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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
Unstable angina
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
Cause of unstable angina
Atheromatous plaque with acute changes like fissuring , rupture , ulceration and Thrombosis ( mural not occlusive) Vasospasm over plaque Dynamic stenosis
27
Other types of angina
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
Myocardial infarction
Myocardial necrosis following cessation, decrease in or interference with myocardial blood supply
29
What disease is myocardial infarction associated with
Atherosclerosis
30
Population more at risk of dying from myocardial infarction
Males
31
Two forms of myocardial infarction
Acute regional transmural infarct Diffuse subendocardial infarct
32
Acute regional transmural infarction
Involves full or nearly full thickness of the ventricular myocardium Infarct vary in size
33
Pathogenesis of Acute regional transmural infarction
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
Clinical course of myocardial infarction
``` Sudden cardiac death arrythmias left ventricular failure thromboembolism rupture of infected myocardium cardiac aneurysm Postinfarct mitral incompetence Pericarditis Dressler syndrome ```
35
Sudden cardiac death after myocardial infarction
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
Arrythmias after myocardial infarction
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
Left ventricular failure after myocardial infarction
Can cause cardiogenic shock ( more than 40% of left ventricle infarcted) Chronic cardiac failure may occur
38
Thromboembolism after myocardial infarction
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
Rupture of infarcted myocardium
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
Cardiac aneurysm after myocardial infarction
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
Post infarct mitral incompetence after myocardial infarction
Due to papillary muscle fibrosis and shortening of Ventricular dilatation
42
Pericarditis after myocardial infarction
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
Dressler syndrome
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
Right coronary artery obstruction
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
left anterior descending coronary artery occlusion
50% cases Anterior wall infarction of left ventricle Often -> anterior wall of the right ventricle Often-> anterior 2/3 of interventricular septum
46
Left circumflex coronary artery occlusion
20% of cases | lateral wall infarction of left ventricle
47
Most come on location and size of regional infarct
Transmural | 2 cm at least
48
Morphology of myocardial infarction up to 18 hours
No gross appearance | No observable microscopic changes
49
MI morphology 24 to 48 hours after
Grossly -> pale edematous muscle Microscopically - Edema, myocyte necrosis , acute inflammatory cell infiltration
50
MI morphology 3 to 4 days after
Gross-> yellow rubbery center, sharply defined hemorrhagic border Microscopically -> coagulative necrosis, Inflammatory infiltrates in the center, granulation tissue formation at the periphery
51
MI morphology 1-3 weeks after
Grossly -> infarcted area paler and thinner than normal area Microscopically -> Well formed granulation tissue, fibrosis in healing
52
MI morphology 3-6 weeks afrr
Grossly -> scar tissue looking tough and white Microscopically-> dense fibrosis
53
Cardiac enzyme demonstrating myocardial infarction
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
Diffuse subendocardial infarction l
Inner part of the left ventricular myocardium affected Necrosis patchy or confluent
55
Diffuse subendocardial infarction pathogenesis
Major coronary arteries all severely narrowed by atheroma
56
Pathophysiological basis of subendocardial MI
``` Decrease in perfusion of left ventricle Decrease perfusion pressure Decrease diastolic interval Compromise flow to myocardium Left ventricle hypertrophic ```
57
Causes of subendocardial MI
Aortic valve disease Cardiogenic shock End stages of dilated cardiomyopathy
58
Clinical course of subendocardial MI
Pericarditis Rupture of ventricular wall or septum Subendocardial fibrosis in healing
59
Sudden cardiac death
Death occurring instantaneously or within 1,2,6,12,24h after onset of symptoms Exclude unnatural causes
60
Percentage of IHD under sudden cardiac death
40%

Cardiovascular Module (21 decks)

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