Inflammations

1. Inflammations assistant-professor Volodymyr Voloshyn (inaccordancewith Ya.Ya. Bodnar et al., Rubin & Farber, Serov et al.; Frank Netter’s illustrations)

2. Inflammation is a typical pathological process which arises up as a reflex to the destroing agent action. It was made in the phylogenesis process and has the protection & adaptation value.

3. Etiology. • exogenous: • biological • physical • chemical • endogenous: - the structures of own tissue and cells - the metabolism’s products -immune complexes

4. histion: • morphofunktional unit of connecting tissue, which includes cellular elements, fibers, basic matter, nerves and their completions, haemomicrocirculation channel and lymphatic ways

5. Inflammation Indications (markers) • Morphological: • Alterations (A): (primary, secondary); • Exudation (B); • Proliferation (C). • Clinical: • temperature; • tumor; • hyperaemia; • pain; • function lose.

6. I Alteration Pathogeny of inflammation Dystrophy Necrosis II Exudation Microcirculation changes Plasma infiltration Blood cells emigration Phagocytosis Spasm Endotelio-cells activation Leuco-diapedesis Completed Paresis Uncompleted Marginal leucocellsplacing Erythro- diapedesis Plasmo-rrhagy Endocytobiosis III Proliferation Mitosis Amitosis

7. Inflammation Alteration Exudation Proliferation Dys tro phy Microcir culation changes Necrosis Plasma infiltration Cells Emmig- ration Phagocitosis

8. Reasons of exudation: • a) an increasing of pressure at arterial and venous hyperemia; • b) increase of vascular wall permeability under neurohumors act of inflammation, hydrogen and potassium ions, ATP acid, milk and other acids; • c) oncotic pressure growthing outside vessels as a result of disintegration of albuminous molecules and output of albumin.

9. Types of exudates inflammation: • serosal (2 % protein) • fibrinoid (crouposis or diphtheritic) • purulent (festered): (acute or chronic) (abscess, phlegmon, empyema) • putrid • hemorrhagic • catarrhal: • acute: serosal, mucus, festering, putrid, hemorrhagic; • chronic: atrophic, hypertrophic; • mixed.

10. Serosal inflammation (acute motion)

11. Fibrinous inflammation

12. Fibrinous pericarditis May occur at uremia, rheumatic disease, transmural myocardial infarction, lobar pneumonia. Macroscopically:Epicardium dull, covered with grayish-yellow rough overlays in the form of threads and resembles hair "hairy heart." Overlay can be easily removed.Consequence: Reunion formed between the sheets of pericardium, often heart cavity obliteration shirts, sometimes sklerozovani shell pertryfikuyutsya or osyfikuyutsya "armored heart."

13. CROUPOUS (LOBAR) PNEUMONIA Croupous pneumonia - an acute disease caused by pneumococcus (occasionally Klebsiella), which develops holdings fibrinous pneumonia. Macroscopically: affected lobe is increased, it’s density like hepatic tissue, on the cute surface is gray, slightly granular (stage of gray hepatization), pleural membrane is covered by fibrinous film which is easily removed (fibrinous pleuritis - a characteristic feature of lobar pneumonia).

14. CROUPOUS (LOBAR) PNEUMONIA Microscopically: at the stage of gray hepatization all alveoli are filled with exudate consisting of fibrin, PMNL and alveolar macrophages. Capillaries of interalveolar septa contain fibrin thrombi. Histochemical reaction stains the fibrin in the exudate in purple color. Consequence: The exudate mainly dissolve by proteolytic enzymes of leukocytes and macrophages and excreted in the sputum.Complications . At insufficient of proteolytic activity there is organization of exudate (replacing into connective tissue). At increasing of proteolytic activity there is purulent fusion with the formation of abscesses in lung.

15. Diphtheritic Inflammation of Pharynx Diphtheritic inflammation of the pharynx (diphtheritic angina) occurs at diphtheria.Microscopic picture: visible necrotic areas of mucosa and underlying tissues of the tonsils are filled by fibrin and PMNL. On the periphery of the fibrinous inflammation - the demarcation zone with advanced full-blooded vessels and the accumulation of PMNL. Consequence of diphtheritic inflammation: the scars formed in place of deep ulcers that occur when the films are removed.

16. Types of purulent inflammation • There are two types: phlegmon &abscess. • Specific forms: empyema & cold abscess

17. Catarrhal inflammation acute: serosal, mucus, festering, putrid, hemorrhagic; chronic: atrophic, hypertrophic;

18. A Alteration Pathogeny of inflammation Dystrophy Necrosis B Exudation Microcirculation changes Plasma infiltration Blood cells emigration Phagocytosis Spasm Endotelio-cells activation Leuco-diapedesis Completed Paresis Uncompleted Marginal leucocellsplacing Erythro- diapedesis Plasmo-rrhagy Endocytobiosis C Proliferation Mitosis Утворення ексудату Amitosis

19. Periods of Emigration • marginate • penetration is through a vascular wall • motion in tissue

20. Infiltration types (and signs): • by polymorphonuclear leucocytes (gray-green tint) • roundcells • macrophage (pale-grayinfiltration) • eosinofilic • hemorrhagic (erythrocytes infiltration)

21. A Alteration Pathogeny of inflammation Dystrophy Necrosis B Exudation Microcirculation changes Plasma infiltration Blood cells immigration Phago-cytosis Spasm Endotelio-cells activation Leuco-diapedesis Completed Paresis Uncompleted Marginal leucocellsplacing Erythro- diapedesis Plasmo-rrhagy Endocytobiosis C Proliferation Mitosis Утворення ексудату Amitosis

22. Stages of phagocytosis: • approaching • adhesion • absorption • digestion

23. A Alteration Pathogeny of inflammation Dystrophy Necrosis B Exudation Microcirculation changes Plasma infiltration Blood cells immigration Phagocytosis Spasm Endotelio-cells activation Leuco-diapedesis Completed Paresis Uncompleted Marginal leucocellsplacing Erythro- diapedesis Plasmo-rrhagy Endocytobiosis C Proliferation Mitosis Утворення ексудату Amitosis

24. Consequences of inflammation: • a) complete restore; • b) scarring formed; • c) chronic form; • d) death.

25. Classifications of inflammation: • Etiology: a) banal; b) specific; • Process rate: a) lightning; b) subacute; c) acute; d) chronic • Process predominance ofbanal inflamation: a) exsudative; b) productive.

26. Acute inflammation---- 1) hyperemia, peristasis and stasis) 2) edema, fibrinous exudates Suppurative inflammationabscesses Endotoxemia circulatory shock.

27. 20 Serous rhinitis in allergic nasal polyp Pseudomembranous enteritis Serous rhinitis in allergic nasal polyp; note the severe edematous swelling of the stroma (arrow). Pseudomembranous enteritis (serofibrinous exudate) in small intestine of baby with staphylococcal food poisoning; note the loose yellowish membranes covering the mucosa (arrow). b a

28. Suppurative microcarditis with abscess formation and bacterial colonies, gross (left) and microscopic (right). note the well-circumscribed yellow necroses (arrow) and fine granular bacterial colonies (arrow).

29. Bronchopneumonia (hemorrhagic)

30. Bronchopneumonia (hemorrhagic) • the prominent extravasation of erythrocytes (arrow)

31. Necrotizing pneumonia, microscopic view; note the pale granular destruction of lung tissue (arrow).

32. Virus pneumonia (hemorrhagic defeat of Lung)

33. Virus pneumonia (defeat of Kidney)

34. Virus pneumonia (hemorrhagic defeat of Liver)

35. Chronic Inflammation

36. Types of productive (proliferative) inflammation • interstitial (acute or chronic) • with polypus and pointed kondilom formation • granulomatosic (acute or chronic) • hyperplastic of lymphoid tissue • Around animal parasites 26

37. Productive Inflammation Miocarditis Interstitial Granulematic Hyperplastic growthing kondilomes Around animal parasites

38. Interstitial inflammation Interstitial inflammation occurs in the stroma of parenchymal organs - myocardium, liver, kidneys and lungs.  Interstitial myocarditis occurs at many infectious diseases (influenza, diphtheria, typhus). Microscopic picture: in the stroma of the myocardium is infiltrate consisting of macrophages, lymphocytes, plasma cells, isolated PMNL , epithelioid cells, fibroblasts. In cardiomyocytes expressed dystrophic, necrobiotic change places sometimes . In areas of infiltration observed formed collagen fibers . Consequence: diffuse small focuses cardiosclerosis.

39. Phases of granulomesorganizing: • Accumulation young mononuclear; • their transformation into macrophages; • formation of mature granulomaes.

40. Tuberculosis granulomas Tuberculosis granulomasare observed at miliary tuberculosis of lung and other organs. Macroscopic picture: thay are revealed numerous white and yellow tubercles in the lung tissue. Their size are like millet grains.

41. Tuberculosis granulomas Microscopic picture :In lung tissue are observed numerous granulomas. In its center there are small areas of caseous necrosis, and around its - the shaft of epithelioid cells. Between epithelioid cells are observed giant multinuclear cells Pirogov - Langhans (which often contain tuberculosis Mycobacterium (at Tsil – Nielsen staining can be detect)). On the periphery of granulomas are observed shaft of lymphocytes.Consequence : a small connective tissue scar formed in the place of tuberculosis granulomas (rarer – can be formed petrificates).Tuberculous granuloma should be differentiated from granulomas at sarkoidosis , histoplasmosis , and some other diseases with similar pathohistology.

42. Unspecific Specific Tuberculosis Acute Chronic Syphilis (Luis) Typhus, spotted fever Rheumatism Leprosy Brucellosis Typhoid (fever) Rinoscleroma Tularemia Glanders Hydrophobia Sarcoidosis Granulamatosisinflammation

43. Granulomatous (fungal) pneumonitis, gross (left) and microscopic (right) with fungal organisms {histoplasma sp. red in PAS stain) in giant cells (arrows).

44. Chronic (lymphocytic) gastritis • Severe chronic fibrosing pneumonitis ("carnification"), gross appearance microscopic (right) with fungal organisms {histoplasma sp. red in PAS stain) in giant cells (arrows).

45. Granulation tissue Granulation tissue (skin wound) preceding repair with fibrosis; note the edematous stroma with mixed inflammatory infiltration and proliferation of capillaries (arrow).

46. note the fibrosing granulomas and the surrounding interstitial lymphocytic infiltration with progressive fibrosis (arrow). • Fibrosing granulomatous pneumonitis in autoimmune disease (Wegener granulomatosis) • Chronic atrophic enteritis (Crohn's) with mucosal atrophy in a patient with Crohn's disease; note the fibrous thickening of the terminal ileum with loss of mucosal structure (arrow).

47. Granulomatous pneumonitis showing gross (left) and microscopic (right) features of pulmonary tuberculosis; note the well-circumscribed granulomas with giant cells and central (caseous) necrosis (arrow).

48. Tuberculosis

49. Syphilis

50. Rinoscleroma