism of unclassified drugs like digoxin and adenosine?
Answer:
Digoxin: Increases vagal tone to slow AV node conduction.
Adenosine: Hyperpolarizes cells by activating potassium channels, rapidly terminating SVT. (2 marks)
279
List two common adverse effects of antiarrhythmic drugs.
Answer:
Amiodarone: Thyroid dysfunction, pulmonary toxicity.
Verapamil: Bradycardia, hypotension. (2 marks)
280
Answer:
Amiodarone: Thyroid dysfunction, pulmonary toxicity.
Verapamil: Bradycardia, hypotension. (2 marks)
Answer: Inhibits Vitamin K epoxide reductase (VKORC1), reducing activation of clotting factors II, VII, IX, and X.
281
SBA: Which anticoagulant directly inhibits Factor Xa?
Answer: Apixaban.
282
SBA: What is the primary adverse effect associated with SGLT2 inhibitors in heart failure management?
Answer: Genital fungal infections.
283
SBA: What is the therapeutic use of neprilysin inhibitors like sacubitril?
Answer: Enhances blood pressure-lowering peptides (e.g., natriuretic peptides) to treat chronic heart failure.
284
SBA: What functional group in aspirin irreversibly inhibits COX-1?
Answer: Acetyl group.
285
SBA: What is the mechanism of action of thrombolytic drugs like alteplase?
Answer: Activates plasminogen to plasmin, which degrades fibrin clots.
286
SBA: Which loop diuretic inhibits the Na+/K+/2Cl− symporter in the nephron?
Answer: Furosemide.
287
SBA: What is the clinical significance of the S-isomer of warfarin?
Answer: It is 4 times more potent than the R-isomer as an anticoagulant.
288
SBA: Which P2Y12 receptor antagonist is reversible?
Answer: Ticagrelor.
289
SBA: What does the hydrophobic interaction in Factor Xa inhibitors like rivaroxaban achieve?
Answer: Stabilizes binding to the S1 and S4 pockets of Factor Xa.
290
EMQ: Match the drug class to its mechanism of action.
Vitamin K antagonists: Inhibit VKORC1 (e.g., warfarin).
Factor Xa inhibitors: Directly inhibit Factor Xa (e.g., apixaban).
P2Y12 receptor antagonists: Inhibit ADP-induced platelet aggregation (e.g., clopidogrel).
291
EMQ: Match the drug to its therapeutic use.
Alteplase: Acute ischemic stroke.
Aspirin: Primary prevention of myocardial infarction.
Sacubitril: Chronic heart failure with reduced ejection fraction.
292
EMQ: Match the drug to its major adverse effect.
Warfarin: Bleeding risk.
SGLT2 inhibitors: Genital fungal infections.
Ticagrelor: Dyspnea.
293
EMQ: Match the drug to its molecular target.
Dabigatran: Direct thrombin (Factor IIa) inhibitor.
Rivaroxaban: Factor Xa inhibitor.
Aspirin: COX-1 inhibitor.
294
EMQ: Match the drug to its clinical consideration.
Warfarin: Requires INR monitoring.
Apixaban: No routine monitoring required.
Clopidogrel: Activated by CYP2C19.
295
Outline the primary pharmacological strategies for MI and stroke.
Answer:
MI: Restore blood flow using thrombolytics (e.g., alteplase) and prevent recurrence with antiplatelets (e.g., aspirin) and anticoagulants (e.g., DOACs).
Stroke: Use antiplatelets for secondary prevention, anticoagulants for cardioembolic stroke. (2 marks)
296
Describe the mechanism of action of aspirin and clopidogrel.
Answer:
Aspirin: Irreversibly inhibits COX-1, reducing thromboxane A2 synthesis and platelet aggregation.
Clopidogrel: Irreversibly inhibits P2Y12 receptors, preventing ADP-induced platelet aggregation. (2 marks)
297
Explain the differences between warfarin and DOACs.
Answer:
Warfarin: Narrow therapeutic index, requires INR monitoring, delayed onset.
DOACs: Fixed dosing, faster onset, fewer interactions, no routine monitoring. (2 marks)
298
Discuss the role of thrombolytics in acute MI and stroke.
Answer:
Activate plasminogen to plasmin, degrading fibrin clots. Used within 3–4.5 hours of symptom onset. (2 marks)
299
List three potential adverse effects of these drugs and their management strategies.
Answer:
Bleeding: Monitor and adjust dose (e.g., warfarin).
Dyspepsia: Use enteric-coated aspirin.
Drug interactions (e.g., warfarin with CYP inhibitors): Monitor INR closely. (2 marks)
300
SBA: What is the primary cause of stable angina?
Answer: Atherosclerosis leading to reduced coronary artery capacity.
301
SBA: Which type of angina is caused by coronary artery spasms?
Answer: Variant (Prinzmetal’s) angina.
302
SBA: What diagnostic marker is elevated in STEMI but not in unstable angina?
Answer: Troponin.
303
SBA: Which enzyme is activated in platelets by thrombin during clot formation?
Answer: Protease-activated receptor (PAR).
304
SBA: What is the mechanism of action of nitrates in angina management?
Answer: They increase nitric oxide levels, leading to vasodilation.
305
SBA: What does a prolonged occlusion of an epicardial coronary artery lead to?
Answer: Myocardial infarction.
306
SBA: Which drug class blocks the P2Y12 receptor to inhibit platelet aggregation?
Answer: P2Y12 receptor antagonists (e.g., clopidogrel).
307
SBA: What is the primary treatment for acute STEMI?
Answer: Percutaneous coronary intervention (PCI).
308
Answer: Percutaneous coronary intervention (PCI).
Answer: Von Willebrand factor.
309
SBA: What is the main diagnostic marker for fibrinolysis?
Answer: D-dimer.
310
EMQ: Match the type of angina to its features.
Stable angina: Exertion-induced chest pain, relieved by rest.
Unstable angina: Chest pain at rest with ST depression on ECG.
Variant angina: Transient chest pain with ST elevation on ECG.
311
EMQ: Match the drug class to its mechanism in angina.
Beta-blockers: Decrease heart rate and myocardial oxygen demand.
Calcium channel blockers: Reduce vascular resistance and prevent coronary spasms.
Nitrates: Reduce preload and afterload via vasodilation.
312
EMQ: Match the process in clot formation to its associated factor.
Platelet adhesion: Von Willebrand factor.
Platelet activation: Thromboxane A2.
Fibrin stabilization: Factor XIII.
313
EMQ: Match the drug to its specific use.
Clopidogrel: Prevent platelet aggregation in coronary artery disease.
Alteplase: Dissolve thrombi in acute MI.
GTN: Relieve acute angina attacks.
314
EMQ: Match the coronary artery pathology to its treatment.
STEMI: PCI or fibrinolytics.
Stable angina: Beta-blockers and nitrates.
Unstable angina: Dual antiplatelet therapy.
315
Outline the pathogenesis of CAD.
Answer:
Atherosclerosis due to endothelial dysfunction.
Fatty plaque formation reduces coronary artery capacity.
Plaque rupture leads to thrombosis, causing ischemia or infarction. (3 marks)
316
What are the clinical features of stable angina, unstable angina, and STEMI?
Answer:
Stable angina: Chest pain on exertion, relieved by rest.
Unstable angina: Chest pain at rest, no troponin elevation.
STEMI: Severe chest pain, troponin elevation, and ST elevation on ECG. (3 marks)
317
Describe the pharmacological management of stable angina.
Answer:
First-line: Beta-blockers (reduce heart rate).
Second-line: Calcium channel blockers or nitrates.
Adjunct: Aspirin and statins to prevent progression. (2 marks)
318
How is STEMI managed acutely?
Answer:
Percutaneous coronary intervention (PCI).
Thrombolytics if PCI unavailable.
Dual antiplatelet therapy and anticoagulants. (2 marks)
319
SBA: What is the mechanism of action of warfarin?
Answer: Inhibits Vitamin K epoxide reductase, reducing the synthesis of clotting factors II, VII, IX, and X.
320
SBA: Which drug is a direct and reversible inhibitor of Factor Xa?
Answer: Apixaban.
321
SBA: Which drug is used to reverse the effects of heparin-induced thrombocytopenia?
Answer: Danaparoid sodium.
322
SBA: What is the primary adverse effect of fibrinolytics like alteplase?
Answer: Hemorrhage.
323
SBA: Which glycoprotein IIb/IIIa inhibitor is a monoclonal antibody used in high-risk percutaneous coronary intervention?
Answer: Abciximab
324
SBA: Which anticoagulant binds to antithrombin III to inhibit thrombin activity?
Answer: Heparin.
325
SBA: What is the function of fibrinolytics in thromboembolic disease management?
Answer: Activate plasminogen to plasmin, which dissolves fibrin clots.
326
SBA: What is the primary clinical use of low molecular weight heparins (LMWHs)?
Answer: Prevention and treatment of deep vein thrombosis (DVT).
327
SBA: What is the advantage of direct oral anticoagulants (DOACs) over warfarin?
Answer: Fixed dosing and no routine INR monitoring.
328
SBA: What is the reversal agent for dabigatran?
Answer: Idarucizumab.
329
EMQ: Match the drug to its mechanism of action.
Warfarin: Inhibits Vitamin K epoxide reductase.
Apixaban: Direct Factor Xa inhibitor.
Dabigatran: Direct thrombin inhibitor.
330
EMQ: Match the anticoagulant to its clinical consideration.
Warfarin: Requires INR monitoring.
DOACs (e.g., rivaroxaban): No routine monitoring.
Heparin: Administered intravenously or subcutaneously.
331
EMQ: Match the antiplatelet drug to its target receptor.
Clopidogrel: P2Y12 receptor.
Aspirin: COX-1.
Abciximab: Glycoprotein IIb/IIIa receptor.
332
EMQ: Match the fibrinolytic to its property.
Alteplase: Fibrin-specific.
Streptokinase: Can induce antibody formation.
Tenecteplase: Longer half-life.
333
EMQ: Match the condition to the appropriate treatment.
STEMI: Alteplase or PCI.
DVT: LMWH or DOACs.
Pulmonary embolism: Fibrinolytics.
334
lassify antithrombotic drugs and give examples.
Answer:
Anticoagulants: Warfarin, DOACs (e.g., apixaban).
Antiplatelets: Aspirin, clopidogrel.
Fibrinolytics: Alteplase, streptokinase. (2 marks)
335
Describe the mechanism of action for warfarin and DOACs.
Answer:
Warfarin: Inhibits Vitamin K epoxide reductase.
DOACs: Directly inhibit Factor Xa or thrombin. (2 marks)
336
List two clinical indications for each drug class.
Answer:
Anticoagulants: DVT, atrial fibrillation.
Antiplatelets: Prevention of MI, stroke.
Fibrinolytics: Acute MI, pulmonary embolism. (3 marks)
337
Discuss major adverse effects and their management.
Answer:
Warfarin: Bleeding, managed with Vitamin K.
Heparin: HIT, managed with danaparoid.
Fibrinolytics: Hemorrhage, monitor closely. (3 marks)
338
SBA: Which beta-blocker is non-selective and inhibits both β1 and β2 receptors?
Answer: Propranolol.
339
SBA: What structural feature distinguishes aryloxypropanolamines from arylethanolamines in beta-blockers?
Answer: Presence of an aryloxypropanolamine side chain increases potency.
340
SBA: Which beta-blocker has cardio-selective β1 affinity and is hydrophilic?
Answer: Atenolol.
341
SBA: What functional group in norepinephrine binds ionically to the β-adrenoceptor at physiological pH?
Answer: Amine group.
342
SBA: What property allows lipophilic beta-blockers like propranolol to penetrate the CNS?
Answer: High partition coefficient (LogP).
343
SBA: Which beta-blocker exhibits mixed β1, β2, and α1 antagonistic effects?
Answer: Carvedilol.
344
SBA: What is the main mechanism of action of beta-blockers in hypertension management?
Answer: Decrease heart rate and myocardial contractility by blocking β1 receptors.
345
SBA: Why are hydrophilic beta-blockers less likely to cause CNS side effects?
Answer: They have a low partition coefficient and cannot easily cross the blood-brain barrier.
346
SBA: What is the mechanism of action of amiodarone?
Answer: Blocks potassium channels, prolonging the refractory period and action potential.
347
SBA: What structural modification in dronedarone reduces the risks of thyroid and neurotoxicity compared to amiodarone?
Answer: Removal of iodine groups and addition of a methylsulfonamide group.
348
EMQ: Match the beta-blocker to its property.
Atenolol: Cardio-selective β1 blocker, hydrophilic.
Propranolol: Non-selective β blocker, lipophilic.
Carvedilol: Mixed β1, β2, and α1 antagonist.
349
EMQ: Match the functional group to its binding site.
Amine group: Ionic bond with Asp113.
Catechol aromatic ring: Hydrophobic interaction with Phe290.
Alcohol group: Hydrogen bond with Asn293.
350
EMQ: Match the drug to its clinical use.
Amiodarone: Ventricular and supraventricular arrhythmias.
Atenolol: Hypertension and angina.
Dronedarone: Atrial fibrillation/flutter.
351
EMQ: Match the beta-blocker to its classification.
Timolol: Non-selective beta-blocker.
Bisoprolol: Cardio-selective beta-blocker.
Labetalol: Mixed alpha and beta antagonist.
352
EMQ: Match the structural modification to its effect.
Addition of bulky N-alkyl substituents: Increases selectivity for β-adrenoceptors over α-adrenoceptors.
Aryloxypropanolamine group: Increases β-blocker potency.
Methylsulfonamide group: Reduces lipophilicity and toxicity.
353
Explain the mechanism of action of beta-blockers.
Answer: Block β-adrenoceptors, reducing the effects of catecholamines (epinephrine and norepinephrine) on the heart. Leads to decreased heart rate, myocardial contractility, and renin secretion. (2 marks)
354
Differentiate between selective and non-selective beta-blockers.
Answer:
Selective: Target β1 receptors (e.g., atenolol).
Non-selective: Block both β1 and β2 receptors (e.g., propranolol). (2 marks)
355
What are the clinical applications of beta-blockers?
Answer: Hypertension, angina, myocardial infarction, arrhythmias, and heart failure. (2 marks)
356
Describe the SAR of beta-blockers.
Answer:
Lipophilicity increases CNS penetration (e.g., propranolol).
Hydrophilic groups reduce CNS effects (e.g., atenolol).
Bulky N-alkyl substituents increase β1 selectivity. (2 marks)
357
What are the structural differences between amiodarone and dronedarone?
Answer:
Amiodarone: Contains iodine groups, leading to thyroid toxicity.
Dronedarone: Lacks iodine and has a methylsulfonamide group, reducing lipophilicity and toxicity. (2 marks)
358
SBA: What is the key difference between crystalline and amorphous solids?
Answer: Crystalline solids have a long-range molecular order, while amorphous solids have a random molecular arrangement.
359
SBA: What is the main advantage of salt formation in drug development?
Answer: It increases the solubility and dissolution rate of acidic and basic drugs.
360
SBA: Which particle property most directly affects flowability during drug manufacturing?
Answer: Particle shape.
361
SBA: What does the term “hydrate” refer to in solid-state chemistry?
Answer: A crystalline structure that includes water molecules within its lattice.
362
SBA: What is the main application of co-crystals in pharmaceutical formulations?
Answer: Enhancing the dissolution rate and bioavailability of poorly water-soluble drugs.
363
SBA: What type of diameter is used to describe the equivalent volume sphere of a particle?
Answer: Volume-equivalent diameter.
364
SBA: Which theory is used to measure the surface area of irregular particles using gas adsorption?
Answer: Brunauer–Emmett–Teller (BET) theory.
365
SBA: How does a larger specific surface area affect drug dissolution rate?
Answer: Increases the dissolution rate due to greater contact with the dissolution medium.
366
SBA: What is the main drawback of amorphous drug formulations?
Answer: They are less stable and more prone to moisture sensitivity compared to crystalline forms.
367
SBA: Which equation describes the relationship between dissolution rate, surface area, and diffusion layer thickness?
Answer: Noyes-Whitney equation.
368
EMQ: Match the particle property to its impact on drug formulation.
Surface area: Dissolution rate.
Particle size: Content uniformity.
Particle shape: Flowability and mixing.
369
EMQ: Match the type of solid-state modification to its example.
Hydrate: Lisinopril dihydrate.
Solvate: Ethanolate of a drug.
Co-crystal: Sildenafil and aspirin co-crystal.
370
EMQ: Match the particle diameter to its application.
Aerodynamic diameter: Inhalation drug deposition.
Stokes’ diameter: Sedimentation properties.
Sieve diameter: Particle size distribution analysis.
371
EMQ: Match the solid-state form to its feature.
Crystalline: Higher stability, lower solubility.
Amorphous: Lower stability, higher solubility.
Polymorphic: Same chemical composition, different molecular packing.
372
EMQ: Match the method to its application in particle analysis.
Laser diffraction: Determines particle size distribution.
BET theory: Measures surface area of irregular particles.
Microscopy: Visualizes particle shape.
373
Explain the significance of particle size and surface area.
Answer:
Smaller particles have a larger surface area, increasing the dissolution rate and bioavailability (Noyes-Whitney principle).
Uniform particle size ensures content uniformity in formulations. (3 marks)
374
Describe the impact of particle shape on powder behavior.
Answer:
Spherical particles: Better flowability and mixing.
Irregular or flaky particles: Poor flowability and increased cohesiveness. (2 marks)
375
What are the roles of polymorphs and co-crystals in pharmaceutical formulations?
Answer:
Polymorphs: Allow control over stability and solubility.
Co-crystals: Enhance dissolution and bioavailability of poorly soluble drugs. (2 marks)
376
Discuss the practical implications of hydrates and solvates.
Answer:
Hydrates: Improved stability but lower solubility.
Solvates: Can alter dissolution behavior and bioavailability. (2 marks)
377
What is the role of BET theory in particle characterization?
Answer: Measures the surface area of irregular particles to predict dissolution and adsorption properties. (1 mark)
378
SBA: What is the key difference between normal and lognormal distributions in particle size analysis?
Answer: Normal distributions are symmetric with mean = median = mode, while lognormal distributions are positively skewed with a logarithmic scale normalizing the data.
379
SBA: What does D90/D10 represent in particle size analysis?
Answer: It represents the ratio of particle sizes at 90% and 10% undersize, indicating the degree of dispersion.
380
SBA: Which particle sizing method measures the aerodynamic diameter of particles?
Answer: Cascade impactor.
381
SBA: What type of diameter does laser diffraction measure?
Answer: Equivalent diameter based on the diffraction pattern.
382
SBA: Which particle sizing method uses Stokes’ Law to measure particle size?
Answer: Andreasen pipette (sedimentation).
383
SBA: What is the most significant limitation of microscopy in particle size analysis?
Answer: Non-representative selection of particles.
384
SBA: What does the Coefficient of Variation (CV%) indicate in particle size distribution?
Answer: It normalizes the standard deviation by dividing it by the mean, indicating the degree of variance.
385
SBA: How does sieving classify particles?
Answer: By sieve equivalent diameter, determined by the size of apertures in the sieve mesh.
386
SBA: What does photon correlation spectroscopy (dynamic light scattering) measure?
Answer: Hydrodynamic diameter of particles in suspension.
387
SBA: What is the main application of the D90/D10 ratio in pharmaceutical powders?
Answer: To assess polydispersity of powders for consistency in formulations
388
EMQ: Match the particle size analysis method to its application.
Sieving: Measures sieve equivalent diameter of powders.
Andreasen pipette: Determines Stokes’ diameter via sedimentation.
Cascade impactor: Measures aerodynamic diameter for inhalation products.
389
EMQ: Match the dispersion measure to its definition.
Standard deviation: Variation of particle sizes around the mean.
Coefficient of variation: Normalized standard deviation (%).
D90/D10: Ratio indicating dispersion irrespective of distribution model.
390
EMQ: Match the particle size technique to its limitation.
Laser diffraction: Struggles with non-spherical particles.
Microscopy: Non-representative selection of particles.
Photon correlation spectroscopy: Affected by aggregates or dust.
391
EMQ: Match the type of particle diameter to its definition.
Volume diameter: Measured by electrical sensing zone methods.
Aerodynamic diameter: Used in respiratory particle analysis.
Hydrodynamic diameter: Determined by dynamic light scattering.
392
EMQ: Match the type of distribution to its property.
Normal distribution: Mean = median = mode.
Lognormal distribution: Data normalized using a logarithmic scale.
Bimodal distribution: Has two distinct modes.
393
Explain the principles of particle size analysis.
Answer:
Represents the size distribution of particles in a sample.
Central tendency measures: mean, mode, median.
Dispersion measures: standard deviation, D90/D10 ratio. (2 marks)
394
Describe three particle sizing techniques and their applications.
Answer:
Sieving: Classifies powders based on sieve equivalent diameter.
Andreasen pipette: Measures Stokes’ diameter using sedimentation.
Cascade impactor: Analyzes aerodynamic diameter for inhalation products. (3 marks)
395
Discuss the limitations of particle sizing methods.
Answer:
Laser diffraction: Inaccurate for non-spherical particles.
Microscopy: Prone to sampling bias.
Dynamic light scattering: Sensitive to aggregates or dust. (2 marks)
396
What is the significance of D90/D10 and CV% in pharmaceutical formulations?
Answer:
D90/D10: Indicates polydispersity, essential for uniform drug delivery.
CV%: Compares variance across sample populations. (2 marks)
397
How are particle size distributions typically visualized?
Answer:
Histograms for incremental distributions.
Cumulative graphs for undersize/oversize percentages. (1 mark)
398
SBA: What is the primary purpose of granulation in pharmaceutical formulations?
Answer: To improve powder flowability and prevent segregation of constituents.
399
SBA: How does granulation reduce dust in powder formulations?
Answer: By aggregating fine powder particles into denser granules
400
SBA: What is the angle of repose used to measure in powder flowability?
Answer: The flowability of powders and granules.
401
SBA: Which liquid component is commonly used in wet granulation?
Answer: Water or ethanol.
402
SBA: What is a common binder used in wet granulation?
Answer: Polyvinylpyrrolidone (PVP).
403
SBA: What is the primary limitation of wet granulation for thermolabile drugs?
Answer: Potential degradation due to moisture and heat.
404
SBA: What is the main disadvantage of dry granulation?
Answer: High compaction force increases dust generation and cross-contamination risks.
405
SBA: Which equipment is used in wet granulation for spraying binder solutions?
Answer: Fluid-bed granulator.
406
SBA: What is the main difference between small granules and large granules?
Answer: Small granules (~0.2–0.4 mm) are used as intermediates, while large granules (~1–4 mm) are often final dosage forms.
407
SBA: What happens if the mass is too dry during wet granulation?
Answer: Granules will fall apart.
408
EMQ: Match the granulation process to its description.
Wet granulation: Uses a liquid binder to aggregate powder particles.
Dry granulation: Compacts powders under high pressure without liquid.
Extrusion-spheronization: Produces spherical granules for uniform dosing.
409
EMQ: Match the method to its equipment.
High-shear granulation: Impeller for mixing, densification, and agglomeration.
Fluid-bed granulation: Sprays binder onto a fluidized powder bed.
Sieve shaker: Separates granules by size.
410
EMQ: Match the limitation to the granulation process.
Wet granulation: Not suitable for moisture-sensitive drugs.
Dry granulation: Generates dust and potential cross-contamination.
Spray drying: High cost of equipment and energy.
411
EMQ: Match the granule property to its benefit.
Denser particles: Improves flowability.
Uniform granules: Prevents segregation.
Reduced dust: Minimizes toxic exposure.
412
EMQ: Match the particle characteristic to its measurement.
Angle of repose: Flowability of powders.
Tapped density: Compressibility of powders.
Bulk density: Volume occupied by powder under normal conditions.
413
Explain the purpose of granulation in pharmaceutical formulations.
Answer:
Prevents segregation of powder mix.
Improves flow properties and compressibility.
Reduces toxic dust. (2 marks)
414
Describe the process of wet granulation.
Answer:
Mix powders with a binder solution.
Pass moist mass through a sieve or extruder.
Dry granules to form solid bridges between particles. (2 marks)
415
Describe the process of dry granulation.
Answer:
Compact powder under high pressure to form slugs.
Mill and sieve slugs into granules. (2 marks)
416
What are the advantages and disadvantages of wet granulation?
Answer:
Advantages: Improves uniformity and reduces dust.
Disadvantages: Expensive, unsuitable for moisture-sensitive drugs. (2 marks)
417
Compare dry granulation to wet granulation.
Answer:
Dry granulation: Less expensive but generates dust.
Wet granulation: Better granule uniformity but costly and complex. (2 marks)
418
SBA: What is the primary mechanism of action for ACE inhibitors?
Answer: Inhibit ACE-mediated conversion of angiotensin I to angiotensin II, leading to vasodilation and reduced aldosterone secretion.
419
SBA: Why are ACE inhibitors associated with a persistent dry cough?
Answer: Due to bradykinin accumulation.
420
SBA: Which class of drugs is most commonly used in African-Caribbean patients for hypertension first-line therapy?
Answer: Calcium channel blockers.
421
SBA: What is the main adverse effect of thiazide diuretics?
Answer: Hypokalaemia.
422
SBA: Which enzyme do statins inhibit to reduce cholesterol?
Answer: HMG-CoA reductase.
423
SBA: Which drug class activates PPARα to treat hypertriglyceridemia?
Answer: Fibrates.
424
SBA: What is the first-line drug for stable angina?
Answer: Beta-blockers.
425
SBA: Which drug selectively inhibits the If current in the sinoatrial node?
Answer: Ivabradine.
426
SBA: What is the primary action of aspirin in thromboembolic disorders?
Answer: Irreversible inhibition of thromboxane synthesis in platelets.
427
SBA: What does an elevated troponin level indicate?
Answer: Myocardial ischemia or infarction.
428
SBA: Which ECG change indicates ST-elevation myocardial infarction (STEMI)?
Answer: ST elevation.
429
SBA: What type of arrhythmia is characterized by a saw-tooth pattern on the ECG
Answer: Atrial flutter.
430
SBA: Which drug is contraindicated in combination with statins due to increased risk of myopathy?
Answer: Fibrates.
431
SBA: What is the most common adverse effect of nitrates?
Answer: Headache.
432
SBA: What type of diuretic is spironolactone?
Answer: Aldosterone receptor antagonist.
433
SBA: What is the mechanism of action of ranolazine in angina?
nswer: Blocks late inward sodium currents.
434
SBA: What is the mechanism of action of nicorandil?
Answer: Activates ATP-sensitive potassium channels.
435
SBA: What does a prolonged QT interval on ECG indicate?
Answer: Risk of ventricular arrhythmias.
436
SBA: Why is grapefruit juice contraindicated with statins?
Answer: It inhibits CYP450 enzymes, increasing statin plasma levels.
437
SBA: What is the most common adverse effect of antiplatelet drugs like clopidogrel?
Answer: Bleeding.
438
EMQ: Match the antihypertensive drug to its mechanism.
ACE inhibitors: Blocks angiotensin II synthesis.
Beta-blockers: Reduce heart rate and cardiac output.
Thiazide diuretics: Promote sodium excretion in the distal tubule.
439
EMQ: Match the lipid-lowering drug to its effect.
Statins: Reduce LDL cholesterol.
Fibrates: Lower triglycerides, increase HDL.
Ezetimibe: Inhibits cholesterol absorption.
440
EMQ: Match the anti-anginal drug to its target.
Nitrates: Vascular smooth muscle.
Beta-blockers: Heart rate and contractility.
Ivabradine: Sinoatrial node.
441
MQ: Match the ECG finding to its diagnosis.
ST elevation: STEMI.
Inverted T wave: Ischemia.
Prolonged QT interval: Risk of torsades de pointes.
442
EMQ: Match the thromboembolic drug to its mechanism.
Aspirin: Inhibits thromboxane synthesis.
Heparin: Activates antithrombin.
Warfarin: Inhibits vitamin K-dependent clotting factors.
443
EMQ: Match the drug to its adverse effect.
ACE inhibitors: Dry cough.
Statins: Myopathy.
Nitrates: Headache.
444
EMQ: Match the cholesterol pathway to its description.
Exogenous: Dietary cholesterol absorption.
Endogenous: Cholesterol synthesis in the liver.
Reverse transport: HDL-mediated clearance.
445
EMQ: Match the arrhythmia to its treatment.
Atrial fibrillation: Warfarin or DOACs.
Ventricular tachycardia: Amiodarone.
Paroxysmal supraventricular tachycardia: Adenosine.
446
EMQ: Match the nitrate to its feature.
Isosorbide mononitrate: Oral, long-acting.
Glyceryl trinitrate: Sublingual, short-acting.
Sodium nitroprusside: IV, used in hypertensive crises.
447
EMQ: Match the anti-platelet to its mechanism.
Clopidogrel: P2Y12 receptor inhibitor.
Aspirin: Thromboxane inhibitor.
Abciximab: Glycoprotein IIb/IIIa inhibitor.
448
Define hypertension (1 mark).
Answer: Persistent elevation of blood pressure ≥140/90 mmHg.
449
List two classes of antihypertensives with examples (2 marks).
Answer: ACE inhibitors (ramipril), CCBs (amlodipine).
450
Explain why ACE inhibitors are less effective in African-Caribbean populations (2 marks).
Answer: Low renin activity, age-related nephron loss.
451
State one adverse effect of thiazide diuretics and its management (2 marks).
Answer: Hypokalaemia, managed with potassium supplements.
452
Outline lifestyle changes recommended in hypertension (3 marks).
Answer: Low-sodium diet, regular exercise, weight loss.
453
What is the mechanism of action of statins (2 marks)?
Answer: Inhibits HMG-CoA reductase, reducing cholesterol synthesis.
454
Why is grapefruit juice contraindicated (2 marks)?
Answer: Inhibits CYP450 enzymes, increasing myopathy risk.
455
Compare LDL and HDL particles (2 marks).
Answer: LDL carries cholesterol to tissues, HDL facilitates reverse cholesterol transport.
456
What is the primary indication for fibrates (2 marks)?
Answer: Hypertriglyceridemia.
457
Name one cholesterol absorption inhibitor (1 mark).
Answer: Ezetimibe.
458
State one adverse effect of statins (1 mark).
Answer: Myopathy.
459
List two drug classes used for angina (2 marks).
Answer: Nitrates, beta-blockers.
460
What is the mechanism of action of nitrates (2 marks)?
Answer: Release NO, causing vasodilation.
461
Why are long-acting nitrates preferred for chronic angina (2 marks)?
Answer: Sustained effect reduces episodes.
462
State two adverse effects of nitrates (2 marks).
Answer: Headache, hypotension.
463
What ECG changes indicate ischemia (2 marks)?
Answer: ST depression, T wave inversion.
464
Differentiate arterial and venous thrombi (2 marks).
Answer: Arterial: Platelet-rich; Venous: RBC-rich.
465
Outline aspirin’s mechanism of action (2 marks).
Answer: Irreversibly inhibits thromboxane synthesis in platelets.
466
Name one DOAC and its target (2 marks).
Answer: Apixaban, Xa inhibitor.
467
List one advantage of DOACs over warfarin (2 marks).
Answer: No routine INR monitoring.
468
What is the most common adverse effect of anticoagulants (2 marks)?
Answer: Bleeding.
469
