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Pharmacy - Year 2 > Pharm CVS > Flashcards

Pharm CVS Flashcards

1
Q

SBA: What is the primary equation for calculating blood pressure?

A

Answer: Blood pressure = Cardiac output × Peripheral resistance.

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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.

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3
Q

SBA: Which part of the brain regulates cardiovascular responses to blood pressure changes?

A

Answer: Medulla and pons (cardiovascular center).

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4
Q

SBA: What is the primary vasoconstrictor in the renin-angiotensin-aldosterone system (RAAS)?

A

Answer: Angiotensin II.

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5
Q

SBA: What triggers the release of erythropoietin (EPO)?

A

Answer: Hypoxia in the kidneys.

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6
Q

SBA: Which adrenergic receptor subtype increases heart rate and force of contraction?

A

Answer: Beta-1 adrenergic receptors.

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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.

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8
Q

SBA: Which hormone is released in response to hypovolemia to retain water?

A

Answer: Antidiuretic hormone (ADH, also known as vasopressin).

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9
Q

SBA: What is the physiological impact of systemic vasodilation on blood pressure?

A

Answer: Decreases peripheral resistance and lowers blood pressure.

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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.

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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.

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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.

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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.

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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.

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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.

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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)

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17
Q

What are the main triggers for baroreceptor activation?

A

Answer: Changes in arterial pressure, such as hypotension or hypertension. (2 marks)

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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)

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19
Q

What is the physiological response to hypotension due to hypovolemia?

A

Answer: ADH release, vasoconstriction, and increased water retention. (2 marks)

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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)

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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.

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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).

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23
Q

SBA: Which hypertension drug class is contraindicated in asthmatic patients?

A

Answer: Beta-blockers.

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24
Q

SBA: What lifestyle modification is recommended for sodium intake in hypertension management?

A

Answer: Reduce salt intake to below 6 g/day.

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25
Q

SBA: Which drug class reduces blood pressure by blocking angiotensin II receptors?

A

Answer: ARBs (e.g., Losartan).

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26
Q

SBA: What side effect is most commonly associated with dihydropyridine calcium channel blockers like Amlodipine?

A

Answer: Peripheral oedema.

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27
Q

SBA: What is the target BP for patients under 80 years with hypertension?

A

Answer: <140/90 mmHg.

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28
Q

SBA: Which electrolyte imbalance is a common side effect of thiazide-like diuretics?

A

Answer: Hypokalaemia.

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29
Q

SBA: What is the mechanism of action of spironolactone in hypertension management?

A

Answer: Blocks aldosterone receptors, promoting sodium excretion and potassium retention.

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30
Q

SBA: What is the significance of a >15 mmHg difference between arms when measuring BP?

A

Answer: Use the higher reading for future measurements and investigate for vascular disease.

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31
Q

EMQ: Match the antihypertensive drug to its side effect.

A

ACE inhibitors: Dry cough.
Beta-blockers: Bradycardia.
Calcium channel blockers: Flushing.
Thiazide diuretics: Hyperglycaemia.
Spironolactone: Gynaecomastia.

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32
Q

EMQ: Match the hypertension drug to its monitoring requirement.

A

ACE inhibitors: Renal function and potassium.
ARBs: Renal function and potassium.
Thiazide diuretics: Sodium and potassium levels.
Beta-blockers: Heart rate.
Spironolactone: Potassium levels.

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33
Q

EMQ: Match the patient group to their recommended first-line antihypertensive therapy.

A

Under 55 years: ACE inhibitors or ARBs.
Over 55 years or Black patients: Calcium channel blockers.
Resistant hypertension: Spironolactone or Alpha-blockers.

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34
Q

EMQ: Match the BP measurement method to its application.

A

Clinic BP: Initial diagnosis.
Ambulatory BP monitoring (ABPM): Confirming diagnosis.
Home BP monitoring (HBPM): Alternative to ABPM.
Manual BP measurement: Pulse irregularity.

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35
Q

EMQ: Match the lifestyle modification to its cardiovascular benefit.

A

Exercise: Reduces resting blood pressure.
Weight loss: Improves BP control.
Salt reduction: Lowers BP by reducing water retention.
Smoking cessation: Reduces cardiovascular risk.

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36
Q

Describe the initial steps for BP measurement.

A

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)

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37
Q

What assessments are made alongside BP measurement?

A

Answer: Assess cardiovascular risk (e.g., QRISK3), target organ damage (e.g., kidneys, heart, eyes), and perform relevant blood tests. (2 marks)

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38
Q

What are the key lifestyle modifications recommended?

A

Answer: Reduce salt intake, increase exercise, achieve a healthy BMI, and limit alcohol consumption. (2 marks)

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39
Q

Describe the stepwise pharmacological treatment for hypertension.

A

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)

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40
Q

What is the target BP for patients under and over 80 years?

A

Answer: <140/90 mmHg (under 80 years) and <150/90 mmHg (over 80 years). (1 mark)

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41
Q

SBA: What is the first-line pharmacological treatment for primary prevention of CVD in patients with a QRISK3 score ≥10%?

A

Answer: Atorvastatin 20 mg daily.

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42
Q

SBA: What is the main treatment goal in lipid modification therapy?

A

Answer: Achieve a ≥40% reduction in non-HDL cholesterol levels.

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43
Q

SBA: What condition is characterized by high cholesterol levels due to a defective gene?

A

Answer: Familial hypercholesterolaemia.

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44
Q

SBA: Which statin intensity category is atorvastatin 80 mg classified under?

A

Answer: High-intensity statin.

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45
Q

SBA: What non-statin medication inhibits intestinal cholesterol absorption?

A

Answer: Ezetimibe.

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46
Q

SBA: What is the role of PCSK9 inhibitors in hyperlipidaemia treatment?

A

Answer: Increase LDL receptor recycling, enhancing LDL cholesterol clearance.

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47
Q

Answer: Increase LDL receptor recycling, enhancing LDL cholesterol clearance.

A

Answer: Liver function tests and lipid profile.

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48
Q

SBA: What lifestyle modification is essential in hyperlipidaemia management to reduce saturated fat intake?

A

Answer: Limit saturated fat to <7% of total daily energy intake.

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49
Q

SBA: What is a common side effect of statins?

A

Answer: Myopathy or muscle pain.

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50
Q

SBA: Which medication is contraindicated in pregnancy for hyperlipidaemia treatment?

A

Answer: Statins.

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51
Q

EMQ: Match the condition to its associated hyperlipidaemia risk.

A

Familial hypercholesterolaemia: Genetic defect in LDL receptor.
Diabetes mellitus: Increased triglycerides and LDL cholesterol.
Chronic kidney disease: Dysregulation of lipid metabolism.

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52
Q

EMQ: Match the medication to its mechanism of action.

A

Statins: Inhibit HMG-CoA reductase.
Ezetimibe: Inhibits cholesterol absorption in the intestine.
Bempedoic acid: Inhibits ATP citrate lyase.

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53
Q

EMQ: Match the side effect to the lipid-lowering drug.

A

Muscle pain: Statins.
Gout: Bempedoic acid.
Injection site reactions: Inclisiran.

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54
Q

EMQ: Match the non-pharmacological intervention to its benefit.

A

Smoking cessation: Reduces cardiovascular risk.
Weight loss: Improves lipid profile and BP.
Exercise: Increases HDL cholesterol.

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55
Q

EMQ: Match the hyperlipidaemia drug to its indication.

A

Inclisiran: High-risk patients with LDL-C ≥4.0 mmol/L.
Atorvastatin: First-line for primary and secondary prevention.
Fibrates: Severe hypertriglyceridemia.

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56
Q

Describe lifestyle modifications for hyperlipidaemia management.

A

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)

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57
Q

What baseline tests are required before starting statin therapy?

A

Answer: Non-fasting lipid profile, liver function tests, renal function, HbA1c, creatine kinase, and thyroid-stimulating hormone (if indicated). (2 marks)

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58
Q

Answer: Non-fasting lipid profile, liver function tests, renal function, HbA1c, creatine kinase, and thyroid-stimulating hormone (if indicated). (2 marks)

A

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)

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59
Q

What are the contraindications and monitoring requirements for statin use?

A

Answer: Contraindicated in pregnancy and active liver disease. Monitor liver function and lipid profile 3 months after initiation and annually. (2 marks)

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60
Q

SBA: What is the primary route of administration for most antihypertensive drugs?

A

Answer: Oral.

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61
Q

SBA: Which antihypertensive drug undergoes significant first-pass metabolism, reducing its bioavailability?

A

Answer: Propranolol.

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62
Q

SBA: What is the key enzyme involved in the metabolism of calcium channel blockers like amlodipine?

A

Answer: CYP3A4.

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63
Q

SBA: Which class of antihypertensive drugs is most affected by reduced renal function?

A

Answer: ACE inhibitors (e.g., Ramipril).

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64
Q

SBA: Why should grapefruit juice be avoided with calcium channel blockers?

A

Answer: Grapefruit juice inhibits CYP3A4, increasing plasma drug levels.

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65
Q

SBA: What is the mechanism of action of ARBs?

A

Answer: Block angiotensin II at the AT1 receptor.

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66
Q

SBA: What type of interaction occurs when NSAIDs reduce the efficacy of ACE inhibitors?

A

Answer: Pharmacodynamic interaction.

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67
Q

SBA: Which antihypertensive drug is a prodrug activated in the liver?

A

Answer: Enalapril.

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68
Q

SBA: What is the primary organ responsible for the excretion of ARBs?

A

Answer: Kidneys.

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69
Q

SBA: Which antihypertensive drug has the highest risk of causing bradycardia when combined with verapamil?

A

Answer: Beta-blockers (e.g., Atenolol).

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70
Q

EMQ: Match the antihypertensive drug to its absorption characteristic.

A

Captopril: Food reduces absorption.
Amlodipine: High oral bioavailability.
Propranolol: Significant first-pass metabolism.

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71
Q

EMQ: Match the antihypertensive drug class to its metabolism.

A

Beta-blockers (e.g., Metoprolol): CYP2D6.
CCBs (e.g., Verapamil): CYP3A4.
ACE inhibitors (e.g., Lisinopril): Active in administered form (no liver metabolism).

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72
Q

EMQ: Match the interaction type to the example.

A

Pharmacokinetic: Grapefruit juice with amlodipine.
Pharmacodynamic: Thiazide diuretics with ACE inhibitors causing severe hypotension.
Drug-food: Captopril with food reducing efficacy.

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73
Q

EMQ: Match the adverse effect to the antihypertensive drug class.

A

Hyperkalaemia: ARBs and potassium-sparing diuretics.
Hypokalaemia: Thiazide diuretics.
Peripheral oedema: Calcium channel blockers.

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74
Q

EMQ: Match the elimination route to the drug.

A

Renal: Losartan.
Hepatic: Amlodipine.
Mixed (renal and hepatic): Metoprolol.

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75
Q

Describe the absorption of antihypertensive drugs.

A

Answer: Most are orally administered; factors like food and gastric pH can influence bioavailability (e.g., captopril). (2 marks)

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76
Q

Explain the metabolism of ACE inhibitors and beta-blockers.

A

Answer:
ACE inhibitors: Most are prodrugs activated in the liver, except Lisinopril.
Beta-blockers: Metabolised by CYP2D6 enzymes. (2 marks

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77
Q

What is the impact of renal function on antihypertensive drug elimination?

A

Answer: Drugs like ACE inhibitors and ARBs rely on renal excretion, making dosage adjustments necessary in renal impairment. (2 marks)

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78
Q

List two examples of drug-drug interactions involving antihypertensive drugs.

A

Answer:
NSAIDs reduce the antihypertensive effect of ACE inhibitors.
Verapamil and beta-blockers increase the risk of severe bradycardia. (2 marks)

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79
Q

Why should patient education include warnings about grapefruit juice with certain antihypertensives?

A

Answer: Grapefruit juice inhibits CYP3A4, increasing the plasma concentration of calcium channel blockers and raising the risk of adverse effects. (2 marks)

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80
Q

SBA: What is the primary action of ACE inhibitors in hypertension?

A

Answer: Reduce the conversion of angiotensin I to angiotensin II, leading to vasodilation and reduced blood pressure.

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81
Q

SBA: What common side effect is associated with ACE inhibitors and caused by bradykinin accumulation?

A

Answer: Dry cough.

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82
Q

SBA: What is the mechanism of action of ARBs?

A

Answer: Block angiotensin II at AT1 receptors, preventing vasoconstriction and aldosterone release.

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83
Q

SBA: What class of drugs inhibits L-type calcium channels to manage hypertension?

A

Answer: Calcium channel blockers (CCBs).

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84
Q

SBA: What adverse effect is commonly associated with dihydropyridine CCBs like amlodipine?

A

Answer: Peripheral oedema.

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85
Q

SBA: What diuretic class is considered first-line in hypertension management?

A

Answer: Thiazide-like diuretics.

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86
Q

SBA: What is the mechanism of action of spironolactone in hypertension treatment?

A

Answer: Antagonizes aldosterone receptors, promoting sodium excretion and potassium retention.

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87
Q

SBA: What antihypertensive drug class is contraindicated during pregnancy?

A

Answer: ACE inhibitors and ARBs.

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88
Q

SBA: What type of beta-blocker is propranolol classified as?

A

Answer: Non-selective beta-blocker.

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89
Q

SBA: Which diuretic is most effective at reducing blood pressure by blocking sodium reabsorption in the distal convoluted tubule?

A

Answer: Thiazide-like diuretics (e.g., indapamide).

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90
Q

EMQ: Match the antihypertensive drug class to its adverse effect.

A

ACE inhibitors: Dry cough
Beta-blockers: Bradycardia
Calcium channel blockers: Flushing and headache
Thiazide diuretics: Hypokalaemia

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91
Q

EMQ: Match the drug to its primary mechanism of action.

A

Captopril: Inhibits ACE.
Losartan: Blocks AT1 receptors.
Amlodipine: Blocks L-type calcium channels.

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92
Q

EMQ: Match the clinical scenario to the most appropriate antihypertensive drug.

A

Hypertension with diabetes: ACE inhibitors (renal protection).
Resistant hypertension: Spironolactone.
Elderly patients: Calcium channel blockers.

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93
Q

EMQ: Match the antihypertensive drug class to its renal effect.

A

Thiazides: Reduce calcium excretion.
Potassium-sparing diuretics: Increase potassium retention.
ACE inhibitors: Reduce proteinuria.

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94
Q

EMQ: Match the contraindication to the drug.

A

Pregnancy: ACE inhibitors.
Bradycardia: Beta-blockers.
Bilateral renal artery stenosis: ARBs.

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95
Q

Describe the mechanism of action of ACE inhibitors and ARBs.

A

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)

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96
Q

List two common adverse effects of ACE inhibitors.

A

Answer: Dry cough and hyperkalaemia. (1 mark)

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97
Q

Explain the role of thiazide-like diuretics in hypertension.

A

nswer: Block sodium-chloride symporters in the distal convoluted tubule, reducing blood volume and lowering blood pressure. (2 marks)

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98
Q

What are the clinical considerations for prescribing beta-blockers?

A

Answer: Use caution in asthma, bradycardia, and in combination with calcium channel blockers (risk of severe bradycardia). (2 marks)

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99
Q

Discuss the monitoring requirements for patients on ACE inhibitors.

A

Answer: Regularly check renal function (serum creatinine) and potassium levels to prevent hyperkalaemia and renal impairment. (2 marks)

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100
Q

SBA: What is the primary mechanism of action of statins?

A

Answer: Inhibition of HMG-CoA reductase.

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101
Q

SBA: Which lipoprotein is referred to as “good cholesterol”?

A

Answer: High-Density Lipoprotein (HDL).

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102
Q

SBA: What is the main role of PCSK9 inhibitors in lipid management?

A

Answer: Increase LDL receptor recycling, reducing circulating LDL cholesterol.

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103
Q

SBA: What lipid parameter is targeted for ≥40% reduction in patients on statin therapy?

A

Answer: Non-HDL cholesterol.

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104
Q

SBA: What is the primary cause of familial hypercholesterolaemia?

A

Answer: Genetic mutations in LDL receptor or PCSK9.

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105
Q

SBA: Which lipoprotein is the main carrier of triglycerides in the bloodstream?

A

Answer: Very Low-Density Lipoprotein (VLDL).

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106
Q

SBA: What is the key characteristic of reverse cholesterol transport?

A

Answer: Movement of cholesterol from peripheral tissues back to the liver via HDL.

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107
Q

SBA: What is the main side effect of fibrates?

A

Answer: Myopathy, especially when combined with statins.

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108
Q

SBA: What is a contraindication for statin therapy?

A

Answer: Pregnancy.

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109
Q

SBA: Which lipid-lowering drug can cause flushing as a common side effect?

A

Answer: Niacin (nicotinic acid).

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110
Q

EMQ: Match the drug to its mechanism of action.

A

Statins: Inhibit HMG-CoA reductase.
PCSK9 inhibitors: Prevent LDL receptor degradation.
Ezetimibe: Inhibits cholesterol absorption in the intestine.

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111
Q

EMQ: Match the lipoprotein to its function.

A

LDL: Delivers cholesterol to peripheral tissues.
HDL: Mediates reverse cholesterol transport.
Chylomicrons: Transport dietary lipids from the intestine.

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112
Q

EMQ: Match the lipid-lowering drug to its adverse effect.

A

Statins: Myopathy.
Fibrates: Gallstones.
Niacin: Flushing.

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113
Q

EMQ: Match the lipid abnormality to the associated drug therapy.

A

Elevated LDL: Statins or PCSK9 inhibitors.
Elevated triglycerides: Fibrates or omega-3 fatty acids.
Mixed dyslipidaemia: Combination of statins and fibrates.

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114
Q

EMQ: Match the lipid-lowering drug to its clinical consideration.

A

Statins: Monitor liver function tests.
Fibrates: Avoid in severe renal impairment.
Niacin: Take aspirin to reduce flushing.

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115
Q

Explain the role of lipoproteins in lipid transport.

A

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)

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116
Q

Describe the pathophysiology of atherosclerosis in dyslipidaemia.

A

Answer:
LDL oxidation in the arterial wall leads to foam cell formation.
Chronic inflammation results in plaque development and narrowing of arteries. (2 marks)

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117
Q

Outline the pharmacological management of dyslipidaemia.

A

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)

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118
Q

What lifestyle interventions support pharmacological treatment in dyslipidaemia?

A

Answer:
Diet low in saturated fats.
Regular physical activity.
Smoking cessation. (2 marks)

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119
Q

What are the monitoring requirements for statin therapy?

A

Answer:
Check lipid profile 3 months after initiation and then annually.
Monitor liver enzymes before starting and periodically. (1 mark)

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120
Q

SBA: What is the primary target of ACE inhibitors in the treatment of hypertension?

A

Answer: Angiotensin-Converting Enzyme (ACE).

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121
Q

SBA: What is the common side effect of ACE inhibitors due to bradykinin accumulation?

A

Answer: Dry cough.

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122
Q

SBA: Which functional group in captopril enhances binding to the zinc ion in ACE?

A

Answer: Sulfhydryl (SH) group.

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123
Q

Answer: Sulfhydryl (SH) group.

A

Answer: Sulfhydryl (SH) group.

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124
Q

SBA: Which ARB has a tetrazole ring to enhance metabolic stability and bioavailability?

A

Answer: Losartan.

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125
Q

SBA: Which drug class inhibits L-type calcium channels to manage hypertension?

A

Answer: Calcium channel blockers (CCBs).

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126
Q

SBA: What is the mechanism of action of HMG-CoA reductase inhibitors (statins)?

A

Answer: Inhibit the rate-limiting step in cholesterol biosynthesis.

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127
Q

SBA: What chemical feature allows atorvastatin to bind effectively to HMG-CoA reductase?

A

Answer: Open lactone ring mimicking the tetrahedral intermediate.

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128
Q

SBA: What adverse effect is commonly associated with statins?

A

Answer: Myopathy.

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129
Q

SBA: What is the primary site of action for thiazide-like diuretics?

A

Answer: Distal convoluted tubule.

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130
Q

EMQ: Match the antihypertensive drug to its mechanism of action.

A

ACE inhibitors: Block conversion of angiotensin I to angiotensin II.
ARBs: Block AT1 receptors.
CCBs: Block L-type calcium channels.

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131
Q

EMQ: Match the drug to its adverse effect.

A

Statins: Myopathy.
ACE inhibitors: Dry cough.
Thiazides: Hypokalaemia.

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132
Q

EMQ: Match the drug to its structural feature.

A

Losartan: Tetrazole ring.
Captopril: Sulfhydryl group.
Enalapril: Ester prodrug.

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133
Q

EMQ: Match the drug class to its therapeutic use.

A

ARBs: Hypertension in ACE inhibitor-intolerant patients.
Statins: Hyperlipidaemia.
Thiazides: First-line for hypertension.

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134
Q

EMQ: Match the calcium channel blocker to its subclass.

A

Nifedipine: 1,4-Dihydropyridine.
Verapamil: Phenylalkylamine.
Diltiazem: Benzothiazepine.

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135
Q

Describe the mechanism of action of ACE inhibitors.

A

Answer: Inhibit ACE, preventing conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion.

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136
Q

Explain why enalapril is preferred over enalaprilat for oral administration.

A

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)

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137
Q

What is the role of the tetrazole ring in ARBs like losartan?

A

What is the role of the tetrazole ring in ARBs like losartan?

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138
Q

List two adverse effects of calcium channel blockers and the associated subclasses.

A

Answer: Peripheral oedema (1,4-dihydropyridines) and bradycardia (phenylalkylamines). (2 marks)

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139
Q

How do statins achieve their lipid-lowering effects?

A

Answer: Inhibit HMG-CoA reductase, reducing cholesterol synthesis and increasing LDL receptor expression for enhanced clearance of LDL cholesterol. (2 marks)

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140
Q

SBA: What is the primary diagnostic marker for myocardial infarction?

A

Answer: Troponin.

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141
Q

SBA: What is the first-line treatment for stable angina?

A

Answer: Glyceryl trinitrate (GTN) for symptom relief.

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142
Q

SBA: Which drug class is used for secondary prevention post-MI to reduce lipid levels?

A

Answer: Statins.

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143
Q

SBA: What is the gold standard treatment for STEMI if performed within 120 minutes of medical contact?

A

Answer: Percutaneous coronary intervention (PCI).

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144
Q

SBA: Which medication is contraindicated in acute MI due to its ability to increase heart rate?

A

Answer: Ivabradine.

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145
Q

SBA: What is the typical dose of aspirin given in the initial management of ACS?

A

Answer: 300 mg.

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146
Q

SBA: Which beta-blocker is commonly used for secondary prevention post-MI?

A

Answer: Bisoprolol.

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147
Q

SBA: What is the mechanism of action of fibrinolytics in STEMI management?

A

Answer: Activation of plasminogen to form plasmin, which breaks down fibrin clots.

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148
Q

SBA: What is the GRACE score used for in ACS management?

A

Answer: Predicts the 6-month mortality risk in patients with ACS.

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149
Q

SBA: Which medication is often used as a second-line treatment for angina if beta-blockers are contraindicated?

A

Answer: Calcium channel blockers (e.g., amlodipine).

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150
Q

EMQ: Match the ACS condition to its typical presentation.

A

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.

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151
Q

EMQ: Match the medication to its role in ACS management.

A

Aspirin: Antiplatelet therapy.
Enoxaparin: Anticoagulation.
Ticagrelor: P2Y12 inhibitor for dual antiplatelet therapy.

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152
Q

EMQ: Match the drug to its contraindication in ACS.

A

ACE inhibitors: History of angioedema.
Beta-blockers: Severe bradycardia.
Nitrates: Severe hypotension.

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153
Q

EMQ: Match the diagnostic test to its role in ACS.

A

ECG: Identifies ischemic changes like ST elevation.
Troponin levels: Confirms myocardial necrosis.
GRACE score: Risk stratification.

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154
Q

EMQ: Match the lifestyle advice to the outcome in ACS management.

A

Smoking cessation: Reduces risk of recurrent MI.
Mediterranean diet: Improves lipid profile.
Physical activity: Enhances exercise capacity and reduces mortality.

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155
Q

List the key symptoms and diagnostic tests for STEMI.

A

Answer:
Symptoms: Severe chest pain, radiating to jaw/arm, nausea, sweating. (1 mark)
Tests: ECG showing ST elevation; raised troponin levels. (1 mark)

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156
Q

Describe the pharmacological treatment during initial STEMI management.

A

Answer:
Aspirin 300 mg STAT (antiplatelet). (1 mark)
Ticagrelor or prasugrel STAT (dual antiplatelet therapy). (1 mark)
Fondaparinux or enoxaparin for anticoagulation. (1 mark)

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157
Q

Outline the reperfusion therapy options for STEMI.

A

Answer:
PCI within 120 minutes of contact (gold standard).
Fibrinolysis (if PCI unavailable) using alteplase or streptokinase. (2 marks)

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158
Q

What lifestyle interventions are recommended post-STEMI?

A

Answer:
Smoking cessation.
Mediterranean diet.
Regular physical activity (20–30 mins/day). (2 marks)

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159
Q

What is the rationale for statin therapy in STEMI patients?

A

Answer:
Reduces LDL cholesterol, stabilizes plaques, and decreases the risk of recurrent events. (1 mark)

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160
Q

SBA: What is the most common cause of heart failure?

A

Answer: Left ventricular dysfunction following myocardial infarction.

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161
Q

SBA: Which peptide is used to confirm or rule out heart failure diagnosis?

A

Answer: NT-proBNP.

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162
Q

SBA: What is the first-line pharmacological therapy for heart failure with reduced ejection fraction (HFrEF)?

A

Answer: ACE inhibitor and beta-blocker.

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163
Q

SBA: What is the typical dose range for furosemide in managing oedema in heart failure?

A

Answer: Up to 80 mg/day, titrated as needed.

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164
Q

SBA: Which drug class reduces mortality and hospitalisation when added to ACE inhibitors and beta-blockers in HFrEF?

A

Answer: Mineralocorticoid receptor antagonists (MRAs).

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165
Q

SBA: Which heart failure medication is a combination of sacubitril and valsartan?

A

Answer: Entresto®.

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166
Q

SBA: What is a common side effect of digoxin that requires monitoring?

A

Answer: Digitalis toxicity (e.g., nausea, vomiting, confusion).

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167
Q

SBA: Which functional classification system is used to assess the severity of heart failure symptoms?

A

Answer: New York Heart Association (NYHA) classification.

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168
Q

SBA: What lifestyle advice should be given to a stable heart failure patient regarding exercise?

A

Answer: Regular, supervised exercise within functional limitations.

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169
Q

SBA: What is the role of SGLT2 inhibitors in heart failure?

A

Answer: Reduce cardiovascular death and hospitalisation for HFrEF patients.

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170
Q

EMQ: Match the drug to its mechanism of action.

A

ACE inhibitors: Inhibit conversion of angiotensin I to angiotensin II.
MRAs: Antagonise aldosterone receptors.
Digoxin: Inhibit Na+/K+ ATPase to increase contractility.

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171
Q

EMQ: Match the symptom to the heart failure feature.

A

Fatigue: Decreased cardiac output and oxygen delivery.
Peripheral oedema: Fluid retention.
Orthopnoea: Redistribution of fluid to the lungs when lying down.

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172
Q

EMQ: Match the drug to its specialist use in HFrEF.

A

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.

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173
Q

EMQ: Match the diagnostic test to its purpose in heart failure.

A

NT-proBNP: Confirms/rules out diagnosis.
Echocardiography: Assesses ventricular function.
ECG: Identifies underlying causes like arrhythmias or ischemia.

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174
Q

EMQ: Match the lifestyle advice to its benefit in heart failure.

A

Balanced diet: Maintains healthy weight and reduces strain on the heart.
Timed diuretic use: Improves sleep by reducing nocturia.
Smoking cessation: Reduces disease progression.

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175
Q

List the key symptoms and diagnostic tools for heart failure.

A

Answer:
Symptoms: Fatigue, breathlessness, oedema.
Diagnostics: NT-proBNP levels, echocardiography, ECG. (2 marks)

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176
Q

Describe the first-line pharmacological management for HFrEF.

A

Answer:
ACE inhibitor (e.g., Ramipril).
Beta-blocker (e.g., Bisoprolol).
Add MRA (e.g., Spironolactone) if symptoms persist. (3 marks)

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177
Q

What are the specialist treatment options for HFrEF?

A

Answer:
Ivabradine for patients with sinus rhythm and HR ≥75 bpm.
Entresto® as a substitute for ACE inhibitors.
Digoxin for severe cases. (2 marks)

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178
Q

What lifestyle advice should be provided to heart failure patients?

A

Answer:
Regular exercise within limits.
Balanced diet, reduced salt intake, and weight management.
Smoking cessation and limited alcohol consumption. (2 marks)

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179
Q

How is heart failure treatment monitored?

A

Answer:
Monitor renal function, electrolytes, and NT-proBNP levels.
Regular assessment of symptoms and medication compliance. (1 mark)

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180
Q

SBA: What is the most common sustained arrhythmia in clinical practice?

A

Answer: Atrial fibrillation (AF).

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181
Q

SBA: Which scoring system is used to assess stroke risk in patients with AF?

A

Answer: CHA₂DS₂-VASc score.

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182
Q

SBA: Which drug is a direct thrombin inhibitor used for anticoagulation in AF?

A

Answer: Dabigatran.

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183
Q

SBA: What is the mechanism of action of warfarin?

A

Answer: Vitamin K antagonist, inhibiting the synthesis of clotting factors II, VII, IX, and X.

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184
Q

SBA: Which type of AF resolves spontaneously within 48 hours?

A

Answer: Paroxysmal AF.

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185
Q

SBA: What is the first-line drug class for rate control in AF?

A

Answer: Beta-blockers (e.g., bisoprolol).

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186
Q

SBA: Which drug is recommended for pharmacological cardioversion in AF patients with structural heart disease?

A

Answer: Amiodarone.

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187
Q

SBA: What is the target INR range for patients on warfarin for stroke prevention in AF?

A

Answer: 2.0–3.0.

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188
Q

SBA: What is a contraindication for beta-blockers in AF management?

A

Answer: Severe bradycardia.

189
Q

SBA: Which anticoagulant is associated with the risk of gastrointestinal bleeding but does not require INR monitoring?

A

Answer: Rivaroxaban (a DOAC).

190
Q

EMQ: Match the type of AF to its definition.

A

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
Q

EMQ: Match the drug to its mechanism of action.

A

Dabigatran: Direct thrombin inhibitor.
Rivaroxaban: Factor Xa inhibitor.
Warfarin: Vitamin K antagonist.

192
Q

EMQ: Match the AF treatment to the associated monitoring requirement.

A

DOACs: Renal function monitoring annually.
Warfarin: Regular INR checks.
Amiodarone: Thyroid and liver function monitoring.

193
Q

EMQ: Match the risk stratification score to its purpose.

A

CHA₂DS₂-VASc: Stroke risk.
HAS-BLED: Bleeding risk.
ORBIT: Assessing overall anticoagulation safety.

194
Q

EMQ: Match the patient scenario to the anticoagulant recommendation.

A

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
Q

List three common symptoms of AF.

A

Answer: Palpitations, breathlessness (dyspnoea), and fatigue. (1 mark)

196
Q

What tests are used to diagnose AF?

A

Answer: ECG (to confirm arrhythmia), blood tests (e.g., thyroid function), and echocardiography (to assess ventricular function). (2 marks)

197
Q

Explain the CHA₂DS₂-VASc scoring system for stroke risk in AF.

A

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
Q

Outline pharmacological options for rate control in AF.

A

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
Q

Discuss the benefits of DOACs compared to warfarin in AF management.

A

Answer: DOACs have a fixed dose, no routine INR monitoring, and a lower risk of intracranial bleeding. (2 marks)

200
Q

SBA: What is the most common mechanism for pharmacokinetic drug interactions?

A

SBA: What is the most common mechanism for pharmacokinetic drug interactions?

201
Q

SBA: Which drug interaction resource provides the most detailed explanation for interaction mechanisms?

A

Answer: Stockley’s Drug Interactions

202
Q

SBA: What is the primary clinical concern when combining NSAIDs with DOACs?

A

Answer: Increased risk of gastrointestinal bleeding.

203
Q

SBA: Which enzyme does grapefruit juice inhibit, leading to increased drug plasma levels?

A

Answer: CYP3A4.

204
Q

SBA: What is the effect of inducing CYP450 enzymes on drug metabolism?

A

Answer: Increased metabolism, leading to reduced plasma concentrations of the drug.

205
Q

SBA: Which food component interacts with MAOIs and can cause a hypertensive crisis?

A

Answer: Tyramine.

206
Q

SBA: What is the recommendation for administering levothyroxine with calcium-containing antacids?

A

Answer: Separate administration by 2-4 hours.

207
Q

SBA: Which protein plays a major role in drug transport and can be inhibited by certain drugs like amiodarone?

A

Answer: P-glycoprotein.

208
Q

SBA: What is a potential interaction when warfarin is combined with cranberry juice?

A

Answer: Increased bleeding risk due to CYP450 inhibition.

209
Q

SBA: What characteristic of a drug increases the likelihood of protein binding interactions?

A

Answer: High protein-binding (>90%).

210
Q

EMQ: Match the drug to the common interaction mechanism.

A

Warfarin: CYP450 inhibition by other drugs or food (e.g., cranberry juice).
Ciprofloxacin: Chelation with calcium-containing products.
Amiodarone: P-glycoprotein inhibition.

211
Q

EMQ: Match the patient characteristic to the increased risk of drug interactions.

A

Elderly: Reduced renal and hepatic function.
Children: Underdeveloped metabolism.
Polypharmacy: Higher risk of adverse drug interactions.

212
Q

EMQ: Match the pharmacodynamic interaction to the drug pair.

A

DOAC + NSAIDs: Increased bleeding risk.
Beta-blockers + Verapamil: Severe bradycardia.
Antihypertensives + Diuretics: Excessive hypotension.

213
Q

EMQ: Match the resource to its feature.

A

Stockley’s: Detailed explanation of interaction mechanisms.
BNF paper: Pharmacodynamic interaction tables.
SPC: Scientific data from clinical trials.

214
Q

EMQ: Match the interaction type to its management.

A

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
Q

Differentiate between pharmacokinetic and pharmacodynamic drug interactions.

A

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
Q

Explain the clinical significance of CYP450 inhibitors and inducers.

A

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
Q

List three examples of food-drug interactions and their outcomes.

A

Answer:
Grapefruit juice + simvastatin: Increased statin toxicity.
Green leafy vegetables + warfarin: Reduced anticoagulant effect.
Tyramine-rich foods + MAOIs: Hypertensive crisis. (3 marks)

218
Q

Outline management strategies for drug interactions.

A

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
Q

What is the pharmacist’s role in minimizing drug interactions?

A

Answer:
Anticipate interactions using resources like BNF and Stockley’s.
Educate patients on signs of toxicity or reduced efficacy. (1 mark)

220
Q

SBA: Which coronary artery supplies the sinoatrial (SA) node in most individuals?

A

Answer: Right coronary artery.

221
Q

SBA: What is the primary pacemaker of the heart?

A

Answer: Sinoatrial (SA) node.

222
Q

SBA: What ion influx is responsible for the depolarization phase in cardiac pacemaker cells?

A

Answer: Calcium (Ca²⁺)

223
Q

SBA: What does the P wave on an ECG represent?

A

Answer: Atrial depolarization.

224
Q

SBA: What is the normal duration of the PR interval on an ECG?

A

Answer: 0.12–0.20 seconds.

225
Q

SBA: What is the most common cause of prolonged QT interval?

A

Answer: Hypocalcaemia.

226
Q

SBA: Which part of the ECG corresponds to ventricular depolarization?

A

Answer: QRS complex.

227
Q

SBA: What is the normal heart rate range for sinus rhythm?

A

SBA: What is the normal heart rate range for sinus rhythm?

228
Q

SBA: What condition is characterized by a heart rate <60 beats per minute with regular rhythm?

A

Answer: Sinus bradycardia.

229
Q

SBA: Which formula is used to calculate the corrected QT interval (QTc)?

A

Answer: Bazett’s formula.

230
Q

EMQ: Match the cardiac rhythm to its ECG feature.

A

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
Q

EMQ: Match the ion to its effect on cardiac action potential.

A

Sodium (Na⁺): Rapid depolarization.
Calcium (Ca²⁺): Plateau phase in ventricular action potential.
Potassium (K⁺): Repolarization.

232
Q

EMQ: Match the part of the ECG to its corresponding event.

A

P wave: Atrial depolarization.
QRS complex: Ventricular depolarization.
T wave: Ventricular repolarization.

233
Q

EMQ: Match the condition to its ECG change.

A

Hypercalcaemia: Shortened QT interval.
Hypocalcaemia: Prolonged QT interval.
Myocardial infarction: ST elevation.

234
Q

EMQ: Match the cardiac pacemaker to its intrinsic rate.

A

SA node: 60–100 bpm.
AV node: 40–60 bpm.
Purkinje fibers: 20–40 bpm.

235
Q

Outline the key components of the ECG and their significance.

A

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
Q

Explain the role of the SA node in cardiac rhythm.

A

Answer: Primary pacemaker; generates impulses at 60–100 bpm. (1 mark)

237
Q

What is the significance of QT interval prolongation?

A

Answer: Increased risk of ventricular arrhythmias, such as Torsades de Pointes. Causes include hypocalcaemia, medications (e.g., amiodarone), and genetic mutations. (2 marks)

238
Q

How is heart rate calculated from an ECG strip?

A

Answer: Count the number of large boxes between consecutive R waves and divide 300 by this number. (1 mark)

239
Q

List three factors that can alter the QT interval.

A

Answer: Plasma calcium levels (hyper/hypocalcaemia), medications (e.g., amiodarone), and genetic mutations (e.g., LQT1, LQT2). (2 marks)

240
Q

What are the criteria for normal sinus rhythm on an ECG?

A

Answer:
Regular rhythm.
Heart rate of 60–100 bpm.
1 P wave for every QRS complex.
PR interval <0.20 seconds. (2 marks)

241
Q

SBA: What is the hallmark ECG feature of atrial fibrillation?

A

Answer: Absence of P waves with an irregularly irregular rhythm.

242
Q

SBA: What ion imbalance is most commonly associated with Torsades de Pointes?

A

Answer: Hypokalemia or hypomagnesemia.

243
Q

SBA: Which arrhythmia presents with a sawtooth pattern on ECG?

A

Answer: Atrial flutter.

244
Q

SBA: What is the ventricular rate in atrial fibrillation if not controlled?

A

Answer: 120–200 beats per minute.

245
Q

SBA: What is the primary treatment for pulseless ventricular tachycardia?

A

Answer: Immediate CPR and defibrillation.

246
Q

SBA: Which drug is used to manage symptomatic bradycardia?

A

Answer: Atropine.

247
Q

SBA: What ECG feature differentiates ventricular tachycardia from supraventricular tachycardia?

A

Answer: Wide QRS complexes in ventricular tachycardia.

248
Q

SBA: What is the most common cause of ventricular fibrillation?

A

Answer: Myocardial infarction.

249
Q

SBA: What is the rate of the sinoatrial (SA) node under normal physiological conditions?

A

Answer: 60–100 beats per minute.

250
Q

SBA: What arrhythmia can result in sudden cardiac death without immediate treatment?

A

Answer: Ventricular fibrillation.

251
Q

EMQ: Match the arrhythmia to its ECG characteristic.

A

Atrial fibrillation: Irregular rhythm with no P waves.
Ventricular tachycardia: Wide QRS complexes, no P waves.
Atrial flutter: Sawtooth P wave pattern.

252
Q

EMQ: Match the arrhythmia to its primary treatment.

A

Atrial fibrillation: Rate control with beta-blockers or digoxin.
Ventricular fibrillation: CPR and defibrillation.
Sinus bradycardia: Atropine.

253
Q

EMQ: Match the arrhythmia to its cause.

A

trial fibrillation: Hypertension or heart failure.
Torsades de Pointes: Prolonged QT interval.
Supraventricular tachycardia: Reentrant circuit in AV node.

254
Q

EMQ: Match the arrhythmia to its symptoms

A

Sinus bradycardia: Fatigue, lightheadedness.
Ventricular tachycardia: Syncope, dyspnea.
Atrial fibrillation: Palpitations, breathlessness.

255
Q

EMQ: Match the arrhythmia to its associated risk.

A

Atrial fibrillation: Stroke.
Ventricular fibrillation: Sudden cardiac death.
Torsades de Pointes: Progression to ventricular fibrillation.

256
Q

List the main mechanisms of arrhythmias.

A

Answer:
Disturbances in impulse formation.
Disturbances in impulse conduction.
Combination of both. (2 marks)

257
Q

Outline the symptoms of supraventricular arrhythmias.

A

Answer:
Atrial fibrillation: Palpitations, breathlessness.
Atrial flutter: Chest discomfort, fatigue.
Supraventricular tachycardia: Dizziness, syncope. (2 marks)

258
Q

What are the key differences in ECG features between ventricular and supraventricular arrhythmias?

A

Answer:
Ventricular: Wide QRS complexes, no P waves.
Supraventricular: Narrow QRS complexes, normal or absent P waves. (2 marks)

259
Q

Describe the management of ventricular tachycardia.

A

Answer:
If pulseless: CPR and defibrillation.
If with a pulse: Antiarrhythmic drugs (e.g., amiodarone) or synchronized cardioversion. (2 marks)

260
Q

Explain the risk of stroke in atrial fibrillation and its prevention.

A

Answer:
Irregular rhythm causes blood pooling in the atria, leading to thrombus formation.
Prevented with anticoagulants (e.g., warfarin or DOACs). (2 marks)

261
Q

SBA: What is the primary mechanism of action for Class I antiarrhythmic drugs?

A

Answer: Sodium channel blockade.

262
Q

SBA: Which Class I antiarrhythmic drug is contraindicated in ischemic heart disease?

A

Answer: Flecainide.

263
Q

SBA: What is the primary effect of beta-blockers (Class II) on cardiac action potential?

A

Answer: Decrease conduction velocity through the AV node and reduce heart rate.

264
Q

SBA: What is the effect of calcium channel blockers (Class IV) on pacemaker cells?

A

Answer: Decrease firing rate and conduction velocity in the SA and AV nodes.

265
Q

SBA: Which Class III drug is used for both supraventricular and ventricular arrhythmias?

A

Answer: Amiodarone.

266
Q

Answer: Decrease firing rate and conduction velocity in the SA and AV nodes.

A

Answer: Adenosine.

267
Q

SBA: What is the Vaughan Williams classification based on?

A

Answer: Electrophysiological effects of drugs on cardiac cells.

268
Q

SBA: Which drug class prolongs the refractory period by blocking potassium channels?

A

Answer: Class III.

269
Q

SBA: What is the primary adverse effect of amiodarone due to its iodine content?

A

Answer: Thyroid dysfunction.

270
Q

SBA: What is the role of magnesium sulfate in arrhythmias?

A

Answer: Used in Torsades de Pointes to stabilize cardiac repolarization.

271
Q

EMQ: Match the drug to its mechanism of action.

A

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
Q

EMQ: Match the class of drugs to their ECG effects.

A

Class I: Widen QRS complex.
Class III: Prolong QT interval.
Class IV: Prolong PR interval.

273
Q

EMQ: Match the drug to its therapeutic indication.

A

Adenosine: Paroxysmal supraventricular tachycardia.
Amiodarone: Ventricular fibrillation.
Digoxin: Atrial fibrillation with heart failure.

274
Q

EMQ: Match the antiarrhythmic drug to its contraindication.

A

Verapamil: AV block.
Flecainide: Structural heart disease.
Propranolol: Severe bradycardia.

275
Q

EMQ: Match the phase of the cardiac action potential to the drug action.

A

Phase 0: Class I - Sodium channel blockers.
Phase 3: Class III - Potassium channel blockers.
Phase 4: Class IV - Calcium channel blockers.

276
Q

List the Vaughan Williams classes and their primary mechanisms.

A

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
Q

Provide two examples of arrhythmias treated by each class.

A

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
Q

What is the mechanism of unclassified drugs like digoxin and adenosine?

A

Answer:
Digoxin: Increases vagal tone to slow AV node conduction.
Adenosine: Hyperpolarizes cells by activating potassium channels, rapidly terminating SVT. (2 marks)

279
Q

List two common adverse effects of antiarrhythmic drugs.

A

Answer:
Amiodarone: Thyroid dysfunction, pulmonary toxicity.
Verapamil: Bradycardia, hypotension. (2 marks)

280
Q

Answer:
Amiodarone: Thyroid dysfunction, pulmonary toxicity.
Verapamil: Bradycardia, hypotension. (2 marks)

A

Answer: Inhibits Vitamin K epoxide reductase (VKORC1), reducing activation of clotting factors II, VII, IX, and X.

281
Q

SBA: Which anticoagulant directly inhibits Factor Xa?

A

Answer: Apixaban.

282
Q

SBA: What is the primary adverse effect associated with SGLT2 inhibitors in heart failure management?

A

Answer: Genital fungal infections.

283
Q

SBA: What is the therapeutic use of neprilysin inhibitors like sacubitril?

A

Answer: Enhances blood pressure-lowering peptides (e.g., natriuretic peptides) to treat chronic heart failure.

284
Q

SBA: What functional group in aspirin irreversibly inhibits COX-1?

A

Answer: Acetyl group.

285
Q

SBA: What is the mechanism of action of thrombolytic drugs like alteplase?

A

Answer: Activates plasminogen to plasmin, which degrades fibrin clots.

286
Q

SBA: Which loop diuretic inhibits the Na+/K+/2Cl− symporter in the nephron?

A

Answer: Furosemide.

287
Q

SBA: What is the clinical significance of the S-isomer of warfarin?

A

Answer: It is 4 times more potent than the R-isomer as an anticoagulant.

288
Q

SBA: Which P2Y12 receptor antagonist is reversible?

A

Answer: Ticagrelor.

289
Q

SBA: What does the hydrophobic interaction in Factor Xa inhibitors like rivaroxaban achieve?

A

Answer: Stabilizes binding to the S1 and S4 pockets of Factor Xa.

290
Q

EMQ: Match the drug class to its mechanism of action.

A

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
Q

EMQ: Match the drug to its therapeutic use.

A

Alteplase: Acute ischemic stroke.
Aspirin: Primary prevention of myocardial infarction.
Sacubitril: Chronic heart failure with reduced ejection fraction.

292
Q

EMQ: Match the drug to its major adverse effect.

A

Warfarin: Bleeding risk.
SGLT2 inhibitors: Genital fungal infections.
Ticagrelor: Dyspnea.

293
Q

EMQ: Match the drug to its molecular target.

A

Dabigatran: Direct thrombin (Factor IIa) inhibitor.
Rivaroxaban: Factor Xa inhibitor.
Aspirin: COX-1 inhibitor.

294
Q

EMQ: Match the drug to its clinical consideration.

A

Warfarin: Requires INR monitoring.
Apixaban: No routine monitoring required.
Clopidogrel: Activated by CYP2C19.

295
Q

Outline the primary pharmacological strategies for MI and stroke.

A

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
Q

Describe the mechanism of action of aspirin and clopidogrel.

A

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
Q

Explain the differences between warfarin and DOACs.

A

Answer:
Warfarin: Narrow therapeutic index, requires INR monitoring, delayed onset.
DOACs: Fixed dosing, faster onset, fewer interactions, no routine monitoring. (2 marks)

298
Q

Discuss the role of thrombolytics in acute MI and stroke.

A

Answer:
Activate plasminogen to plasmin, degrading fibrin clots. Used within 3–4.5 hours of symptom onset. (2 marks)

299
Q

List three potential adverse effects of these drugs and their management strategies.

A

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
Q

SBA: What is the primary cause of stable angina?

A

Answer: Atherosclerosis leading to reduced coronary artery capacity.

301
Q

SBA: Which type of angina is caused by coronary artery spasms?

A

Answer: Variant (Prinzmetal’s) angina.

302
Q

SBA: What diagnostic marker is elevated in STEMI but not in unstable angina?

A

Answer: Troponin.

303
Q

SBA: Which enzyme is activated in platelets by thrombin during clot formation?

A

Answer: Protease-activated receptor (PAR).

304
Q

SBA: What is the mechanism of action of nitrates in angina management?

A

Answer: They increase nitric oxide levels, leading to vasodilation.

305
Q

SBA: What does a prolonged occlusion of an epicardial coronary artery lead to?

A

Answer: Myocardial infarction.

306
Q

SBA: Which drug class blocks the P2Y12 receptor to inhibit platelet aggregation?

A

Answer: P2Y12 receptor antagonists (e.g., clopidogrel).

307
Q

SBA: What is the primary treatment for acute STEMI?

A

Answer: Percutaneous coronary intervention (PCI).

308
Q

Answer: Percutaneous coronary intervention (PCI).

A

Answer: Von Willebrand factor.

309
Q

SBA: What is the main diagnostic marker for fibrinolysis?

A

Answer: D-dimer.

310
Q

EMQ: Match the type of angina to its features.

A

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
Q

EMQ: Match the drug class to its mechanism in angina.

A

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
Q

EMQ: Match the process in clot formation to its associated factor.

A

Platelet adhesion: Von Willebrand factor.
Platelet activation: Thromboxane A2.
Fibrin stabilization: Factor XIII.

313
Q

EMQ: Match the drug to its specific use.

A

Clopidogrel: Prevent platelet aggregation in coronary artery disease.
Alteplase: Dissolve thrombi in acute MI.
GTN: Relieve acute angina attacks.

314
Q

EMQ: Match the coronary artery pathology to its treatment.

A

STEMI: PCI or fibrinolytics.
Stable angina: Beta-blockers and nitrates.
Unstable angina: Dual antiplatelet therapy.

315
Q

Outline the pathogenesis of CAD.

A

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
Q

What are the clinical features of stable angina, unstable angina, and STEMI?

A

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
Q

Describe the pharmacological management of stable angina.

A

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
Q

How is STEMI managed acutely?

A

Answer:
Percutaneous coronary intervention (PCI).
Thrombolytics if PCI unavailable.
Dual antiplatelet therapy and anticoagulants. (2 marks)

319
Q

SBA: What is the mechanism of action of warfarin?

A

Answer: Inhibits Vitamin K epoxide reductase, reducing the synthesis of clotting factors II, VII, IX, and X.

320
Q

SBA: Which drug is a direct and reversible inhibitor of Factor Xa?

A

Answer: Apixaban.

321
Q

SBA: Which drug is used to reverse the effects of heparin-induced thrombocytopenia?

A

Answer: Danaparoid sodium.

322
Q

SBA: What is the primary adverse effect of fibrinolytics like alteplase?

A

Answer: Hemorrhage.

323
Q

SBA: Which glycoprotein IIb/IIIa inhibitor is a monoclonal antibody used in high-risk percutaneous coronary intervention?

A

Answer: Abciximab

324
Q

SBA: Which anticoagulant binds to antithrombin III to inhibit thrombin activity?

A

Answer: Heparin.

325
Q

SBA: What is the function of fibrinolytics in thromboembolic disease management?

A

Answer: Activate plasminogen to plasmin, which dissolves fibrin clots.

326
Q

SBA: What is the primary clinical use of low molecular weight heparins (LMWHs)?

A

Answer: Prevention and treatment of deep vein thrombosis (DVT).

327
Q

SBA: What is the advantage of direct oral anticoagulants (DOACs) over warfarin?

A

Answer: Fixed dosing and no routine INR monitoring.

328
Q

SBA: What is the reversal agent for dabigatran?

A

Answer: Idarucizumab.

329
Q

EMQ: Match the drug to its mechanism of action.

A

Warfarin: Inhibits Vitamin K epoxide reductase.
Apixaban: Direct Factor Xa inhibitor.
Dabigatran: Direct thrombin inhibitor.

330
Q

EMQ: Match the anticoagulant to its clinical consideration.

A

Warfarin: Requires INR monitoring.
DOACs (e.g., rivaroxaban): No routine monitoring.
Heparin: Administered intravenously or subcutaneously.

331
Q

EMQ: Match the antiplatelet drug to its target receptor.

A

Clopidogrel: P2Y12 receptor.
Aspirin: COX-1.
Abciximab: Glycoprotein IIb/IIIa receptor.

332
Q

EMQ: Match the fibrinolytic to its property.

A

Alteplase: Fibrin-specific.
Streptokinase: Can induce antibody formation.
Tenecteplase: Longer half-life.

333
Q

EMQ: Match the condition to the appropriate treatment.

A

STEMI: Alteplase or PCI.
DVT: LMWH or DOACs.
Pulmonary embolism: Fibrinolytics.

334
Q

lassify antithrombotic drugs and give examples.

A

Answer:
Anticoagulants: Warfarin, DOACs (e.g., apixaban).
Antiplatelets: Aspirin, clopidogrel.
Fibrinolytics: Alteplase, streptokinase. (2 marks)

335
Q

Describe the mechanism of action for warfarin and DOACs.

A

Answer:
Warfarin: Inhibits Vitamin K epoxide reductase.
DOACs: Directly inhibit Factor Xa or thrombin. (2 marks)

336
Q

List two clinical indications for each drug class.

A

Answer:
Anticoagulants: DVT, atrial fibrillation.
Antiplatelets: Prevention of MI, stroke.
Fibrinolytics: Acute MI, pulmonary embolism. (3 marks)

337
Q

Discuss major adverse effects and their management.

A

Answer:
Warfarin: Bleeding, managed with Vitamin K.
Heparin: HIT, managed with danaparoid.
Fibrinolytics: Hemorrhage, monitor closely. (3 marks)

338
Q

SBA: Which beta-blocker is non-selective and inhibits both β1 and β2 receptors?

A

Answer: Propranolol.

339
Q

SBA: What structural feature distinguishes aryloxypropanolamines from arylethanolamines in beta-blockers?

A

Answer: Presence of an aryloxypropanolamine side chain increases potency.

340
Q

SBA: Which beta-blocker has cardio-selective β1 affinity and is hydrophilic?

A

Answer: Atenolol.

341
Q

SBA: What functional group in norepinephrine binds ionically to the β-adrenoceptor at physiological pH?

A

Answer: Amine group.

342
Q

SBA: What property allows lipophilic beta-blockers like propranolol to penetrate the CNS?

A

Answer: High partition coefficient (LogP).

343
Q

SBA: Which beta-blocker exhibits mixed β1, β2, and α1 antagonistic effects?

A

Answer: Carvedilol.

344
Q

SBA: What is the main mechanism of action of beta-blockers in hypertension management?

A

Answer: Decrease heart rate and myocardial contractility by blocking β1 receptors.

345
Q

SBA: Why are hydrophilic beta-blockers less likely to cause CNS side effects?

A

Answer: They have a low partition coefficient and cannot easily cross the blood-brain barrier.

346
Q

SBA: What is the mechanism of action of amiodarone?

A

Answer: Blocks potassium channels, prolonging the refractory period and action potential.

347
Q

SBA: What structural modification in dronedarone reduces the risks of thyroid and neurotoxicity compared to amiodarone?

A

Answer: Removal of iodine groups and addition of a methylsulfonamide group.

348
Q

EMQ: Match the beta-blocker to its property.

A

Atenolol: Cardio-selective β1 blocker, hydrophilic.
Propranolol: Non-selective β blocker, lipophilic.
Carvedilol: Mixed β1, β2, and α1 antagonist.

349
Q

EMQ: Match the functional group to its binding site.

A

Amine group: Ionic bond with Asp113.
Catechol aromatic ring: Hydrophobic interaction with Phe290.
Alcohol group: Hydrogen bond with Asn293.

350
Q

EMQ: Match the drug to its clinical use.

A

Amiodarone: Ventricular and supraventricular arrhythmias.
Atenolol: Hypertension and angina.
Dronedarone: Atrial fibrillation/flutter.

351
Q

EMQ: Match the beta-blocker to its classification.

A

Timolol: Non-selective beta-blocker.
Bisoprolol: Cardio-selective beta-blocker.
Labetalol: Mixed alpha and beta antagonist.

352
Q

EMQ: Match the structural modification to its effect.

A

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
Q

Explain the mechanism of action of beta-blockers.

A

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
Q

Differentiate between selective and non-selective beta-blockers.

A

Answer:
Selective: Target β1 receptors (e.g., atenolol).
Non-selective: Block both β1 and β2 receptors (e.g., propranolol). (2 marks)

355
Q

What are the clinical applications of beta-blockers?

A

Answer: Hypertension, angina, myocardial infarction, arrhythmias, and heart failure. (2 marks)

356
Q

Describe the SAR of beta-blockers.

A

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
Q

What are the structural differences between amiodarone and dronedarone?

A

Answer:
Amiodarone: Contains iodine groups, leading to thyroid toxicity.
Dronedarone: Lacks iodine and has a methylsulfonamide group, reducing lipophilicity and toxicity. (2 marks)

358
Q

SBA: What is the key difference between crystalline and amorphous solids?

A

Answer: Crystalline solids have a long-range molecular order, while amorphous solids have a random molecular arrangement.

359
Q

SBA: What is the main advantage of salt formation in drug development?

A

Answer: It increases the solubility and dissolution rate of acidic and basic drugs.

360
Q

SBA: Which particle property most directly affects flowability during drug manufacturing?

A

Answer: Particle shape.

361
Q

SBA: What does the term “hydrate” refer to in solid-state chemistry?

A

Answer: A crystalline structure that includes water molecules within its lattice.

362
Q

SBA: What is the main application of co-crystals in pharmaceutical formulations?

A

Answer: Enhancing the dissolution rate and bioavailability of poorly water-soluble drugs.

363
Q

SBA: What type of diameter is used to describe the equivalent volume sphere of a particle?

A

Answer: Volume-equivalent diameter.

364
Q

SBA: Which theory is used to measure the surface area of irregular particles using gas adsorption?

A

Answer: Brunauer–Emmett–Teller (BET) theory.

365
Q

SBA: How does a larger specific surface area affect drug dissolution rate?

A

Answer: Increases the dissolution rate due to greater contact with the dissolution medium.

366
Q

SBA: What is the main drawback of amorphous drug formulations?

A

Answer: They are less stable and more prone to moisture sensitivity compared to crystalline forms.

367
Q

SBA: Which equation describes the relationship between dissolution rate, surface area, and diffusion layer thickness?

A

Answer: Noyes-Whitney equation.

368
Q

EMQ: Match the particle property to its impact on drug formulation.

A

Surface area: Dissolution rate.
Particle size: Content uniformity.
Particle shape: Flowability and mixing.

369
Q

EMQ: Match the type of solid-state modification to its example.

A

Hydrate: Lisinopril dihydrate.
Solvate: Ethanolate of a drug.
Co-crystal: Sildenafil and aspirin co-crystal.

370
Q

EMQ: Match the particle diameter to its application.

A

Aerodynamic diameter: Inhalation drug deposition.
Stokes’ diameter: Sedimentation properties.
Sieve diameter: Particle size distribution analysis.

371
Q

EMQ: Match the solid-state form to its feature.

A

Crystalline: Higher stability, lower solubility.
Amorphous: Lower stability, higher solubility.
Polymorphic: Same chemical composition, different molecular packing.

372
Q

EMQ: Match the method to its application in particle analysis.

A

Laser diffraction: Determines particle size distribution.
BET theory: Measures surface area of irregular particles.
Microscopy: Visualizes particle shape.

373
Q

Explain the significance of particle size and surface area.

A

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
Q

Describe the impact of particle shape on powder behavior.

A

Answer:
Spherical particles: Better flowability and mixing.
Irregular or flaky particles: Poor flowability and increased cohesiveness. (2 marks)

375
Q

What are the roles of polymorphs and co-crystals in pharmaceutical formulations?

A

Answer:
Polymorphs: Allow control over stability and solubility.
Co-crystals: Enhance dissolution and bioavailability of poorly soluble drugs. (2 marks)

376
Q

Discuss the practical implications of hydrates and solvates.

A

Answer:
Hydrates: Improved stability but lower solubility.
Solvates: Can alter dissolution behavior and bioavailability. (2 marks)

377
Q

What is the role of BET theory in particle characterization?

A

Answer: Measures the surface area of irregular particles to predict dissolution and adsorption properties. (1 mark)

378
Q

SBA: What is the key difference between normal and lognormal distributions in particle size analysis?

A

Answer: Normal distributions are symmetric with mean = median = mode, while lognormal distributions are positively skewed with a logarithmic scale normalizing the data.

379
Q

SBA: What does D90/D10 represent in particle size analysis?

A

Answer: It represents the ratio of particle sizes at 90% and 10% undersize, indicating the degree of dispersion.

380
Q

SBA: Which particle sizing method measures the aerodynamic diameter of particles?

A

Answer: Cascade impactor.

381
Q

SBA: What type of diameter does laser diffraction measure?

A

Answer: Equivalent diameter based on the diffraction pattern.

382
Q

SBA: Which particle sizing method uses Stokes’ Law to measure particle size?

A

Answer: Andreasen pipette (sedimentation).

383
Q

SBA: What is the most significant limitation of microscopy in particle size analysis?

A

Answer: Non-representative selection of particles.

384
Q

SBA: What does the Coefficient of Variation (CV%) indicate in particle size distribution?

A

Answer: It normalizes the standard deviation by dividing it by the mean, indicating the degree of variance.

385
Q

SBA: How does sieving classify particles?

A

Answer: By sieve equivalent diameter, determined by the size of apertures in the sieve mesh.

386
Q

SBA: What does photon correlation spectroscopy (dynamic light scattering) measure?

A

Answer: Hydrodynamic diameter of particles in suspension.

387
Q

SBA: What is the main application of the D90/D10 ratio in pharmaceutical powders?

A

Answer: To assess polydispersity of powders for consistency in formulations

388
Q

EMQ: Match the particle size analysis method to its application.

A

Sieving: Measures sieve equivalent diameter of powders.
Andreasen pipette: Determines Stokes’ diameter via sedimentation.
Cascade impactor: Measures aerodynamic diameter for inhalation products.

389
Q

EMQ: Match the dispersion measure to its definition.

A

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
Q

EMQ: Match the particle size technique to its limitation.

A

Laser diffraction: Struggles with non-spherical particles.
Microscopy: Non-representative selection of particles.
Photon correlation spectroscopy: Affected by aggregates or dust.

391
Q

EMQ: Match the type of particle diameter to its definition.

A

Volume diameter: Measured by electrical sensing zone methods.
Aerodynamic diameter: Used in respiratory particle analysis.
Hydrodynamic diameter: Determined by dynamic light scattering.

392
Q

EMQ: Match the type of distribution to its property.

A

Normal distribution: Mean = median = mode.
Lognormal distribution: Data normalized using a logarithmic scale.
Bimodal distribution: Has two distinct modes.

393
Q

Explain the principles of particle size analysis.

A

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
Q

Describe three particle sizing techniques and their applications.

A

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
Q

Discuss the limitations of particle sizing methods.

A

Answer:
Laser diffraction: Inaccurate for non-spherical particles.
Microscopy: Prone to sampling bias.
Dynamic light scattering: Sensitive to aggregates or dust. (2 marks)

396
Q

What is the significance of D90/D10 and CV% in pharmaceutical formulations?

A

Answer:
D90/D10: Indicates polydispersity, essential for uniform drug delivery.
CV%: Compares variance across sample populations. (2 marks)

397
Q

How are particle size distributions typically visualized?

A

Answer:
Histograms for incremental distributions.
Cumulative graphs for undersize/oversize percentages. (1 mark)

398
Q

SBA: What is the primary purpose of granulation in pharmaceutical formulations?

A

Answer: To improve powder flowability and prevent segregation of constituents.

399
Q

SBA: How does granulation reduce dust in powder formulations?

A

Answer: By aggregating fine powder particles into denser granules

400
Q

SBA: What is the angle of repose used to measure in powder flowability?

A

Answer: The flowability of powders and granules.

401
Q

SBA: Which liquid component is commonly used in wet granulation?

A

Answer: Water or ethanol.

402
Q

SBA: What is a common binder used in wet granulation?

A

Answer: Polyvinylpyrrolidone (PVP).

403
Q

SBA: What is the primary limitation of wet granulation for thermolabile drugs?

A

Answer: Potential degradation due to moisture and heat.

404
Q

SBA: What is the main disadvantage of dry granulation?

A

Answer: High compaction force increases dust generation and cross-contamination risks.

405
Q

SBA: Which equipment is used in wet granulation for spraying binder solutions?

A

Answer: Fluid-bed granulator.

406
Q

SBA: What is the main difference between small granules and large granules?

A

Answer: Small granules (~0.2–0.4 mm) are used as intermediates, while large granules (~1–4 mm) are often final dosage forms.

407
Q

SBA: What happens if the mass is too dry during wet granulation?

A

Answer: Granules will fall apart.

408
Q

EMQ: Match the granulation process to its description.

A

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
Q

EMQ: Match the method to its equipment.

A

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
Q

EMQ: Match the limitation to the granulation process.

A

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
Q

EMQ: Match the granule property to its benefit.

A

Denser particles: Improves flowability.
Uniform granules: Prevents segregation.
Reduced dust: Minimizes toxic exposure.

412
Q

EMQ: Match the particle characteristic to its measurement.

A

Angle of repose: Flowability of powders.
Tapped density: Compressibility of powders.
Bulk density: Volume occupied by powder under normal conditions.

413
Q

Explain the purpose of granulation in pharmaceutical formulations.

A

Answer:
Prevents segregation of powder mix.
Improves flow properties and compressibility.
Reduces toxic dust. (2 marks)

414
Q

Describe the process of wet granulation.

A

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
Q

Describe the process of dry granulation.

A

Answer:
Compact powder under high pressure to form slugs.
Mill and sieve slugs into granules. (2 marks)

416
Q

What are the advantages and disadvantages of wet granulation?

A

Answer:
Advantages: Improves uniformity and reduces dust.
Disadvantages: Expensive, unsuitable for moisture-sensitive drugs. (2 marks)

417
Q

Compare dry granulation to wet granulation.

A

Answer:
Dry granulation: Less expensive but generates dust.
Wet granulation: Better granule uniformity but costly and complex. (2 marks)

418
Q

SBA: What is the primary mechanism of action for ACE inhibitors?

A

Answer: Inhibit ACE-mediated conversion of angiotensin I to angiotensin II, leading to vasodilation and reduced aldosterone secretion.

419
Q

SBA: Why are ACE inhibitors associated with a persistent dry cough?

A

Answer: Due to bradykinin accumulation.

420
Q

SBA: Which class of drugs is most commonly used in African-Caribbean patients for hypertension first-line therapy?

A

Answer: Calcium channel blockers.

421
Q

SBA: What is the main adverse effect of thiazide diuretics?

A

Answer: Hypokalaemia.

422
Q

SBA: Which enzyme do statins inhibit to reduce cholesterol?

A

Answer: HMG-CoA reductase.

423
Q

SBA: Which drug class activates PPARα to treat hypertriglyceridemia?

A

Answer: Fibrates.

424
Q

SBA: What is the first-line drug for stable angina?

A

Answer: Beta-blockers.

425
Q

SBA: Which drug selectively inhibits the If current in the sinoatrial node?

A

Answer: Ivabradine.

426
Q

SBA: What is the primary action of aspirin in thromboembolic disorders?

A

Answer: Irreversible inhibition of thromboxane synthesis in platelets.

427
Q

SBA: What does an elevated troponin level indicate?

A

Answer: Myocardial ischemia or infarction.

428
Q

SBA: Which ECG change indicates ST-elevation myocardial infarction (STEMI)?

A

Answer: ST elevation.

429
Q

SBA: What type of arrhythmia is characterized by a saw-tooth pattern on the ECG

A

Answer: Atrial flutter.

430
Q

SBA: Which drug is contraindicated in combination with statins due to increased risk of myopathy?

A

Answer: Fibrates.

431
Q

SBA: What is the most common adverse effect of nitrates?

A

Answer: Headache.

432
Q

SBA: What type of diuretic is spironolactone?

A

Answer: Aldosterone receptor antagonist.

433
Q

SBA: What is the mechanism of action of ranolazine in angina?

A

nswer: Blocks late inward sodium currents.

434
Q

SBA: What is the mechanism of action of nicorandil?

A

Answer: Activates ATP-sensitive potassium channels.

435
Q

SBA: What does a prolonged QT interval on ECG indicate?

A

Answer: Risk of ventricular arrhythmias.

436
Q

SBA: Why is grapefruit juice contraindicated with statins?

A

Answer: It inhibits CYP450 enzymes, increasing statin plasma levels.

437
Q

SBA: What is the most common adverse effect of antiplatelet drugs like clopidogrel?

A

Answer: Bleeding.

438
Q

EMQ: Match the antihypertensive drug to its mechanism.

A

ACE inhibitors: Blocks angiotensin II synthesis.
Beta-blockers: Reduce heart rate and cardiac output.
Thiazide diuretics: Promote sodium excretion in the distal tubule.

439
Q

EMQ: Match the lipid-lowering drug to its effect.

A

Statins: Reduce LDL cholesterol.
Fibrates: Lower triglycerides, increase HDL.
Ezetimibe: Inhibits cholesterol absorption.

440
Q

EMQ: Match the anti-anginal drug to its target.

A

Nitrates: Vascular smooth muscle.
Beta-blockers: Heart rate and contractility.
Ivabradine: Sinoatrial node.

441
Q

MQ: Match the ECG finding to its diagnosis.

A

ST elevation: STEMI.
Inverted T wave: Ischemia.
Prolonged QT interval: Risk of torsades de pointes.

442
Q

EMQ: Match the thromboembolic drug to its mechanism.

A

Aspirin: Inhibits thromboxane synthesis.
Heparin: Activates antithrombin.
Warfarin: Inhibits vitamin K-dependent clotting factors.

443
Q

EMQ: Match the drug to its adverse effect.

A

ACE inhibitors: Dry cough.
Statins: Myopathy.
Nitrates: Headache.

444
Q

EMQ: Match the cholesterol pathway to its description.

A

Exogenous: Dietary cholesterol absorption.
Endogenous: Cholesterol synthesis in the liver.
Reverse transport: HDL-mediated clearance.

445
Q

EMQ: Match the arrhythmia to its treatment.

A

Atrial fibrillation: Warfarin or DOACs.
Ventricular tachycardia: Amiodarone.
Paroxysmal supraventricular tachycardia: Adenosine.

446
Q

EMQ: Match the nitrate to its feature.

A

Isosorbide mononitrate: Oral, long-acting.
Glyceryl trinitrate: Sublingual, short-acting.
Sodium nitroprusside: IV, used in hypertensive crises.

447
Q

EMQ: Match the anti-platelet to its mechanism.

A

Clopidogrel: P2Y12 receptor inhibitor.
Aspirin: Thromboxane inhibitor.
Abciximab: Glycoprotein IIb/IIIa inhibitor.

448
Q

Define hypertension (1 mark).

A

Answer: Persistent elevation of blood pressure ≥140/90 mmHg.

449
Q

List two classes of antihypertensives with examples (2 marks).

A

Answer: ACE inhibitors (ramipril), CCBs (amlodipine).

450
Q

Explain why ACE inhibitors are less effective in African-Caribbean populations (2 marks).

A

Answer: Low renin activity, age-related nephron loss.

451
Q

State one adverse effect of thiazide diuretics and its management (2 marks).

A

Answer: Hypokalaemia, managed with potassium supplements.

452
Q

Outline lifestyle changes recommended in hypertension (3 marks).

A

Answer: Low-sodium diet, regular exercise, weight loss.

453
Q

What is the mechanism of action of statins (2 marks)?

A

Answer: Inhibits HMG-CoA reductase, reducing cholesterol synthesis.

454
Q

Why is grapefruit juice contraindicated (2 marks)?

A

Answer: Inhibits CYP450 enzymes, increasing myopathy risk.

455
Q

Compare LDL and HDL particles (2 marks).

A

Answer: LDL carries cholesterol to tissues, HDL facilitates reverse cholesterol transport.

456
Q

What is the primary indication for fibrates (2 marks)?

A

Answer: Hypertriglyceridemia.

457
Q

Name one cholesterol absorption inhibitor (1 mark).

A

Answer: Ezetimibe.

458
Q

State one adverse effect of statins (1 mark).

A

Answer: Myopathy.

459
Q

List two drug classes used for angina (2 marks).

A

Answer: Nitrates, beta-blockers.

460
Q

What is the mechanism of action of nitrates (2 marks)?

A

Answer: Release NO, causing vasodilation.

461
Q

Why are long-acting nitrates preferred for chronic angina (2 marks)?

A

Answer: Sustained effect reduces episodes.

462
Q

State two adverse effects of nitrates (2 marks).

A

Answer: Headache, hypotension.

463
Q

What ECG changes indicate ischemia (2 marks)?

A

Answer: ST depression, T wave inversion.

464
Q

Differentiate arterial and venous thrombi (2 marks).

A

Answer: Arterial: Platelet-rich; Venous: RBC-rich.

465
Q

Outline aspirin’s mechanism of action (2 marks).

A

Answer: Irreversibly inhibits thromboxane synthesis in platelets.

466
Q

Name one DOAC and its target (2 marks).

A

Answer: Apixaban, Xa inhibitor.

467
Q

List one advantage of DOACs over warfarin (2 marks).

A

Answer: No routine INR monitoring.

468
Q

What is the most common adverse effect of anticoagulants (2 marks)?

A

Answer: Bleeding.

469
Q
A

Pharmacy - Year 2 (11 decks)

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