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arteriolosclerosis

By Mike Wallace,2014-05-31 13:15
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arteriolosclerosis

    Chapter7 Diseases of Cardiovascular System

OBSERVATIONAL METHODS OF SPECIMEN

    Heart. (Fig.7-01) The normal heart assumes cone form flatted slightly in front and back; its size resembles ones right fist, and the heart of an adult

    man weights 240gm in females and 270gm in males. The inner endocardium

    and outer epicardium is smooth. The expected thickness of the free wall of the

    right ventricle is 0.3-0.4cm and that of the left ventricle 0.8-1.2cm. The

    perimeter of mitral valve is l0cm, of tricuspid valve l2cm, of aortic valve

    7.5cm and of pulmonary valve 8.5cm. The valve is very thin; the cordae

    tendineae is fine and long with full of flexibility.

    Gross examination. Note the size, morphology, color and smooth degree of

    the heart. Section surface: To observe whether each heart cavity is dilated, the

    thickness, degree of hardness and color and luster of the cardiac muscle is

    changed, and there are myocardial infarct, hemorrhage and scar formation;

    whether the endocardium is smooth, whether there are mural thrombi and

    hemorrhagic point in the endocardium; whether the perimeter of each valve is

    changed; whether there are edema, thickness and/or scarring, ulcer and

    perforation in the valve; whether there are adhered vegetations in valve and

    how is its quantity, size, morphology, color and arrangement; whether the

    cordae tendineae is thickness, shortening and fusion; whether the papillary

    muscle is hypertrophy; whether there are defect in the auricular and

    ventricular septum; whether the foramen ovale is closed and pathological

    changes in the coronary artery.

    Light microscope examination. Note whether there is inflammation, what

    kind of inflammation and characteristic lesions on each layer of heart wall;

    whether the myocardial cells are hypertrophy, atrophy, and whether cross

    striation is clear; whether the pigment and the other foreign materials are

    deposited in the myocardial plasma; whether the endothelial cells are integrity

    and there are mural thrombi in the endocardium, and the adhered vegetations

    in valve constitute with what kinds of composition.

    Blood vessel. Three basic structural constituents make up the walls of

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blood vessels: endothelium, smooth muscle, and connective tissue. They are

    arranged in concentric layers (or tunicas) - an intima, a media, and an

    adventitia - most clearly distinguished in the larger vessels. Arteries are

    divided into three types: ?Large or elastic arteries, including aorta and its

    major branches; ?Medium-sized or muscular arteries(such as the coronary or renal arteries), also referred to as distributing arteries; and ?Small arteries

    (usually less than 2 mm in diameter).

    Gross examination. To observe that whether the shape (such as saccular protrusion, fusiform expansion, flexion and tubercle, etc.), thickness and

    hardness of blood vessel are changed; whether the vascular intima is smooth

    and has the sclerosis plaque; whether the vascular lumen is narrow, and

    thrombus and the other foreign materials.

    Light microscope examination. (Fig. 7-02a,b) To observe whether the

    vascular endothelial are integrity, and there are intimal thickness and

    deposition of abnormal materials in the intima; whether the elastic fibers are

    break, increase or decrease, and the smooth muscle cells have what kind of

    changes in the media; and whether there is inflammation in each layer of

    vascular wall and narrow of the lumen.

AIMS

1. To grasp the basic pathological changes of atherosclerosis; the

    characteristics of pathological changes of atherosclerosis of coronary and

    brain artery; and the type, pathological changes and consequence of the

    coronary heart disease.

    2. To grasp the pathological changes and outcome of main organs of the

    primary hypertension, and the relationship between atherosclerosis and

    hypertension.

    3. To grasp the basic pathological changes of rheumatic disease and the

    pathological changes of rheumatic heart disease; to master the pathological

    features of chronic valvular heart disease and its influence on

    hemodynamics.

    4. To be familiar with the pathological changes and its consequence of

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    infective endocarditis.

    5. To understand the concept, pathological changes and its consequence of

    myocarditis and cardiomyopathy.

CONTENTS

     Gross specimen Tissue section

    Atherosclerosis of the aorta Atherosclerosis of the aorta Atherosclerosis

    Atherosclerosis of the brain Coronary atherosclerosis

    Coronary atherosclerosis

    Myocardial infarction Myocardial infarction Coronary heart

    disease

    Hypertensive heart disease Arteriolar nephrosclerosis Primary hyper- tension

    Arteriolar nephrosclerosis Hyaline degeneration of the

    spleen artery

    Brain hemorrhage Necrotizing arteriolitis

     Hyperplastic arteriolosclerosis

    Rheumatic endocarditis Rheumatic endocarditis Rheumatic heart

    disease

    Rheumatic pericaditis Rheumatic myocarditis

     Rheumatic pericaditis

    Mitral valve stenosis Valvlar vitium of

    the heart

    Mitral valve stenosis and

    insufficiency

    Acute bacterial endocarditis Acute bacterial endocarditis Infective endo- carditis

    Subacute bacterial endocar- Subacute bacterial endocar-

    ditis ditis

    Dilated cardiomyopathy Hypertrophic cardiomyopathy Cardiomyopathy

    Hypertrophic cardiomyopathy Keshan disease

    Keshan disease

     Viral myocarditis Myocarditis

     Bacterial myocarditis

KEY POINTS OF SPECIMEN OBSERVATION

1. Atherosclerosis

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Basic pathologic changes

    (1) Gross morphology

    ?Fatty streak and spot: Multiple yellow, flat spots, flatten or slightly

    raised, are visible on the tunica intima of the arteries. Some of the spots

    coalesce into enlongated streaks

    ?Fibous plaque: Yellow or porcelain white (wax drop shape) plaque

    slightly raised above the surrounding intimal surface.

    ?Atheromatous plaque: The plaque appears white or whitish yellow,

    slightly raised and impinge on the lumen of the artey. On section, the

    superificial portion of these lesions at the luminal surface tend to be firm

    and white (the fibrious cap) and the deep portions yellow or whitish

    yellow and soft, the centers contain yellow, grumous debris. Its bottom is

    atrophied media. The atheroma may complicate ulceration or

    calcification.

    ?Complicated lesions: Hemorrhage into a plaque; focal rupture or gross

    ulceration; thrombosis; calcification; aneurysm; media weakening; and

    the lumen is narrowed in different degree.

    (2) Histopathology

    ?Fatty streak: A collection of lipid-filled foam cells in the intima.

    ?Fibrous plaque: The surface of plaque is the fibrous cap under that

    contains smooth muscle cells, macrophages, foam cells, and extracellular

    lipid and matrix.

    ?Atheroma: The surface layer of atheroma is hyaline degenerated fibrous

    cap, the deep layer is lots of amorphism necrotic mass in which has

    cholesterol crystal and calcium salt, and the bottom and edge of lesion

    has granulation tissue, a little of foam cells, mononuclear cells and

    lymphocytes.

    Specimen observation

    Case abstract: Male, 55-year-old. He suffered the intermittent substernal

    ache and/or precordial chest ache accompanying with the short breath and

    heartthrob for 4 years. In the last 2 months, the symptoms were more serious.

    3 hours ago, paroxysmal acute angina pectoris was happened after hard work

    and the radiating pain was emitted to left shoulder and arm. Myocardial

    infarct was diagnosed by electrocardiogram, showing pathologic Q waves in

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leads V1-V5. The emergency treatment didnt work. Patient was dead. Serious

    atherosclerosis of the aorta and its main branches, coronary artery, the circle

    of Willis and myocardial infarct of the left ventricle wall were observed in

    autopsy.

    (?)Atherosclerosis of the aorta

    Gross specimen: (Fig. 7-03a, b) There are many grey and yellow plaques,

    slight elevated on tunica intima of the aorta. Pin-size yellow flecks are fatty

    streak, gray hunch is fibrous plaque; yellow white one is atheromatous plaque.

    What is the main pathological change and where is the most serious lesion?

    What complications are there?

    Tissue section: (Fig. 7-04a,b, c) First, ascertain the tunica intima of the aorta and to observe the characteristic lesions of the intima.(a)Plenty of foam cells

    congregated under endothelium, which is fatty streak.(b) Fibrous plaque. The

    surface of intima is fibrous cap, under which there are plenty of foam cells. (c)

    Atheromatous plaque. Local intemia thicken apparently; surface of intima is

    fibrous cap with hyaline degeneration. The light stained area is necrotic

    substance, cholesterol crytstal and calcification under the cap. Media is

    compressed and become thinner.

    Question: What kinds of complicated lesions are there in atherosclerosis of

    the aorta? Which is the most feared?

(?) Coronary atherosclerosis

    Gross specimen: (Fig.7-05a,b) It is coronary artery sliced transversely or vertically ?Note the characteristics lesions in the tunica intima; ?Note the

    changes of the lumen.

    Tissue section: (Fig. 7-06a,b) ?Note the changes of thickness and lumen;

    ?Note characteristics lesions in the vascular wall.

    Question: What is the most dangerous lesion of coronary atherosclerosis for

    the patient?

(?) Atherosclerosis of the basal artery

    Gross specimen: (Fig. 7-07) Opened or unopened the basal artery (some with the brain tissue). ?See through the adventitia; there is yellow white plaques

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    on intima; ?Wall thichen with luminal narrowing. Question: What kind of influence does atherosclerosis of the brain on the cerebral cortex? What outcome could it be? What kinds of clinical

    manifestation are there?

(?) Myocardial infarction

    Gross specimen: (Fig.7-08a, b) Horizontal section of the heart.(a) Gray

    infarctive focuses are visible at anterial wall of left ventricle and anterior

    1/3 of interventrical septum, which involve all layers.(b)It is left ventricular

    aneurysm. The wall of left ventricle become thin, protrude, complicated from

    myocardial infarct.

    Question: What complications and results may be having?

    Section: (Fig. 7-09a, b, c) To ascertain and observe the region of damage.(a)

    Light microscope of 1 day of myocardial infarct.The cytoplasm of myocytes

    are granular with loss of nuclei and striations; and cytoplasm of some

    myocytes are coagulative and hypereosinophilic showing wave-like striation.

    Interstitial vessels dilate and congest. (b) Necrotized cardiac muscle cells

    dissolve presenting netlike. (c)In the seventh daysperipheral granulation

    tissues grow into replacing the infarct.

    Question: What are the reasons of myocardial infarct? What are the main manifestations in clinic? Which complications and results may be having?

2. Primary hypertension

    Basic pathologic changes

    The following pathological changes could be seen at the stage 2, 3 or

    complications stage respectively.

    (1) Gross morphology

    ?The artery

    ? Wall of arterioles thicken and is sclerosis, and the lumen is narrow;

    ? Wall of small artery thicken, and lumen contracts in different degree;

    ? Large artery: often accompanying atherosclerosis.

    ?Heart: concentric hypertrophy or eccentric hypertrophy of the left

    ventricle.

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    ?Kidney: primary granular atrophy of the kidney. The kidneys are reduced

    in size, and the cortical surfaces show fine, even granularity. On cut

    surface, the renal cortex becomes thin, and dividing line between the

    cortex and medulla is not clear.

    ?Brain: edema, cerebral softening or cerebral lacunar infarct, and

    hemorrhage.

    ?Retina: arteriosclerosis of the central artery, papilledema, ratinal

    exudates and hemorrhage.

    (2) Histopathology

    ? The artery

    1) Benign hypertension

    ? The vascular lesion consists of a homogenous, pink, hyaline

    thickening of the walls of arterioles with loss of underlying

    structural detail and narrowing of the lumen.

    ? Elastic fibers and collagenous fibers in the intima of the small artery

    (musclar artery) increase; the internal elastic laminas reduplicate;

    and smooth muscle cells and elastic fibers in the media increase.

    2) Malignant hypertension: fibrinoid necrosis of arterioles, proliferation

    of smooth muscle cells of the small artery yielding onion-skin

    appearance.

    ?Myocytes: hypertrophy.

    ?Kidney: focal atrophy and disappearance of nephrons, hyperplasia of the

    connective tissue and infiltration of the lymphocytes in the interstitial.

    The rest glomeruluses are hyprothy accompanying with the renal tubules

    dilation and protein cast formation in the tubular lumen.

    ?Brain: cerebral edema, focal liquefactive necrosis and hemorrhage.

    Specimen observation

    (?) Benign hypertension

    Case abstract: Female, 55-year-old. She often suffered headache and

    dizziness for 6 years, and these symptoms aggravated after emotional

    excitement and hard work. In recent one year, she occasionally felt the chest

    distress and palpitation, amount of urine increased, and the blood pressure

    was 200/130mmHg(26.7/17.3kPa). Urinary albumin (+), chest-X-ray:

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    hypertrophy of the heart as “boot” shape. One day ago, she suddenly fainted at working and the left limbs paralyzed. The emergency treatment didnt work.

    Patient was dead.

    (1) Hypertensive heart disease (HHD)

    Gross specimen: (Fig. 7-10) To pay attention to observe the size, shape of the

    heart, thickness of the ventricular wall, and the changes of papillary muscles,

    valves and cavity of the left ventricles.

    Question: How do these changes of the heart take place? What influence will it

    make on human body?

    Tissue section: (Fig. 2-07) To observe the change of the cardiac muscles and think of the causation of these changes.

    (2) Arteriolar nephrosclerosis

    Gross specimen: (Fig. 7-11) ?How do the size, shape and surface of the kidney change? ?What changes have happened in the renal cortex and medulla?

    ?Do the renal pelvis and its surrounding tissues have any changes? ?What

    characteristics does transected small artery have?

    Tissue section: (Fig.7-12a,b) The afferent glomerular arteriole suffered

    homogeneous, red-stained hyaline degeneration, and vascular wall thicken with

    stricture or obstruction of the lumen; wall of interlobular arteries thicken,

    lumen of that stricture. Some of glomeruli suffered fibrosis, hyaline

    degenerationcorresponding glomeruli atrophy, disappear and is replaced by

    fibrous tissue. Other glomeruli suffered compensatory hypertrophy; renal

    tubule dilateand protein cast can be seen.

    Question: What serious consequence, can be caused by pathologic changes of

    the kidney and what are the clinical manifestations?

    (3) Brain Hemorrhage

    Gross specimen: (Fig. 7-13) Note the position, scope of the hemorrhage in

    the brain tissue, and then to infer the patient’s clinical manifestations.

    (4) Hyaline degeneration of the spleen artery

    Gross specimen: (Fig. 7-14) To observe carefully the changes of the central

    arterial wall in the white pulp.

(?) Malignant hypertension (Accelerated hypertension)

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Tissue sections:(Fig. 7-15a,b) (a) Interlobular arteries suffered fibrinoid

    necorsis. (b) Hyperplastic ateriolosclerosis is identified with its onion-skin,

    concentric, laminated thickening of the walls of arterioles, caused by

    increase of smooth muscle and collagen fibers in the wall of interlobular

    arteries.

    Question: What are the characteristic lesions of arteriole and small atery? What manifestations would patient show? What is the main cause of death?

3. Rheumatism heart disease (RHD)

    Basic pathologic changes

    ?Alteration and exudative stage

    There are mucoid degeneration of connective tissue matrix, fibrinoid

    necrosis of collagen and a little of serous fluid and infiltration of plasma

    cells.

    ?Proliferative stage (granulomatous stage)

    The basic pathological change is formation of Aschoff body (rheumatic

    body or rheumatic granuloma).

    Aschoff body is large, round or oval, consists of central fibrinoid

    necrosis with a perimeter of Aschoff cell (rheumatic cell), lymphocyte,

    plasma cell and monocyte.

    Aschoff cells have abundant basophilic cytoplasm and single or multiple central round-to-ovoid nuclei in which the chromatin is disposed in the

    central zone. In cross section these nuclei have an “owl eye” appearance,

    and when cut longitudinally they resemble a “caterpillar”.

    ?Scar stage (healing stage)

    The rheumatic granuloma is replaced by the fibroblast, and finally

    become fibrous scar.

    ?Hereinabove pathological changes could appear at the same time.

    ?The rheumatic lesion in tunica serosa is mainly serous and/or fibrinous

    inflammation.

    (1) Gross morphogogy

    ?Rheumatic endocarditis

    It mainly involves the mitral valve. Vegetations (verrucae) are visible

    along the line of closure of the valve leaflet. The valve leaflets become

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    fibrous thickening, hardening or fusion. The irregular MacCallum

    plaques may be visible in the left atrium.

    ?Rheumatic myocarditis: the myocardial interstitium inflammation, the

    heart may dilate.

    ?Rheumatic pancarditis: cor villosum or hydropericardium could be seen.

    (2) Histopathology

    ?Rheumatic endocarditis: the vegetations are white thrombus, composed

    of pink platelet trabeculae and dark-red fibrin.

    ?Rheumatic myocarditis: scattered Aschoff bodies within the interstitial

    connective tissue, often perivascular. Besides, degeneration, exudation

    and focuses of scar may be seen.

    ?Rheumatic pancarditis: a fibrinous or serofibrinous inflammation.

    Specimen observation

    (?) Rheumatic endocarditis

    Case abstractFemale, 10 years old. She had fever and migratory joint ache for 2 months, palpitation and hard breath for 1 week. She also sufferen from

    lower extremities edema, hepatomegly and splenomegly, ascitis, and

    pink-white froth sputum was coughed. She was dead after effectless treatment.

    Gross specimen: (Fig. 7-16a,b) (a) Acute rheumatic endocarditis. The mitral valve is thin. There is a row of small irregular, warty gray vegetations

    (verrucae) on the line of closure of atrial surface of mitral valve; cordae

    tendineae thicken. (b) Recurrent rheumatic endocarditis. The mitral valve and

    the tendinous cords thicken apparently, a few of small brown warty

    vegetations are visible alone the line of closure of valve leaflet.

    Tissue section: (Fig. 7-17) First to recognize the valve and to observe the pathological changes of the valve.

    Question: What is the essence of the lesion? What kind of serious results will

    be happened if the lesion relapsed?

(?)Rheumatic myocarditis

    Tissue section: (Fig. 7-18a,b) The myocardial interstitium especially besides vessels has circumscribed collection of cells, the Aschoff body.

    Question: Whats lesion in this stage? How many stage of lesions in the

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