Ischemic Heart Disease

Question 1

Mention basic underlying causes of IHD

Answer 1

1. Reduction of coronary blood flow
2. Increased myocardial demands for oxygen
3. Dec O2 carrying capacity of blood

Question 2

Mention causes of IHD related to dec coronary blood flow

Answer 2

1. Atherosclerosis
2. Occlusive coronary thrombosis
3. Coronary embolism due to mural thrombosis/valve vegetations
4. Coronary spasm
5. Dissecting aneurysm
6. Syphilitic Osteal stenosis or aortic incampetence
7. Polyarteritis nodosa
8. Dec blood volume (hypotension & shock)
9. Calcific aortic stenosis

Question 3

Mention causes of IHD related to inc myocardial needs

Answer 3

1. Exercise & inc HR
2. Coarctation of aorta which leads to LV hypertrophy
3. Valvular disease
4. Hypertension (due to ven hypertrophy)

Question 4

Define angina pectoris

Answer 4

It is intermittentent chest pain caused by transient reverisble myocardial ischemia.
Anginal pain is due to release of ichemia-induced adenosine & bradykinin that stimulate autonomic afferents

Question 5

Compare typical and crescendo angina

Answer 5

T:
-It is predictable episodic anginal pain associated with particular leveles of exertion, relieved by nitroglycerine & rest. It is described as crushing/squeezing substernal chest pain radiate to left arm or left jaw.
C:
-it is increasingly frequent anginal pain associated with less exertion or at rest. It is oreinfarctiona angina. It is associated with plaque disruption, superimposed thrombosis, distal embolization of thromus & vasospasm.

Question 6

Define Prinzmetal angina

Answer 6

It occurs at rest due to coronary artery spasm, although it usually occurs on or near atherosclerosis, normal vessels may be affected. Promptly responds to VDs as nitroglycerine & Ca channel blockers

Question 7

Describe G&M features of CHD

Answer 7

G, Dilated & hypertrophied left ventricle with discrete grey-white areas from previously healed infarcts, there is moderate to severe athersclerosis of coronary vessels or complete occlusion
M, include myocardial hypertrophy diffuse subendocardial myocyte vacuolizations & fibrosis from previously healed infarcts.

Question 8

CHF parients have history of …

Answer 8

MI

Question 9

Describe pathogenesis of MI

Answer 9

-MI is due to sudden thrombotic occlusion of coronaries by atherosclerosis (acute plaque changes)
Vasospasm & platelet aggregation can contribute

Question 10

Reversible changes of MI occur during first …..

They are …..

Answer 10

1 & 1/2 hrs

Myofibril relaxation, glycogen loss & mitochondrial swelling

Question 11

GR: Out of 90% patients with thrombosis after 4 hrs, only 60% still after 12-24 hrs

Answer 11

Because at least some occlusion clear spontaneously through lysis of thromus orcrelaxation of spasm.

Question 12

Thrombolysis is done by …..

Answer 12

Streptokinase or tPA

Question 13

Describe G&M changes during:

1. 0.5 - 4 hrs
2. 4 - 12 hrs

Answer 13

1. G, none . M, usually none with variable waviness of fibers at border.
2. G, occasional dark mottling. M, beginning of coagukative necrosis & edema hemorrhage.

Question 14

Describe G&M changes during:

1. 12 - 24 hrs
2. 1 - 3 days

Answer 14

1. G, dark mottling. M, coagukative necrosis, cytoplasmic eosinophilia, nuclear pyknosis, marginal contraction band necrosis, beginning of neutrophilic infiltrate.
2. G, mottling with yellow tan infarct center. M, coagulative necrosis with loss of nuclei & striations, interstitial neutrophilic infiltrate.

Question 15

Describe G&M changes during:

1. 3 - 7 days
2. 7 - 10 days

Answer 15

1. G, hyperemic border + yellow tan central softening. M, beginning of disintegration of dead myofibers with dying neutrophils, & early phagocytosis of dead cells at infarct border.
2. G, maximally yellow tan soft with depressed red tan margins. M, well-developed phagocytosis if dead cells with ealy formation of fibrovascular granulation tissue at border.

Question 16

Describe G&M changes during:

1. 10-14 days
2. 2-8 weeks
3. > 2 months

Answer 16

1. G, red gray depressed infarct borders. M, well-established granulation tissue with new blood vessels & collagen deposition
2. G, gray white scar profressive from border towars infarct core. M, increasing collagen deposition & dec cellularity.
3. G, scarring complete. M, dense collagenous scar.

Question 17

Mention the cardiac markers useful for diagnosis of MI

Answer 17

CK & CK-MB
LDH
c-TnI

Question 18

GR: MI causes arrhythmias.

Answer 18

By causing electrical instability (irritability) of ischemic regions of the heart.

Question 19

MI reaches full size in …..

Answer 19

3 to 6 hrs

Question 20

Write a short note on site & effect in transmural infarction (coronary vessel)

Answer 20

1. Acute occulsion of proximal LAD (40-50%) affects ant wall if left vent, apex & ant 2/3 of IV septum.
2. Acute occlusion of right coronary (30-40%) affects most of rt vent, post wall of lt vent & post 1/3 of IV septum
3. Accute occlusion of proximal left circumflex (15-20%) affects lat lt vent.

Question 21

Describe factors affecting size & rate of development of MI

Answer 21

1. Size & distribution of involved vessel
2. Rate of development & duration of occlusion
3. Metabolic demands of myocardium (BP & HR)
4. Extent of collateral supply

Question 22

Describe patterns of MI

Answer 22

1. Subendocardial infarction (limitef to inner third of myocardium)
2. Transmural infarction (full thickness of ventricle)
3. Microscopic infarcts: in small vessels due to vasculitis, embolizations, vessel spasm due to elevated CA endogenous (pheochormocytoma or extreme stress) or exogenous (cocaine)

Question 23

Mention complications of infarction

Answer 23

1. Arrhythmia
2. Acute LV heart failure & sudden cardiac death
3. Rupture of papillary muscle, ventricle or perforation of IV septum resulting in acute mitral regurgitation, cardiac tamponade or left to right shunt respectively.
4. Mural thrombosis (embolization)
5. Aneurysmal dilatation
6. Pericarditis (fibrinous/hemorrhagic)
7. Progressive HF
8. Mitral valve insufficiency