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Cardiovascular Module > Pathologu Ischemic Heart Disease > Flashcards

Pathologu Ischemic Heart Disease Flashcards

1
Q

Ischaemic Heart disease

A

Conditions resulting from in balance between supply and demand of heart for oxygenated blood

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2
Q

Single most important factor in imbalance between oxygen supply and demand

A

Reduction in coronary perfusion

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3
Q

Disorders that can cause partial or complete coronary Obstruction

A

Atherosclerosis

platelet aggregation and thrombosis

vasospasm

Infectious Inflammatory disorders (syphilis tuberculosis etc.)

Non-infectious inflammatory disorders ( Polyarteritis nodosa, takayasus disease , kawasakis disease, SLE, rheumatoid vasculitis)

Shock
 embolism 
neoplasm 
trauma 
Aneurysm
 congenital anomalies
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4
Q

Most important factor causing Reduced coronary perfusion

A

Coronary Atherosclerosis (90% of IHD with at least 75% luminal narrowing )

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5
Q

Coronary arteries affected by Atherosclerosis

A

Left anterior descending artery ( first 2 cm)

Left coronary artery (first 2 cm)

Right coronary artery (proximal and distal third )

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6
Q

…. is Released by activated platelets which cause vasoconstriction and reduce coronary perfusion

A

Thromboxane A2

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7
Q

Vasospasm impact in astherosclerosis

A

Vasoconstriction leading to reduced lumen size which increase local mechanical forces contributing to plaque rupture

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8
Q

Vasospasm is induced by

A

Adrénergic agonist

Released please content

Impaired secretion of endothelial cell relaxing factors such as NO

Cocaine

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9
Q

Vasculitis impact in atherosclerosis

A

Narrowing and super added Thrombosis leading to occlusion of lumen

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10
Q

Factors that can affect blood flow which will reduce coronary perfusion

A

Blood pressure Drop during shock

Aortic stenosis

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11
Q

Pathogenesis of IHD

A

Increase demand in oxygen without increase in supply ( high HR , ventricular hypertrophy)

Decreased oxygen carrying capacity of blood ( severe anemia, CO poisoning)

Decreased Oxygenation of blood (advance pulmonary disease)

Decreased coronary blood flow so perfusion defect (90% of IHD)

Anaerobic glycolysis accelerated
ATP depletion

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12
Q

Consequences of declining ATP concerns

A

Lots of sodium and potassium gradients
calcium overload
activation of endogenous phospholipase and professes which can damage cytoskeletal supports
accumulation of catabolite such as lactates which inhibit ATP production
products of lipids degradation act as detergents to damage cell membranes
Adenine nucleosides and bases accumulates and become source of free Radicals via the xanthine oxidase reaction

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13
Q

Presentation of IHD

A

Angina pectoris
myocardial infarction
Chronic ischemic heart disease with heart failure
sudden cardiac death

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14
Q

Angina pectoris

A

Attacks of sudden substernal or precordial chest discomfort or pain

Transient episodes of myocardial ischemia that falls just precariously shorts of inducing infarction but has reversible myocyte injury

Chest pain is :
constricting 
vice like 
squeezing 
gripping 
crushing 
choking
 knife like
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15
Q

Angina pectoris subtypes

A

Stable or chronic angina

variant or printzmetals angina

stable or Cresendo or pre-infarction angina

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16
Q

Commonest form of angina

A

Stable

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17
Q

When do you get chest pain in stable angina

A 
Physical activity 
exposure to cold 
strong emotions 
heavy meal 
serious injury 
shock 
anemia
 thyrotoxicosis
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18
Q

Characteristics of stable angina

A

Fixed -degree of coronary stenosis

blood flow adequate for resting metabolic needs

No coronary reserve to allow increased perfusion when demands increase

ST segment depression on ECG because subendocardium affected

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19
Q

Major cause of a stable angina

A

Stenosis due to atheroma

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20
Q

5% of stable angina due to

A

Left ventricular hypertrophy

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21
Q

Less common reason for stable angina

A

Spasm of epicardial arteries
Myocarditis
intrinsic metabolic defect
disease of the small intramyocardial vessels (syndrome X , microvascular angina)

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22
Q

Syndrome X population affected

A

Woman especially after hysterectomy

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23
Q

Variant or prinzmetals angina

A

Occurs at rest
Not related to physical exertion emotional stress or any of the factors know to cause ischemia
Mostly due to vasospasm
Increased risk of sudden cardiac death

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24
Q

Treatment of variant agina

A

Vasodilators such as nitroglycerin

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25
Q

Unstable angina

A

Unpredictable episodes of pain

accelerate in intensity and frequency overtime

Can’t happen with less and less effort and sometimes at rest overtime

Results in myocardial infarction or sudden cardiac death

26
Q

Cause of unstable angina

A

Atheromatous plaque with acute changes like fissuring , rupture , ulceration and Thrombosis ( mural not occlusive)

Vasospasm over plaque
Dynamic stenosis

27
Q

Other types of angina

A

Nocturnal angina (Chest pain during sleep caused by increased heart rate associated with dreams or underlying congestive cardiac failure)

decubitus or resting angina ( happens to person at rest lying down and frequently at the same time every day . reduced when the person sits or standups).

post infarction angina ( Occurs after MI when residual ischemia triggers angina)

28
Q

Myocardial infarction

A

Myocardial necrosis following cessation, decrease in or interference with myocardial blood supply

29
Q

What disease is myocardial infarction associated with

A

Atherosclerosis

30
Q

Population more at risk of dying from myocardial infarction

A

Males

31
Q

Two forms of myocardial infarction

A

Acute regional transmural infarct

Diffuse subendocardial infarct

32
Q

Acute regional transmural infarction

A

Involves full or nearly full thickness of the ventricular myocardium

Infarct vary in size

33
Q

Pathogenesis of Acute regional transmural infarction

A

Initial events acute change in atheroma ( 50%/75% luminal narrowing )

Recent occlusion of the coronary artery by Thrombosis ( Platelet aggregation over exposed subendothelial collagen)
Underlying ulcerated or Stenotic atheroma

vasospasm

Increased myocardial demands reducing cardiac blood flow such as shock

34
Q

Clinical course of myocardial infarction

A 
Sudden cardiac death 
arrythmias 
left ventricular failure 
thromboembolism 
rupture of infected myocardium 
cardiac aneurysm 
Postinfarct mitral incompetence 
Pericarditis 
Dressler syndrome
35
Q

Sudden cardiac death after myocardial infarction

A

25% of patients die before hospital

Mostly due to left ventricular failure , cardiac arrhythmias (Ventricular fibrillation)

Cigarette smoking increase risk of sudden cardiac death after myocardial infarction

36
Q

Arrythmias after myocardial infarction

A

Most important factor for survival and frequency

Manifest mostly as Ventricular fibrillation

Can lead to 
heart block 
Ventricular premature contractions 
sinus bradycardia 
sinus tachycardia 
Ventricular Tachycardia
37
Q

Left ventricular failure after myocardial infarction

A

Can cause cardiogenic shock ( more than 40% of left ventricle infarcted)

Chronic cardiac failure may occur

38
Q

Thromboembolism after myocardial infarction

A

Systemic emboli from mural Thrombosis

Most important is systemic venous Thrombosis especially in legs

Can lead to massive pulmonary embolism which can lead to death

39
Q

Rupture of infarcted myocardium

A

5% of cases

mostly in the free wall of the left ventricle
lead to hemopericardium
death from cardiac tamponade

Loud pansystolic murmurs in rupture of papillary muscle of the interventricular septum

Rapidly fatal mostly occurs in first week when infarct is soft

40
Q

Cardiac aneurysm after myocardial infarction

A

During healing stage

Hills infarct is a thin fibrous tissue which can bulge or stretch under systolic pressure force

Mostly located near Apex because commonest sites of interaction

Laminated thrombus is in cavity
calcification of the wall of the aneurysm
spontaneous rupture not common

41
Q

Post infarct mitral incompetence after myocardial infarction

A

Due to papillary muscle fibrosis and shortening of Ventricular dilatation

42
Q

Pericarditis after myocardial infarction

A

Epicardial manifestation of myocardial inflammation

Fibrinous or finbrinosanguinous pericarditis

Develops 2 to 3 days after transmural infarction

Sharp chest pain with movement and respiration

Resolve over time

43
Q

Dressler syndrome

A

Weeks to months after acute MI

Chest pain 
 pericardial friction rub 
Pleurisy
 pulmonary infiltrates 
fever 
malaise 
leucocytosis 
pericardial effusion which is fibrinous

Due to autoimmune reaction to myocardial damage

Aspirin treatment , corticosteroids if recurrent

44
Q

Right coronary artery obstruction

A

30% cases

Inferior or posterior wall infarction of left ventricle
Often -> Posterior third of interventricular septum
right ventricular free wall in some cases

ECG changes in leads II III aVF

45
Q

left anterior descending coronary artery occlusion

A

50% cases

Anterior wall infarction of left ventricle

Often -> anterior wall of the right ventricle

Often-> anterior 2/3 of interventricular septum

46
Q

Left circumflex coronary artery occlusion

A

20% of cases

lateral wall infarction of left ventricle

47
Q

Most come on location and size of regional infarct

A

Transmural

2 cm at least

48
Q

Morphology of myocardial infarction up to 18 hours

A

No gross appearance

No observable microscopic changes

49
Q

MI morphology 24 to 48 hours after

A

Grossly -> pale edematous muscle

Microscopically - Edema, myocyte necrosis , acute inflammatory cell infiltration

50
Q

MI morphology 3 to 4 days after

A

Gross-> yellow rubbery center, sharply defined hemorrhagic border

Microscopically -> coagulative necrosis, Inflammatory infiltrates in the center, granulation tissue formation at the periphery

51
Q

MI morphology 1-3 weeks after

A

Grossly -> infarcted area paler and thinner than normal area

Microscopically -> Well formed granulation tissue, fibrosis in healing

52
Q

MI morphology 3-6 weeks afrr

A

Grossly -> scar tissue looking tough and white

Microscopically-> dense fibrosis

53
Q

Cardiac enzyme demonstrating myocardial infarction

A

CK rises 2 to 4 hours ( peak in 24 hour , normal after 72 hours)

CK-MB - Specific, rises within 4-8 hours, peak at 18 hours , normal 48 to 72 hours after

Troponin I & T normally not detectable in the serum , seen at same time as CK—MB and persists 7-10 days

54
Q

Diffuse subendocardial infarction l

A

Inner part of the left ventricular myocardium affected

Necrosis patchy or confluent

55
Q

Diffuse subendocardial infarction pathogenesis

A

Major coronary arteries all severely narrowed by atheroma

56
Q

Pathophysiological basis of subendocardial MI

A 
Decrease in perfusion of left ventricle 
Decrease perfusion pressure 
Decrease diastolic interval 
Compromise flow to myocardium 
 Left ventricle hypertrophic
57
Q

Causes of subendocardial MI

A

Aortic valve disease

Cardiogenic shock

End stages of dilated cardiomyopathy

58
Q

Clinical course of subendocardial MI

A

Pericarditis

Rupture of ventricular wall or septum

Subendocardial fibrosis in healing

59
Q

Sudden cardiac death

A

Death occurring instantaneously or within 1,2,6,12,24h after onset of symptoms

Exclude unnatural causes

60
Q

Percentage of IHD under sudden cardiac death

A

40%

Cardiovascular Module (21 decks)

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