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. hystion: • 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. 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

7. 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

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. 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

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

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

13. 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

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

15. 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

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

17. 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.

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

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

20. 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

21. 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).

22. Bronchopneumonia (hemorrhagic)

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

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

25. Chronic Inflammation

26. 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

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

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

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

30. 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).

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

32. 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).

33. Type I (allergic) reaction, bronchial asthma with prominent bullous emphysema of the lung Type II (toxic) reaction, necrotizing glomerulus and vasculitis with fibrinoid necrosis in patient with panarteritis nodosa,

34. type II reactive • necrotic the homogeneous red necroses of glomerular vessels and arteries

35. Type I (allergic) reaction, bronchial asthma with prominent bullous emphysema of the lung (left), and typical eosinophilic bronchitis with sclerosis of epithelial basement membrane Type I (allergic) reaction (bronchial asthma): typical eozinophilic bronchitis with sclerosis of epithelial basement membrane (arrow).

36. Type III (immune complex) reaction, membranous glomerulus with immune complex deposits.

37. Type III (immune complex) reaction (membranous glomerulus)note the prominent thickening of glomerular capillary basement membranes (arrow).

38. Kidney transplant rejection (lymphocytic), gross appearance of kidney (left), interstitial lymphocytic infiltration with tubular damage (right, arrow).

39. 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).

40. Morphological markers of specific granulomaes Tuberculosis Syphilis Leprosy Necrosis Vasculites Epitelioid cells Epitelioid cells Necrosis Virkhov;s cells Epitelioid cells Lymphocytes Fibroblastes Solitary plasmocytes Lymphocytes Plasmocytes Multitude plasmocytes Gigantic cells of Pirohov’ & Langans’ Lymphocytes Gigantic cells of Pirohov’ & Langans’

41. Morphological markers of specific granulomaes Rinoscleroma Glanders Epitelioid cells Granulation tissue Plasmocytes Neutrophyles Leucocytes Mikulch’ cells necrosis with kariorexis Hyaline globes Microabscesses

42. AIDS(acquired immune deficiency syndrome). Periods: • incubate (asymptomatic carrier) • limphadenopathic syndrome (LAS) • pre – AIDS (syndromewhich is associative with AIDS) • acquired immune deficiency syndrome (AIDS). 38

43. AIDS Syndromes: • lymphatic nodes defeat • injury, which formed at opportunistic infections • development of malignant tumors.

44. AIDS stages • Follicular hyperplasia • Diffuse hyperplasia by angioimmunoblastic lymphadenopatic type • Lymphoid emaciation (виснаження).

45. AIDS finishes by death always!!!and there is the end…

46. Thank you for attention!