Ischaemic Heart Disease pharm

Question 1

What is the main etiology of ischemic heart disease?

Answer 1

Atherosclerosis

Question 2

What are some causes of IHD?

Answer 2

1) Atherosclerosis
2) Embolism
3) Dissecting aneurysm
4) Trauma
5) Arteritis
6) Hypoxemia
7) Ostial stenosis (syphilitic aortitis)
8) Anomalous origin of LCA

Question 3

What are 4 complications of IHD?

Answer 3

1) Ventricles
- LV failure → CHF
- Ruptured myocardium → cardiac tamponade
- Fibrosis and aneurysm
- thrombus

2) Arrhythmias → sudden cardiac death
3) Pericarditis (post-MI: Dressler’s syndrome)
4) Valves (ruptured papillary muscle)

Question 4

What are 3 factors that contribute to the pathogenesis of IHD?

Answer 4

1) ↓coronary flow (occlusion)
2) ↑ metabolic Dd (eg. exercise, pregnancy, infection, hyperthyroidism, myocardial hypertrophy)
3) ↓O2 availability in blood (eg. anemia, CO poisoning, pulmonary diseases, L→R shunt)

Question 5

What is Prinzmetal angina?

Answer 5

A form of episodic myocardial ischemia
- secondary to coronary arterial spasm
- **unrelated to exertion HR, BP
- responds to vasodilators

Question 6

How does chronic IHD lead to HF?

Answer 6

Chronic atherosclerotic narrowing of coronary arteries
→ loss of myocardial fibres → generalised myocardial fibrosis
→ insidious cardiac failure → death

Question 7

What are 2 causes of sudden cardiac death?

Answer 7

1) Pronounced stenosis of 1 or more major arteries
2) Acute plaque change

Question 8

For how long would a MI not be visible macro and micreoscopically?

Answer 8

12 hours

Question 9

What are the 3 histological characteristics of an myocardial infarction and when would they occur?

Answer 9

12-24hrs
1) Coagulative necrosis (ghost outlines, no nuclei)
2) Intercellular oedema (spacing)
3) Bright eosinophilic infarcted myocytes

Question 10

How would an MI appear macroscopically 12-24hrs after it occurs?

Answer 10

Pale with blotchy discolouration

Question 11

When would neutrophil infiltration occur after an MI?

Answer 11

24-72 hrs

Question 12

How would an MI appear macroscopically 24-72hrs after it occurs?

Answer 12

Soft pale and yellow

Question 13

When would granulation tissue form after an MI?

Answer 13

3-10 days

Question 14

How would an MI appear macroscopically 3-10 days after it occurs?

Answer 14

Hyperemic border surrounding yellow infarcted area

Question 15

How would an MI appear macroscopically 6-8 weeks after it occurs?

Answer 15

Fibrous scar

Question 16

What are the drugs used in angina?

Answer 16

1) Vasodilators (nitrates, Ca channel blockers)
2) Cardiac depressants (Ca channel blockers, ß-blockers)
3) Cardiac pacemaker retardant (Ivabradine)

Question 17

What are the moa of nitrates used in angina treatment?

Answer 17

Nitrates release NO → (Guanylyl cyclase → cGMP )→ ↑myosin LC (inactive)
1) venodilation → blood pools in veins → ↓ preload
2) arteriolar dilation → ↓peripheral R → ↓ afterload
→ ↓ workload on myocardium → ↓ O2 consumption

Question 18

Which nitrate is used for emergency angina therapy?

Answer 18

Sublingual nitroglycerin

Question 19

What is the difference between sublingual and transdermal nitroglycerin?

Answer 19

Onset:
Sublingual: 1-5min
Transdermal: 30-60min

Duration:
Sublingual:10-30min
Transdermal: 7-10hrs

Question 20

Nitroglycerin is metabolised to (active/inactive metabolite)?

Answer 20

Active but less active

Question 21

What nitrate is used for angina pectoris prophylaxis and HF?

Answer 21

ISMN/ISDN

Question 22

How is ISDN/ISMN adminstered?

Answer 22

Oral

Question 23

ISDN has a (faster/slower) onset of action than ISMN?

Answer 23

Slower (mononitrate faster)

Question 24

How does the PD of ISDN/ISMN differ at different plasma concentrations?

Answer 24

Low Pc: venous dilation → ↓preload
High Pc: also dilate arteries → ↓preload + ↓afterload

Question 25

Which of the nitrates used in angina treatment have a direct dilatory effect on the coronary arteries, thereby lowering the intramural pressure and improving subendocardial blood flow?

Answer 25

ISMN/ISDN

Question 26

What are 3 AEs of nitrates?

Answer 26

1) Reflex tachycardia (baroreflex engaged by vasorelaxation)
2) Hypotension
3) Headache (meningeal artery vasodilation)

Question 27

How do the different types of calcium channel blockers differ in their ability to lower BP?

Answer 27

Verapimil=diltiazem=nifedipine

Question 28

How do the different types of calcium channel blockers differ in their vasodilatory effects?

Answer 28

Verapimil < diltiazem < nifedipine

Question 29

How do the different types of calcium channel blockers differ in their cardiac depressant effects?

Answer 29

Verapimil > diltiazem > nifedipine

Question 30

What are 3 AEs of calcium channel blockers used in angina treatment?

Answer 30

Cardiac depression:
1) Bradycardia
2) AV blocker
3) HF

Question 31

What are the clinical uses for DHP Ca channel blockers?

Answer 31

1) HTN
2) Stable angina (amlopidine)
3) ↓ risk of MI and stroke (amlopidine)

Question 32

What are 3 AEs of DHP Ca channel blockers?

Answer 32

1) Hypotension
2) HF
3) MI

Question 33

What is Ivabradine used for?

Answer 33

Stable angina pectoris and chronic HF with systolic dysfunction (sinus rhythm >75bpm)

Question 34

What is the moa of Ivabradine?

Answer 34

“Pure” HR lowering agent:
inhibition cardiac pacemaker I(F) current that controls spontaneous diastolic depolarisation in the sinus node and thus regulates HR
→ ↓cardiac workload and O2 consumption

Question 35

What are 3 AEs of Ivabradine?

Answer 35

1) Visual problems: luminous phenomena, transient enhanced brightness in a limited area of vision
2) Dizziness, fatigue, malaise
3) Hypotension