Drugs used in the treatment of ischaemic heart disease

Question 1

Ischemic Heart Disease (IHD)

Answer 1

Ischemic Heart Disease (IHD) results from inadequate coronary perfusion relative to myocardial demand.

Question 2

Pre-existing (“fixed”) Atherosclerotic Occlusion:

Answer 2

his refers to the chronic, stable narrowing of the coronary arteries due to the buildup of atherosclerotic plaques.

Question 3

Acute Plaque Change

Answer 3

sudden alterations in the atherosclerotic plaque, which can lead to:
Thrombosis: Formation of a blood clot at the site of the plaque.
Vasospasm: Sudden constriction of the coronary artery.

Question 4

Which of the following best describes the primary underlying causes of ischemic heart disease (IHD)?

a. Chronic high blood pressure and diabetes
b. Fixed atherosclerotic occlusion and acute plaque change with thrombosis
c. Pulmonary embolism and chronic obstructive pulmonary disease
d. Heart failure and atrial fibrillation

Answer 4

Fixed atherosclerotic occlusion and acute plaque change with thrombosis
Rationale: IHD is mainly caused by pre-existing atherosclerotic occlusion and acute plaque change with superimposed thrombosis and/or vasospasm.

Question 5

What is the primary mechanism leading to acute coronary syndrome (ACS) in most patients?

a. Chronic myocardial ischemia due to long-standing hypertension
b. Abrupt plaque change followed by thrombosis
c. Progressive heart failure and fluid overload
d. Intermittent episodes of atrial fibrillation

Answer 5

Answer:
b. Abrupt plaque change followed by thrombosis
Rationale: ACS typically occurs due to sudden changes in the atherosclerotic plaque, leading to thrombosis.

Question 6

.A 58-year-old man with a history of stable angina presents with sudden onset of severe chest pain. Which pathophysiological change is most likely responsible for his condition?

a. Gradual worsening of coronary artery stenosis
b. Acute plaque rupture with superimposed thrombosis
c. Development of pulmonary embolism
d. Sudden onset of atrial fibrillation

Answer 6

Answer:
b. Acute plaque rupture with superimposed thrombosis
Rationale: Sudden severe chest pain in a patient with a history of stable angina is often due to acute plaque rupture and thrombosis, leading to an acute coronary syndrome.

Question 7

Characteristic chest pain (burning or heavy discomfort behind the sternum), of duration <
15 minutes, due to myocardial ischaemia, usually occurring on exercise and relieved by
rest.

Answer 7

Angina pectoris

Question 8

Stepwise treatment for angina pectoris (stable)

Answer 8

Beta-blocker:
Atenolol

Add 2nd agent:
Long-acting
calcium channel
blocker:
amlodipine

Add 3rd agent:
Isosorbide
mononitrate /
dinitrate

Question 9

Organic nitrates

Answer 9

• Glyceryl trinitrate
• Isosorbide mononitrate
• Isosorbide dinitrat

Question 10

Dilation of collateral vessels that bypass narrowed coronary artery segment

Answer 10

caused by organic nitrates.

Question 11

Which of the following best describes the function of collateral vessels in the context of coronary artery disease (CAD)?

A) They directly increase the diameter of narrowed coronary arteries.
B) They provide an alternative pathway for blood flow to ischemic myocardium.
C) They create new coronary arteries that replace occluded ones.
D) They do not play a significant role in myocardial blood supply during CAD.

Answer 11

B) They provide an alternative pathway for blood flow to ischemic myocardium.

Question 12

What is the primary clinical significance of well-developed collateral vessels in a patient with significant coronary artery stenosis?

A) They eliminate the need for any further medical intervention.
B) They contribute to the progression of coronary artery disease.
C) They help preserve myocardial function despite occlusive coronary artery disease.
D) They indicate a higher risk of myocardial infarction.

Answer 12

C) They help preserve myocardial function despite occlusive coronary artery disease.

Question 13

Organic nitrates: anti-anginal actions
How do medications that reduce pre-load and after-load help in managing CAD?

A) By increasing the diameter of the coronary arteries.
B) By reducing oxygen demand of the myocardium.
C) By stimulating the formation of new coronary arteries.
D) By increasing heart rate.

Answer 13

Answer: B) By reducing oxygen demand of the myocardium.

Question 14

Which mechanism allows for the redistribution of coronary flow to ischemic areas in CAD?

A) Formation of new coronary arteries.
B) Increased cardiac output.
C) Development of collateral vessels.
D) Vasoconstriction of epicardial arteries

Answer 14

C) Development of collateral vessels

Question 15

How do collateral vessels contribute to myocardial perfusion in areas affected by coronary artery stenosis?

A) By eliminating the stenosis.
B) By providing an alternative route for blood flow to ischemic regions.
C) By causing vasoconstriction in unaffected arteries.
D) By increasing systemic blood pressure.

Answer 15

By providing an alternative route for blood flow to ischemic regions.

Question 16

ane’s medication regimen aims to reduce pre-load. Which of the following describes pre-load?

A) The resistance the heart must overcome to eject blood.
B) The volume of blood in the ventricles at the end of diastole.
C) The rate at which the heart beats.
D) The oxygen content of arterial blood.

Answer 16

B) The volume of blood in the ventricles at the end of diastole.

Question 17

In the management of CAD, why is it important to reduce after-load?

A) To increase the heart rate.
B) To decrease the workload on the heart.
C) To induce coronary artery spasms.
D) To increase myocardial oxygen consumption.

Answer 17

B) To decrease the workload on the heart.

Question 18

What is the clinical significance of the redistribution of coronary flow to ischemic areas via collaterals?

Answer 18

It enhances blood supply to areas of the myocardium deprived of oxygen.

Question 19

Which therapeutic strategy is most likely to benefit Jane by reducing both pre-load and after-load?

A) Beta-blockers.
B) Calcium channel blockers.
C) ACE inhibitors.
D) Statins.

Answer 19

c

Question 20

What role does nitric oxide play in the mechanism of action of organic nitrates?

A) It increases myocardial oxygen consumption.
B) It activates guanylyl cyclase, leading to cGMP formation.
C) It decreases the formation of cGMP.
D) It causes smooth muscle contraction.

Answer 20

B

Question 21

How does cGMP contribute to smooth muscle relaxation in the context of organic nitrate therapy?

A) By increasing calcium levels in smooth muscle cells.
B) By activating kinases that increase myosin phosphatase activity.
C) By increasing myosin phosphate levels.
D) By inhibiting nitric oxide production.

Answer 21

B

Question 22

Which enzyme is responsible for the formation of cGMP in response to nitric oxide?

A) Adenylate cyclase.
B) Phosphodiesterase.
C) Guanylyl cyclase.
D) Myosin phosphatase.

Answer 22

C

Question 23

tolerance and adverse effects

Answer 23

organic nitrates adverse effect are
Hypotension and headache

Question 24

Organic nitrates: pharmacokinetic and pharmaceutical
aspects: Glyceryl trinitrate

Answer 24

apidly inactivated by hepatic metabolism * Route of administration: sublingual – onset of action = few minutes
converted to di- and mononitrates
* Absorbed through the skin – transdermal patch
* Ineffective if administered orally – first pass metabolism by the liver * Duration of action: 30 minutes
* Due to volatility of the active ingredient, if tablets are opened, the
volatile substance evaporates
* Spray is better, more stable

Question 25

longer acting organic nitrate, absorbed and metabolised more slowly.

Answer 25

Isosorbide mononitrates

Route of administration: oral * Take twice daily in the morning (8:00) and at lunch (14:00) to allow
for the nitrate free period (to avoid tolerance)

Question 26

A least lipophilic beta1 blocker cardia selective drug?

Answer 26

Atenolol

loses selectivity at high doses.

Question 27

Which of the following best describes the pharmacokinetic property of the cardio-selective β1 Atenolol

A) Highly lipophilic and metabolized in the liver.
B) Least lipophilic and excreted mainly unchanged in the urine.
C) Highly lipophilic and excreted mainly unchanged in the urine.
D) Least lipophilic and extensively metabolized in the liver.

Answer 27

B

Question 28

Why is the prescribed β1 blocker given once daily?

Answer 28

Because it has a long duration of action. he drug’s pharmacokinetics are not affected by liver disease.

Question 29

At high doses, what happens to the cardio-selectivity of the prescribed β1 blocker?

Answer 29

It loses its cardio-selectivity

Question 30

Acute coronary syndrome (ACS

Answer 30

Acute reduction in coronary blood flow most often due to a ruptured
atherosclerotic plaque and subsequent formation of an intracoronary
thrombus. The reduction in coronary blood flow produces myocardial
ischemia and, if left untreated, may lead to myocardial infarction (MI)

Question 31

The spectrum of Acute coronary syndrome.

Answer 31

Unstable angina (UA) * Non-ST-segment elevation myocardial infarction (NSTEMI) * ST-segment elevation myocardial infarction (STEMI),

Question 32

Unstable angina is a medical emergency and if untreated can progress
to NSTEMI. Presents as chest pain or discomfort like stable angina but
with the following additional characteristics:

Answer 32

• angina at rest or minimal effort * angina occurring for the first time, particularly if it occurs at rest * prolonged angina > 10 minutes, not relieved by sublingual nitrates
• the pattern of angina accelerates and gets worse

Question 33

Short-term goals:ACS: goals of treatmen

Answer 33

Early restoration of blood flow to the infarct-related artery to prevent
infarct expansion (in the case of MI) or prevent complete occlusion and MI
(in UA); * Prevention of death and other MI complications; * Prevention of coronary artery re-occlusion
* Relief of ischemic chest discomfort

Question 34

Long-term goals:

Answer 34

Control of atherosclerosis risk factors, * Prevention of additional MACE, including reinfarction, stroke, and HF
* Improvement in quality of life.

Question 35

Thrombolytic therapy for acute MI & STEMI

Answer 35

After administration, monitor continuously:
* Pulse
* BP
* Respiration depth and rate (count for a full minute)
* ECG

Question 36

Antiplatelet treatment.

Answer 36

Clopidogrel * Aspirin, oral, 150 mg stat, then as daily single dose, continued
indefinitely in the absence of contraindications