Thrombosis is blood clotting within the vascular system or the cardiac chambers of a living organism. Thrombus is the product of thrombosis. Classifications 1.1 red or stasis thrombus (venous thrombosis or phlebothrombosis); 1.2 gray-white thrombus (arterial thrombosis); 1.3 mixed thrombus (aortic or cardiac chamber thrombosis); 1.4 hyaline thrombus (microcirculatory thrombosis). 2.1 mural thrombus (aorta, vessels, cardiac chamber); 2.2 occlusive thrombus (vessels).

1 The thrombus may be obstructive into the artery and the cause of infarction in the organs, into the vein –it may be the cause of edema and ulcer.

2The thrombus into deep veins of low extremity may be embolising in pulmonary artery causing death. The thrombus into the aorta or the heart may be embolising in artery system of lots of organs.Etiology: Virchov’s triad as local causes: 1) destruction of integrity of the vascular wall (endothelial injury); 2) impairment; 3) disturbance of blood flow.The systemic (generalized) factors: 1 imbalance between coagulation and anticoagulation systems; 2 increase of viscosity and amount of regular blood elements. Pathogenesis: stages of thrombus formation:1Agglutination of the thrombocytes (platelets); 2 coagulation of fibrinogen; 3 agglutination of the erythrocytes; 4 precipitations of the plasma proteins. Results of thrombus are in:1 organization; 2 canalization; 3 calcification (phleboliths); 4 septic dissolution;5 embolisms; 6 aseptic dissolution.Diseases: 1 Atherosclerosis; 2 Vasculitis; 3 Malignant tumors; 4 Vegetation of the valves; 5 Nonbacterial endocarditis; 6 DIC-syndrome; 7 Traumas.

№ 26 MIXED THROMBUS WITH THE START OF OPRGANISATION H & E des.Microscopically: the thrombus contains fibrin, red cells, platelets, leukocytes and precipitation proteins. It is attached to a vascular wall where the connective tissue grows into thrombus. Grossly the thrombus consists of head, body, and tail.It is characterized by firm adherent, gray-white and red stripes, also friable.

The diseases: see above. Clinical correlations: Thrombosis may be as complication of a lot of diseases.

1The thrombus may be obstructive into artery and be the cause of infarction and gangrene of the organs; in case of the vein it may cause hemorrhage, edema, and trophic ulcer. 2 The thrombus into deep veins of the leg may be embolising in the pulmonary artery causing death.3 The thrombus into the aorta or the heart may be embolising in arterial system of many organs.4 The favorable outcome: organization of the thrombus when thrombus consolidation on the wall and decreases thromboembolism development.

5 The favorable outcome: canalization gives the partial resumption of blood stream

Definition: There is a group of stromal vascular disproteinosis with destruction of the connective tissue and deposits of abnormal proteins in the stroma.Classification of stromal vascular dystrophy: 1 amyloidosis; 2 hyalinosis; 3 mucoid swelling; 4 fibrinoid swelling/Definition: Amyloidosis is the pathologic process characterized by developing of amyloid - pertinacious substance deposited between cells in various tissues and organs of the body. Amyloidosis is the group of diseases, with a common sign of amyloid depositions. Amyloidosis is a pathologic process of the stromal vascular disproteinosis.Classifications of amyloidosis:

1. Based on chemical composition:1.1. AL-amyloid: composed of immunoglobulin light chains (amyloid light chain) associated with multiple myeloma and other

monoclonal B-cell proliferations.1.2. AA-amyloid: made up of immunoglobulin protein absence (amyloid associated) composed by the liver.2. Based on the associated clinical setting:2.1. Immunocyte dyscrasias with amyloidosis;2.2. Reactive systemic amyloidosis;2.3. Heredofamilial amyloidosis;2.4. Localized amyloidosis;2.5. Senile Amyloid.

3 Based on anatomic distribution:Major organ involvements are the following: amyloidosis of the kidney, spleen, liver, heart, endocrine organs.

№ 42 AMYLOIDOSIS OF THE SPLEEN (“SAGO SPLEEN”). Congo red stain desMicroscopically: amyloid deposits associated with capillaries end reticuloendothelial cells in the marginal zone of the lymphoid follicles are seen as amorphous pink casts. Congo-red stained amyloid shows pink or red colour of the deposits. Under polarized light the Congo red-stained amyloid shows green birefringence. This reaction is shared by all forms of amyloid and is due to the crossed beta-pleated configuration of amyloid fibres.

Grossly: amyloidosis of the spleen often causes moderate or even marked enlargement. Amyloid deposits virtually limited to the splenic follicles produce tapioca-like granules on gross examination (“sago spleen”). The spleen appears firm in consistency and reveals pale, grey, waxy deposits on the cut surface.One more gross type of spleen amyloidosis is named “lardaceous spleen” when amyloid deposits maybe seen within the splenic sinuses and all splenic pulps. Etiology: several aspects of amyloid origins are still not clear.Pathogenesis: Systemic amyloidosis (generalized) may be primarily connected with Immunocyte dyscrasias or secondary as the complication of chronic inflammations or destructive process of the tissue. Heredofamilial amyloidosis forms a separate heterogenic group of the diseases.Diseases: Amyloidosis.Clinical signs: Splenomegaly may be rare. Biopsy followed by Congo red stainingis the most important tool in the diagnosis of amyloidosis.

Hemorrhage is blood outcome from the vessel or the heart. There are three mechanisms of bleeding: 1 per rhexin- with rupture of the vessel; 2 per diapedesin- with hyperpermobility of the small vessels (capillaries, arterioles, venules); 3 per diabrosin- with erosion (corrosive) of the vascular wall (pus, enzymes of the tumor, gastric juice). Classification of hemorrhage: 1) According to the vessel & heart: 1 venous, 2 arterial, 3capillaries, 4 parenchymal, 5 flow from cardiac chambers. 2) According to the site: 1 external, 2 internal: a) into the organ; b) into the body cavity.1definition: external hemorrhage is the blood outflow to environment. EXTERNAL hemorrhage: 1 nasal hemorrhage – epistaxis; 2 blood vomiting - hematemesis; 3 irregular bleeding between the periods – metrorrhagia;4 the presence of blood in the urine – hematuria;5 tarry stool as a sign of bleeding in the gastrointestinal tract- melena; 6 the presence of blood in the phlegm- hemapthoe.

INTERNAL hemorrhages within the organs are 1 hemorrhagic infiltration; 2 hematoma; 3 petechii; 4 ecchymosi (see abridged dictionary of medical terms).

The types of the internal hemorrhage into the body cavities are: 1 hemothorax; 2 hemopericardium; 3 hemoperitoneum; 4 hemarthrosis.

Hemorrhagic diathesis is an increased tendency to hemorrhage within lots of organs

№16A HEMORRHAGIC INFILTRATION WITHIN THE BRAIN H&E desMicroscopically: Blood saturates within the cerebral tissue without its destruction.This type of the intraorganic hemorrhage is named hemorrhagic infiltration.Grossly: Another type of the intraorganic hemorrhage is referred to as hematoma. Hematoma is the cavity filled with Blood with drawn from the cerebral tissue.Definition: hemorrhagic infiltration is the blood saturation of the tissue.

The mechanisms of their formation is rupture of the vessels (Latin term is per rhexin) Diseases: Essential and symptomatic Arterial hypertension; Atherosclerosis; Aneurisms; Tumor; Leukemia; Trauma; Sepsis; Rheumatism; DIC-syndrome; Typhus fever Result of hemorrhage into the brain may be a cyst. Clinical signs: neuralgic symptoms or death of the patient many occur.

Definition: Hypertrophy is an increase in the size of an organ or tissue due to enlarged size of cells.The size of the ventricular chamber may be normal or some with constricted as concentric hypertrophy or extended:a) in vertical size – tonogenic dilation b) in cross (transversal) size – myogenic dilation.Phase of compensation is characterized by Hypertrophy of the myocardium and tonogenic dilation of the chamber. Phase of decompensation is characterized by concentric hypertrophy of the myocardium and myogenic dilation of the chamber. In this phase myocardium is soft in consistency. Subendocardial surface shows apparent bands of yellow myocardium alternating with bands of darker, red-brown, the so-called “tiger heart.” Cause is a mild hypoxia. If subendocardial surface shows apparent diffusion of yellow myocardium, the cause is severe hypoxia. Some causes of decompensation hypertrophic heart are as follows:1. Disparity between adequate blood supply of the hypertrophic and limiting capability of the vasculature. It leads to chronic hypoxia.2. Progressive destruction of mitochondrions in hypertrophic myocardiocytes.3. Increase of cytosol free calcium in myocardiocytes is due to dilation of endoplasmic reticulum.Classification: 1.Adaptive hypertrophy 1.1. Neuro- humoral hypertrophy 1.2. Hypertrophic growth 2. Compensative hypertrophy 2.1. Working hypertrophy 2.2. Vicar hypertrophy.

№73 MYOCARDIAL HYPERTROPHY. H & E. des.Microscopically: The myocardiocytes are enlarged and contain large, hyper chromatic nuclei.Grossly: The heart is enlarged; the weight of the heart usually exceeds 350-400gm. and over. Thickness of the left ventricular wall is over 1.2 cm (normal thickness is 0.7 to 1.2cm), the one of the right ventricular wall is over 0.5cm thick (normal thickness is 0.2-0.5 cm). Etiology: Myocardial hypertrophy is usually working hypertrophy.Pathogenesis: Working hypertrophy is caused by increased Functional demand (increased work load). The myocardial cells (myocardiocytes) become hypertrophic. The nuclei of myocardiocytes are enlarged, rich in chromatin. The whole

intracellular structures increased in number (mitochondrions, muscular filaments, ribosomes). Endoplasmic reticulum is dilation enlarged. The myocardial stroma, nervous filaments and vessels become also hypertrophic.With increase of hypertrophy, the metabolic requirements continue to increase but the capability of the heart to meet adequate requirements is decreased.It leads to fatty dystrophy of the heart and decompensation.Diseases: 1. Left ventricular hypertrophy shows:1.1. Essential hypertension.1.2. Secondary hypertension.1.3. Heart valve disease aortic stenosis and insufficiency.1.4 Congenital malformation valve disease: coarctation of the aorta.Diseases: 2. Right ventricular hypertrophy shows:2.1. Diffuse lung diseases with pulmonary hypertension (Chronic bronchitis, obstructive chronic diffuse emphysema, diffuse pneumosclerosis and others).2.2 Rheumatic mitral valve diseases.2.3 Congenital malformation valve diseases (tetralogy of Fallot, patent ductus arteriosus, septal defects and others).Clinical signs: Accidental or consolidate (compensative) phase of myocardial hypertrophy may be a symptomatic. In decompensation phase of myocardial hypertrophy, clinical manifestations of heart failure occur.

Definition: Inflammation is the complex local cyclic vascular mesenchimal reaction of the organism developed during process of evolution. This is a response to lesion, leading to elimination of causality agent with regeneration of the tissue as a completion phase. Classifications of inflammation: 1.1. Acute 2.1. Exudative 1.2. Subacute 2.2. Productive 1.3. Chronic Etiology: of inflammation:

1. Infectional (viral, bacterial, fungal, parasitic, rickettsiae, protozoan);2. Noninfectional factors (chemical and physical factors, foreign body);3. Immune factors. 4. Unknown factors. PATHOGENESIS of inflammation may by of three- component phases: - Alteration - Exudation - cells proliferations. The inflammatory response includes 1 circulating cells, plasma proteins, vascular wall cells, cells and extracellular matrix of the surrounding connective tissue.

Nomenclature: stomatitis- inflammation of the mouth; amygdalitis (angina, tonsillitis)- inflammation of the palatine tonsil; laryngitis- inflammation of the larynx; pneumonia-the inflammation of the lung; myositis- the inflammation of the muscles; hepatitis- the inflammation of the liver; nephritis- the inflammation of the kidney; leptomeningitis- the inflammation of the pia mater of the brain; pachymeningitis- dura mater of brain, pancarditis- the inflammation of all membranes of the heart;

“Pery” means inflammation of the serous membrane or vascular adventitia(pericarditis; periflebitis). “Para” means inflammation of fatty tissues surrounding an organ (paranephritis).

Definition of exudative inflammation: Exudative inflammation is the type of inflammation, characterized by predominance of exudation over alteration and proliferation. Classification: The types of exudative inflammation are as follows:1. Serous, 2. Fibrinous, 3. Purulent. 4. Hemorrhaged, 5. Putrid, 6. Catarrhal, 7. Mixed. OUTCOME of exudative inflammation:

1. Complete resolution. 2. Scarring (fibrosis). 3. Progression to other types of inflammation. Fibrinous inflammation Definition: Fibrinous inflammation is the type of exudative inflammation,

characterized by a fibrin rich exudation. Classification: there are two types of fibrinous inflammation of the mucous membranes1croupous; 2 diphtheritic.Purulent (suppurative) inflammation Definition: Purulent (suppurative) inflammation is characterized by a purulent exudate (pus), consisting of neutrophils, parenchymal cell debris, neutrophils debris and micro organisms. Classification: of purulent inflammation: 1 Phlegmonon; 2 Abscess; 3 Empyema.Phlegmonon is diffuse purulent exudative inflammation of friable connective tissue.

Abscess is the local purulent inflammation with degradation of the tissue and the formation of a cavity enclosed by a pyogenic membrane.Empyema is the purulent (suppurative) inflammation of the anatomic cavity walls with the accumulation of pus in the anatomic cavity.Etiology: 1.Pyogenic microorganisms (staphylococcus, streptococcus, gonococcus, meningococcus, E. coli and other). 2. Some chemical factors (turpentic, mustard) as Aseptic purulent Inflammation.

№ 81 FIBRINOUS PERYCARDITIS H & E des Microscopically: Pink masses of fibrin exudate lie over the pericardial surface. Neutrophil infiltration and inflammatory hyperemia are seen in the thick epicardium. Grossly: The thick epicardium covered with friable gray masses with hair- like spongeous form,. Figurative name is “Hair heart”.

Definition: Fibrinous inflammation is the type of exudative inflammation, characterized by a fibrin rich exudate.

Etiology: 1. Toxic factors. 2. Bacterial infection. Pathogenesis: This occurs as a consequence of severe injuries, with resultant greater vascular permeability to allow larger molecules (specifically fibrinogen)

to pass the endothelial barrier. The diseases: 1. Uremia. 2. Rheumatism. 3. Complication of Tuberculosis. 4. Fibrinous lobar pneumonia. 5. Complication of Transmural or subepicardial myocardial infarcts.

Outcome: 1. Resolution of the exudate with restoration of the normal tissue struc- ture. 2. Organization of the exudate to form focal scar tissue and lead to the development

of fibrous strands bridging the pericardial space.3. Organization of the exudate with obliteration of the pericardial space.4. Calcification of the pericardium the so-called “Shell heart”.Clinical signs: acute and chronic heart failure.

№ 129 FIBROADENOMA OF THE BREAST H & E des.Microscopically: There is a loose fibroblastic stroma containing duct like epithelium with lined spaces of various forms and sizes.Classification: there are two types of Fibroadenoma: 1 pericanalicular and 2 intracanalicular. Pericanalicular Fibroadenoma contains open, round to oval, fairly regular ductal spaces. Intracanalicular Fibroadenoma contains ductal spaces compressed by extensive proliferation of the stroma, on cross-section there appear slits or irregular, star-shaped structures.Grossly: It is discrete, solitary, freely movable nodule of 1 to 10 cm in dia, easily “shelled out”. The tumor is firm, of white tan color on cut surface.Definition: Fibroadenoma is a benign epithelial tumor derived from the ducts of the breast rich fibrous stroma. It is mature with single tissue atypia; its growth is named expansive; it has no metastases, no recidives. Its malignant analogue is named adenocarcinoma.An absolute or relative increase in estrogen activity plays some role in its development

№ 125 SQUAMOUS CELL (EPIDERMAL) CARCINOMA WITH KERATOSIS OF THE OESOPHAGUS H & E des. Microscopically: there are multiple nest- like structures consisting of atypical polygonal cells with keratinization in the structural centers named keratin pearls.Grossly: there are three forms: 1 Polyp like; 2 diffuse infiltrative as entophytic; 3 ulcerous. Grey-white plaque-like initial overt lesion thickens with elevation of mucosa. Thickening and rigidity of the wall combined with carcinoma growthinto the respiratory tree, aorta can be revealed. The background diseases are chronic esophagitis due to tobacco and alcoholic abuse; gastric-esophagus reflux. Precancer is named dysplasia and leukoplakia. The onset form is named carcinoma in situ. Definition: Squamous cell carcinoma is a malignant tumor derived from squamous cells. The tumor may be keratinous as well-differentiated squamous cell carcinomas and non keratinous as poorly differentiated one.It has cellular and tissue atypia, it is immature with infiltrative growth. The tumor localizations are according to anatomic luminal narrowing: 1 proximal at the cricoid cartilage; 2 downwards direction the anterior crossing of the left main bronchus; 3 distal where esophagus penetrates the diaphragm. The carcinoma spreads to paraesophageal lymph nodes.The tumor in the upper and middle part of thoracic esophagus spreads along hematogenous pathway to the lungs; the low part of esophagus carcinoma spreads to the liver. Organs: Squamous cell carcinoma is a nonspecific tumor and may occur within the cervix of the uterus, lung, skin, larynx, rectum etc. Complications: fistula between the esophagus and trachea may be revealed when the tumor grows and aspiration pneumonia; may occur cachexy; intoxication, stenosis with alimentary cachexy, hematemesis. Causes of death are complications.

№ 137 ADENOCARCINOMA OF THE STOMACH H & E des.Microscopically: Malignant cells are formed neoplastic glands, well or poorly differentiated. Classification of microscopical forms: 1 adenocarcinoma; 2 “signet-rings” cells carcinoma; 3) scirrh; 4) solid carcinoma.Grossly: There are five macroscopical forms: 1 polyp-like; 2 fungal like, 3 diffuse or linitis plastica; 4 flat or depressed; 5 excavated (ulcer-like). The tumor is solid or soft, white-grey, may grow through the wall of the stomach. Adenocarcinoma may grow into adjacent organs: the liver, colon, pancreas, spleen.Definition: Adenocarcinoma is a malignant tumor derived from glandular epithelium. Organs: Adenocarcinoma is nonspecific tumor and may occur within other organs: the large intestine, uterus, pancreas, liver etc.It is an immature tumor, with cellular and tissue atypia, of invasive growth.Its growth may be into lumina of the hollow organ named exophytic growth and into the organ wall named endophytic. The background diseases are: chronic gastritis; adenomas; peptic ulcer.Precancer is named dysplasia and large intestinal metaplasia of the gastric glandular cells. The tumor within only mucous membrane is named early gastric cancer.Carcinoma of the stomach gives lymph metastases; first of all it spreads to lymph nodes in minor and major curvatures. It first hematogenic metastasis is within the liver.There are three retrograde metastases of the gastric carcinoma: 1 Krukenberg tumor designates metastases into the ovary; 2 Shnitsler metastases designate metastases gastric carcinoma into the lymph nodes of pararectal adipose tissue; 3 Virchow’s node designates metastasis into left supraclavicular lymph node. Complications: 1 hemorrhage as melena; 2 perforation; 3 peritonitis; 4 penetration withcontact metastases; 5 stenosis of the pyloric part of the stomach; 6 intoxication; 7 cachexy.Causes of death are complications.

Definitions: Hemoblastosis is a total term to designate tumors of the hematopoietic and lymphoid systems. 1 Leukemias (syn. Leucosis) are the systemic neoplasms to arise in the bone marrow and circulate in the peripheral blood.

Leukemias are classified as follows:I. In accordance with the state of maturity of the leukemic cells: 1 Acute Leukemias are characterized with replacement of the bone marrow with immature cells (called “blasts” Leukemias). 2 Chronic Leukemias-are characterized with replacement of the bone marrow with mature cells (called “cytics” leukemias).II. Of the cell type involved (according to the cytogenesis): Acute Chronic:1 Lymphoblastic leukemia 1.Lymphocytic leukemia2 Myeloblastic leukemia 2.Myelocytic leukemia3 Monoblastic leukemia 3.Monocytic leukemia4 undifferentiated cell leukemia 4.Erythremia (polycythemia vera).(immature cells without cytochemical identification).

Etiology: 1.Ionizing radiations. 2. Chemicals. 3. Viruses (HTLV-1 and EBV).Pathogenesis: Leukemias are primary disorders of the bone marrow. There is initiation of neoplastic proliferation of white blood cells. Bone marrow becomes pyoid. The leukemic cells spread from bone marrow into the blood, in large amounts. These cells also infiltrate the liver, spleen, lymph nodes and other tissues throughout the body, causing enlargement of these organs.As the leukemic cells accumulate in the marrow, they suppress normal hematopoietic stem cells development.Leukemic infiltrate- is local metastasis with the growth of leukemic cells.Complications: The patients have anemia, thrombocytopenia, infection complications (pneumonia, sepsis), bleeding (petechiae, ecchymoses, epistaxis, gum bleeding and others), and necrotic complications (ulcer, necrotic tonsillitis and others). These complications may be the cause of death.

Clinical features and Signs:1 Philadelphia chromosome is found within leukemic cells.2 Blood test shows increase of leukocytes anemia, cases of thrombocytopenia.3 Bone marrow becomes pyoid.4 Spleen is enlarged mass up to 4-5 kg with myelocytic leukemic infiltration. Lymphoid cells are atrophic. There may be ischemic infarction and scar area within the spleen.5 Lymph nodes are enlarged as well. There is myeloid leukemic infiltration within lymph nodes. Lymphoid cells are atrophic.

2 Lymphomas are tumor masses within either lymph nodes or other organs.

Definition: Lymphoma is a regional tumor disease of the peripheral lymphoreticular tissue, particularly in lymph nodes.Classification Lymphomas are classified as follows:1 Non-Hodgkin’s lymphomas -small lymphocytic lymphomas -large cell lymphomas -Lymphoblastic lymphomas -Burkitt’s lymphoma.2 Hodgkin’s disease (Lymphogranulomatosis).

Radiation sickness is injury produced by ionizing radiation.Classification: a) acute; b) chronic.All types of radiation exert their effects on cells causing alterations of the cells. The most important direct or indirect targets are DNA, lipids

(membranes) and proteins ( enzymes). Biological effect depends on the physical properties of the radiation factors 1) type of radiation; 2) absorbed dose; 3) direct or indirect action; 4) time of action.

Biological effect depends on the cellular properties: 1) mitotic phase; 2) type of the cell; 3) water concentration; 4) cumulative effect of the cell.

№258 LIVER WITH LYMPHATIC LEUKEMIA (chronic lymphocytic leukemia) H and E. des. Microscopically: Leukemic infiltrations mainly of prolymphocytes and lymphocytes are localized in the portal tract, periportal connective tissue and in the stroma between lobules. Leukemic infiltrations with small, mature- like lymphocytes manifest lymphomas. Grossly: The liver is enlarged, of gray-brown color.

Definition: chronic lymphocytic leukemia (CLL) is a systemic malignant tumor disease of hematopoietic tissue, characterized by diffuse replacement of the bone marrow by mature neoplastic cells of the lymphoid stem (prolymphocytes and lymphocytes).Clinical Sings:1 CLL typically affects individuals over 50.2 In more than 95% of cases, CLL is a neoplasm of B cells and only 5% - are tumors of T –cells.3 The leukemic B cells fail to respond to antigene stimulation. Patients have hypogammaglobulinemia and they show increased susceptibility to bacterial infections.4 15% of patients have antibodies against red cells, giving rise to an autoimmune hemolytic anemia.5 The patients have generalized lymphadenopathy and heptosplenomegaly.

The thyroid gland may be enlarged and named goiter or struma. Macroscopic classification as follows: diffuse, nodular and mixed. Microscopic classification as follows: colloidal, parenchymatous and mixed. Clinical classification follows: euthyroid (normal function), hypothyroid (decreasing function) and hyperthyroid (increasing function). Diseases occur as endemic goiter, sporadic goiter, diffuse toxic goiter (Basedov’s disease, Grave’s disease). Endemic goiter occurs in geographic areas where soil, water and food supply contain low levels of iodine. Morphologically it is a diffuse non-toxic goiter, colloid goiter. Sporadic goiter occurs in most cases when the cause is not evident. Morphologically it is diffuse or nodular non-toxic colloid goiter.Diffuse toxic goiter (Basedov’s disease, Grave’s disease) is an autoimmune disease with production of antibodies to TCG-receptors. It is a diffuse, toxic goiter with follicles hyperplasia, mixed goiter.Goiter may occur as Hashimoto’s thyroiditis or Riedel’s thyroiditis.

№ 278 DIFFUSE TOXIC GOITRE (Basedov’s disease, Graves’s disease) H & E des Microscopically: There are diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells. They are tall, columnar and more crowned than usual, with formation of small papillae which project into follicular lumen. The colloid within the follicular lumen is pale with scalloped margins, lymphoid infiltrates of predominantly of T cells with fewer B cells and mature plasma cells present throughout the interstitium, germinal centers are common. Grossly: The thyroid gland is diffusely enlarged, smooth, and soft, its capsule is intact. Microscopical picture of the extrathyroid changes:There is generalized lymphoid hyperplasia is evident. Ophthalmopathy is caused by oedematous orbital tissues with presence of hydrophilic glycosaminoglycans and infiltration by lymphocytes, mostly T cells. The heart muscles may be hypertrophic with serous myocarditis to result in sclerosis. The liver may be with serous inflammation and lymphocyte infiltration to result in sclerosis and rarely cirrhosis. The derma thickening due to deposition of glycosaminoglycans and lymphocyte infiltration is shows. Clinical signs: 1 thyrotoxicosis (tachycardia, heart failure, ophthalmopathy (proptosis or exophthalmia);2 Serum TSH concentrations are decreased; 3 increase of free T4 and T3. Causes of death: 1 heart failure; 2 liver failure; 3 cahexia; 4 acute adrenal insufficiency with total thyroid ectomy to follow.

Atherosclerosis is a chronic disease with the lipid and protein abnormal metabolisms and destruction of the large aorta and arteries (elastic type and myoelastic types) with the formation of atherosclerotic (fibrofatty) plaques.Manifestation of the atherosclerosis is in Atherosclerotic plaque. Forms of atherosclerosis: 1) cerebral and carotid arterial injury (as cerebrovascular disease); 2) cardiac arterial injury (ischemic heart disease); 3) renal arterial injury; 4) injury of the aorta; 5) injury of the intestinal arteries; 6) injury of the extremity arteries. Clinical signs are in development of Atherosclerosis into other diseases of the principal organs. Myocardial infarction is a form of ischemic heart disease with development of myocardial necrosis area caused by the local insufficiency of blood supply. Ischemic heart disease refers to a group of closely related diseases caused by imbalance between myocardial oxygen demand and blood supply.

162b TRANSMURAL MYOCARDIAL INFARCTION WITH STATING OF ORGANISATION H&E des. Microscopically: the cardiac muscle cells are bright and eosinophilic, due to coagulate necrosis. The myocardial cells may show contraction bands. Nuclei are absent. Within10 days after the event necrotic myocytes at the periphery of the infarct are replaced by granulation (as young connective) tissue with numerous macrophages remnants (debris) of necrotic myocytes. Definition: Infarct as the pathologic process is an area of ischemic necrosis within a tissue or an organ produced by occlusion of its arterial supply.The causes of the infarct are 1) thrombus; 2) embolus; 3) atherosclerotic plaque; 4) prolonged spasm.There are three stages of infarct progression: 1 ischemia; 2 necrosis 3 sclerosis(as the formation of the scar). There are four forms of infarct according to the left wall thickness: 1) subendocardial; 2) transmural; 3) intramural; 4) subepicardial. The result is sclerosis (formation of the scar). Complication: 1 rupture of the infarct; 2 mural thrombi; 3 acute fibrinous pericarditis; 4 papillary muscle dysfunction; 5 ventricular aneurysms (acute and chronic). Causes of death: 1) cardiac arrhythmias; 2) left ventricular failure; 3) cardiac shock; 4) rupture of the wall, the septum or the papillary muscle; 5) thromboembolism.

160b ATHEROSCLEROTIC PLAQUE (ATHEROMA) H&E des. Microscopically: one can observe the intimal thickening with cell migration,

proliferation and extracellular matrix elaboration in the intimae. Atherosclerotic plaque has three principal components: 1) cells (smooth muscle cells, macrophages, other leukocytes);2) extracellular matrix (collagen, elastic fibers, proteoglycans); 3) intra- and extra cellular lipid.All components can be seen within the fibrous cap of the plaque. The necrotic center consists of cell debris, cholesterol crystals, foam cells and calcium. There are two types of atherosclerotic plaques: 1 vulnerable plaques; 2 stable plaques. Grossly: Aorta demonstrates multiple fatty and fibrous plaques, some of them with diffuse and complicated lesions (calcinosis, ulceration, thrombosis). There are six stages of atherosclerotic plaques: 1) prelipidosis; 2) lipidosis;3) atheromatosis; 4) ulceration; 5) sclerosis; 6) calcinosis.Complication of the atherosclerotic plaque: 1) calcinosis; 2) ulceration; 3) rupture with hemorrhage; 4) thrombosis; 5) aneurismal dilatation; 6) embolism ( thromboembolism and fatty embolism).Clinical significance according to the complications: 1 atherosclerotic plaque oc-cludes lumina of blood flow compromise to distal parts of organs and causeischemic injury. Thrombi, thromboemboli and fatty emboli may also obstruct blood flow too. 2 aneurisms may rupture with hemorrhage. Causes of death: 1) rupture with hemorrhage; 2) thrombo- and fatty embolism with occlusion of the lumina blood flow compromise of the principal organs.

AppendicitisAppendicitis is a disease with inflammation of the appendix. Classification is as follows 1 acute; 2 chronic.Acute appendicitis is revealed as simple, superficial, phlegmonous, phlegmonous and ulcerous, gangrenous and apostematous. Complications of acute appendicitis are as follows: 1 perforation; 2 suppurative peritonitis; 3 periappendicular abscess; 4 empyema; 5 pyleflebitis; 6 abscesses of the liver. Chronic appendicitis occurs as a result of acute simple and superficial appendicitis.There can be seen growth of granulate tissue and formation of scar with obliteration of the appendicular lumen. Complications of chronic appendicitis are as follows:a)hydrocele;b)mucocele; d)myxoglobulosis. № 263 PHLEGMONOUS ULCEROUS APPENDICITIS H & E des Microscopically: All layers of the wall are infiltrated by exudate consisting of numerous granulocytes. The tissue structures are subjected to suppurative fusion. The mucous membrane is fully destroyed in some foci with ulceration. Grossly: appendix is red, swollen, dull, covered with a fibrinous purulent exudate of grey- yellow color. Definition: appendicitis is inflammation of the appendix. Etiology: a) obstruction with coprostasis and invasive of microorganisms; b) disintegration of the nervous system of the appendix; c) secondary with generalization of infectious diseases; d) coprostasis.Result is complication with intoxication.

Hepatitis Definition: Hepatitis is a disease connected with injury of hepatocytes associated with an influx of inflammatory cells into the liver.Etiology: Continuous infections of viral hepatitis; alcoholism, drugs, Wilson’s disease. The classifications are as follow: 1a) primary hepatitis; b) secondary hepatitis.Primary hepatitis is an original disease. Secondary one develops with other diseases. 2 a) acute; b) chronic. Primary hepatitis according to etiology: a) viral; b) alcoholic; c) autoimmune; d) drug-induced.Viral hepatitis: 1) acute may be: HAV, HBV, HCV, HDV, HEV, and HGV; 2) chronic may be: HBV, HCV, HDV, HEV, HGV (excluding HAV). Pathogenesis of hepatitis B : 1 acute infection: a) 60% subclinical disease; b) 25% acute hepatitis; c) 10% “ healthy” carrier; d) 5% persistent infection; Subclinical disease –100% recovery; acute hepatitis –99% recovery & 1% fulminant hepatitis and death. Persistent infection 90% recovery and 10% chronic hepatitis. Chronic hepatitis- 50% cirrhosis and death; cirrhosis 10% -hepatocellular carcinoma.Acute hepatitis: Grossly the liver is enlarged, of red color. Microscopically: 1) hydropic and ballooning cell degeneration; b) bridge and piecemeal necrosis; c) apoptotic bodies (Councilman bodies); d) infiltration of portal and lobular stroma with lymphocytes, macrophages, some granulocytes; e) proliferation of reticuloendoteliocytes; g) cholestasis; h) regeneration of the hepatocytes. The right markers of HBV infection are “ground –glass” hepatocytes with HbsAg; “sanded” nuclei with HbcAg. Clinical morphologic forms of acute viral hepatitis lead to a) cyclic jaundice; b) without jaundice; c) fulminant; d) cholestatic. Results of acute viral hepatitis are: a) recovery; b) acute hepatic and renal failure with death; c) chronic hepatitis; d) cirrhosis. Chronic hepatitis: etiologic Classification is as follows: 1 viral; 2 autoimmune; 3 medical; 4 cryptogenic. Classification according to activity is as follows: 1 hepatitis with minimal activity and mild activity (persistence); 2 hepatitis with moderate and severe degrees of activity (aggressive). Classification according to stage: 0 –absence of fibrosis; 1- flabby fibrosis; 2- moderate fibrosis; 3- severe fibrosis. Microscopical picture of chronic hepatitis B: Hydropic and balloon dystrophies; Councilman’s bodies are as apoptotic bodies; necrotic hepatocytes; Lymphomacrophageal infiltration; Hyperplasia and proliferation of Kupffer cells; Fibrosis of periportal tracts.

№ 202 MASSIVE HEPATIC NECROSIS (TOXIC DYSTROPHY OF THE LIVER) H & E des. Microscopically: the structure of the liver is destroyed with necrosis of the hepatocytes. Only a collapsed reticulin framework and preserved portal tracts may occur. There are a lot of macrophages and new connective tissue. The regenerative hepatocytes can be seen. Grossly: the liver is smaller than normal, shrink, soft, of red, yellow color and spotted and with wrinkled capsule.

Definition: Massive hepatic necrosis is an acute Hepatosis with necrosis of hepatocytes. Etiology: 1) exogenic agents (mushroom, arsenic, heliotrope, phosphorus, drugs); 2) endogenic intoxications (gestosis, thyrotoxicosis);3) viral hepatitis (fulminate forms). Morphological stages: 1-st week – fatty) of the hepatocytes into lobular centers. The liver is smaller than normal, soft, of yellow color.2-d week – yellow stage. Necrosis within lobules occurs. 3-th week – red degeneration (dystrophy) stage. The resorption of fatty-protein detritus with naked hyperemic sinusoids, collapse of the stroma, the liver is of red color. Results are hepatic or hepatic renal failure as a cause of death or may be postnecrotic macronodular cirrhosis of the liver. Clinical signs: Fulminant hepatic failure with clinical hepatic insufficiency progressing to hepatic encephalopathy.

Sepsis Definition: Sepsis is a polyetiologic, non contagious disease characterized by generalized [systemic] infection, acyclic clinical course, and special significance of changed reactivity. Etiology: Staphylococcus, streptococcus, esherichia coli, blue pus bacillus, proteus,klebsiella, Gram negative bacteria and fungi. Classification depends on entry of infection: 1 therapeutic sepsis; 2 surgical sepsis; 3 gynecologic sepsis; 4 umbilical sepsis;5 tonsilogenic sepsis; 6 odontogenic sepsis; 7 otogenic sepsis; 8 urogenic sepsis; 9 cryptogenic sepsis (without entry of infection).Four forms of sepsis course occur: 1fulminant (1 day); 2 acutissimus (1-3 days); 3 acute (2-3 weeks); 4 lingering (more than 3 weeks).There are four clinical – morphologic forms of sepsis: 1 septic pyemia;2 septicemia; 3 septic (bacterial) endocarditis; 4 chroniosepsis.Septic pyemia is a form of sepsis with microbial embolism into the organs and multiple abscesses within the organs. Pathogenesis: entry of infection and the septic primary focus produce thrombophlebitis, then lymphangitis and lymphadenitis with multiple abscesses within the organs to follow. Complications are revealed by pleural empyema, purulent peritonitis, purulentparanephritis and acute septic polypous ulcerous endocarditis. Acute septic Polypous ulcerous endocarditis may develop during septic pyemia with pus on the valvular endocardium of the heart. This pus shows acute septic endocarditis as a part of septic pyemia as that from the clinical morphologic form of sepsis, i.e. septic (bacterial) endocarditis.

Possible causes of death are complications.Septicemia is the form with hypereaction of the organism with DIC-syndrome, Jaundice, hemorrhagic diathesis, necrosis of the organs, reversible injury of the organs. Bacterii are in the blood stream. The spleen called “septic spleen” may weigh 500gr and even 1500gr. with myeloid methaplasia.Septicemia is considered to be a toxic infectious Shock. Clinical course may occur as fulminant or acute. Patients die within 1 to3 days. Possible causes of death are intoxication and multiple organ failures.Septic (bacterial) endocarditis is the form of sepsis when cardiac valve is used for entry of infection. Septic focus is localized on valvular leaflets. Rheumatic, brucellous, syphilitic, atherosclerotic valvular diseases and heart malformation may take priority over septic endocarditis, termed secondary septic (bacterial) endocarditis. Primary septic endocarditis develops on intact valvular leaflets termed Tchernogubov’s disease. Course of disease may occur as 1 acute form; 2 subacute form and3 chronic form termed lingering septic endocarditis or sepsis lenta. Pathogenesis of septic endocarditis is connected with blood circulation of immune complex formed of antigens, antibodies, and compliment with lesions of valves, vessels, kidneys and spleen. Thromboembolic syndrome may develop as a complication.

Possible cause of death may be complications.Modern conception of chroniosepsis. Chroniosepsis is characterized by primary purulent focus organ atrophy, cahexia Causes of death are cahexia, amyloidosis and other diseases. Purulent-absorption fever is termed by I.V. Davidovsky. Clinical presentations and pathological manifestations of local purulent and necrotic processes with demarcate border. Modern term is intoxication or endotoxicosis. Meningococcosis Definition: Meningococcosis is an infective disease in three forms: 1 acute nasopharingitis; 2 purulent leptomeningitis; 3 meningococcemia. Etiology: Nesseria meningitidis. Pathogenesis: Meningococcosis is a respiratory infection and Nesseria meningitidis can overcome hemato-encephalic barrier. The entries of infection are mucous membranes of the nose and the fauces.Acute nasopharingitis develops in a mild clinical course.Leptomeningitis is an inflammation of pia mater of the brain, and arachnoid of the brain. Leptomeningitis is characterized by four clinical courses: 1 fulminant, 2 acute, 3 subacute, 4 chronic. Leptomeningitis occurs as spinal and craniocerebral. Complications: purulent meningoencephalitis, thrombophlebitis, hemorrhagic infarction of the brain, fibrous adhesions and hydrocephalus. Meningococcemia develops in a clinical course as meningococcal sepsis and manifested in DIC- syndrome, hemorrhagic diathesis, and necrosis of the organs.Severe course may take a fulminant form. Sometimes fulminant form reveals hemorrhage within bilateral adrenal with acute adrenal insufficiency, described as Waterhouse –Friderichsen syndrome. The syndrome may be the cause of death.

№ 90 ACUTE PYOGENIC (MENINGOCOCCAL) MENINGITIS H & E des.

Microscopically: subarachnoid space is filled with neutrophils in severely affected areas and they are found predominantly around the leptomeningeal blood vessels in less severe cases. Grossly: normally clear, cerebral spinal fluid is cloudy and sometimes franklypurulent. The exudate is evident within the leptomeninges over the surface of the brain. The meningeal vessels are engorged and stand out prominent.Pyogenic meningitis is caused by Nesseria meningitidis. Results are 1 complete resorption; 2 organization with leptomeningeal fibrosis and consequently hydrocephalus. The complications of acute pyogenic meningitis are: 1 encephalitis; 2 pyocephalus. Causes of death may be: 1edema of the brain; 2 intoxication; 3 hydrocephalus.

Acute pneumonia is the exudative inflammation of the lungs.Classifications are as follows:I. Etiology: 1.1. Viral. 1.2. Bacterial. 1.3. Fungal. 1.4. Protozoa. 1.5. Physical agents. 1.6. Chemistry agents.II. Pathogenesis: 2.1. Primary. 2.2. Secondary as complications of other disease 2.3 Contagious and nosocomial [hospital-acquired] pneumoniaIII.Clinical-morphological forms:3.1Lobar (crupous) pneumonia 3.2Bronchopneumonia. 3.3 Acute interstitial pneumonia (pneumonitis).Lobar (crupous) pneumonia Synonyms: 1.LOBAR pneumonia- the whole lobe is involved. 2. CRUPOUS (as a type OF FIBRINOUS INFLAMMATION) pneumonia.3. PLEUROPNEUMONIA - pleura is involved.Definition: Acute infectious allergic inflammatory disease of the lungs involving one or more lobes of the lung.Etiology: 1, 2, 3 types Pneumococcus and Klebsiella pneumonia (rarely).Pathogenesis: It is caused by hypersensitivity reaction induced by pneumococci and Klebsiella with immunocomplex disorders of microcirculation. Intraalveolar fibrinous exudation occurs. Consolidation of lung parenchyma is the result of the whole lobe being involved. Stages are revealed as: Congestions (Influx) occurs within the First day. Microscopically: vascular congestion with serous exudate within alveolar can be seen and many bacteria occur in the alveoli. Grossly: the affected lobe is heavy, red and boggy.Red hepatization (2 – 3 DAYS). Microscopically: alveolar spaces are airless, packed with red cells and fibrin.Grossly: The lung lobe is of liver-like consistency, of red color. Pleura demonstrates a fibrinous or fibrinous-purulent exudate.Gray hepatization (4 – 6 days). Microscopically: The alveolar spaces are airless, packed with neutrophils and fibrin. Septal between alveoli are thickened with neutrophils infiltration. Vascular congestion can be seen. The pleura demonstrates fibrinous or fibrinopurulent exudates. Grossly: The affected lobe of the lung is dry, grey and firm (the lung lobe is of liver-like consistency). Pleura is thickened, with gray fibrinous membranes on the surface. Resolution (9 – 11 DAYS). Exudates within the alveoli is enzymatically digested and either resorbed or expectorated, leaving the basic architecture intact. ATYPICAL FORMS OF CRUPOUS PNEUMONIA: 1. Central. 2. Massive. 3. Total. 4. Migratory. 5. Klebsiella pneumonia. Complications are as follows: Pulmonary complications: 1Carnification of the lung. 2 Abscess of the lung.3 Gangrene of the lung. 4 Empyema of the pleura. Extra pulmonary complications: 1 Purulent mediastinitis. 2 Purulent pericarditis (infective endocarditis). 3 Purulent peritonitis. 4 Purulent arthritis. 4 Purulent meningitis (abscess of the brain). Bronchopneumonia (local pneumonia) Definition: bronchopneumonia (local pneumonia) is characterized by local acute inflammation amount from acinus to segment connected with acute bronchiolitis.

Etiology: 1 viral infection (influenza, parainfluenza, measles, respiratory-syncytial infection, adenoviral infection and others). 2 Bacterial infections (pneumococcus, streptococcus, staphylococcus, pseudomonas, eroginosa, escherichia coli and others). 3 Fungal infections. 4 Protozoan infections (pneumocystis). 5 Mixed infections. 6 Physical and chemistry agents (uremic, lipid, dusty, radiation pneumonia). Morphological changes in the lung depending on the character of stimulus (etiology)of pneumonia. VIRAL pneumonia is usually serous or serous – hemorrhagic pneumonia (influenza). BACTERIAL pneumonia is usually purulent. Staphylococcal and Klebsiella pneumonia is characterized by considerable alveolar wall damage, leading to necrosis with abscess formation. It may lead to empyema (pus in the pleural cavity). Classification: LOCAL PNEUMONIA may be as follows:1 according to amount of foci inflammation: 1.1 Acinar. 1.2 Lobular. 1.3 Confluent lobular (multilobular) 1.4 Segmental.1.5 Polysegmental. 1.6 Bilateral.1.7 Subtotal. 2 according to pathogenesis:

2.1Aspirate.2.2Hypostatic. 2.3Postoperative. Complications: 1Carnification of the lung. 2 Abscess of the lung. 3 Gangrene of the lung. 4 Pleuritis.

Acute interstitial pneumonia (acute pneumonitis) Definition: Acute interstitial pneumonia is characterized by primary acute inflammation within interstitium of respiratory regions of the lungs and within alveolar septa.Etiology: 1Viruses: micoplasma, L. pneumophphilia, cytomegalovirus, pneumocystis carini. 2 Fungal. Measles Definition: Measles is a viral contagious disease with cough, sneeze, fever, and conjunctivitis and maculopapulous rash. Etiology: measles Virus.Complications: false croup (acute laryngitis and laryngotracheitis with larynx edema), bronchiolitis, local pneumonia, bronchiectatic disease, enteropathy, encephalitis and hemorrhages of the brain. Influenza (grippe)

Definition: Influenza is an acute viral severe contagious epidemic disease. Etiology: three serologic types of virus occur as A, B, C RNA viruses.Action of virus includes 1 citolytic action to the respiratory epithelium, 2 immunodepressive action, 3 vasoparalitic action, 4 naturopathic action. Classification: there are three clinic forms of influenza (mild, medium and severe)Severe influenza consists of a) toxic form; b) influenza with pulmonale complications.Toxic form includes hemorrhagic pneumonia, hemorrhagic syndrome, and acute hyperplasia lymphoid organs.Complications: a) pulmonale complications (bronchiectatic disease, pneumosclerosis, local carnification, chronic obstructive emphysema); b) extra pulmonale complications (hemorrhagic, fibrinous or purulent pleuritis, purulent mediastinitis, pericarditis, meningitis, purulent encephalitis, glomerulonephritis).

Causes of death: intoxication or bacterial bronchopneumonia and complications.

№220. LOCAL PNEUMONIA (BRONCHOPNEUMONIA) H & E desMicroscopically: there can be seen airless inflammative foci with focal suppurative exudate that fills the bronchi, bronchioles and adjacent alveolar spaces. Grossly: In the lung one can see multiple airless small and large inflammative foci of dark red to gray – yellow color, protruded over cut surface, of hard consistency. Definition: Bronchopneumonia is a disease, characterized by local inflammation of the lung resulting from an initial inflammation of the bronchi and bronchioles with extension into the adjacent alveoli. Results are 1Resorption of the exudates and complete recovery (usually).2 Diffuse pneumosclerosis. 3 Carnification of the lung.

Possible causes of death are as follows: 1 Purulent complication. 2 Cardiac and respiratory insufficiency.

Chronic diffuse inflammative pulmonary diseases are divided into three groups:1 obstructive; 2 restrictive; 3 mixed.Chronic obstructive pulmonary diseases are diseases with airflow obstruction.Classification: They include chronic obstructive bronchitis, chronic obstructive emphysema, bronchiectatic disease and chronic bronchiolitis.Chronic restrictive pulmonary diseases are interstitial diseases characterized by reduced volume pulmonary parenchyma and vital capacity with respiratory dysfunction.Morphogenesis of Chronic diffuse inflammative pulmonary diseases develops via three pathways: 1 bronchitogenic; 2 pneumonitogenic; 3 pneumoniogenic.Chronic obstructive bronchitisChronic obstructive bronchitis is a disease with chronic inflammation, hyperplasia of mucus producing goblet cells and mucous glands.Chronic obstructive bronchitis occurs as simple and obstructive.Obstructive chronic bronchitis occurs with obstruction of peripheral bronchi with bronchiolitis to follow.Bronchiectasis Bronchiectasis is termed dilation of bronchus lumen. Classification of bronchiectasis:According to the anatomic nature of the lesion bronchiectases are divided into 2 types: Sac-like (destructive), and Cylinder-like (retention) bronchiectasis. Etiology: The conditions that most commonly predispose to bronchiectasis include:Bronchial obstruction. Common causes are tumors, foreign bodies, and occasional mucous impaction. Under these conditions, the bronchiectasis is localized to the obstructed lung segment. Bronchiectasis can also complicate atopic asthma and chronic bronchitis.2. Congenital or hereditary conditions. For example, in 1) Cystic fibrosis, widespread severe bronchiectasis results from obstruction and infection due to the secretion of abnormally viscid mucus. 2) In immunodeficiency states, particularly immunoglobulin deficiencies, bronchiectasis tends to develop due to increased susceptibility to repeated bacterial infections. 3) Kartagener's syndrome, an autosomal recessive disorder, is frequently associated with bronchiectasis and sterility in males. Structural abnormalities of the cilia impair mucociliary clearance in the airways, leading to persistent infections, and reduce the mobility of spermatozoa.3. Necrotizing, or suppurative, pneumonia may predispose to bronchiectasis. Sometimes it may be a sequela of childhood pneumonias complicating measles, whooping cough, and influenza. Pathogenesis of bronchiectasis:The pathogenesis of bronchiectasis shows two critical and interconnected processes, there are: 1) obstruction, and 2) chronic persistent infection. Either of these two processes may come first. Normal clearance mechanisms are hampered by obstruction, so secondary infection soon follows; conversely, barely chronic infection causes damage to bronchial walls, leading to weakening and dilation. For example, obstruction due to a bronchogenic carcinoma or a foreign body impairs clearance of secretions, providing fertile superimposed infection. The

resultant inflammatory damage to the bronchial wall and the accumulating exudate further distend the airways, leading to irreversible dilation. Conversely, a persistent necrotizing inflammation in the bronchi or bronchioles may cause obstructive secretions, inflammation throughout the wall (with peribronchial fibrosis and scarring traction on the walls).In the usual case mixed flora can be cultured from the involved bronchi, including staphylococci, streptococci, pneumococci, enteric organisms, anaerobic and microaerophilic bacteria, and (particularly in children) haemophilus inftuenzae and Pseudomonas aeruginosa. Clinical course and complications: The clinical manifestations consist of severe,persistent cough with expectoration of mucopurulent, sometimes fetid, sputum. The sputum may contain flecks of blood; frank hemoptysis can occur. Symptoms are often episodic and are precipitated by upper respiratory tract infections or the introduction of new pathogenic agents. Clubbing of the fingers may develop. In cases of severe, widespread bronchiectasis, significant obstructive ventilatory defects develop, with hypoxemia, hypercapnia, pulmonary hypertension, and (rarely) “cor pulmonale.” Metastatic brain abscesses and reactive amyloidosis are other, less frequent complications of bronchiectasis. Bronchiectasis disease is termed multiple bronchiectasis with “cor pulmonale”.

№214 CHRONIC BRONCHITIS ACCOMPANIED BY BRONCHIECTASIS H & E des Microscopically: Intense acute and chronic inflammatory exudate within the walls of the bronchi and bronchioles, and desquamation of lining epithelium, cause extensive areas of ulceration. Hyperplasia of mucous glands is seen. As usual, fibrosis of the bronchial walls and peribronchial fibrosis is observed. The lumen is abnormally dilated, and scarring also persists. Lining epithelium shows prominent squamous methaplasia.

Grossly: the most severe involvement is found in the distal bronchi and bronchioles. The airways are dilated to as much as 4 times their usual diameter, and on gross examination of the lung, they can involve almost the pleural surfaces. Definition: Bronchiectasis is the permanent dilation of bronchi and bronchiolesdue to destruction of the muscle and elastic supporting tissue, resulting from or associated with chronic necrotizing infections. Complications may be pulmonale: bronchopneumonia, atelectasis, obstructive emphysema, and pneumofibrosis. Complications may be extra pulmonale: right-side heart failure or “cor pulmonale” and amyloidosis.

TUBERCULOSIS.Definition: Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis, characterized by involving of the lungs but may affect any organor tissue in the body. Course of tuberculosis is as follows: exudative inflammation and caseous necrosis during acute phase and proliferative inflammation with specific granulomas formation and fibrosis during chronic phase. Classification: Principally tuberculosis is divided into 3 main clinical-morphologic types: 1Primary tuberculosis develops as a result of primary infection and appears as a primary tuberculous complex (Ghon complex), 2 Hematogenous tuberculosis, and 3 Secondary tuberculosis Etiology: Tuberculosis is a mycobacterium infectious disease. There are a lot of types of Mycobacterium, but only 3 of them are a human pathogens.They are Mycobacterium tuberculosis, Mycobacterium bovis, and Mycobacterium africanum, included in the Mycobacterium tuberculosis complex. These organisms are the etiologic agents of human tuberculosis.There are two pathways for infection to follow: 1 aerogenic; 2 alimentary. Pathogenesis: Immunity to a tubercular infection is primarily mediated by T cells and is characterized by development of hypersensitivity and resistance to the organism. The chief implications of primary tuberculosis are 1) it induces hypersensitivity and increased resistance; 2) the foci of scarring may harbor viable bacilli for years, perhaps life long, and thus, be a site for reactivation later when host defenses are compromised; and 3) uncommonly, the disease may develop without interruption into the so-called progressive primary tuberculosis or disseminated disease.The process of primary tuberculosis development begins in the primary lung focus (Ghon focus) with elimination of surrounding inflammation. Proliferation replaces exudation. The rim of epithelioid and lymphoid cells, appears around the focus of caseative pneumonia. Outside the rim numerous of tubercles appear. So, the primary focus undergoes encapsulation. Outcome: The process represents an outcome of the primary tuberculosis, persisting life long. Morphologic appearance: Aerogenic contamination leads to primary tuberculosis complex (Ghon complex) within the lung, consisting of three parts.1 Primary focus or affection occurs within the right lung under pleura, in 3, 8, 9, 10 segments. Primary focus (Ghon focus) consists of caseousnecrosis with serous-fibrinous pleuritis. 2 Tubercular lymphangitis includeslymphostasis and tubercular granulomas within perivascular tissue. 3 Lymphadenitis of bronchipulmonal, bronchial and byfurcar lymph nodes. Alimentary contamination leads to primary tuberculosis complexwithin the small intestine, this consists of three parts. 1 Primary focus (affection) occurs as ulcer of the intestinal wall. 2 Tubercular lymphangitis. 3 Lymphadenitis of mesenteric lymph nodes. Clinical course of primary tuberculosis includes three variants:1 primary tuberculosis loss with healing of primary tuberculosis complex; 2 progressive primary tuberculosis with process of generalization; 3 chronic primarytuberculosis.Progress of primary tuberculosis may spread to: 1 lymphogenic pathway; 2 hematogenic pathway; 3 growth of primary affect; 4mixed.Hematogenic tuberculosis is characterized by predominance of productive tissuereaction, hematogenic generalization, lesion of various tissues. There are three types of hematogenic tuberculosis: 1 generalized tuberculosis; 2 hematogenic tuberculosis with predominant pulmonary lesion; 3 hematogenic tuberculosis with predominant extra pulmonary lesion. 1 generalized tuberculosis includes three forms: 1.1 fulminant Tuberculous Sepsis;1.2 acute common miliary tuberculosis; 1.3 acute common large local Tuberculosis; 1.4 chronic common miliary tuberculosis.2 hematogenic tuberculosis with predominant pulmonary lesion includes:

2.1 acute and chronic miliary tuberculosis of the lungs; 2.2 hematogenic disseminated large local tuberculosis of the lungs.3 hematogenic tuberculosis with predominant extra pulmonary lesion includes: 3.1 bone- joint form; 3.2 urinary- infiltrative tuberculosis genital form;3.3 tuberculous meningitis; 3.4 skin form.Secondary tuberculosis consists of high morphologic forms, to extend along several different forms called stages. 1 acute local tuberculosis (foci of Abricosov’s reinfection) occurs in 1, 2 segments of right (rare left) lung as caseous pneumonia. Healing with encapsulated petrifica- tion is termed Aschoff-Pule foci; 2 fibrous- local tuberculosis includes foci of healing and acute condition; 3 infiltrative tuberculosis (Assman-Redecker foci) consists of small Focus of caseous necrosis with perifocal serous exudate and cellular infiltration; 4 tuberculema is encapsulated focus of caseous necrosis of 5cm in dia.; 5 caseous pneumonia is characterized by massive caseous necrosis. 6 acute cavernous tuberculosis develops with cavity formation within caseous masses. Cavity of 2-7cm in dm is formed in 1-2 segments of the lungs connected with bronchus. 7 fibrous-cavernous tuberculosis (pulmonary consumption) includes chroniccavity, pneumosclerosis, petrification, foci of caseous pneumonia;8 cirrhotic tuberculosis is characterized by scar formation, local-diffused pneumosclerosis and bronchiectasis.

№244 MILIARY TUBERCULOSIS OF THE LUNG H & E des. Microscopically: multiple small nodules are seen within the lung tissue composed of central caseation, surrounded by the rim of epithelioid cells with admixture of some Pirogov-Langhans giant cells. Peripherally a thin rim of lymphoid cells is present. Grossly: the lung is slightly enlarged, soft, with disseminated miliary (millet-like) gray-white to yellow colored granulomas, not more than 2 mm in diameter. Pathogenesis: Miliary lung tuberculosis results as follows:1 Progressive primary tuberculosis in the cases of hematogenous generalization from the Ghon focus,2 Hematogenous tuberculosis in the cases of reactivation in the foci of scarring (healed Ghon foci) when the host defense is compromised.3 In very rare cases secondary tuberculosis may develop a miliary disease as a result of intracanalicular or hematogenous spread in weakened persons.

Outcome: Outcome of tuberculous granulomas depends on immunologic status of the host and may show 1) total necrosis in immunodeficient patients, or 2) fibrosis in sufficient immunity.

№242 Caseous pneumonia (Predominance of exudative reaction) H & E des. Microscopically: Confluent massive foci of exudative inflammation occur within the lung. Alveolar exudate includes serous fluid, fibrin, leukocytes and lymphocytes. Caseous necrosis can be seen in the center of inflammatory focus. Pulmonary structure is not revealed (vague lung marking of violet color as kariorrhexis is noted). Grossly: the lung is enlarged, firm, with prominent amounts of fibrin, covering pleura. The cross-section is yellow-grey colored. The process may show acinar component to lobar affect. Definition: changes described beyond represent a manifestation of secondary lung tuberculosis. Secondary tuberculosis is the pattern of the disease arising in a previously sensitized host from reactivation of dormant primary lesions or exogenous re-infection. Pathogenesis: Secondary pulmonary tuberculosis is classically localized of the apex of one or both upper lobes. The reason is obscure but may be related to high oxygen tension in the apices. Due to preexistence of hypersensitivity, the bacilli produce a prompt and marked tissue response that tends to approach the wall of the focus. Cavitation occurs readily in the secondary form, resulting in dissemination along the airways. Erosion into an airway becomes an important source of infectivity because the patient now produces sputum containing bacilli. Complications in secondary tuberculosis are usually connected with cavitation and represent bleeding (hemoptysis), pneumothorax, purulent pleuritis (empyema of pleura). Amyloidosis may also complicate the disease as a result to prolonged pro- cess. Rarely, in the terminal stages of the disease, hematogenous dissemination may take place with meningitis development, especially in marked immunodeficient per- sons. Sometimes extra pulmonary isolated organ tuberculosis may occur.Possible causes of death: lung and heart failure, bleeding, amyloidosis with uremia.

Thrombosis is blood clotting within the vascular system or the cardiac chambers of a living organism. Thrombus is the product of thrombosis. Classifications 1.1 red or stasis thrombus (venous thrombosis or phlebothrombosis); 1.2 gray-white thrombus (arterial thrombosis); 1.3 mixed thrombus (aortic or cardiac chamber thrombosis); 1.4 hyaline thrombus (microcirculatory thrombosis). 2.1 mural thrombus (aorta, vessels, cardiac chamber); 2.2 occlusive thrombus (vessels).

1 The thrombus may be obstructive into the artery and the cause of infarction in the organs, into the vein –it may be the cause of edema and ulcer.

2The thrombus into deep veins of low extremity may be embolising in pulmonary artery causing death. The thrombus into the aorta or the heart may be embolising in artery system of lots of organs.

Etiology: Virchov’s triad as local causes: 1) destruction of integrity of the vascular wall (endothelial injury); 2) impairment; 3) disturbance of blood flow.The systemic (generalized) factors: 1 imbalance between coagulation and anticoagulation systems; 2 increase of viscosity and amount of regular blood elements. Pathogenesis: stages of thrombus formation:1Agglutination of the thrombocytes (platelets); 2 coagulation of fibrinogen; 3 agglutination of the erythrocytes; 4 precipitations of the plasma proteins. Results of thrombus are in:1 organization; 2 canalization; 3 calcification (phleboliths); 4 septic dissolution;5 embolisms; 6 aseptic dissolution.Diseases: 1 Atherosclerosis; 2 Vasculitis; 3 Malignant tumors; 4 Vegetation of the valves; 5 Nonbacterial endocarditis; 6 DIC-syndrome; 7 Traumas. Embolism is the circulation with blood or lymph stream of abnormal masses (emboli) to occur in any site within the cardiovascular system. Classification1 the volume of emboli: 1 single; 2 multiple; 3 repeated.2 according to the type of embolus: 1 thromboembolism; 2 fatty; 3 bubble of air; 4 nitrogen; 5tissue embolism; 6 foreign bodies; 7 microbial ( bacterial ).3 according to movement of emboli with blood flow: 1 direct embolism; 2 retrograde, (backward); 3 paradoxical embolism.

№ 91 METASTATIC ABSCESSES IN THE KIDNEY H & E des. MicroscopicallyThere are a lot of microbial emboli into the lumen of multiple small vessels of the kidney. Leukocyte infiltration surrounds microbial emboli with dissolution of the tissue is named abscess.GrosslyThere are multiple small green- yellow purulent foci on the cut and the surface of the kidneyDefinitionEmbolism is the circulation with blood or lymph stream of abnormal mass (emboli) to occur anywhere with blood within the cardiovascular system.Metastasis shows the development of secondary purulent foci discontinued with the primary purulent focus.Etiology: Bacterial colony, fungus.Pathogenesis: the primary focus may be anywhere, from purulent thrombophlebitis microbial emboli in the small vessels of the lung and then other organs: the kidney;the heart; the brain; the spleen; the liver.Result is in multiple purulent metastases as abscesses.Diseases: 1 sepsis; 2 appostematous nephritis; 3 bacterial endocarditis; 4 acute pyelonephritis (as hematogenic pathway).Clinical correlations: 1 acute renal failure; 2 pyuria; 3 high temperature4 low back pains; 5 disuria.

№259 LYMPH NODE (OR SPLEEN №260) WITH LYMPHOGRANULOMATOSIS (OR HODGKIN’S DISEASE) H & E. des. Microscopically-The lymphoid tissue is depleted. The tumor is composed of atypical binucleate Reed - Sternberg – Berezovsky cells surrounded by multiple cell types, including atypical histiocytes –

Hodgkin’s cells, eosinophies, lymphocytes, plasma cells, benign histiocytes. The Foci of the necrosis and sclerosis may be seen in lymph node.It is lymphogranulomatosis, mixed cellular type.Grossly: lymph nodes are enlarged, painless, rich, of grey-pink color and may be joined in conglomerates (packets).the spleen with lymphogranulomatosis is the so-called “Porphyric” spleen.There are small splenic enlargements with grey sites of necrosis and sclerosis between red spleen tissues.Definition: Lymphogranulomatosis is a malignant tumor of lymphoid tissue with lesion of lymph nodes and organs, characterized by growth of the giant cells called Reed-Sternberg – Beresovsky cells, large and small atypical histiocytes (Hodgkin’s cells) and inflammatory infiltration. The lymphoid tissue is depleted due to the development of necrosis and sclerosis.Etiology: EBV infection.Classification: Lymphogranulomatosis may be:1. Local lymphogranulomatosis, involving a single node or chain of nodes in one group of lymph nodes (usually neck nodes).2. Generalized lymphogranulomatosis, characterized by spreading of pathological process to other groups of lymph nodes and organs (spleen).Histological variants of the lymphogranulomatosis.1 With lymphocyte predominance.2 Nodular scleroses.3 Mixed cellularity.4 With lymphocyte depletion.Clinical significance: 3 and 4 variants are characterized by unfavorable prognosis.

№ 93 PHLEGMON OF THE SUBCUTANEOUS FAT H & E des Microscopically: Diffuse neutrophil infiltration and inflammatory hyperemia are seen in the subcutaneous fat. See Definition, classification and etiology above.The diseases: 1. Trauma. 2. Wound formation. 3. Typhoid Fever. 4 Sepsis.Complications: Dissemination of the purulent inflammation may lead to fistula or leakage.

Outcome: 1. Resolution of the exudate with restoration of the normal tissue structure. 2. Scarring. Additionally: Phlegmonous inflammation may occur also in the appendix, in the bile cyst and other organs.

Definition: Necrosis is one of the morphological patterns of death: the death of cells or tissue parts or organ parts in a living organism. There are two patterns of death in the living organism: a) necrosis; b) apoptosis.Classification is according to etiology: 1 Hypoxia; 2 Physical agents; 3 chemical agents and drugs; 4 Infectious agents; 5 genetic injury; 6 malnutrition.Classification is according to pathogenesis: 1 direct action; 2 indirect action.Clinic pathologic forms: 1 coagulation necrosis; 2 liquefactive necrosis; 3 gangrenous necrosis; 4 infarct; 5 sequester; 6 fatty necrosis.Classification: there are two types of necrosis according to denaturation of proteins and enzyme digestion: 1 coagulation is necrosis with a

predominance of proteins. Its variety is named caseous necrosis; 2 liquefactive one is necrosis with a predominance of enzymes and water.

Classification of gangrenous necrosis: 1 dry 2 wet gangrene. Wet gangrene is associated with microorganisms.

Classification of wet gangrene: 1 bedsore ( syn. Decubitus ) is the type of wet gangrenous necrosis of the skin and soft tissues exposed to long

term pressure; 2 noma is the type of wet gangrenous necrosis of cheeks or the perineum developed in debilitated children.

Results of necrosis: 1 restitution; 2 scar; 3 cyst formation; 4 myolysis; 5 rupture;

6 petrifaction; 7 ossification; 8 encapsulation; 9 fistula formation

№7 NECROSIS OF THE SKELETAL MUSCLES WITH PETRIFICATION H & E des. Microscopically: This is coagulation necrosis of the skeletal muscles without nuclei, without banding striatura of bright pink color and deposition of calcium salt.Grossly: The skeletal muscle is solid of yellow color, waxy like, the so-called Zenker’s necrosis.The definition: coagulation necrosis is necrosis of the tissue in which denatured proteins are richer than enzymes and water.Cause: right toxin actions.

Diseases: Typhus fever; typhoid fever; toxic dysentery; toxic diphtheria.

Pathogenesis: proteins and enzymes are denatured by the cellular injury and intracellular acidosis.

Results: organization with scarring, formation petrification.

Clinical signs: pains; loss of muscular contractility.

Definition: PIGMENTS are coloured substances.Classification of pigments: 1 exogenous; 2 endogenous.Endogenous pigments: 1 haemoglobin-derived pigments; 2 lipidogenic pigment (lipofuscin); 3 tyrosinogenic pigment (melanin)There are normal haemoglobin-derived pigments: 1 hemosiderin; 2 bilirubin; 3 ferritin.There are abnormal haemoglobin-derived pigments: 1 hematoidin; 2 hemomelanin; 3 hematin.Hemosiderosis is a condition, characterized by hemosiderin deposition in many organs and tissues in systemic overload of iron.Hemosiderin is a haemoglobin-derived granular pigment that is brown and accumulated in tissues (cells), with a local or systemic excess of iron.Classification:1.1 .Systemic Hemosiderosis (in diseases, accompanied by intravascular haemolysis),1.2 . Local Hemosiderosis (accompanied by haemorrhages).2.1. Primary Hemosiderosis (Idiopathic pulmonary hemosiderosis),2.2 Secondary Hemosiderosis (Congestion-associated hemosiderosis).EtiologyIncreased contents of ferritin in blood and tissues caused by intravascular and extra vascular haemolysis.PathogenesisLocal excess of iron, and consequently hemosiderin, results from gross hemorrhage or myriad minute hemorrhages accompanying severe vascular congestion. After lysis of the erythrocytes at the site of hemorrhage, the red cell debris parts are phagocytosed by macrophages; the haemoglobin content is then catabolized by lysosomes with accumulation of the heme iron in hemosiderin. The same process is seen in the ordinary bruise. The array of colours through which the bruise passes reflects these transformations. The original red-blue colour of haemoglobin is transformed to various shades of green-blue by the local formation of biliverdin (green bile) and bilirubin (red bile) from the heme moiety; the iron ions of haemoglobin are accumulated as golden-yellow hemosiderin.Abnormality of melanin metabolism may increase or look decrease this pigment.Classification: 1.1 Hereditary and 1.2 Acquired; 2.1 local and 2.2 generalised; 3.1 hyper pigmentation and 3.2 hypo pigmentation. Hyper pigmentation: pigmental Xeroderma, Addison’s disease, melanodermia, lentigo,Pigmented nevus. Hypo pigmentation: Albinism, vitiligo.PATHOLOGIC CALCIFICATION.

Definition: Pathologic calcification is referred to as abnormal precipitation of calcium salts.Classification: There are dystrophic and metastatic calcifications.

№63 LIVER IN MECHANICAL JAUNDICE. H & E des.Microscopically elongated green-brown plugs of bile are visible in dilated bile canaliculi. Rupture of canaliculi leads to extravasation of bile, which is quickly phagocytosed by Kupffer cells. Droplets of bile pigment also accumulate within hepatocytes, which can take on a wispy appearance (foamy degeneration). Duct epithelial cells proliferation is observed as well as looping and reduplication of ducts. Associated portal tract findings include edema and periductal infiltrations of neutrophils. Prolonged obstructive cholestasis leads to focal destruction of the parenchyma, giving rise to bile lakes (pools) filled with cellular debris and pigment.Grossly the liver is enlarged, dense, green-brown coloured.Definition: Jaundice is yellow pigmentation of the skin, sclerae, mucous membranes and organ parenchyma with both unconjugated and conjugated bilirubin in hyperbilirubinemia (blood level of bilirubin over 1.2 mg/dl).Classification

1. Hemolytic jaundice (subhepatic) is characterized by excessive production of bilirubin, accompanied with increased lysis of erythrocytes, and reduced hepatocellular uptake. These mechanisms produce unconjugated hyperbilirubinemia.

2. Obstructive jaundice (mechanical or infrahepatic) is characterized by impaired bile flow and decreased hepatocellular excretion, leading to conjugated hyperbilirubinemia.

3. Parenchymatous jaundice (hepatic) is associated with hepatocytes injury, which may operate due to any of the named above mechanisms and produce both unconjugated and conjugated hyperbilirubinemia.

Etiology and pathogenesisExtrahepatic biliary obstruction leads to dilation and rupture of bile canaliculi and extravasation of bile, which accumulates in Kupffer cells and hepatocytes. Accumulation of bile leads to degeneration, injury and necrosis of hepatocytes and portal tract fibrosis, which initially extends into and subdivides the parenchyma with relative preservation of hepatic architecture. Ultimately, in the final stage bile-stained cirrhotic liver occurs.Diseases:Gallstone obstruction of biliary tree; carcinomas of head of pancreas, extrahepatic bile ducts, ampulla of Vater; extrahepatic biliary atresia; biliary strictures and choledochal cysts; primary sclerosing cholangitis; liver fluke infestation.Complications and outcome:Cholestatic condition, which result from extrahepatic biliary obstruction and leads to biliary cirrhosis and may be complicated by hepatic failure, multiple organ failure, coagulopathy, hepatic encephalopathy, hepatorenal syndrome, portal hypertension from cirrhosis, esophageal varices and risk of rupture, hepatocellular carcinoma.Clinical correlations:1) Conjugated hyperbilirubinemia, 2) hypoalbuminemia, 3) bilirubinuria, leading to renal tubular necrosis, 4) yellow discoloration of skin, sclerae, mucous membranes, 5) pruritus, 6) hemorrhagic syndrome.

Definition: Parenchymal disproteinosis is the reversible injury of the cells connected with abnormality of protein metabolism. Definition: Dystrophy is the pathologic process connected with disturbances of tissue metabolism, leading to structural disorders.Classification 1 parenchymal disproteinosis: a) hydropic dystrophy; b) hyaline droplet dystrophy; c) hyperkeratosis (or horny dystrophy).2 according to the sites of structural changes: a) parenchymal dystrophy; b) stromal vascular dystrophy; c) mixed dystrophy.3 according to the metabolic changes: a) disproteinosis; b) lipidosis; c) carbohydrates abnormality; d) mineral and pigmental abnormality.4 according to the nature: a) acquired; b) hereditary.5 according to a spread: a) general; b) local.Lysosomal storage diseases caused by mutations in enzyme proteinsIn Glycogenoses, enzymatic defects in the synthesis or breakdown (degradation) of glycogen result in massive stockpiling, with secondary injury and cell death.1 Glycogen storage diseases or Glycogenoses; 2 Sphingolipoidoses is Tay-Sachs disease with accumulation of GM2 gangliosides; 3 Gaucher disease with accumulation of glucocerebrosides; 4 Sulfatidoses is Niemann- Pick disease with accumulation of sphingomyelin.

34 HYDROPIC DYSTROPHY OF THE KIDNEY H&E des.Microscopically: small clear vacuoles may be seen within the cytoplasm; Electron microscopically: These represent distended and pinched-off segments of the endoplasmic reticulum.Grossly: When all cells in an organ are affected, there is pallor, with increased turgor and: weight.Definition: Hydropic dystrophy or degeneration is a type of parenchymal disproteinosis with the cellular swelling and with fluid babbles in the cytoplasm to appear.Etiology: a) hypoxia, b) high temperature; c) starvation; d) infectious diseases; e) exotoxins. Pathogenesis of the Hydropic dystrophy: cells are incapable of maintaining ionic and fluid homeostasis. K-Na pomp component of the cellular membranes is destroyed and Na ions are accumulated within cellular plasma. Accumulation of the protein within cell plasma may also occur : 1 nephrotic syndrome appears in membrane and enzyme systems destruction with disturbance of reabsorption of the water and the protein. The mechanisms are called infiltration.The diseases: glomerulonephritis, nephrotic syndrome.Organs: the kidney, the liver, the skin, the adrenals, nervous system, muscles.Outcome: 1 if the etiologic agent is not manifested, the cells return to normal state; 2 if the etiologic agent acts, there may be liquefactive necrosis as irreversible injury. Clinical correlations: 1proteinuria; 2 polyuria; 3 hypoproteinemia;