MP323 - Management of Cardiovascular Conditions Flashcards
(270 cards)
1
Q
Physiological Risk factors of CVD?
A
Obesity, High blood pressure, diabetes, and blood cholesterol
2
Q
Behavioural Risk Factors of CVD?
A
Smoking, poor diet, inactivity, alcohol consumption
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.
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.
5
Q
What is a key step in atherogenesis?
A
Thrombosis - inhibition of platelets is a key strategy for reducing atherosclerotic disease development.
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.
7
Q
Treatment for CVD
A
Lifestyle modification and pharmacotherapy
- Primary prevention to reduce lipid and platelet contribution
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
9
Q
What is a ligand?
A
A substance (whether it be a drug or an endogenous substance) which binds and activates a receptor
10
Q
Which molecules absorb UV-Vis radiation?
A
Molecules with double bonds
11
Q
A
12
Q
What is the pharmacotherapeutic basis of treating cardiovascular disease?
A
Understanding existing pharmacotherapeutic approaches and treatment guidelines.
13
Q
What does pharmacodynamics refer to?
A
Effects of drugs on the body.
14
Q
What does pharmacokinetics refer to?
A
What the body does to a drug.
15
Q
What are the key components of pharmacokinetics?
A
- Absorption
- Distribution
- Metabolism
- Elimination
16
Q
What factors affect drug absorption?
A
- Molecular weight
- Ionization
- Solubility
- Formulation
- Route of administration
- Gastric pH
- Contents of GI tract
17
Q
What is meant by ‘volume of distribution’?
A
A measure of the extent to which a drug is distributed in body tissues.
18
Q
What is the primary route of drug metabolism?
A
Liver.
19
Q
What are the types of metabolic reactions in drug metabolism?
A
- Phase I (Cytochrome P450 system)
- Phase II
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)
21
Q
What is ‘steady state’ in pharmacokinetics?
A
Condition where drug administration equals drug elimination, resulting in a constant serum drug level.
22
Q
What is a loading dose?
A
A higher initial dose of a drug to rapidly achieve therapeutic serum levels.
23
Q
What does efficacy refer to in pharmacodynamics?
A
Degree to which a drug is able to produce the desired response.
24
Q
What is ‘potency’ in pharmacology?
A
Amount of drug required to produce 50% of the maximal response.
25
What is the therapeutic index?
Measure of the safety of a drug, calculated as LD50/ED50.
26
What is the definition of an agonist?
A ligand that binds and activates a receptor.
27
What are cell surface receptors?
Proteins or glycoproteins present on cell surfaces or within the cell that mediate drug action.
28
What is the renin-angiotensin-aldosterone axis?
A hormone system that regulates blood pressure and fluid balance.
29
What are ACE inhibitors used for?
First-line treatment in hypertension (under 55 and not black/ carribean).
30
What is the role of diuretics in heart failure management?
To increase cardiac efficiency and reduce cardiac oxygen demand.
31
What is the primary goal of primary prevention in pharmacotherapy for atherosclerosis?
To calculate risk and prevent health events.
32
True or False: All drugs have a single effect.
False.
33
Fill in the blank: The concentration of the drug which induces a specified clinical effect in 50% of subjects is called _______.
Effective Concentration 50% (ED50)
34
Terms to remember related to pharmacokinetics include _______.
* Absorption
* Distribution
* Metabolism
* Elimination
* Clearance
35
What does CV disease include?
Coronary heart disease, angina, myocardial infarction, heart failure, and stroke
36
What are the central components in the pathogenesis of CV disease?
Atherosclerosis and hypertension
37
What is the definition of prehypertension?
120-139/80-89
38
What are the blood pressure ranges for Stage I hypertension?
140-159/90-99
39
What are the blood pressure ranges for Stage II hypertension?
160-179/100-109
40
What defines Stage III hypertension?
>180/>110
41
What is MAP and how is it calculated?
Mean systemic arterial pressure, calculated as MAP = CO x TPR
42
What percentage of hypertension cases is classified as primary?
90-95%
43
What are some causes of secondary hypertension?
* Renal or renovascular disease
* Endocrine disease
* Phaeochromocytoma
* Cushing's syndrome
* Conn's syndrome
* Acromegaly and hypothyroidism
* Coarctation of the aorta
* Iatrogenic factors
44
What are common causes of secondary hypertension?
* Intrinsic renal disease
* Renovascular disease
* Mineralocorticoid excess
* Sleep breathing disorder
45
List some risk factors for the development of CVD and hypertension.
* Family history
* Ethnicity
* Smoking
* Diabetes
* Obesity
* Hypercholesterolaemia
* Physical inactivity
* Stress
* Infection
* Microalbuminuria
* Age (older than 55 for men, 65 for women)
46
What organs are primarily affected by hypertension?
* CVS (Heart and Blood Vessels)
* The kidneys
* Nervous system
* The eyes
47
What are the effects of hypertension on the cardiovascular system?
* Ventricular hypertrophy
* Dysfunction and failure
* Arrhythmias
* Coronary artery disease
* Acute myocardial infarction
* Arterial aneurysm, dissection, and rupture
48
What is the major risk factor for ischemic heart disease related to hypertension?
Left ventricular hypertrophy
49
What leads to impaired kidney function due to hypertension?
Glomerular sclerosis
50
What neurological consequences can hypertension cause?
* Stroke
* Intracerebral and subarachnoid hemorrhage
* Cerebral atrophy
* Dementia
51
What are the components of blood pressure?
Cardiac output (CO) and total peripheral vascular resistance (TPvR)
52
What factors determine cardiac output?
* Heart rate
* Stroke volume
53
What is the primary long-term control mechanism for blood pressure?
The kidneys controlling blood volume (via RAAS axis)
54
What is the renin-angiotensin-aldosterone system (RAAS) important for?
Blood pressure regulation
55
What triggers the activation of the RAAS?
Reduced blood flow
56
What does angiotensin II do?
* Causes direct constriction of renal arterioles
* Stimulates aldosterone synthesis
57
Fill in the blank: Blood pressure is a _________ killer.
silent
58
True or False: Hypertension is a major driver of cardiovascular disease.
True
59
What is the primary function of baroreceptor reflexes?
Regulation of arterial blood pressure
60
What influences vascular resistance?
Sympathetic and parasympathetic activity
61
What are the short-term effects of the autonomic nervous system on blood pressure?
Affects heart and blood vessels
62
What are the long-term effects of the kidneys on blood pressure?
* Sodium excretion
* Renal water excretion
* Water intake
63
What do enzymes catalyze by lowering?
Activation energy
64
What concept describes how binding at the active site brings specificity?
Induced fit
65
What do competitive inhibitors mimic?
Active site
66
What is EC50 a measure of?
Potency
67
What happens to intermolecular bonds during induced fit?
Bonds are strained and not optimum length for maximum bonding
68
What type of residues act as nucleophiles in catalysis?
Serine, Cysteine, Threonine
69
What stabilizes the transition state in enzymatic reactions?
Catalytic triad of serine, histidine, and aspartate
70
What is the purpose of enzymes?
Powerful catalysts that increase the rate of a reaction
71
What is the nature of the transition state in a reaction?
Highly unstable and energetically unfavorable
72
What do enzymes lower in a reaction?
Activation energy
73
What mechanism does serine use in enzyme catalysis?
Nucleophilic attack
74
What type of site do agonists bind to in enzymes?
Orthosteric site
75
What is the definition of uncompetitive inhibition?
Inhibitor and enzyme bind to different sites, but inhibitor only binds to enzyme-substrate complex (ESI)
76
What is the difference between non-competitive and competitive inhibition?
Non-competitive can bind simultaneously; competitive resembles substrate and binds at active site
77
What does IC50 represent?
Concentration of inhibitor that reduces enzyme activity to 50% of uninhibited value
78
What is Km in enzyme kinetics?
Michaelis constant, concentration of S that gives half max enzymatic reaction rate
79
What does a positive allosteric modulator do?
Increases orthosteric activity
80
What is the role of cofactors in enzyme catalysis?
Assist in enzyme function, e.g., Zn2+ or small organic molecules like NAD+
81
What does the term 'induced fit' refer to?
Active site alters shape to maximize intermolecular bonding
82
What is the role of the active site in enzymes?
Accepts reactants and catalyzes the reaction
83
Fill in the blank: The _______ method describes how the enzyme's active site is nearly the correct shape for the substrate.
Induced fit
84
True or False: Enzymes change the equilibrium of a reaction.
False
85
What is the significance of the dissociation constant (Kd)?
It is the ratio of ligand's off & on binding - equilibrium
86
What happens during acid/base catalysis in enzymes?
Protons are accepted or donated by residues like histidine
87
What is the effect of a high substrate concentration on a competitive inhibitor?
It can compensate for inhibition
88
What is the role of the catalytic triad in enzyme activity?
Facilitates the stabilization of the transition state
89
What are the three main mechanisms of enzyme catalysis?
* Acid/base catalysis * Nucleophilic attack * Stabilization of transition state
90
What is the definition of hypertension?
A condition where blood pressure is elevated to an extent where clinical benefit is obtained from blood pressure lowering.
## Footnote
Hypertension is a key risk factor for various cardiovascular and other complications.
91
List three complications associated with hypertension.
* Coronary heart disease
* Stroke
* Heart failure
## Footnote
Other complications include renal failure and retinopathy.
92
What is the impact of blood pressure lowering in hypertension?
Reduces mortality and complications.
## Footnote
The absolute benefit depends on the individual’s overall risk.
93
Which groups have a higher risk of hypertension complications?
* Existing cardiovascular disease (CVD)
* Elderly
* Diabetic
* Smoker
* Obese
* Hyperlipidaemia
* Inactive
## Footnote
These factors significantly increase the overall risk.
94
How is hypertension typically diagnosed?
Usually asymptomatic; often an incidental finding or found through screening.
## Footnote
Blood pressure should be measured in both arms, taking the mean of at least 2 readings.
95
What blood pressure measurement indicates the need for treatment?
BP ≥ 140/90mmHg; treat if high risk.
## Footnote
High risk includes target organ damage, existing CVD, diabetes, or a 10-year CVD risk ≥ 20%.
96
What is the recommended target blood pressure for most patients?
≤140/≤90mmHg.
## Footnote
For diabetic patients with complications or existing CVD, the target is ≤130/≤80mmHg.
97
What non-pharmacological management strategies can lower blood pressure?
* Weight management
* Smoking cessation
* Regular exercise
* Reduced salt intake
* Limited alcohol consumption
* Healthy diet
## Footnote
These lifestyle changes should be offered to all patients with high or borderline high blood pressure.
98
What are the first-line pharmacological options for hypertension management?
* ACE-I/ARB
* Beta-blocker
* Calcium channel blocker
* Diuretic (thiazide-like/thiazide)
## Footnote
Other options include alpha-blockers, vasodilators, and centrally acting agents.
99
What does the A(B)/C(D) rule refer to?
A guideline for selecting antihypertensive agents based on renin status.
## Footnote
Start with the agent most likely to be effective and progress to logical combinations.
100
What are the compelling indications for using beta-blockers in hypertension?
Use if there is a compelling indication; less effective for routine initial treatment.
## Footnote
They are linked to the development of diabetes and should not be combined with diuretics.
101
What is the definition of pharmaceutical care?
The responsible provision of drug therapy for the purpose of achieving definite outcomes that improve a patient's quality of life.
## Footnote
This definition is attributed to Hepler & Strand (1990).
102
What is an essential component of pharmaceutical care?
Monitoring and follow-up are essential.
## Footnote
Choosing the drug based on patient need and counseling on concordance/side effects are also important.
103
What is the recommended daily dose of aspirin for secondary prevention?
75mg daily.
## Footnote
For primary prevention, consider for patients aged ≥50 years old with controlled BP and target organ damage.
104
What is the goal for LDL cholesterol in secondary prevention with statins?
Aim for <4mmol/L or LDL <2mmol/L.
## Footnote
Statins should be commenced regardless of cholesterol levels.
105
List some drugs that can exacerbate hypertension.
* NSAIDs
* Oestrogens
* Sympathomimetics
* Corticosteroids
* Medicines with high sodium content
## Footnote
Examples include certain antacids and soluble tablets.
106
True or False: The A(B)/C(D) rule is a strict guideline that must always be followed.
False.
## Footnote
It is a guide; compelling indications or contraindications may override it.
107
What is the focus of health education?
Health education focuses on prevention and health protection
## Footnote
It encompasses various aspects including preventive services, health education for preventive health protection, and positive health education.
108
List the components of preventive health education.
* 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
109
What model is referred to as Tannahill's model?
A model that categorizes health promotion into three domains: health education, health protection, and preventive health services
## Footnote
It was developed by Downie et al. in 1990.
110
Who is responsible for risky behavior related to smoking?
* Individuals (choice)
* Communities (norms regarding smoking)
* Health policymakers (distribution of resources)
* Legislators & tax assessors
* Tobacco company executives
* Decision-makers in marketing companies
111
True or False: Changing behavior is considered an event.
False
## Footnote
Changing one's behavior is a process, not an event.
112
What are the components of the Health Belief Model?
* Perceived susceptibility
* Perceived severity
* Perceived benefits
* Perceived barriers
* Cues to action
* Self-efficacy
113
What does SIMD stand for?
Scottish Index of Multiple Deprivation
## Footnote
It is a tool for identifying areas suffering from deprivation.
114
What are the domains and indicators of deprivation in SIMD?
* Employment
* Income
* Health
* Education, Skills, and Training
* Geographic Access to Services
* Crime
* Housing
115
What lifestyle modification is suggested in the Diabetes Prevention Program?
Includes 7% weight loss and at least 150 minutes of physical activity per week
## Footnote
This was based on a study involving 3,234 patients with elevated glucose levels.
116
Fill in the blank: The Stages of Change Model emphasizes that changing behavior is a _______.
process
117
What is the significance of BMI in cardiovascular disease risk?
BMI is calculated as weight in kilograms divided by body surface area in meters squared
## Footnote
It is used to assess risk levels for cardiovascular diseases.
118
What are the recommendations for weight management based on BMI?
* Start weight management and physical activity as appropriate
* Initiate caloric restriction and increase caloric expenditure if BMI is above goal
119
What is the role of community in health promotion?
Communities influence norms regarding health behaviors, such as smoking
## Footnote
They can establish social networks and standards that affect individual choices.
120
What is one of the challenges of inequality in health promotion?
Identifying and addressing disparities in health education and access to resources
## Footnote
This includes understanding how social class impacts health behaviors.
121
True or False: Compliance is not an important factor in health promotion.
False
## Footnote
Engagement and compliance are crucial for the success of health interventions.
122
What are some treatment options for cardiovascular disease (CVD)?
* Drug therapy
* Lifestyle modifications
* Behavioral change
123
What is the definition of atheroma?
Atheroma is the accumulation of intracellular and extracellular lipid in the intima of large and medium sized arteries
## Footnote
Atheroma is a key component in the development of atherosclerosis.
124
What does atherosclerosis refer to?
The thickening and hardening of arterial walls as a consequence of atheroma in large and medium sized arteries.
125
At what stage of life does atherosclerosis begin to develop?
Atherosclerosis can start as early as infancy and childhood.
126
List common sites where atherosclerosis occurs.
* Aorta - especially abdominal
* Coronary arteries
* Carotid arteries
* Cerebral arteries
* Leg arteries
127
How is atherosclerosis typically detected?
Atherosclerosis is typically asymptomatic and is often found after it manifests as a heart attack or stroke.
128
What is the primary cause of the atherosclerotic process?
The process is initiated by endothelial dysfunction.
129
What are the main components of an atherosclerotic plaque?
* Lipid containing macrophages
* Extracellular matrix
* Proliferating smooth muscle cells
130
What role does LDL play in atherosclerosis?
LDL with its high cholesterol content is believed to play an active role in the pathogenesis of the atherosclerotic lesion.
131
Fill in the blank: Cholesterol synthesis in the liver occurs via _______.
HMG-CoA reductase
132
What happens when LDL levels exceed receptor availability?
The amount of LDL that is removed by scavenger cells is greatly increased.
133
True or False: Oxidized LDL forms when LDL particles react with free radicals.
True
134
What are the major cellular events in the progression of atherosclerosis?
* Endothelial permeability
* Monocyte adhesion and transmigration
* Macrophage transformation into foam cells
* Smooth muscle cell migration
135
What is the role of macrophages in atherosclerosis?
Macrophages transform into foam cells and accumulate cholesterol, contributing to plaque formation.
136
What are the non-pharmaceutical methods for preventing atheroma?
* No smoking
* Reduce fat intake
* Diet high in fruits and vegetables
* Not too much alcohol
* Regular exercise/weight control
137
List two secondary prevention treatments for atheroma.
* Antiplatelets
* Statins
138
What is the mechanism of action of aspirin as an antiplatelet agent?
Aspirin blocks production of thromboxane A2 by inhibiting the platelet enzyme cyclooxygenase-1 (COX-1).
139
What class of drugs are statins and what is their primary function?
Statins are HMG-CoA reductase inhibitors that reduce plasma LDL.
140
What happens to smooth muscle cells during atherosclerosis?
Smooth muscle cells undergo phenotypic modulation, migrate, and deposit extracellular matrix in the lesions.
141
Fill in the blank: The most widely used antiplatelet agent worldwide is _______.
aspirin
142
What is the role of thromboxane A2 in platelet function?
Thromboxane A2 is a platelet agonist that activates and recruits more platelets to the site of vascular injury.
143
Describe the process of platelet adhesion following blood vessel injury.
Endothelial damage results in a loss of antithrombotic functions, allowing platelets to adhere to exposed subendothelial connective tissues.
144
What is the effect of lifestyle changes on atherosclerosis?
Lifestyle changes such as diet, exercise, and smoking cessation can reduce the risk of developing atheroma.
145
What leads to smooth muscle phenotypic modulation in atherosclerosis?
Endothelial damage, recruitment of macrophage, and lipid accumulation
## Footnote
These factors contribute to the altered behavior of smooth muscle cells in atherosclerotic plaques.
146
What is the result of smooth muscle phenotypic modulation?
Changed behavior of smooth muscle and growth of plaque
## Footnote
This modulation affects the stability and progression of atherosclerotic lesions.
147
What do antiplatelet therapies block?
ADP receptors or thromboxane A2 receptors
## Footnote
These receptors are involved in platelet aggregation and thrombus formation.
148
What is the effect of statins on cholesterol?
Reduce cholesterol production
## Footnote
Statins are commonly used in the management of hyperlipidemia and cardiovascular disease.
149
Fill in the blank: Smooth muscle phenotypic modulation results in _______.
[changed behavior of smooth muscle and growth of plaque]
150
What does 'ischemia' refer to?
An insufficiency in blood supply
## Footnote
Ischemia specifically relates to the coronary arteries being the only source of blood for the heart muscle.
151
What is angina pectoris?
A result of ischemia caused by an imbalance between myocardial blood supply and oxygen demand
## Footnote
It is a common presenting symptom among patients with coronary artery disease, often manifested as chest pain.
152
What are the three main types of angina?
* Stable angina
* Unstable angina
* Prinzmetal’s angina
153
What characterizes stable angina?
Impaired coronary perfusion by fixed or stable atheroma of coronary arteries
154
What is unstable angina?
Characterized by rapidly worsening chest pain on minimal exertion or at rest
## Footnote
It is associated with an ulcerated atheroma and thrombus formation.
155
What causes Prinzmetal’s angina?
Coronary artery spasm
## Footnote
This spasm temporarily narrows the coronary artery, causing transient impairment of blood supply.
156
What symptoms are associated with exertional angina?
Chest pain during exertion or emotion, relieved by rest and nitroglycerine
157
What is anginal equivalent syndrome?
Myocardial ischemia causing symptoms like shortness of breath or pain at a site other than the chest
158
What is syndrome X?
Typical exertional angina with anatomically normal large coronary arteries
## Footnote
It is also known as microvascular angina due to reduced capacity of vasodilation in microvasculature.
159
What is silent ischemia?
Common condition where more episodes of silent than painful ischemia occur
## Footnote
It is difficult to diagnose.
160
What is decubitus angina?
Chest pain occurring only while lying down, relieved by standing or sitting
161
What is nocturnal angina?
Angina that awakens the patient from sleep, possibly provoked by vivid dreams
162
What causes angina?
* 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
What assessment methods are used for stable angina?
* History grading scale
* Exercise testing
* Electrocardiogram
164
What are the classes of the Canadian Cardiovascular Society grading scale for angina severity?
* 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
What is unstable angina characterized by?
Angina at rest, not responding readily to therapy, and may indicate an impending heart attack
166
What is the role of exercise testing in stable angina assessment?
To induce a controlled, temporary ischemic state during clinical and ECG observation
167
What is the purpose of nitrates in angina treatment?
Relax coronary arteries and increase perfusion of the myocardium
## Footnote
Nitrates donate nitric oxide, stimulating cGMP to reduce intracellular calcium levels.
168
What is the mechanism of beta-blockers in treating angina?
Decrease the oxygen demands of the myocardium by lowering heart rate and force of contraction
169
What do calcium channel blockers do in angina treatment?
Prevent calcium entry into cardiac and smooth muscle cells, protecting tissue during ischemia
170
What is the dual action of nicorandil?
Acts as a nitrate and K+ ATP channel agonist
## Footnote
It hyperpolarizes the membrane and decreases calcium entry.
171
What are the surgical treatment options for angina?
* Stenting
* Angioplasty
* Bypass surgery
172
What is the goal of angina treatment?
* Feel better
* Live longer
173
True or False: Unstable angina is associated with a stable atheroma.
False
174
Fill in the blank: Angina is diagnosed via ______ and ______.
Exercise + ECG
175
What lifestyle changes can help prevent angina?
* No smoking
* Diet high in fruits and vegetables
* Moderate alcohol consumption
* Regular exercise/weight control
176
What is the primary learning outcome regarding stable angina?
To update on the current and evidence-based pharmacological management of stable angina
## Footnote
This includes understanding treatment options and their effects.
177
What is the primary learning outcome regarding acute coronary syndrome?
To update on the current and evidence-based management of acute coronary syndrome
## Footnote
This involves exploring effective treatment strategies.
178
What is a key distinction about stable angina?
Stable angina is not a disease – it is a symptom
## Footnote
It indicates underlying coronary artery disease.
179
What are the first and second choice tests for diagnosing stable angina?
1st choice: Exercise Tolerance Test (ETT), 2nd choice: Stress echocardiogram
## Footnote
CT angiogram is also a second choice.
180
What is the first-line medication to reduce cardiac workload in stable angina?
Beta-blocker
## Footnote
It is used to prevent or reduce chest pain.
181
What is the role of aspirin in the management of stable angina?
To prevent/reduce chest pain and provide long-term benefit
## Footnote
It is part of secondary prevention strategies.
182
What are the side effects of potassium channel activators like Nicorandil?
Ulcers, headache, and palpitations
## Footnote
Nicorandil is a 3rd/4th line treatment.
183
What is the purpose of Ivabradine in stable angina management?
Lowers heart rate through effect on SA node
## Footnote
It is used if beta-blocker is not tolerated or in combination.
184
What is the significance of the GRACE score?
Used for risk calculation in unstable angina and NSTEMI management
## Footnote
Helps determine inpatient vs outpatient care.
185
What does MONA stand for in NSTEMI management?
Morphine, Oxygen, Nitrates, Aspirin
## Footnote
It is a mnemonic for initial treatment steps.
186
What is the importance of 'Time is Muscle' in STEMI management?
Highlights the urgency of re-perfusion therapy
## Footnote
The goal is to restore blood flow quickly to minimize heart damage.
187
What are common clinical features of acute coronary syndrome?
Dyspnoea, chest pain, nausea, palpitations, hypotension
## Footnote
These symptoms may vary by patient.
188
What are the indications for eplerenone after acute myocardial infarction?
LVSD (EF ≤ 40%) and clinical evidence of heart failure
## Footnote
It requires monitoring of U+Es and BP.
189
What are common side effects of ACE inhibitors?
Cough, angioedema, potassium excess, taste changes, orthostatic hypotension
## Footnote
Remember the acronym CAPTOPRIL.
190
Fill in the blank: The treatment of stable angina typically includes _______ as a first-line medication.
beta-blocker
191
True or False: Stable angina can be treated with short-acting calcium channel blockers.
False
## Footnote
Short-acting calcium channel blockers should be avoided.
192
What lifestyle factors are considered risk factors for coronary heart disease?
Smoking, obesity, diet, lack of exercise, alcohol
## Footnote
Modifying these factors is crucial for prevention.
193
What is the recommended duration for aspirin therapy after NSTEMI/STEMI?
Lifelong at 75mg OD
## Footnote
This is part of secondary prevention strategies.
194
What is the significance of troponin release in NSTEMI and STEMI?
Indicates myocardial injury
## Footnote
Troponin levels help differentiate between unstable angina and myocardial infarction.
195
What is the role of GTN spray in angina management?
Used for immediate relief of angina symptoms
## Footnote
It can be used as needed.
196
What are some complications within the first 72 hours of an acute coronary syndrome event?
Death, cardiogenic shock, heart failure, ventricular arrhythmia
## Footnote
These complications require immediate attention.
197
What are the goals of secondary prevention in patients with a history of myocardial infarction?
Modification of risk factors, lifelong medications like aspirin and statins
## Footnote
It aims to prevent further cardiovascular events.
198
What is the clinical syndrome characterized by symptoms like breathlessness and ankle swelling?
Heart Failure
## Footnote
Heart failure is caused by structural and/or functional cardiac abnormalities leading to reduced cardiac output.
199
What is the prevalence of heart failure in the adult population of developed countries?
Approximately 1–2%
## Footnote
This prevalence rises to ≥10% among individuals over 70 years of age.
200
List some common aetiological factors for heart failure.
* Myocardial Infarction
* Hypertension
* Atrial Fibrillation
* Alcohol / drugs
* Valve diseases
* Viral / thyroid issues
201
What are common clinical symptoms of heart failure?
* Breathlessness
* Nocturnal symptoms
* Fatigue
* Ankle oedema
* Poor exercise tolerance
202
What is the New York Heart Association (NYHA) classification for heart failure?
* I - Asymptomatic
* II - Symptoms on exercise
* III - Symptoms on mild exercise
* IV - Symptoms at rest
203
True or False: Heart failure is associated with a better prognosis than many cancers.
False
## Footnote
Heart failure has a worse prognosis than many cancers.
204
What are the non-pharmacological management strategies for heart failure?
* Education for patients and carers
* Self-management advice
* Dietary measures
* Weight reduction if obese
* Smoking cessation
* Exercise
205
What are some therapeutic options for pharmacological management of heart failure?
* ACE-inhibitors / Angiotensin receptor blockers
* Beta-blockers
* Aldosterone antagonists
* Sacubitril/valsartan
* Dapagliflozin / empagliflozin
* Diuretics
206
What is the place of diuretics in heart failure therapy?
Symptom control
## Footnote
Loop diuretics are usually required and require monitoring of renal function and electrolytes.
207
What is the effect of ACE-inhibitors on heart failure?
Improve survival and symptoms, reduce hospitalisation
## Footnote
Indicated for all grades of heart failure unless contraindicated.
208
What are the practical points regarding beta-blockers in heart failure treatment?
* Start low and titrate slow
* Patient’s heart failure should be stable at initiation
* Avoid abrupt withdrawal
209
Fill in the blank: Spironolactone reduces morbidity and mortality when added to usual treatment in advanced heart failure patients (NYHA class ______).
III-IV
210
What are the indications for Sacubitril/Valsartan in heart failure?
* NYHA II-III (IV)
* Symptomatic despite optimized therapy
* Minimum 1 hospitalisation in the past year
* Ejection fraction < 35%
211
What are the main therapeutic effects of SGLT-2 inhibitors?
Reduce mortality and hospitalisation
## Footnote
SGLT-2 inhibitors also have a mechanism that reduces sodium and glucose flow into the blood.
212
True or False: Digoxin is indicated for patients with atrial fibrillation combined with heart failure.
True
213
What is the role of vasodilators in heart failure therapy?
Improve survival compared to placebo
## Footnote
Only indicated if the patient remains symptomatic or if all other options have been considered.
214
List some drugs that can exacerbate heart failure.
* NSAIDs / COX-2 inhibitors
* Rate-limiting calcium channel blockers
* Chemotherapy (e.g., doxorubicin)
* Cough/cold medicines
* Anti-psychotic drugs (e.g., clozapine)
215
What are the main responsibilities of pharmacists in heart failure management?
* Chronic management
* Monitoring contraindicated medication
* Interactions with OTC drugs
* Compliance and patient education
216
What is myocardial infarction (MI)?
Interruption of blood supply to part of the heart, causing some heart cells to die.
## Footnote
Also known as acute myocardial infarction (AMI) or heart attack.
217
What is the most common underlying condition in patients with MI?
Coronary atherosclerosis.
## Footnote
This condition involves the buildup of plaques in the coronary arteries.
218
What is the triggering mechanism for thrombus formation in MI?
Plaque rupture.
## Footnote
This occurs at the site of an atherosclerotic lesion.
219
What factors influence the risk of plaque rupture?
Plaque type (composition) rather than plaque size (volume).
## Footnote
Soft extracellular lipids make plaques more vulnerable.
220
What are the two main types of myocardial infarction?
* NSTEMI (Non–ST-segment elevation myocardial infarction)
* STEMI (ST-segment elevation myocardial infarction)
221
How does NSTEMI occur?
By developing a complete occlusion of a minor coronary artery or a partial occlusion of a major coronary artery.
## Footnote
This leads to partial thickness damage of the heart muscle.
222
How does STEMI occur?
By developing a complete occlusion of a major coronary artery.
## Footnote
This results in full thickness damage of the heart muscle.
223
What is the time frame for irreversible damage to the myocardium after blood flow interruption?
Begins as early as 20 to 40 minutes.
## Footnote
Damage can continue to evolve for several hours.
224
What cellular changes may follow an initial MI?
* Infarct extension
* Infarct expansion
* Ventricular remodeling
225
What are common symptoms of myocardial infarction?
* Chest pain
* Nausea
* Vomiting
* Sweating
* Breathing difficulty
226
What is a typical description of chest pain during an MI?
Patients often describe it as 'someone sitting on my chest'.
227
What biochemical markers are indicative of myocardial necrosis?
* Troponin
* Creatine kinase (CK)
* Myoglobin
* Lactate dehydrogenase (LDH)
228
When do troponin I and T levels typically rise after MI?
* Troponin I: rises in about 3 hours, peaks at 14 to 18 hours
* Troponin T: rises in 3 to 5 hours
229
What is the significance of the CK-MB2 to CK-MB1 ratio in MI?
A ratio greater than one indicates myocardial infarction.
230
How quickly can myoglobin levels elevate after an MI?
Within 1 to 2 hours.
## Footnote
However, elevated myoglobin is not specific for MI.
231
What does the ECG show during the earliest stage of MI?
Tall and narrow T waves, referred to as hyperacute T waves.
232
What changes occur to the T waves within a few hours of myocardial ischemia?
The T waves become inverted.
233
What is indicated by the presence of pathologic Q waves on an ECG?
Tissue necrosis and provides evidence of a previous myocardial infarction.
234
What is the universal definition of myocardial infarction according to the European Society of Cardiology?
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
What is the time frame in which a substantial amount of myocardial tissue can be salvaged after coronary occlusion?
Within 6 hours.
236
True or False: The pain of myocardial infarction is often relieved by rest or sublingual GTN.
False.
237
Fill in the blank: The initial downward deflection of the QRS complex is referred to as _______.
Q waves.
238
What is the primary cause of myocardial infarction (MI)?
Coronary atherosclerosis
## Footnote
Atherosclerosis is the buildup of fats, cholesterol, and other substances in and on the artery walls.
239
What are the three main components relied upon for the diagnosis of myocardial infarction?
Symptoms, biochemical markers, electrocardiographic findings
## Footnote
These components help in identifying the occurrence and severity of an MI.
240
How long does it typically take for Q waves to develop after a myocardial infarction?
Hours to days
## Footnote
Q waves indicate the presence of dead tissue and provide ECG evidence of a previous MI.
241
What is the time frame in which substantial myocardial tissue can be salvaged during an MI?
Within 6 hours
## Footnote
Quick intervention can prevent further damage to heart tissue.
242
What symptoms are commonly associated with myocardial infarction?
Often more prolonged and not relieved by rest or sublingual GTN
## Footnote
Symptoms may include chest pain, discomfort, and other signs of heart distress.
243
Which biochemical markers are used in the diagnosis of myocardial infarction?
Troponin I/T, CK-MB, Myoglobin, LDH-1
## Footnote
These markers are proteins released when the heart muscle is damaged.
244
What are the key ECG findings in a myocardial infarction?
Peaked/inverted T wave, ST elevation, pathologic Q wave
## Footnote
These changes indicate different phases and types of myocardial infarction.
245
Fill in the blank: Tissue necrosis in myocardial infarction starts in _______.
20-40 mins
## Footnote
This rapid onset emphasizes the urgency of treatment in MI cases.
246
What are the two types of myocardial infarction classified under MI?
NSTEMI, STEMI
## Footnote
NSTEMI refers to non-ST elevation myocardial infarction, while STEMI refers to ST elevation myocardial infarction.
247
True or False: The presence of pathologic Q waves is a temporary finding in ECG after an MI.
False
## Footnote
Pathologic Q waves are considered permanent indicators of previous myocardial infarction.
248
What is heart failure?
Characterized by impaired cardiac pumping such that the heart is unable to pump adequate amount of blood to meet metabolic needs.
249
What are the two types of heart failure?
* Systolic Heart Failure
* Diastolic Heart Failure
250
What are common signs and symptoms of heart failure?
* Shortness of breath
* Excessive tiredness
* Leg swelling
251
What is the prevalence of heart failure in individuals aged 75-84 years?
7%
252
What percentage of hospital bed-days does heart failure account for?
2%
253
What is the median survival for males and females with heart failure?
* 1.7 years for males
* 3.2 years for females
254
What are the underlying causes of heart failure?
* Ischemic heart disease (CAD)
* Hypertension
* Myocardial infarction (MI)
* Valvular heart disease
* Congenital heart disease
* Dilated cardiomyopathy
255
What is preload?
The amount of fiber stretch in the ventricles at the end of diastole.
256
What factors increase preload?
* Increase in blood volume
* Vasoconstriction
257
What is Starling's Law?
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
What is afterload?
The resistance against which the ventricle must pump.
259
What factors increase afterload?
* Hypertension
* Vasoconstriction
260
What is contractility?
The ability of the heart muscle to contract.
261
What can decrease contractility?
* Infarcted tissue
* Ischemic tissue
262
What compensatory mechanisms occur in heart failure?
* Sympathetic nerve stimulation
* Myocardial hypertrophy
* Hormonal response
263
What is the role of the renin-angiotensin-aldosterone system (RAAS) in heart failure?
It is central to altering the disease in patients with reduced ejection fraction.
264
What are common drug classes used in the pharmacology of heart failure treatment?
* ACE inhibitors
* Angiotensin II receptor blockers
* Beta-adrenergic blockers
* Aldosterone antagonists
* Diuretics
* Vasodilators
* Neprilysin antagonists
265
What do ACE inhibitors do?
Block the conversion of angiotensin I to angiotensin II, relax blood vessels, and decrease cardiac output.
266
What is the effect of beta-blockers in heart failure?
Reduce excessive sympathetic stimulation, decrease heart rate, and decrease force of contraction.
267
What do loop diuretics do?
Inhibit the reabsorption of sodium, chloride, and potassium, decreasing intravascular volume.
268
What is the function of neprilysin inhibitors?
Prevent the breakdown of natriuretic peptides, maintaining their ability to decrease intravascular volume and increase vasodilation.
269
True or False: Compensatory mechanisms always improve heart failure.
False
270
Fill in the blank: The average GP will suspect a new diagnosis of HF in _____ people annually.
10
