Lecture 18 cardiovascular system

Prof.Dr.
Khalil Hassan Zenad
Aljeboori
Copyrights©2017lAliraqiaUniversitylDentistrylPathologylProf.Dr.KhalilHassanZenadAljeboori.
Lecture 18
CARDIOVASCULAR SYSTEM

1.Coronary sclerosis:
Arteriosclerosis involving coronary vessels is of atherosclerotic type, intimal fibrosis,
thickening, lipoid deposition, calcium deposits all of which narrow the lumen of large
vessels near the surface of heart, the left coronary artery is more severely affected
than the right. The etiology of coronary arteriosclerosis is obscure but hereditary, sex
and race are factors of importance. Diabetic women and men also had a high
incidence of coronary disease. Hypertension appear to be no have direct relation
with coronary diseases. So it is separated disorders. Coronary arteriosclerosis is
associated with decrease blood supply to myocardium cause ischemic degeneration
and necrosis, with patchy fibrosis in myocardium resulted into myocardial anoxemia
and pain of angina pectoris which more prominent during heavy work, such coronary
insufficiency result in myocardial damage which resemble an infarction.
Diseases of myocardium:

Complete occlusion result from:
1. Thrombosis
2. Progression of the arteriosclerotic process
3. Embolism
4. Intramural hemorrhage
5. Syphilitic lesion around coronary opening.
2.Coronary occlusion:

Is invariable on the basis of coronary arteriosclerosis, it is a final event blocking a lumen of
already narrowed.
Artery, also there is a relation between intimal hemorrhage in sclerotic artery and
thrombosis of lumen.
The intimal capillaries in atheromatous lesion subjected to high intracapillary blood
pressure, then prone to rupture and resulting small hematoma may precipitate thrombosis
or by itself close the lumen of sclerotic artery, so both sclerotic thickening and thrombosis
is important for artery occlusion which occur gradually. Syphilis of aorta when involve
region of coronary artery may also narrow the opening of coronary artery similar to
atherosclerosis.
Coronary occlusion by emboli may occur but rare it occur when fragment of vegetation
from adjacent aortic valve. In small cases coronary occlusion cause death due to ischemia
of myocardium which lead to ventricular fibrillation or a systole.
3.Coronary thrombosis:

It occur following coronary occlusion when occlusion of anterior
descending left coronary artery produce scarring of anterior part
interventricular septum and apical part of left ventricle
obstruction of circumflex branch of left coronary artery affect
the wall of left ventricle, obstruction of the right coronary artery
produce scarring of posterior half of interventricular septum
extending back to curve around on the posterior part of wall of
left ventricle.
Myocardial infraction:

Appearance:
If death following coronary thrombosis no lesion. In early stage the infract area dark red, hemorrhagic later
on yellow opaque with necrosis.
Microscopically:
Necrotic muscle fiber swollen, hyaline, loss striation, leukocytes infiltration, infract area become soft, and
rupture.
Healing:
by replacement of necrosis and inflammatory reaction by connective tissue which appear depressed area,
the C.T lay down collagen and area become grayish, firm, scar. This process completed within 5-8weeks.
Complication:
1. Rupture of heart.
2. Mural thrombus with emboli give rising.
3. Congestive circulatory failure, the healthy muscle remaining unable to carry heart work.
4. Mural aneurysm.

Hypertrophy of left ventricle may result from:
1. Hypertension.
2. Aortic regurgitation or stenosis.
3. Mitral regurgitation.
4. Coronary sclerosis.
Hypertrophy of right ventricle resulted from:
1. Mitral stenosis.
2. Pulmonary stenosis or regurgitation.
3. Increase resistance to pulmonary circulation e.g. from emphysema or
pulmonary arteriosclerosis.
4. Coronary sclerosis.
Hypertrophy of heart:
Increase the size of heart due to increase work, hypertrophy may accompanied by cardiac
dilatation.

Peripheral hypertension produce hypertrophy of left ventricle due to
increased work. The hypertension is disturbance of peripheral arterioles,
so the heart unable to cope with increased work so dilatation and
congestive heart failure result.
Systemic hypertension:
1. Primary (benign) hypertension
2. Secondary hypertension
Hypertensive heart disease:

Primary hypertension two types:
a) Benign hypertension,
in which slow progressive rise in blood pressure, more common in male. Five
percent of such patient enter a malignant phase after many years.
Organs changes:
1. Cardiovascular changes:
a) Heart hypertrophy of left ventricle arteries.
b)Atheroma of large arteries.
c) Muscular arteries medial hypertrophy and intimal thickening, small
arteries arteriosclerosis.
2. Brain. Cerebral vascular accident
3. Kidney-nephrosclerosis benign type.

Death due to:
1. Heart failure.
2. Coronary insufficiency or infarction.
3. Cerebral vascular accident.
4. Renal failure.
Prognosis:

Is malignant termination of benign hypertension, more progressive in
which systolic 280 mm Hg, diastolic 180 mm Hg blood pressure.
Organ changes:
1. Cardiovascular heart left ventricular hypertrophy, vessels atheroma in
small arteries. Malignant arteriosclerosis
a) Fibrinoid necrosis.
b) hyperplasia of onion skin type.
2. Kidney-malignant nephrosclerosis.
3. Brain-cerebral vascular accident.
b) Malignant hypertension:

1.Renal failure.
2.Heart failure due to hypertension.
3.Cerebral vascular accident.
Prognosis:

Occur secondary to pre-existing disease:
1. Renal diseases, renal vessels obstruction.
2. Endocrine, Cushing syndrome, phoechromocytoma,
hyperthyroidism Cohn's syndrome due to hyperaldosteronism.
3. Blood polycythemia.
4. Cerebral lesion.
5. Drugs, adrenaline.
6. Cardiovascular (coaraction of aorta, arteriovenous fistulae).
Secondary hypertension:

Myocardium may be involved by septic emboli in cases of acute or subacute bacterial
endocarditis or from pyemia. Tuberculosis and syphilitic gumma rare, granuloma due to
actinomycosis, schistosomiasis are rare acute degenerative changes or cloudy swelling
occur in toxic myocarditis with diphtheria, typhoid fever, pneumonia, interstitial
myocarditis with rickettsial disease (typhus fever), also occur with probable viral
myocarditis and following pneumonitis.
Myocarditis:
Metabolic disease:
Metabolic changes in myocardium occur with toxic goiter, myxedema, Addison's
disease and beriberi also fatty change or degeneration of heart.

Heart block:
Lesions involving special conducting tissue of heart, produce complete or partial heart block i.e. interfere
with conduction of impulses manifested by disturbances in the cardiac rhythm, the lesion are scar due to
the coronary artery disease or rheumatic fever, the left bundle branch block occur due to coronary
sclerosis or hypertension while rare right bundle branch block due to rheumatism syphilitic gumma is a
rare cause of destruction of conducting tissue.
Heart failure:
Failure of adequate circulation is a condition in which cardiac output is too low for metabolic needs and
in relation to venous return. A number of bodily disorders occur in relation to heart failure include
edema, fluid accumulation in serous cavities, chronic passive congestion in spleen, liver, kidneys and
lungs. Edema of heart due to elevated venous pressure and capillary and lymphatic changes, excessive
sodium and chloride intake.
Sudden death without any change but may be due to excessive adrenaline accumulation in heart
muscles.

Diseases of pericardium:
Pericarditis:
Mostly occur with involvement of myocarditis and endocarditis or from neighbouring
organ, lung.
Etiology:
1. Infective bacteria e.g. staph, Aureus, tuberculosis….
2. Aseptic. Rheumatic, uremic, secondary or myocardial infarction.
Types of pericarditis:
1. Serous with non-bacterial infections
2. Serofibrinous or fibrinous occur with rheumatic, myocardial infarction and in
uremia.
3. Purulent or suppurative by pyogenic bacteria.
4. Hemorrhagic, this blood mixed with inflammatory exudates.

Tuberculous pericarditis:
Either miliary, blood borne or from pulmonary T.B or mediastinal lymph
nodes. Fibrinous exudates with granulation tissue cover pericardial sac.
Constrictive pericarditis (pick’s disease):
Due to healed T.B pericarditis but may follow suppurative bacterial disease.
Polyserositis (Concato’s disease):
In which inflammatory serous effusions into periton, pleura, pericardial sac
due to either active T.B but often end into constrictive pericarditis following
the presence of inflammatory serous exudates in serous cavities.

Hydropericardium:
True transudate accumulated in pericardium.
Etiology-
1) Cardiac failure.
2) Chronic renal diseases.
3) Hypoproteinemia associated diseases.
It interfere with heart movement.

Hemopericardium:
Pure blood accumulated in pericardium etiology:
1) Rupture of heart.
2) Rupture of intrapericardial portion of aorta.
3) Hemorrhagic diseases e.g. purpura.
Neoplasms:
Tumors of heart are rare but may be metastasis from carcinoma or
leukemia. Congenital rhabdomyosarcoma is reported. Fibrosarcoma and
mesothelioma of pericardium may occur.

Lecture 18 cardiovascular system

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