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MPharm Year 3 > MP323 - Management of Cardiovascular Conditions > Flashcards

MP323 - Management of Cardiovascular Conditions Flashcards

1
Q

Physiological Risk factors of CVD?

A

Obesity, High blood pressure, diabetes, and blood cholesterol

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2
Q

Behavioural Risk Factors of CVD?

A

Smoking, poor diet, inactivity, alcohol consumption

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3
Q

What is atherosclerosis?

A

Driven by hypertension, hyperlipidemia - this is where fatty tissue lines the vascular smooth muscle, reducing space for blood flow.

Complicated to diabetes, and pro-inflammatory status.

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4
Q

How are statins prescribed?

A

Predominantly prescribed for high cholesterol:HDl ratio’s etc but can also be prescribed for primary prevention for high risk patients such as diabetics.

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5
Q

What is a key step in atherogenesis?

A

Thrombosis - inhibition of platelets is a key strategy for reducing atherosclerotic disease development.

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6
Q

What are anticoagulants?

A

They act similarly to antiplatelets and play a role in reducing blood clots - also useful in reducing risk in atrial fibrillation

Anticoagulants inhibits clotting cascade and thrombus development.

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7
Q

Treatment for CVD

A

Lifestyle modification and pharmacotherapy

  • Primary prevention to reduce lipid and platelet contribution
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8
Q

ADME information on Digoxin?

A

It is a cardiac glycoside, and when orally consumed, 70-80% of an oral dose is absorbed.

Has a half life of 22-45 hours.

Digoxin is extensively distributed in the tissues, as reflected by the large volume of distribution

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9
Q

What is a ligand?

A

A substance (whether it be a drug or an endogenous substance) which binds and activates a receptor

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10
Q

Which molecules absorb UV-Vis radiation?

A

Molecules with double bonds

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11
Q
A
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12
Q

What is the pharmacotherapeutic basis of treating cardiovascular disease?

A

Understanding existing pharmacotherapeutic approaches and treatment guidelines.

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13
Q

What does pharmacodynamics refer to?

A

Effects of drugs on the body.

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14
Q

What does pharmacokinetics refer to?

A

What the body does to a drug.

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15
Q

What are the key components of pharmacokinetics?

A
  • Absorption
  • Distribution
  • Metabolism
  • Elimination
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16
Q

What factors affect drug absorption?

A
  • Molecular weight
  • Ionization
  • Solubility
  • Formulation
  • Route of administration
  • Gastric pH
  • Contents of GI tract
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17
Q

What is meant by ‘volume of distribution’?

A

A measure of the extent to which a drug is distributed in body tissues.

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18
Q

What is the primary route of drug metabolism?

A

Liver.

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19
Q

What are the types of metabolic reactions in drug metabolism?

A
  • Phase I (Cytochrome P450 system)
  • Phase II
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20
Q

What are the primary sites of elimination for drugs?

A
  • Pulmonary (expired air)
  • Bile (excreted in feces)
  • Renal (glomerular filtration, tubular reabsorption, tubular secretion)
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21
Q

What is ‘steady state’ in pharmacokinetics?

A

Condition where drug administration equals drug elimination, resulting in a constant serum drug level.

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22
Q

What is a loading dose?

A

A higher initial dose of a drug to rapidly achieve therapeutic serum levels.

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23
Q

What does efficacy refer to in pharmacodynamics?

A

Degree to which a drug is able to produce the desired response.

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24
Q

What is ‘potency’ in pharmacology?

A

Amount of drug required to produce 50% of the maximal response.

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25
Q

What is the therapeutic index?

A

Measure of the safety of a drug, calculated as LD50/ED50.

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26
Q

What is the definition of an agonist?

A

A ligand that binds and activates a receptor.

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27
Q

What are cell surface receptors?

A

Proteins or glycoproteins present on cell surfaces or within the cell that mediate drug action.

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28
Q

What is the renin-angiotensin-aldosterone axis?

A

A hormone system that regulates blood pressure and fluid balance.

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29
Q

What are ACE inhibitors used for?

A

First-line treatment in hypertension (under 55 and not black/ carribean).

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30
Q

What is the role of diuretics in heart failure management?

A

To increase cardiac efficiency and reduce cardiac oxygen demand.

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31
Q

What is the primary goal of primary prevention in pharmacotherapy for atherosclerosis?

A

To calculate risk and prevent health events.

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32
Q

True or False: All drugs have a single effect.

A

False.

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33
Q

Fill in the blank: The concentration of the drug which induces a specified clinical effect in 50% of subjects is called _______.

A

Effective Concentration 50% (ED50)

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34
Q

Terms to remember related to pharmacokinetics include _______.

A
  • Absorption
  • Distribution
  • Metabolism
  • Elimination
  • Clearance
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35
Q

What does CV disease include?

A

Coronary heart disease, angina, myocardial infarction, heart failure, and stroke

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36
Q

What are the central components in the pathogenesis of CV disease?

A

Atherosclerosis and hypertension

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37
Q

What is the definition of prehypertension?

A

120-139/80-89

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38
Q

What are the blood pressure ranges for Stage I hypertension?

A

140-159/90-99

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39
Q

What are the blood pressure ranges for Stage II hypertension?

A

160-179/100-109

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40
Q

What defines Stage III hypertension?

A

> 180/>110

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41
Q

What is MAP and how is it calculated?

A

Mean systemic arterial pressure, calculated as MAP = CO x TPR

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42
Q

What percentage of hypertension cases is classified as primary?

A

90-95%

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43
Q

What are some causes of secondary hypertension?

A
  • Renal or renovascular disease
  • Endocrine disease
  • Phaeochromocytoma
  • Cushing’s syndrome
  • Conn’s syndrome
  • Acromegaly and hypothyroidism
  • Coarctation of the aorta
  • Iatrogenic factors
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44
Q

What are common causes of secondary hypertension?

A
  • Intrinsic renal disease
  • Renovascular disease
  • Mineralocorticoid excess
  • Sleep breathing disorder
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45
Q

List some risk factors for the development of CVD and hypertension.

A
  • Family history
  • Ethnicity
  • Smoking
  • Diabetes
  • Obesity
  • Hypercholesterolaemia
  • Physical inactivity
  • Stress
  • Infection
  • Microalbuminuria
  • Age (older than 55 for men, 65 for women)
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46
Q

What organs are primarily affected by hypertension?

A
  • CVS (Heart and Blood Vessels)
  • The kidneys
  • Nervous system
  • The eyes
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47
Q

What are the effects of hypertension on the cardiovascular system?

A
  • Ventricular hypertrophy
  • Dysfunction and failure
  • Arrhythmias
  • Coronary artery disease
  • Acute myocardial infarction
  • Arterial aneurysm, dissection, and rupture
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48
Q

What is the major risk factor for ischemic heart disease related to hypertension?

A

Left ventricular hypertrophy

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49
Q

What leads to impaired kidney function due to hypertension?

A

Glomerular sclerosis

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50
Q

What neurological consequences can hypertension cause?

A
  • Stroke
  • Intracerebral and subarachnoid hemorrhage
  • Cerebral atrophy
  • Dementia
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51
Q

What are the components of blood pressure?

A

Cardiac output (CO) and total peripheral vascular resistance (TPvR)

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52
Q

What factors determine cardiac output?

A
  • Heart rate
  • Stroke volume
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53
Q

What is the primary long-term control mechanism for blood pressure?

A

The kidneys controlling blood volume (via RAAS axis)

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54
Q

What is the renin-angiotensin-aldosterone system (RAAS) important for?

A

Blood pressure regulation

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55
Q

What triggers the activation of the RAAS?

A

Reduced blood flow

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56
Q

What does angiotensin II do?

A
  • Causes direct constriction of renal arterioles
  • Stimulates aldosterone synthesis
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57
Q

Fill in the blank: Blood pressure is a _________ killer.

A

silent

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58
Q

True or False: Hypertension is a major driver of cardiovascular disease.

A

True

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59
Q

What is the primary function of baroreceptor reflexes?

A

Regulation of arterial blood pressure

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60
Q

What influences vascular resistance?

A

Sympathetic and parasympathetic activity

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61
Q

What are the short-term effects of the autonomic nervous system on blood pressure?

A

Affects heart and blood vessels

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62
Q

What are the long-term effects of the kidneys on blood pressure?

A
  • Sodium excretion
  • Renal water excretion
  • Water intake
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63
Q

What do enzymes catalyze by lowering?

A

Activation energy

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64
Q

What concept describes how binding at the active site brings specificity?

A

Induced fit

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65
Q

What do competitive inhibitors mimic?

A

Active site

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66
Q

What is EC50 a measure of?

A

Potency

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67
Q

What happens to intermolecular bonds during induced fit?

A

Bonds are strained and not optimum length for maximum bonding

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68
Q

What type of residues act as nucleophiles in catalysis?

A

Serine, Cysteine, Threonine

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69
Q

What stabilizes the transition state in enzymatic reactions?

A

Catalytic triad of serine, histidine, and aspartate

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70
Q

What is the purpose of enzymes?

A

Powerful catalysts that increase the rate of a reaction

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71
Q

What is the nature of the transition state in a reaction?

A

Highly unstable and energetically unfavorable

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72
Q

What do enzymes lower in a reaction?

A

Activation energy

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73
Q

What mechanism does serine use in enzyme catalysis?

A

Nucleophilic attack

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74
Q

What type of site do agonists bind to in enzymes?

A

Orthosteric site

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75
Q

What is the definition of uncompetitive inhibition?

A

Inhibitor and enzyme bind to different sites, but inhibitor only binds to enzyme-substrate complex (ESI)

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76
Q

What is the difference between non-competitive and competitive inhibition?

A

Non-competitive can bind simultaneously; competitive resembles substrate and binds at active site

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77
Q

What does IC50 represent?

A

Concentration of inhibitor that reduces enzyme activity to 50% of uninhibited value

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78
Q

What is Km in enzyme kinetics?

A

Michaelis constant, concentration of S that gives half max enzymatic reaction rate

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79
Q

What does a positive allosteric modulator do?

A

Increases orthosteric activity

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80
Q

What is the role of cofactors in enzyme catalysis?

A

Assist in enzyme function, e.g., Zn2+ or small organic molecules like NAD+

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81
Q

What does the term ‘induced fit’ refer to?

A

Active site alters shape to maximize intermolecular bonding

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82
Q

What is the role of the active site in enzymes?

A

Accepts reactants and catalyzes the reaction

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83
Q

Fill in the blank: The _______ method describes how the enzyme’s active site is nearly the correct shape for the substrate.

A

Induced fit

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84
Q

True or False: Enzymes change the equilibrium of a reaction.

A

False

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85
Q

What is the significance of the dissociation constant (Kd)?

A

It is the ratio of ligand’s off & on binding - equilibrium

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86
Q

What happens during acid/base catalysis in enzymes?

A

Protons are accepted or donated by residues like histidine

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87
Q

What is the effect of a high substrate concentration on a competitive inhibitor?

A

It can compensate for inhibition

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88
Q

What is the role of the catalytic triad in enzyme activity?

A

Facilitates the stabilization of the transition state

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89
Q

What are the three main mechanisms of enzyme catalysis?

A
  • Acid/base catalysis * Nucleophilic attack * Stabilization of transition state
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90
Q

What is the definition of hypertension?

A

A condition where blood pressure is elevated to an extent where clinical benefit is obtained from blood pressure lowering.

Hypertension is a key risk factor for various cardiovascular and other complications.

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91
Q

List three complications associated with hypertension.

A
  • Coronary heart disease
  • Stroke
  • Heart failure

Other complications include renal failure and retinopathy.

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92
Q

What is the impact of blood pressure lowering in hypertension?

A

Reduces mortality and complications.

The absolute benefit depends on the individual’s overall risk.

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93
Q

Which groups have a higher risk of hypertension complications?

A
  • Existing cardiovascular disease (CVD)
  • Elderly
  • Diabetic
  • Smoker
  • Obese
  • Hyperlipidaemia
  • Inactive

These factors significantly increase the overall risk.

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94
Q

How is hypertension typically diagnosed?

A

Usually asymptomatic; often an incidental finding or found through screening.

Blood pressure should be measured in both arms, taking the mean of at least 2 readings.

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95
Q

What blood pressure measurement indicates the need for treatment?

A

BP ≥ 140/90mmHg; treat if high risk.

High risk includes target organ damage, existing CVD, diabetes, or a 10-year CVD risk ≥ 20%.

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96
Q

What is the recommended target blood pressure for most patients?

A

≤140/≤90mmHg.

For diabetic patients with complications or existing CVD, the target is ≤130/≤80mmHg.

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97
Q

What non-pharmacological management strategies can lower blood pressure?

A
  • Weight management
  • Smoking cessation
  • Regular exercise
  • Reduced salt intake
  • Limited alcohol consumption
  • Healthy diet

These lifestyle changes should be offered to all patients with high or borderline high blood pressure.

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98
Q

What are the first-line pharmacological options for hypertension management?

A
  • ACE-I/ARB
  • Beta-blocker
  • Calcium channel blocker
  • Diuretic (thiazide-like/thiazide)

Other options include alpha-blockers, vasodilators, and centrally acting agents.

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99
Q

What does the A(B)/C(D) rule refer to?

A

A guideline for selecting antihypertensive agents based on renin status.

Start with the agent most likely to be effective and progress to logical combinations.

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100
Q

What are the compelling indications for using beta-blockers in hypertension?

A

Use if there is a compelling indication; less effective for routine initial treatment.

They are linked to the development of diabetes and should not be combined with diuretics.

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101
Q

What is the definition of pharmaceutical care?

A

The responsible provision of drug therapy for the purpose of achieving definite outcomes that improve a patient’s quality of life.

This definition is attributed to Hepler & Strand (1990).

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102
Q

What is an essential component of pharmaceutical care?

A

Monitoring and follow-up are essential.

Choosing the drug based on patient need and counseling on concordance/side effects are also important.

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103
Q

What is the recommended daily dose of aspirin for secondary prevention?

A

75mg daily.

For primary prevention, consider for patients aged ≥50 years old with controlled BP and target organ damage.

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104
Q

What is the goal for LDL cholesterol in secondary prevention with statins?

A

Aim for <4mmol/L or LDL <2mmol/L.

Statins should be commenced regardless of cholesterol levels.

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105
Q

List some drugs that can exacerbate hypertension.

A
  • NSAIDs
  • Oestrogens
  • Sympathomimetics
  • Corticosteroids
  • Medicines with high sodium content

Examples include certain antacids and soluble tablets.

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106
Q

True or False: The A(B)/C(D) rule is a strict guideline that must always be followed.

A

False.

It is a guide; compelling indications or contraindications may override it.

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107
Q

What is the focus of health education?

A

Health education focuses on prevention and health protection

It encompasses various aspects including preventive services, health education for preventive health protection, and positive health education.

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108
Q

List the components of preventive health education.

A
  • Preventive services
  • Preventive health education
  • Preventive health protection
  • Health education for preventive health protection
  • Positive health education
  • Positive health protection
  • Health education aimed at positive health protection
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109
Q

What model is referred to as Tannahill’s model?

A

A model that categorizes health promotion into three domains: health education, health protection, and preventive health services

It was developed by Downie et al. in 1990.

110
Q

Who is responsible for risky behavior related to smoking?

A
  • Individuals (choice)
  • Communities (norms regarding smoking)
  • Health policymakers (distribution of resources)
  • Legislators & tax assessors
  • Tobacco company executives
  • Decision-makers in marketing companies
111
Q

True or False: Changing behavior is considered an event.

A

False

Changing one’s behavior is a process, not an event.

112
Q

What are the components of the Health Belief Model?

A
  • Perceived susceptibility
  • Perceived severity
  • Perceived benefits
  • Perceived barriers
  • Cues to action
  • Self-efficacy
113
Q

What does SIMD stand for?

A

Scottish Index of Multiple Deprivation

It is a tool for identifying areas suffering from deprivation.

114
Q

What are the domains and indicators of deprivation in SIMD?

A
  • Employment
  • Income
  • Health
  • Education, Skills, and Training
  • Geographic Access to Services
  • Crime
  • Housing
115
Q

What lifestyle modification is suggested in the Diabetes Prevention Program?

A

Includes 7% weight loss and at least 150 minutes of physical activity per week

This was based on a study involving 3,234 patients with elevated glucose levels.

116
Q

Fill in the blank: The Stages of Change Model emphasizes that changing behavior is a _______.

A

process

117
Q

What is the significance of BMI in cardiovascular disease risk?

A

BMI is calculated as weight in kilograms divided by body surface area in meters squared

It is used to assess risk levels for cardiovascular diseases.

118
Q

What are the recommendations for weight management based on BMI?

A
  • Start weight management and physical activity as appropriate
  • Initiate caloric restriction and increase caloric expenditure if BMI is above goal
119
Q

What is the role of community in health promotion?

A

Communities influence norms regarding health behaviors, such as smoking

They can establish social networks and standards that affect individual choices.

120
Q

What is one of the challenges of inequality in health promotion?

A

Identifying and addressing disparities in health education and access to resources

This includes understanding how social class impacts health behaviors.

121
Q

True or False: Compliance is not an important factor in health promotion.

A

False

Engagement and compliance are crucial for the success of health interventions.

122
Q

What are some treatment options for cardiovascular disease (CVD)?

A
  • Drug therapy
  • Lifestyle modifications
  • Behavioral change
123
Q

What is the definition of atheroma?

A

Atheroma is the accumulation of intracellular and extracellular lipid in the intima of large and medium sized arteries

Atheroma is a key component in the development of atherosclerosis.

124
Q

What does atherosclerosis refer to?

A

The thickening and hardening of arterial walls as a consequence of atheroma in large and medium sized arteries.

125
Q

At what stage of life does atherosclerosis begin to develop?

A

Atherosclerosis can start as early as infancy and childhood.

126
Q

List common sites where atherosclerosis occurs.

A
  • Aorta - especially abdominal
  • Coronary arteries
  • Carotid arteries
  • Cerebral arteries
  • Leg arteries
127
Q

How is atherosclerosis typically detected?

A

Atherosclerosis is typically asymptomatic and is often found after it manifests as a heart attack or stroke.

128
Q

What is the primary cause of the atherosclerotic process?

A

The process is initiated by endothelial dysfunction.

129
Q

What are the main components of an atherosclerotic plaque?

A
  • Lipid containing macrophages
  • Extracellular matrix
  • Proliferating smooth muscle cells
130
Q

What role does LDL play in atherosclerosis?

A

LDL with its high cholesterol content is believed to play an active role in the pathogenesis of the atherosclerotic lesion.

131
Q

Fill in the blank: Cholesterol synthesis in the liver occurs via _______.

A

HMG-CoA reductase

132
Q

What happens when LDL levels exceed receptor availability?

A

The amount of LDL that is removed by scavenger cells is greatly increased.

133
Q

True or False: Oxidized LDL forms when LDL particles react with free radicals.

A

True

134
Q

What are the major cellular events in the progression of atherosclerosis?

A
  • Endothelial permeability
  • Monocyte adhesion and transmigration
  • Macrophage transformation into foam cells
  • Smooth muscle cell migration
135
Q

What is the role of macrophages in atherosclerosis?

A

Macrophages transform into foam cells and accumulate cholesterol, contributing to plaque formation.

136
Q

What are the non-pharmaceutical methods for preventing atheroma?

A
  • No smoking
  • Reduce fat intake
  • Diet high in fruits and vegetables
  • Not too much alcohol
  • Regular exercise/weight control
137
Q

List two secondary prevention treatments for atheroma.

A
  • Antiplatelets
  • Statins
138
Q

What is the mechanism of action of aspirin as an antiplatelet agent?

A

Aspirin blocks production of thromboxane A2 by inhibiting the platelet enzyme cyclooxygenase-1 (COX-1).

139
Q

What class of drugs are statins and what is their primary function?

A

Statins are HMG-CoA reductase inhibitors that reduce plasma LDL.

140
Q

What happens to smooth muscle cells during atherosclerosis?

A

Smooth muscle cells undergo phenotypic modulation, migrate, and deposit extracellular matrix in the lesions.

141
Q

Fill in the blank: The most widely used antiplatelet agent worldwide is _______.

A

aspirin

142
Q

What is the role of thromboxane A2 in platelet function?

A

Thromboxane A2 is a platelet agonist that activates and recruits more platelets to the site of vascular injury.

143
Q

Describe the process of platelet adhesion following blood vessel injury.

A

Endothelial damage results in a loss of antithrombotic functions, allowing platelets to adhere to exposed subendothelial connective tissues.

144
Q

What is the effect of lifestyle changes on atherosclerosis?

A

Lifestyle changes such as diet, exercise, and smoking cessation can reduce the risk of developing atheroma.

145
Q

What leads to smooth muscle phenotypic modulation in atherosclerosis?

A

Endothelial damage, recruitment of macrophage, and lipid accumulation

These factors contribute to the altered behavior of smooth muscle cells in atherosclerotic plaques.

146
Q

What is the result of smooth muscle phenotypic modulation?

A

Changed behavior of smooth muscle and growth of plaque

This modulation affects the stability and progression of atherosclerotic lesions.

147
Q

What do antiplatelet therapies block?

A

ADP receptors or thromboxane A2 receptors

These receptors are involved in platelet aggregation and thrombus formation.

148
Q

What is the effect of statins on cholesterol?

A

Reduce cholesterol production

Statins are commonly used in the management of hyperlipidemia and cardiovascular disease.

149
Q

Fill in the blank: Smooth muscle phenotypic modulation results in _______.

A

[changed behavior of smooth muscle and growth of plaque]

150
Q

What does ‘ischemia’ refer to?

A

An insufficiency in blood supply

Ischemia specifically relates to the coronary arteries being the only source of blood for the heart muscle.

151
Q

What is angina pectoris?

A

A result of ischemia caused by an imbalance between myocardial blood supply and oxygen demand

It is a common presenting symptom among patients with coronary artery disease, often manifested as chest pain.

152
Q

What are the three main types of angina?

A
  • Stable angina
  • Unstable angina
  • Prinzmetal’s angina
153
Q

What characterizes stable angina?

A

Impaired coronary perfusion by fixed or stable atheroma of coronary arteries

154
Q

What is unstable angina?

A

Characterized by rapidly worsening chest pain on minimal exertion or at rest

It is associated with an ulcerated atheroma and thrombus formation.

155
Q

What causes Prinzmetal’s angina?

A

Coronary artery spasm

This spasm temporarily narrows the coronary artery, causing transient impairment of blood supply.

156
Q

What symptoms are associated with exertional angina?

A

Chest pain during exertion or emotion, relieved by rest and nitroglycerine

157
Q

What is anginal equivalent syndrome?

A

Myocardial ischemia causing symptoms like shortness of breath or pain at a site other than the chest

158
Q

What is syndrome X?

A

Typical exertional angina with anatomically normal large coronary arteries

It is also known as microvascular angina due to reduced capacity of vasodilation in microvasculature.

159
Q

What is silent ischemia?

A

Common condition where more episodes of silent than painful ischemia occur

It is difficult to diagnose.

160
Q

What is decubitus angina?

A

Chest pain occurring only while lying down, relieved by standing or sitting

161
Q

What is nocturnal angina?

A

Angina that awakens the patient from sleep, possibly provoked by vivid dreams

162
Q

What causes angina?

A
  • Decrease in myocardial blood supply
  • Increased coronary resistance
  • Coronary spasm
  • Abnormal constriction of resistant vessels
  • Increased extravascular forces
  • Reduction in oxygen-carrying capacity of blood
163
Q

What assessment methods are used for stable angina?

A
  • History grading scale
  • Exercise testing
  • Electrocardiogram
164
Q

What are the classes of the Canadian Cardiovascular Society grading scale for angina severity?

A
  • Class I: Angina only during strenuous activity
  • Class II: Slight limitation during vigorous activity
  • Class III: Moderate limitation with everyday activities
  • Class IV: Severe limitation or angina at rest
165
Q

What is unstable angina characterized by?

A

Angina at rest, not responding readily to therapy, and may indicate an impending heart attack

166
Q

What is the role of exercise testing in stable angina assessment?

A

To induce a controlled, temporary ischemic state during clinical and ECG observation

167
Q

What is the purpose of nitrates in angina treatment?

A

Relax coronary arteries and increase perfusion of the myocardium

Nitrates donate nitric oxide, stimulating cGMP to reduce intracellular calcium levels.

168
Q

What is the mechanism of beta-blockers in treating angina?

A

Decrease the oxygen demands of the myocardium by lowering heart rate and force of contraction

169
Q

What do calcium channel blockers do in angina treatment?

A

Prevent calcium entry into cardiac and smooth muscle cells, protecting tissue during ischemia

170
Q

What is the dual action of nicorandil?

A

Acts as a nitrate and K+ ATP channel agonist

It hyperpolarizes the membrane and decreases calcium entry.

171
Q

What are the surgical treatment options for angina?

A
  • Stenting
  • Angioplasty
  • Bypass surgery
172
Q

What is the goal of angina treatment?

A
  • Feel better
  • Live longer
173
Q

True or False: Unstable angina is associated with a stable atheroma.

A

False

174
Q

Fill in the blank: Angina is diagnosed via ______ and ______.

A

Exercise + ECG

175
Q

What lifestyle changes can help prevent angina?

A
  • No smoking
  • Diet high in fruits and vegetables
  • Moderate alcohol consumption
  • Regular exercise/weight control
176
Q

What is the primary learning outcome regarding stable angina?

A

To update on the current and evidence-based pharmacological management of stable angina

This includes understanding treatment options and their effects.

177
Q

What is the primary learning outcome regarding acute coronary syndrome?

A

To update on the current and evidence-based management of acute coronary syndrome

This involves exploring effective treatment strategies.

178
Q

What is a key distinction about stable angina?

A

Stable angina is not a disease – it is a symptom

It indicates underlying coronary artery disease.

179
Q

What are the first and second choice tests for diagnosing stable angina?

A

1st choice: Exercise Tolerance Test (ETT), 2nd choice: Stress echocardiogram

CT angiogram is also a second choice.

180
Q

What is the first-line medication to reduce cardiac workload in stable angina?

A

Beta-blocker

It is used to prevent or reduce chest pain.

181
Q

What is the role of aspirin in the management of stable angina?

A

To prevent/reduce chest pain and provide long-term benefit

It is part of secondary prevention strategies.

182
Q

What are the side effects of potassium channel activators like Nicorandil?

A

Ulcers, headache, and palpitations

Nicorandil is a 3rd/4th line treatment.

183
Q

What is the purpose of Ivabradine in stable angina management?

A

Lowers heart rate through effect on SA node

It is used if beta-blocker is not tolerated or in combination.

184
Q

What is the significance of the GRACE score?

A

Used for risk calculation in unstable angina and NSTEMI management

Helps determine inpatient vs outpatient care.

185
Q

What does MONA stand for in NSTEMI management?

A

Morphine, Oxygen, Nitrates, Aspirin

It is a mnemonic for initial treatment steps.

186
Q

What is the importance of ‘Time is Muscle’ in STEMI management?

A

Highlights the urgency of re-perfusion therapy

The goal is to restore blood flow quickly to minimize heart damage.

187
Q

What are common clinical features of acute coronary syndrome?

A

Dyspnoea, chest pain, nausea, palpitations, hypotension

These symptoms may vary by patient.

188
Q

What are the indications for eplerenone after acute myocardial infarction?

A

LVSD (EF ≤ 40%) and clinical evidence of heart failure

It requires monitoring of U+Es and BP.

189
Q

What are common side effects of ACE inhibitors?

A

Cough, angioedema, potassium excess, taste changes, orthostatic hypotension

Remember the acronym CAPTOPRIL.

190
Q

Fill in the blank: The treatment of stable angina typically includes _______ as a first-line medication.

A

beta-blocker

191
Q

True or False: Stable angina can be treated with short-acting calcium channel blockers.

A

False

Short-acting calcium channel blockers should be avoided.

192
Q

What lifestyle factors are considered risk factors for coronary heart disease?

A

Smoking, obesity, diet, lack of exercise, alcohol

Modifying these factors is crucial for prevention.

193
Q

What is the recommended duration for aspirin therapy after NSTEMI/STEMI?

A

Lifelong at 75mg OD

This is part of secondary prevention strategies.

194
Q

What is the significance of troponin release in NSTEMI and STEMI?

A

Indicates myocardial injury

Troponin levels help differentiate between unstable angina and myocardial infarction.

195
Q

What is the role of GTN spray in angina management?

A

Used for immediate relief of angina symptoms

It can be used as needed.

196
Q

What are some complications within the first 72 hours of an acute coronary syndrome event?

A

Death, cardiogenic shock, heart failure, ventricular arrhythmia

These complications require immediate attention.

197
Q

What are the goals of secondary prevention in patients with a history of myocardial infarction?

A

Modification of risk factors, lifelong medications like aspirin and statins

It aims to prevent further cardiovascular events.

198
Q

What is the clinical syndrome characterized by symptoms like breathlessness and ankle swelling?

A

Heart Failure

Heart failure is caused by structural and/or functional cardiac abnormalities leading to reduced cardiac output.

199
Q

What is the prevalence of heart failure in the adult population of developed countries?

A

Approximately 1–2%

This prevalence rises to ≥10% among individuals over 70 years of age.

200
Q

List some common aetiological factors for heart failure.

A
  • Myocardial Infarction
  • Hypertension
  • Atrial Fibrillation
  • Alcohol / drugs
  • Valve diseases
  • Viral / thyroid issues
201
Q

What are common clinical symptoms of heart failure?

A
  • Breathlessness
  • Nocturnal symptoms
  • Fatigue
  • Ankle oedema
  • Poor exercise tolerance
202
Q

What is the New York Heart Association (NYHA) classification for heart failure?

A
  • I - Asymptomatic
  • II - Symptoms on exercise
  • III - Symptoms on mild exercise
  • IV - Symptoms at rest
203
Q

True or False: Heart failure is associated with a better prognosis than many cancers.

A

False

Heart failure has a worse prognosis than many cancers.

204
Q

What are the non-pharmacological management strategies for heart failure?

A
  • Education for patients and carers
  • Self-management advice
  • Dietary measures
  • Weight reduction if obese
  • Smoking cessation
  • Exercise
205
Q

What are some therapeutic options for pharmacological management of heart failure?

A
  • ACE-inhibitors / Angiotensin receptor blockers
  • Beta-blockers
  • Aldosterone antagonists
  • Sacubitril/valsartan
  • Dapagliflozin / empagliflozin
  • Diuretics
206
Q

What is the place of diuretics in heart failure therapy?

A

Symptom control

Loop diuretics are usually required and require monitoring of renal function and electrolytes.

207
Q

What is the effect of ACE-inhibitors on heart failure?

A

Improve survival and symptoms, reduce hospitalisation

Indicated for all grades of heart failure unless contraindicated.

208
Q

What are the practical points regarding beta-blockers in heart failure treatment?

A
  • Start low and titrate slow
  • Patient’s heart failure should be stable at initiation
  • Avoid abrupt withdrawal
209
Q

Fill in the blank: Spironolactone reduces morbidity and mortality when added to usual treatment in advanced heart failure patients (NYHA class ______).

A

III-IV

210
Q

What are the indications for Sacubitril/Valsartan in heart failure?

A
  • NYHA II-III (IV)
  • Symptomatic despite optimized therapy
  • Minimum 1 hospitalisation in the past year
  • Ejection fraction < 35%
211
Q

What are the main therapeutic effects of SGLT-2 inhibitors?

A

Reduce mortality and hospitalisation

SGLT-2 inhibitors also have a mechanism that reduces sodium and glucose flow into the blood.

212
Q

True or False: Digoxin is indicated for patients with atrial fibrillation combined with heart failure.

A

True

213
Q

What is the role of vasodilators in heart failure therapy?

A

Improve survival compared to placebo

Only indicated if the patient remains symptomatic or if all other options have been considered.

214
Q

List some drugs that can exacerbate heart failure.

A
  • NSAIDs / COX-2 inhibitors
  • Rate-limiting calcium channel blockers
  • Chemotherapy (e.g., doxorubicin)
  • Cough/cold medicines
  • Anti-psychotic drugs (e.g., clozapine)
215
Q

What are the main responsibilities of pharmacists in heart failure management?

A
  • Chronic management
  • Monitoring contraindicated medication
  • Interactions with OTC drugs
  • Compliance and patient education
216
Q

What is myocardial infarction (MI)?

A

Interruption of blood supply to part of the heart, causing some heart cells to die.

Also known as acute myocardial infarction (AMI) or heart attack.

217
Q

What is the most common underlying condition in patients with MI?

A

Coronary atherosclerosis.

This condition involves the buildup of plaques in the coronary arteries.

218
Q

What is the triggering mechanism for thrombus formation in MI?

A

Plaque rupture.

This occurs at the site of an atherosclerotic lesion.

219
Q

What factors influence the risk of plaque rupture?

A

Plaque type (composition) rather than plaque size (volume).

Soft extracellular lipids make plaques more vulnerable.

220
Q

What are the two main types of myocardial infarction?

A
  • NSTEMI (Non–ST-segment elevation myocardial infarction)
  • STEMI (ST-segment elevation myocardial infarction)
221
Q

How does NSTEMI occur?

A

By developing a complete occlusion of a minor coronary artery or a partial occlusion of a major coronary artery.

This leads to partial thickness damage of the heart muscle.

222
Q

How does STEMI occur?

A

By developing a complete occlusion of a major coronary artery.

This results in full thickness damage of the heart muscle.

223
Q

What is the time frame for irreversible damage to the myocardium after blood flow interruption?

A

Begins as early as 20 to 40 minutes.

Damage can continue to evolve for several hours.

224
Q

What cellular changes may follow an initial MI?

A
  • Infarct extension
  • Infarct expansion
  • Ventricular remodeling
225
Q

What are common symptoms of myocardial infarction?

A
  • Chest pain
  • Nausea
  • Vomiting
  • Sweating
  • Breathing difficulty
226
Q

What is a typical description of chest pain during an MI?

A

Patients often describe it as ‘someone sitting on my chest’.

227
Q

What biochemical markers are indicative of myocardial necrosis?

A
  • Troponin
  • Creatine kinase (CK)
  • Myoglobin
  • Lactate dehydrogenase (LDH)
228
Q

When do troponin I and T levels typically rise after MI?

A
  • Troponin I: rises in about 3 hours, peaks at 14 to 18 hours
  • Troponin T: rises in 3 to 5 hours
229
Q

What is the significance of the CK-MB2 to CK-MB1 ratio in MI?

A

A ratio greater than one indicates myocardial infarction.

230
Q

How quickly can myoglobin levels elevate after an MI?

A

Within 1 to 2 hours.

However, elevated myoglobin is not specific for MI.

231
Q

What does the ECG show during the earliest stage of MI?

A

Tall and narrow T waves, referred to as hyperacute T waves.

232
Q

What changes occur to the T waves within a few hours of myocardial ischemia?

A

The T waves become inverted.

233
Q

What is indicated by the presence of pathologic Q waves on an ECG?

A

Tissue necrosis and provides evidence of a previous myocardial infarction.

234
Q

What is the universal definition of myocardial infarction according to the European Society of Cardiology?

A

Detection of rise and/or fall of troponin associated with at least one of:
* Symptoms of ischemia
* ECG changes indicative of new ischemia
* Evidence of new loss of viable myocardium
* Identification of intra-coronary thrombus

235
Q

What is the time frame in which a substantial amount of myocardial tissue can be salvaged after coronary occlusion?

A

Within 6 hours.

236
Q

True or False: The pain of myocardial infarction is often relieved by rest or sublingual GTN.

A

False.

237
Q

Fill in the blank: The initial downward deflection of the QRS complex is referred to as _______.

A

Q waves.

238
Q

What is the primary cause of myocardial infarction (MI)?

A

Coronary atherosclerosis

Atherosclerosis is the buildup of fats, cholesterol, and other substances in and on the artery walls.

239
Q

What are the three main components relied upon for the diagnosis of myocardial infarction?

A

Symptoms, biochemical markers, electrocardiographic findings

These components help in identifying the occurrence and severity of an MI.

240
Q

How long does it typically take for Q waves to develop after a myocardial infarction?

A

Hours to days

Q waves indicate the presence of dead tissue and provide ECG evidence of a previous MI.

241
Q

What is the time frame in which substantial myocardial tissue can be salvaged during an MI?

A

Within 6 hours

Quick intervention can prevent further damage to heart tissue.

242
Q

What symptoms are commonly associated with myocardial infarction?

A

Often more prolonged and not relieved by rest or sublingual GTN

Symptoms may include chest pain, discomfort, and other signs of heart distress.

243
Q

Which biochemical markers are used in the diagnosis of myocardial infarction?

A

Troponin I/T, CK-MB, Myoglobin, LDH-1

These markers are proteins released when the heart muscle is damaged.

244
Q

What are the key ECG findings in a myocardial infarction?

A

Peaked/inverted T wave, ST elevation, pathologic Q wave

These changes indicate different phases and types of myocardial infarction.

245
Q

Fill in the blank: Tissue necrosis in myocardial infarction starts in _______.

A

20-40 mins

This rapid onset emphasizes the urgency of treatment in MI cases.

246
Q

What are the two types of myocardial infarction classified under MI?

A

NSTEMI, STEMI

NSTEMI refers to non-ST elevation myocardial infarction, while STEMI refers to ST elevation myocardial infarction.

247
Q

True or False: The presence of pathologic Q waves is a temporary finding in ECG after an MI.

A

False

Pathologic Q waves are considered permanent indicators of previous myocardial infarction.

248
Q

What is heart failure?

A

Characterized by impaired cardiac pumping such that the heart is unable to pump adequate amount of blood to meet metabolic needs.

249
Q

What are the two types of heart failure?

A
  • Systolic Heart Failure
  • Diastolic Heart Failure
250
Q

What are common signs and symptoms of heart failure?

A
  • Shortness of breath
  • Excessive tiredness
  • Leg swelling
251
Q

What is the prevalence of heart failure in individuals aged 75-84 years?

A

7%

252
Q

What percentage of hospital bed-days does heart failure account for?

A

2%

253
Q

What is the median survival for males and females with heart failure?

A
  • 1.7 years for males
  • 3.2 years for females
254
Q

What are the underlying causes of heart failure?

A
  • Ischemic heart disease (CAD)
  • Hypertension
  • Myocardial infarction (MI)
  • Valvular heart disease
  • Congenital heart disease
  • Dilated cardiomyopathy
255
Q

What is preload?

A

The amount of fiber stretch in the ventricles at the end of diastole.

256
Q

What factors increase preload?

A
  • Increase in blood volume
  • Vasoconstriction
257
Q

What is Starling’s Law?

A

Describes the relationship between preload and cardiac output; greater fiber stretch leads to a greater force of contraction, but only up to a point.

258
Q

What is afterload?

A

The resistance against which the ventricle must pump.

259
Q

What factors increase afterload?

A
  • Hypertension
  • Vasoconstriction
260
Q

What is contractility?

A

The ability of the heart muscle to contract.

261
Q

What can decrease contractility?

A
  • Infarcted tissue
  • Ischemic tissue
262
Q

What compensatory mechanisms occur in heart failure?

A
  • Sympathetic nerve stimulation
  • Myocardial hypertrophy
  • Hormonal response
263
Q

What is the role of the renin-angiotensin-aldosterone system (RAAS) in heart failure?

A

It is central to altering the disease in patients with reduced ejection fraction.

264
Q

What are common drug classes used in the pharmacology of heart failure treatment?

A
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • Beta-adrenergic blockers
  • Aldosterone antagonists
  • Diuretics
  • Vasodilators
  • Neprilysin antagonists
265
Q

What do ACE inhibitors do?

A

Block the conversion of angiotensin I to angiotensin II, relax blood vessels, and decrease cardiac output.

266
Q

What is the effect of beta-blockers in heart failure?

A

Reduce excessive sympathetic stimulation, decrease heart rate, and decrease force of contraction.

267
Q

What do loop diuretics do?

A

Inhibit the reabsorption of sodium, chloride, and potassium, decreasing intravascular volume.

268
Q

What is the function of neprilysin inhibitors?

A

Prevent the breakdown of natriuretic peptides, maintaining their ability to decrease intravascular volume and increase vasodilation.

269
Q

True or False: Compensatory mechanisms always improve heart failure.

A

False

270
Q

Fill in the blank: The average GP will suspect a new diagnosis of HF in _____ people annually.

A

10

MPharm Year 3 (3 decks)

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