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BAMS Bds2 > đź«€CVS Medicine > Flashcards

đź«€CVS Medicine Flashcards

1
Q

What are the main components of the cardiovascular system?

A

Heart
Arteries
Veins
Capillaries

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2
Q

Which system is the cardiovascular system closely associated with?

A

The respiratory system

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3
Q

What happens when any component of the cardiovascular system is impaired?

A

It results in cardiovascular system (CVS) disease

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4
Q

What are the two main circulations the heart pumps blood to?

A

Pulmonary circulation
Systemic circulation

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5
Q

Which side of the heart pumps blood to the lungs, and through which vessel?

A

The right side of the heart pumps blood to the lungs through the pulmonary artery.

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6
Q

Which side of the heart pumps blood to the systemic circulation, and through which vessel?

A

The left side of the heart pumps blood to the systemic circulation through the aorta.

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7
Q

What is the myocardium?

A

Heart muscle

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8
Q

How many chambers does the heart have? Name them.

A

The heart has 4 chambers:
Right atrium
Right ventricle
Left atrium
Left ventricle

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9
Q

What are the four heart valves and their locations?

A

Aortic valve: Between the left ventricle (LV) and the aorta.
Pulmonary valve: Between the right ventricle (RV) and pulmonary artery.
Tricuspid valve: Between the right atrium (RA) and RV.
Mitral (bicuspid) valve: Between the left atrium (LA) and LV.

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10
Q

What system regulates the heartbeat and coordinates contractions of the heart?

A

The electrical conduction system.

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11
Q

Name the key components of the heart’s electrical conduction system.

A

Sinoatrial (SA) node
Atrioventricular (AV) node
Bundle of His
Purkinje fibers

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12
Q

What type of blood do arteries typically carry, and in which direction?

A

Arteries carry oxygenated blood away from the heart.

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13
Q

What type of blood do veins typically carry, and in which direction?

A

Veins carry deoxygenated blood back to the heart.

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14
Q

What happens when blood vessels narrow and what are the consequences?

A

Narrowing of vessels results in impaired blood flow to and away from tissues.
cons:
Reduced oxygen and nutrient delivery to tissues.
Reduced waste removal from tissues.

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15
Q

What is atherosclerosis?

A

A condition where fatty deposits (plaques) accumulate in the walls of arteries.

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16
Q

What effect does atherosclerosis have on arteries?

A

It causes stiffening and narrowing of the arteries, a condition called stenosis.

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17
Q

Name four non-modifiable risk factors for cardiovascular disease (CVD).

A

Older age
Male
Family history of CVD
Ethnicity

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18
Q

Name at least five modifiable risk factors for cardiovascular disease.

A

Hypertension
Obesity
Diabetes
High lipid levels
Smoking
Alcohol
Stress
Poor sleep

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19
Q

What are the key contributors to the formation of plaques in atherosclerosis?

A

1.Vessel wall damage
2.High LDL cholesterol levels
3.High circulating glucose (diabetes)
4.Immune cell activity

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20
Q

What are two common causes of vessel wall damage that contribute to atherosclerosis?

A

1.Hypertension (high blood pressure)
2.Smoking

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21
Q

What is hypertension?

A

High blood pressure, defined as a reading consistently above 140/90 mmHg.

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22
Q

What are the complications of untreated hypertension?

A

Atherosclerosis
Chronic kidney disease
Heart failure
Stroke
Retinopathy
Vascular dementia

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23
Q

List non-modifiable risk factors for hypertension.

A

Age
Gender
Ethnicity (e.g., black African, black Caribbean)
Family history (genetic predisposition)

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24
Q

List modifiable risk factors for hypertension.

A

Smoking
Alcohol excess
High dietary salt intake
Obesity
Lack of physical exercise
Anxiety
Emotional stress
Caffeine consumption

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25
Q

How is hypertension managed?

A

-Lifestyle modifications:
Obesity, dietary modifications, smoking, alcohol consumption, caffeine, salt intake, stress management

-Medications:
ACE inhibitors
Angiotensin-II receptor blockers (ARBs)
Beta blockers
Calcium channel blockers
Diuretics

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26
Q

What is coronary artery disease?

A

A condition where atherosclerosis causes hardening and narrowing of the coronary arteries, leading to ischemic heart disease.

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27
Q

What are the two main manifestations of ischemic heart disease?

A

Angina
Myocardial infarction (MI)

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28
Q

What is angina, and how is it classified?

A

Angina is chest pain due to myocardial ischemia:

Stable angina: Occurs only during exertion.
Unstable angina: Occurs at rest.

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29
Q

What are the classic symptoms of angina?

A

Central crushing chest pain that radiates to the left arm or jaw.

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30
Q

What lifestyle changes can help manage coronary artery disease?

A

Weight loss.
Healthy diet.
Stop smoking.
Reduce alcohol consumption.

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31
Q

What medication is used for immediate symptom relief in coronary artery disease?

A

GTN (glyceryl trinitrate) spray.

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32
Q

What are the key components of long-term secondary prevention for coronary artery disease?

A

Managing hypertension.
Controlling lipid levels.
Using aspirin as antiplatelet therapy.

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33
Q

What is percutaneous coronary intervention (PCI)?

A

A minimally invasive procedure that uses a balloon to widen diseased coronary arteries, often followed by stent insertion to maintain artery patency.

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34
Q

Through which arteries is percutaneous coronary intervention typically performed?

A

Via the radial or femoral artery.

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35
Q

What is a coronary artery bypass graft (CABG)?

A

A surgical procedure that bypasses narrowed or blocked coronary arteries using a harvested vessel from another part of the body (commonly the leg).

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36
Q

What is the purpose of a stent in PCI?

A

To maintain the widened artery and prevent it from narrowing again.

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37
Q

What is heart failure?

A

A condition where the heart fails to pump blood effectively.

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38
Q

What are the types of heart failure?

A

-Left-sided heart failure: Blood backs up into the lungs, causing pulmonary edema.
-Right-sided heart failure: Blood backs up into systemic circulation, causing peripheral edema.

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39
Q

What are common causes of heart failure?

A

Hypertension
Coronary artery disease (e.g., previous MI)
Valvular heart disease
Arrhythmias
Congenital heart defects

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40
Q

What are the symptoms of heart failure?

A

Shortness of breath (SoB)
Cough (frothy sputum)
Orthopnoea – SoB when lying flat
Paroxysmal nocturnal dyspnoea –suddenly waking at night with SoB
Peripheral oedema – fluid in the legs, abdomen, sacrum
Fatigue

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41
Q

How is heart failure managed?

A

-Lifestyle modifications:
Diet, exercise, smoking cessation.
-Medical management:
Control hypertension.
Off-load fluid with diuretics.
Improve heart function with beta blockers or digoxin.
-Devices:
Cardiac resynchronization therapy (CRT).
-Surgery:
Heart transplant for suitable patients.

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42
Q

What is an arrhythmia?

A

An abnormal heart rhythm caused by interrupted electrical signals that coordinate heart muscle contraction.

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43
Q

What is atrial fibrillation (AF)?

A

A common arrhythmia where disorganized electrical activity in the atria causes fibrillation (random muscle twitching) and an irregular pulse.

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44
Q

Why does atrial fibrillation increase the risk of stroke?

A

Uncoordinated heart activity in AF disrupts smooth blood flow, increasing the likelihood of blood clot formation that can travel to the brain.

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45
Q

How is atrial fibrillation managed?

A

Anticoagulants (e.g., DOACs) to prevent clot formation.
Rate-controlling medications (e.g., bisoprolol).

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46
Q

What is the function of pacemakers in managing arrhythmias?

A

Pacemakers deliver controlled electrical impulses to restore and maintain a normal heart rhythm.

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47
Q

What are the two main types of valvular dysfunction?

A

Stenosis: Valve becomes stiff and doesn’t fully open.
Regurgitation: Valve doesn’t fully close, causing leaks.

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48
Q

What causes valvular disease?

A

Aging (e.g., aortic stenosis due to calcification).
Congenital defects (e.g., bicuspid aortic valve).
Damage from myocardial infarction (e.g., papillary muscle rupture).
Rheumatic heart disease.
Infective endocarditis.

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49
Q

How does rheumatic heart disease cause valvular damage?

A

The immune system attacks heart valves following an untreated Group A streptococcal throat infection, mistaking valve proteins for the bacteria’s M protein.

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50
Q

What are the types of valve replacements?

A

Bioprosthetic valves: Made from pig tissue, lower clot risk, but shorter lifespan.
Metallic valves: Longer lifespan, higher clot risk, require anticoagulation therapy (e.g., warfarin).

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51
Q

What is infective endocarditis?

A

A life-threatening infection of the heart lining (endocardium), particularly affecting heart valves.

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52
Q

How is infective endocarditis related to dental procedures?

A

Bacteria from invasive dental procedures can enter the bloodstream and infect damaged heart valves, especially in predisposed individuals.

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53
Q

What are the three main consequences of infective endocarditis?

A

Impaired heart valve function, leading to heart failure.
Focus of infection, causing sepsis.
Source of emboli, leading to strokes.

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54
Q

How is infective endocarditis managed?

A

4–6 weeks of IV antibiotics.
Surgery may be required to replace damaged valves.

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55
Q

What are the current guidelines for antibiotic prophylaxis in UK dentistry?

A

Antibiotic prophylaxis is not routinely recommended for dental procedures but may be considered for high-risk patients after consulting with their cardiologist.

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56
Q

What preventive measures reduce the risk of infective endocarditis?

A

Regular dental check-ups
Toothbrushing instruction
Dietary advice
High-fluoride toothpaste.

57
Q

What are the dental implications of anticoagulant use in cardiovascular disease patients?

A

Increased bleeding risk during and after dental procedures.

58
Q

How might polypharmacy affect dental patients with cardiovascular disease?

A

Dry mouth from medications.
Lichenoid tissue reactions caused by some antihypertensive drugs.

59
Q

Why is lying back a concern for patients with heart failure?

A

It may cause orthopnea (shortness of breath when lying flat).

60
Q

What is the connection between periodontal disease and cardiovascular disease?

A

Periodontitis is increasingly recognized as a risk factor for cardiovascular disease.

61
Q

What is Acute Coronary Syndrome (ACS)?

A

ACS is an overarching term for 3 diseases that affect the myocardium:

Unstable Angina
ST-elevation Myocardial Infarction (STEMI)
Non-ST-elevation Myocardial Infarction (NSTEMI)

62
Q

What causes ACS?

A

ACS occurs due to a supply/demand mismatch of oxygen to the myocardium, which can result from:
-Blockage or narrowing of coronary arteries
-Increased demand (e.g., arrhythmias, acute illness)

63
Q

What happens to the myocardium in ACS?

A

Atherosclerotic plaque narrows the artery
Plaque may embolize, causing partial or total blockage
Leads to ischemia, and potentially infarction and necrosis of tissue

64
Q

What are the symptoms of ACS?

A

Central, crushing chest pain
Radiating pain to jaw or arm (commonly left)
Nausea, vomiting
Sweating, clamminess
Shortness of breath, palpitations
Feeling of impending doom

65
Q

What are the types of ACS?

A

-Unstable Angina - Partial occlusion, ischemia, no infarction
-NSTEMI - Partial occlusion, ischemia, infarction
-STEMI - Total occlusion, infarction

66
Q

What are the complications of ACS?

A

Death (cardiac arrest)
Arrhythmias
Heart failure
Rupture of heart wall
New valvular disease (papillary muscle infarction)

67
Q

How is ACS diagnosed?

A

ECG: Detects ST-elevation or non-ST-elevation
Troponin test: Measures elevated troponin levels (protein released when heart muscle is damaged)

68
Q

What is the immediate management of ACS in a dental practice?

A

Call an ambulance and get to the hospital
Oxygen (100% via non-rebreather mask)
Glyceryl trinitrate spray (GTN)- 2 puffs, sublingual
Aspirin (300mg) (chewed)

69
Q

What is the role of oxygen in ACS management?

A

Oxygen helps increase oxygen delivery to the ischemic myocardium, limiting infarct size.

70
Q

What is the role of GTN (Glyceryl Trinitrate) in ACS management?

A

Vasodilator: Relaxes blood vessels, improving blood flow
Reduces preload (less workload on the heart)
Increases blood flow to coronary arteries

71
Q

What is the role of aspirin in ACS management?

A

Prevents thrombus enlargement
Reduces platelet aggregation by inhibiting COX enzyme, reducing thromboxane A2 production

72
Q

What are the reperfusion strategies in ACS?

A
  1. Percutaneous Coronary Intervention (PCI):
    Breaks up the clot via angioplasty, places a stent
    Must be done within 120 minutes of onset
  2. Thrombolysis:
    Clot-busting drug (alteplase) administered intravenously
73
Q

What are the secondary prevention strategies for ACS?

A

-Lifestyle changes (e.g., diet, exercise, smoking cessation)
-Medications:
Aspirin (75mg daily)
Antiplatelet (e.g., clopidogrel)
Lipid-lowering drugs (e.g., atorvastatin)
ACE inhibitors (e.g., for blood pressure)
Beta-blockers (e.g., atenolol)

74
Q

What are the dental implications for patients with ACS?

A

Medical emergency management
Stress from dental procedures can trigger ACS events
Smoking cessation advice due to shared risk factors with periodontal disease
Bleeding risk due to antiplatelet medications
Use of local anesthetic with caution (contains adrenaline)

75
Q

When should adrenaline be avoided in dental treatment for ACS patients?

A

Within 6 months of a myocardial infarction (MI)
In cases of severe hypertension or unstable arrhythmia

76
Q

What is Peripheral Arterial Disease (PAD)?

A

PAD refers to the narrowing of arteries supplying the limbs, most commonly the legs, caused by atherosclerosis. It leads to ischemia, infarction, and necrosis of limb tissues.

77
Q

What are the common symptoms/signs of PAD?

A

Cramping pain in the legs, thighs, buttocks, or calves, especially when walking (intermittent claudication)
Non-healing ulcers on the toes, foot, or leg
One leg cooler or paler than the other
Hair loss on the affected leg
Necrosis of skin on the digits

78
Q

What is the pathophysiology of PAD?

A

Atherosclerosis causes narrowing of arteries supplying the limbs
Leads to ischemia, and eventually infarction and necrosis of tissues
Same risk factors as ACS (e.g., smoking, hypertension, diabetes, high cholesterol)

79
Q

How is PAD diagnosed?

A

CT angiography of the limb is commonly used for diagnosis.

80
Q

What is the management of PAD?

A

Lifestyle advice and risk factor management (e.g., smoking cessation, exercise)
Medications:
Antiplatelet (e.g., clopidogrel)
Lipid-lowering agents (e.g., atorvastatin)
Surgical treatments:
Angioplasty and stent placement
Endartectomy
Bypass surgery
Amputation (in severe cases)

81
Q

What is angioplasty and stent placement in PAD surgery?

A

Angioplasty enlarges the blocked artery
A stent is inserted to maintain artery patency (keep it open)

82
Q

What is endarterectomy in PAD surgery?

A

Surgical removal of atherosclerotic plaque from the artery.

83
Q

What is bypass surgery for PAD?

A

A graft is placed to reroute blood flow around the blocked or narrowed artery.

84
Q

What are the dental implications for patients with PAD?

A

Shared risk factors with periodontal disease (e.g., smoking, diabetes)
Antiplatelet medications increase the bleeding risk
Cardiovascular health is a concern, as PAD patients have an increased risk of ACS
Dental stress can potentially trigger cardiovascular events

85
Q

How does PAD affect the cardiovascular system?

A

PAD patients are at a higher risk for Acute Coronary Syndrome (ACS) due to the same atherosclerotic process affecting both peripheral and coronary arteries.

86
Q

How are ACS, PAD, and stroke related in terms of disease mechanism?

A

All three involve occlusion of blood flow due to atherosclerosis (plaque buildup in arteries)
This occlusion results in ischemia and, if untreated, can lead to infarction and tissue necrosis in the heart (ACS), legs (PAD), or brain (stroke)
Shared risk factors include smoking, diabetes, hypertension, and hyperlipidemia

87
Q

What is the formula for blood pressure?

A

Blood pressure = Cardiac Output Ă— Total Peripheral Resistance
(Cardiac Output = Heart Rate Ă— Stroke Volume)

88
Q

How can blood pressure be reduced?

A

Blood pressure can be reduced by lowering any of the following:

Heart rate
Stroke volume
Total peripheral resistance

89
Q

How can blood pressure be reduced?

A

Blood pressure can be reduced by lowering any of the following:

Heart rate
Stroke volume
Total peripheral resistance

90
Q

What does Total Peripheral Resistance (TPR) depend on?

A

TPR depends on how much vasoconstriction vs. vasodilation is present in peripheral circulation.

91
Q

What are the three main areas where anti-hypertensives work to reduce blood pressure?

A

Heart (reduce heart rate or contractility)
Blood vessels (vasodilation)
Kidneys (reduce fluid reabsorption)

92
Q

What is the role of ACE-inhibitors in lowering blood pressure?

A

ACE inhibitors (e.g., ramipril, lisinopril) inhibit the formation of angiotensin-II, which reduces aldosterone production, leading to less fluid reabsorption in the kidneys and thus lower blood pressure.

93
Q

What are common oral implications of ACE inhibitors?

A

Lichenoid tissue reaction
Dry mouth

94
Q

Examples of ACE-inhibitors

A

Ramipril, lisinopril, perindopril

95
Q

How do Angiotensin-II-receptor blockers (ARBs) reduce blood pressure?

A

ARBs (e.g., candesartan, losartan) bind to angiotensin-II receptors, preventing vasoconstriction and reducing aldosterone production, which lowers blood pressure.

96
Q

Examples of Angiotensin-II-receptor blockers (ARBs)

A

Candesartan, losartan, valsartan

97
Q

How do beta blockers lower blood pressure?

A

Beta blockers (e.g., atenolol, propranolol) block beta 1 receptors on cardiac muscle, preventing stimulation by adrenaline, reducing heart rate and contractility, which lowers blood pressure.

98
Q

Why should beta blockers be avoided in asthmatics?

A

Beta blockers can cause broncho-constriction, which is harmful to asthmatics.

99
Q

What are some oral implications of beta blockers?

A

Beta blockers can cause oral lichenoid tissue reactions.

100
Q

Examples of Beta blockers

A

Atenolol, bisoprolol, propranolol, carvedilol

101
Q

What is the mechanism of action of calcium channel blockers in lowering blood pressure?

A

Calcium channel blockers (e.g., amlodipine, nifedipine) reduce vasoconstriction (lower TPR) by inhibiting calcium channels on smooth muscle, reduce heart rate by inhibiting calcium channels in the sino-atrial node, and reduce contractility by inhibiting calcium channels in cardiac muscle

102
Q

What are common oral manifestations of calcium channel blockers?

A

Gingival enlargement (particularly with nifedipine)
Oral lichenoid reactions

103
Q

Examples of calcium channel blockers

A

Amlodipine, nifedipine, felodipine

104
Q

How do diuretics reduce blood pressure?

A

Diuretics (e.g., furosemide, bendroflumethiazide) work by increasing urine output, thereby reducing circulating fluid volume, which leads to lower blood pressure.

105
Q

What are common oral implications of diuretics?

A

Dry mouth
Oral lichenoid reactions

106
Q

What are the mechanisms of action of diuretics?

A

Diuretics work at different parts of the nephron to decrease fluid reabsorption, increasing urination and thereby reducing fluid volume in circulation, which lowers blood pressure

107
Q

Examples of diuretics

A

Furosemide, bendroflumethiazide,bumetanide

108
Q

What is the function of the Renin-Angiotensin-Aldosterone System (RAAS) in regulating blood pressure?

A

When blood pressure is low, the RAAS system increases blood pressure by promoting the production of angiotensin-II, which causes vasoconstriction and stimulates aldosterone production, leading to fluid retention.

109
Q

How do ARBs differ from ACE inhibitors in their mechanism of action?

A

ACE inhibitors block the formation of angiotensin-II, whereas ARBs block the receptors that angiotensin-II binds to, preventing vasoconstriction and aldosterone production, both of which help lower blood pressure.

110
Q

What is a potential side effect of beta blockers, particularly for individuals with anxiety?

A

Beta blockers are often used to manage physical symptoms of anxiety, such as tremors and rapid heart rate, by reducing heart rate and contractility.

111
Q

What are the subtypes of adrenergic receptors that beta blockers target?

A

Beta blockers can be selective or non-selective, targeting:

Beta 1 receptors (primarily in the heart)
Beta 2 receptors (in smooth muscle of the bronchi and bronchioles)
Alpha 1 receptors (in blood vessel smooth muscle)

112
Q

What is the difference between selective and non-selective beta blockers?

A

Selective beta blockers primarily block beta 1 receptors in the heart, while non-selective beta blockers block both beta 1 and beta 2 receptors, which can affect the lungs and blood vessels.

113
Q

What conditions are anti-platelet drugs commonly used for?

A

Coronary artery disease
Secondary prevention following myocardial infarction (MI)
Peripheral artery disease
Secondary prevention following stroke/TIA

114
Q

What is dual anti-platelet therapy (DAPT)?

A

DAPT involves using two anti-platelet drugs together, typically for 12 months, to further reduce the risk of clot formation.

115
Q

What are some examples of anti-platelet drugs?

A

Aspirin
Clopidogrel
Ticagrelor
Dipyridamole

116
Q

How do anti-platelet drugs work?

A

Anti-platelet drugs reduce platelet activation and aggregation, preventing thrombus (clot) formation.

117
Q

What is the common dosage and use of Aspirin for secondary prevention?

A

75 mg once per day for secondary prevention
300 mg for acute myocardial infarction (MI) or stroke

118
Q

What is the mechanism of action of Aspirin?

A

Aspirin inhibits the COX-1 enzyme, reducing the production of thromboxane A2, which decreases platelet aggregation.

119
Q

How long do platelets live, and what implication does this have for anti-platelet therapy?

A

Platelets have a lifespan of 7-10 days, meaning aspirin’s effects last for the same period, reducing platelet aggregation during that time.

120
Q

What is the mechanism of action of Clopidogrel and Ticagrelor?

A

Both drugs bind to P2Y12 receptors on platelets.
This prevents ADP from binding to the receptors, stopping platelet activation and aggregation.

121
Q

What are the dental implications of anti-platelet therapy?

A

Patients on anti-platelets may have prolonged bleeding times.
Patients on dual anti-platelet therapy (DAPT) have an increased bleeding risk.
It’s generally not necessary to stop anti-platelet therapy for dental treatment, but always consider the risk vs. benefit.

122
Q

How should you manage dental treatment for patients on anti-platelet therapy?

A

No need to stop anti-platelet medication for dental treatment unless there’s a significant risk of bleeding.
Consider if treatment can be delayed if the patient is on DAPT (often for 12 months).

123
Q

What is the role of Dipyridamole in anti-platelet therapy?

A

Dipyridamole works by inhibiting platelet activation and aggregation, although its exact mechanism is more complex compared to aspirin or clopidogrel.

124
Q

What are the common Direct Oral Anticoagulants (DOACs) used in atrial fibrillation for stroke prevention?

A

Edoxaban
Rivaroxaban
Apixaban
Dabigatran

125
Q

What are the advantages of DOACs over warfarin?

A

Rapid onset of action
Short half-lives
No need for monitoring
Fewer drug interactions compared to warfarin
Able to miss a dose to facilitate dental treatment

126
Q

What is the role of Warfarin in anticoagulation therapy?

A

Warfarin is commonly used for conditions like metallic valve replacement and works by inhibiting coagulation factors II, VII, IX, and X (2, 7, 9, 10).

127
Q

How is Warfarin monitored, and what is the target INR for metallic valve replacement?

A

Warfarin requires INR monitoring, generally every 4 weeks, with a target INR range of 2.5–3.5 for metallic valve replacement.

128
Q

What is the ideal time frame to check INR before dental treatment for a patient on warfarin?

A

INR should ideally be checked < 24 hours before dental treatment.
If the readings are stable, 72 hours is acceptable.

129
Q

What is the general guideline regarding INR for dental treatment in patients on warfarin?

A

If INR is < 4, dental treatment can proceed.
If INR is higher, dental procedures may need to be postponed or adjusted.

130
Q

What are the dental implications of anti-coagulants?

A

Increased bleeding risk
SDCEP guidelines (Scottish Dental Clinical Effectiveness Programme) may help guide decisions
General principles: Assess if dental treatment is necessary and consider risks of bleeding

131
Q

What are the two types of cholesterol and their roles in cardiovascular disease?

A

LDL (low-density lipoprotein) – “bad” cholesterol, contributes to atherosclerosis.
HDL (high-density lipoprotein) – “good” cholesterol, helps remove LDL from the blood.

132
Q

What are statins and how do they work?

A

Statins (e.g., atorvastatin, simvastatin, rosuvastatin) work by inhibiting the enzyme HMG-CoA reductase in the liver, which stops the production of LDL cholesterol.

133
Q

What is a dangerous side effect of statins and how should it be managed?

A

Rhabdomyolysis (breakdown of skeletal muscle) can occur, leading to the release of myoglobin, which can damage the kidneys and heart.
Symptoms include “coca-cola” colored urine.
Requires emergency medical care.
Avoid interacting drugs or temporarily withhold statins when interacting medications are used.

134
Q

Which drugs can interact with statins to cause rhabdomyolysis?

A

Fluconazole
Miconazole
Clarithromycin

135
Q

What is angina and how do anti-anginal medications help?

A

Angina is chest pain due to the narrowing of coronary arteries.
Anti-anginal medications (like nitrates) relax smooth muscle in coronary vessels, causing vasodilation to improve blood flow to the heart.

136
Q

What are the two main types of nitrates used to treat angina?

A

GTN spray (glycerol trinitrate) – used for acute relief
Isosorbide mononitrate (ISMN) – used daily for prevention

137
Q

What is nicorandil, and what is its potential oral side effect?

A

Nicorandil is a second-line agent for angina management.
It can cause severe oral ulceration (up to 5%), which heals upon discontinuation of the medication.

138
Q

How should oral ulceration caused by nicorandil be managed?

A

Nicorandil-induced oral ulceration usually resolves upon withdrawal of the medication, under the guidance of the medical team.
Symptomatic relief can be provided with benzydamine mouthwash.

BAMS Bds2 (5 decks)

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