Study the electronogram

Myeloma cell, x 16 000.

Pay attention to expansion of endoplasmatic reticulum canals filled with paraprotein. What group of leukemia does multiple myeloma belong to? Name the types of multiple myeloma according to its localization. Name histological variants of multiple myeloma.


1. Name the histogenetic types of acute leukemia: a)..., b)...,c)...,d)...,e)...,f)...,g)....

2. What are pathological changes in chronic myelocytic leukemia: a) the size of the liver and spleen, b) appearance of the bone marrow, c) characteristic cells in hemo- and myelogram.

3. Name the types of multiple myeloma: a) according to the marrow involvement: 1)..., 2)..., b) morphological types: 1)...,2)....

4. Name the types of Hodgkin's disease depending on the degree of generalization: 1) a)..., b)..., 2) name histological types of it: a)..., b)..., c)..., d)....

5. Name the types of anemia according to pathogenesis: a)...,b)...,c)....

6. A child aged 8 developed weakness, increase of body temperature, nasal bleeding and odontorrhagia. The hemogram has demonstrated 20,000 leukocytes (mainly lymphoblasts) per 1 mm2. What type of leukemia is it judging by the level of differentiation of leukemia cell and cytogenesis?

Answers: 1. a) nondifferentiated, b) myeloblasts, c) lymphoblastic, d) monoblastic, e) megacarioblastic, f) erythromyeloblastic g) plas-moblastic. 2. a) increased, b) pyoid, c) myelocytes, promyelocytes.

3. a) osseous, extraosseous, b) solitary, multiple (generalized). 4. a) isolated, generalized, b) lymphohistiocytic, nodular, mixed-cell, with suppression of lymphoid tissue. 5. a) posthemorrhagic, b) owing to infringed hemopoiesis, c) hemolytic. 6. Acute lymphoblastic leukemia.

Questions to control the knowledge

1. Give definition of hemoblastoses.

2. Give definition of leukemia, what is the difference between leukemia and leukocytosis.

3. What factors allow to define leukemia as acute or chronic?

4. Name histo-(cyto-)genetic classification of acute and chronic leukemia; the difference between them.

5. What is the difference in hemo- and myelogram in acute and chronic leukemia?

6. Pathological anatomy of acute and chronic leukemia.

7. Complications and causes of death in leukemia.

8. Pathomorphosis of leukemia.

9. The signs of leukemia in children.

10. Classification of lymphoma. Hodgkin's disease.

11. Anemia, its types.

12. Pathological anatomy of anemia.


Anemia, leukemia, hemoblastoses, lymphoma, leukemic failure, blast crisis, Gunter's glossitis, pyoid marrow, Hodgkin's disease.



Atherosclerosis is a chronic disease affecting primarily the intima of large and medium-sized arteries and is characterized by fibrolipid plaques or atheromas. Atherosclerosis is the commonest arterial diseases.

Epidemiology. It is known that the most common cause of death (40%) is cardiovascular diseases, most of witch are related to atherosclerosis. Epidemiologic investigations on living populations have revealed a number of risk factors, which are associated with increased risk of developing clinical atherosclerosis.

The risk factors are often acting in combination rather than singly.

The first of them is age. Early atherosclerotic lesions may be present in childhood, but clinical manifestations will appear later. In scientific research, which have been performed at our department, morphological signs of atherosclerosis were found in the fetus and new-born aorta.

The second of risk factors is sex. The incidence and severity of atherosclerosis are higher in men than in women.

Genetic factors play a significant role in atherosclerosis. There is familial predisposition to atherosclerosis which may be related to other risk factors like diabetes, hypertension and hyperlipoproteinemia.

Geographic factors also play a role. There is a high incidence of atherosclerosis in the Europe, Australia, and US.

Many studies have demonstrated specific effects of diet including the amount of dietary cholesterol ingested on lipid and lipoprotein levels.

Hypertension is a major risk factor in atherosclerosis development. It acts probably by mechanical injury to the arterial wall due to increased blood pressure.

Other factors are diabetes mellitus, smoking, obesity, etc.

Pathogenesis. There are several patho-genesis theories of atherosclerosis: Virchow's, Rokitansky's, Anychkow's, Benditt's. Historically, two hypotheses for atherogenesis were dominant: one emphasized cellular proliferation in the intima as a reaction to insudation of plasma proteins and lipids from the blood, whereas the other postulated that organization and repetitive growth of thrombi resulted in plaque formation. The contemporary view of the pathogenesis of atherosclerosis incorporates elements of both older theories and is called the response to injury hypothesis. Formulated in 1973 and modified in 1986 and 1993, it states that atherosclerotic lesions are initiated as a

response to some form of injury to arterial endothelium. The injury is a form of endothelial dysfunction without necessary denudation, which increases permeability to plasma constituents, including lipids, and permits blood monocytes and eventually platelets to adhere to endothelium. Monocytes adhere and subsequently enter the intima, transform into macrophages, and accumulate lipid to become foam cells, contributing to the evolution of the lesion. Factors released from activated platelets at the surface or monocytes then cause migration of smooth muscle cells from media into the intima, followed by proliferation and synthesis of extracellular matrix components by smooth muscle cells, leading to the accumulation of collagen and proteoglycans. Single or short-lived injurious events can be followed by restoration of endothelial function and regression of the lesion. Repeated or chronic injury, however, results in the development of an atheromatous plaque, probably by permitting continuing increased permeability, ingress of monocytes, or perhaps platelet interactions.

Morphology. Although the fibrous and complicated plaques are the atherosclerotic lesions associated with disturbances in blood front that cause clinical disease states, the morphologic changes of diffuse intimal thickening and fatty streaks may be either precursors of the basic atherosclerotic lesion or stages in its development.

1. Intimal thickening. Fibromuscular thickening of the intima of arteries may be a part of atherosclerotic process, particularly rapid during the first two decades of life. Macroscopically, the lesions may appear as small white areas of intimal cushion at the bifurcation and branching of arteries, or many be appear as «diffuse intimal thickening». Microscopically, the lesions consist of smooth muscle cells, fibrous tissue, some collagen but no lipid.

2. Fatty streaks especially prominent in the aorta and major arteries, more often on the posterior wall than the anterior wall. Macroscopically, the lesions may appear as flat or slightly elevated and yellow. They may be either in the form of small (about lmm in size) or in the form of elongated, beaded streaks. Microscopically, fatty streaks lying under the endothelium are composed of closely-packed foam cells, lipid-containing elongated smooth muscle cells and a few lymphoid cells. Small amount of extracellular lipid, collagen and proteoglycans are also present. The cholesterol esters in foam cells of fatty streaks differ chemically from those in the lipid core of atheromatous fibrous plague. These dissimilarities might be explained on the basis of two types of fatty streaks, which differ in morphology, cellular genotype, and lipid content, with one type related to the fibrous plague and the other type not related.

3. Fibrous plaque (atheroma). The lesions are raised, pearly white to grey, smooth-surfaced, plaque-

like structures in the intima but may extend into the media, may encroach considerably on the vascular lumen, especially in muscular arteries such as coronary arteries. On cross section a typical lesion has a soft, yellow central zone with gruel-like material covered on the luminal aspect by a layer of dense fibromuscular tissue (fibrous cap).

In general, plaques are found most often in the abdominal aorta, large arteries of the lower limbs, carotid arteries, proximal portions of the coronary arteries and circle of Willis.

The histologic appearance of lesions varies considerably depending on the relative amounts of the different components. The central atheroma of an uncomplicated fibrous plague consist of acellular, amorphous, electron-dense material that contains lipids, cellular debris, fibrin and other plasma proteins. The fibrous cap is composed of avascular connective tissues and elongated smooth muscle cells covered by endothelium. Inflammatory cells, including macrophages, may be present. In older and more advanced lesions the collagen in the fibrous cap may be dense and hyalinised, smooth muscle cells may be atrophic and foam cells are fewer.

4. Complicated plaques develop from preexisting fibrous plaques as a result of one of a combination of several pathologic changes that include calcification, ulceration, thrombosis and haemorrhage. The complicated lesion is the most common type of

atherosclerotic lesion that produces significant circulatory change and clinical disease.

a) Calcification the intima is brittle and cracks like an eggshell when the vessel is opened. Microscopically the dystrophic calcific process involves both the fibrous cap and the atheromatous portion of the plaque.

b) Ulceration and thrombosis. Advanced fibrous plaques with soft pultaceous atheromas, especially those with calcification may ulcerate as a result of mechanical or hemodynamic forces. With ulceration, cholesterol or lipid debris from the atheroma may be discharged and embolize. Murul thrombi may form on the ulcer or at sites of endothelial damage or mural hemorrhage. Such thrombi also may become organised and incorporated within the intimal plaque. Mural thrombi in medium-sized arteries may progress to occlusive thrombi that may reconalize.

c) Hemorrhage into atherosclerotic plaque is a common finding in advanced lesions, especially in the coronary arteries. The blood may reach the lesion from the vascular lumen through surface ulcerations or from rupture of capillaries that vascularized the atheroma from adventitial vasa vasorum.

d) With secondary changes in the media: 1) the internal elastic lamina is attenuated and fragmented; 2) smooth muscle cells and elastic lamina atrophy is connected a form of aneurysmal dilatation, which may follow, especially in elastic arteries.

Microscopically following states of atherosclerosis are distinguished:

1) pre-lipidosis, 2) lipidosis, 3) liposclerosis, 4) atheromatosis, 5) ulceration, 6) atherocalcification.

There are several clinico-morphological types of atherosclerosis according to localization. There are: 1) Atherosclerosis of aorta; 2) Atherosclerosis of coronary arteries; 3) Atherosclerosis of cerebral artery;

4) Atherosclerosis of arteries of lower extremities;

5) Atherosclerosis of arteries of small intestine;

6) Atherosclerosis of renal arteries.

The clinical effects result from the following:

1. Slow luminal narrowing causing ischemia and atrophy.

2. Suddenly luminal occlusion causing infarction necrosis.

3. Propagation of plaque by formation of thrombi and emboli.

4. Formation of aneurysmal dilation and eventual rupture.

The symptomatic atherosclerotic disease involves most often the heart, brain, kidneys, small intestine and lower extremities.

Some of the important effects are listed below: Aorta aneurysm formation, thrombosis and embolization to other organs; Heart — myocardial infarction, ischemic heart disease; Brain — chronic ischemic brain damage, cerebral infarction; Small intestine — ischemic bowel disease, infarction; Lower

extremities — intermittent claudication, gangrene. Kidney — chronic ischemic renal damage, sclerosis, atrophy.

Most of them may be as a cause of death.


Depending upon the suddenness of onset, duration, degree, location and extent of the area affected by myocardial ischemia, there can be 2 types of ischemic manifestation:

1. Myocardial infarction.

2. Non-infarct effects of myocardial ischemia; which include the following:

a) angina pectoris;

b) chronic ischemic heart disease;

c) sudden cardiac death.

Myocardial infarction is the most significant in the human pathology.

In industrialized countries myocardial infarction accounts for 10—25 % of all deaths. About 5 % of heart attacks occur in young people under the age of 40 years, especially with hypertension, diabetes mellitus, cigarette smoking and etc.

The etiologic role of severe coronary atherosclerosis of one or more of the three major coronary arterial trunks in the pathogenesis of about 90% cases

of acute myocardial infarction are caused by non-atherosclerotic factors, such as coronary vasospasm, arteritis, coronary ostial stenosis, embolism, thrombotic diseases, trauma.

Myocardial infarction has been classified in a number of ways by the physicians and the pathologists:

1. According to the anatomic region of the left ventricle involved. They are called anterior, posterior, lateral, septal and circumferential.

2. According to the degree of thickness of the ventricular wall involved:

a) full-thickness or transmural, when they involve the entire thickness of the ventricular wall;

b) subendocardial or lamina, when they occupy the inner subendocardial half of the myocardium.

3. According to the age of infarcts:

a) newly-formed infarcts are called acute, recent or fresh;

b) advanced infarcts are called old, healed or organized.

Infarctions are most frequently located in the left ventricle. Beside it may be located in other parts of the heart. But it is observed rarely. The region of infarction depends upon the area of obstructed blood supply by one or more of the three coronary arterial trunks.

1. Stenosis of the left anterior descending coronary artery is the most common (40—50%).

2. Stenosis of the right coronary artery is the next most frequent (30—40%).

3. Stenosis of the left circumflex coronary artery is seen least frequently (15—20%).

Pathologic changes. The macroscopic and microscopic changes in the myocardial infarction according to the age of the infarct. Macroscopically the majority of infarcts occur singly and vary in size from 4 to 10 cm. During the first week the colour of infarct charges from cyanotic red to bright yellow or yellow-green. The consistency of infarct in this period is soft.

During the second week infarct has red periphery and during the fourth to sixth week it is a thin, grey-white, hard, shrunken fibrous scar.

Microscopically during the first week we may see coagulative necrosis and marginal neutrofilic infiltration, then beginning of resorption of necrosed fibres by macrophages, onset of fibrovascular response; neutrofilic infiltration disappear. During the fourth to sixth week—increased fibrocollagenic tissue, decreased blood supply, fewer pigmented macrophages, lymphocytes and plasma cells. Using special methods such as electron microscopy, chemical and histo-chemical studies, the changes can be demonstrated in early infarcts before detectable light microscopic alterations appear.

Complications. About 10% patients with acute myocardial infarction develop cardiogenic shock, which is characterized by hypertension with systolic blood pressure of 80 mm Hg or less for many days.

Shock may be accompanied by peripheral circulatory failure, oliguria and mental confusion. A lot of patients with myocardial infarction suffer from congestive heart failure, which may be in the form of right ventricular, left ventricular failure or both. This complication is responsible for about 40% of deaths from acute myocardial infarction.

Arrhythmias are the most common form of complication in acute myocardial infarction.

Mural thrombosis and thromboembolism from intracardiac thrombi and from thrombosis in the leg veins is observed 15—45% in cases of acute myocardial infarction.

Usually in the first week heart rupture may develop. It is often fatal.

Cardiac aneurysm often develops in the left ventricle; it impairs the function of the heart and is a site for mural thrombi.

Fibrinous pericarditis appears on about the second day of myocardial infarction. As a rule, this complication develops in the patients with transmural myocardial infarction.

About 3—4% of patients who suffered from acute myocardial infarction develop post-myocardial infarction syndrome. It is characterized by pneumonitis.

The main causes of death are complications of myocardial infarction.

Non-infarct effects of myocardial ischemia

1. Angina pectoris is clinical syndrome of Coronary artery disease. Dystrophy and necrobiosis are revealed in the myocardial cells due to which transient myocardial pain in the substernal or pericardial region of the chest occurs.

2. Chronic Coronary artery disease (Myocardial fibrosis). Myocardial fibrosis may be focal or diffuse. Development mechanism of myocardial fibrosis can be different. Macroscopically the left ventricular wall generally shows the fact of grey-white fibrosis in brown myocardium. Microscopically there are areas of diffuse myocardial fibrosis, especially around the small blood vessels in the interstitial tissue of the myocardium.

3. Sudden cardiac death is defined as sudden death within 24 hours of the onset of cardiac symptoms. In the majority of cases it is caused by Coronary artery disease, coronary vasospasm, calcific aortic stenosis, myocarditis, hypertrophic cardiomyopathy, hereditary and acquired defects of the conduction system.

The autopsy in such cases reveals most commonly critical atherosclerotic coronary narrowing.

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