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InflammationsInflammationsassistant-professor Volodymyr assistant-professor Volodymyr

VoloshynVoloshyn

(in accordance with Ya.Ya. Bodnar et al., Rubin & Farber, Serov et al.; Frank Netter’s illustrations)

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• 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.

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Etiology.• exogenous:

– biological– physical– chemical

• endogenous: - the structures of own tissue

and cells - the metabolism’s products - immune complexes

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hystion:• morphofunktional unit of

connecting tissue, which includes cellular elements, fibers, basic matter, nerves and their completions, haemomicrocirculation channel and lymphatic ways

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Inflammation Indications (markers)

• Clinical:– temperature;– tumor;– hyperaemia;– pain;– function lose.

• Morphological:– Alterations (A):(primary, secondary);– Exudation (B);– Proliferation (C).

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Pathogeny of inflammation

Microcirculation changes

Plasma infiltration

Blood cells immigration

Phagocytosis

Marginal leucocells

placing

Endotelio-cells

activation

Spasm

Paresis

Plasmo-rrhagy

Completed

Erythro-diapedesis

Leuco-diapedesis

Uncompleted

Endocytobiosis

Утворення ексудатуMitosis Amitosis

Dystrophy NecrosisAB

C

Exudation

Proliferation

Alteration

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Pathogeny of inflammationExudation

Microcirculation changes

Plasma infiltration

Blood cells emigration

Phagocytosis

Marginal leucocells

placing

Endotelio-cells

activation

Spasm

Paresis

Plasmo-rrhagy

Completed

Erythro-diapedesis

Leuco-diapedesis

Uncompleted

Endocytobiosis

Утворення ексудатуProliferation

Mitosis Amitosis

Alteration Dystrophy Necrosis

AB

C

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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.

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• 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.

Types of exudates inflammation:

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Pathogeny of inflammationExudation

Microcirculation changes

Plasma infiltration

Blood cells emigration

Phagocytosis

Marginal leucocells

placing

Endotelio-cells

activation

Spasm

Paresis

Plasmo-rrhagy

Completed

Erythro-diapedesis

Leuco-diapedesis

Uncompleted

Endocytobiosis

Утворення ексудатуProliferation

Mitosis Amitosis

Alteration

Dystrophy NecrosisAB

C

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Periods of Emigration

• marginate• penetration is through a vascular

wall• motion is in tissue

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• by polymorphonuclear leucocytes (gray-green tint)

• roundcells• macrophage (pale-gray infiltration)

• eosinofilic

• hemorrhagic (erythrocytes infiltration)

Infiltration types (and signs):

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Pathogeny of inflammationExudation

Microcirculation changes

Plasma infiltration

Blood cells immigration

Phago-cytosis

Marginal leucocells

placing

Endotelio-cells

activation

Spasm

Paresis

Plasmo-rrhagy

Completed

Erythro-diapedesis

Leuco-diapedesis

Uncompleted

Endocytobiosis

Утворення ексудатуProliferation

Mitosis Amitosis

Alteration

Dystrophy NecrosisAB

C

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Stages of phagocytosis:

approachingadhesionabsorptiondigestion

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Pathogeny of inflammationExudation

Microcirculation changes

Plasma infiltration

Blood cells immigration

Phagocytosis

Marginal leucocells

placing

Endotelio-cells

activation

Spasm

Paresis

Plasmo-rrhagy

Completed

Erythro-diapedesis

Leuco-diapedesis

Uncompleted

Endocytobiosis

Утворення ексудатуProliferation

Mitosis Amitosis

Alteration

Dystrophy NecrosisAB

C

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Consequences of inflammation:

• a) complete restore;• b) scarring formed;• c) chronic form;• d) death.

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Classifications of inflammation:

• Etiology: a) banal; b) specific;

• Process rate: a) lightning; b) subacute; c) acute; d) chronic

• Process predominance of banal inflamation: a) exsudative; b) productive.

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• Acute inflammation ---- 1) hyperemia, peristasis and stasis) 2) edema, fibrinous exudates

Suppurative inflammation abscesses

Endotoxemia

circulatory shock.

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• 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.

Types of exudates inflammation:

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Serous rhinitis in allergic nasal polyp

Pseudomembranous Pseudomembranous enteritisenteritis

a b

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).

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• 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).

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Bronchopneumonia

(hemorrhagic)

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Bronchopneumonia (hemorrhagic)

• the prominent extravasation of erythrocytes (arrow)

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Necrotizing pneumonia, microscopic view; note the pale granular destruction of

lung tissue (arrow).

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Chronic Inflammation

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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

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Phases of granulomesorganizing:

• Accumulation young mononuclear;

• their transformation into macrophages;

• formation of mature granulomaes.

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Granulamatosis inflammation

Specific

Tuberculosis

Syphilis (Luis)

Leprosy

Glanders

Rinoscleroma

Unspecific

Acute

Syphilis (Luis)

Typhus, spotted fever

Typhoid (fever)

Hydrophobia

Chronic

Rheumatism

Brucellosis

Tularemia

Sarcoidosis

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Granulomatous (fungal) pneumonitis, gross (left) and

microscopic (right)

with fungal organisms {histoplasma sp. red in PAS stain) in giant cells (arrows).

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• 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).

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• Granulation tissue

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

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• Fibrosing granulomatous pneumonitis in autoimmune disease (Wegener granulomatosis)

• Chronic atrophic enteritis (Crohn's)

note the fibrosing granulomas and the surrounding interstitial lymphocytic infiltration with progressive fibrosis (arrow).

with mucosal atrophy in a patient with Crohn's disease; note the fibrous thickening of the terminal ileum with loss of mucosal structure (arrow).

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• 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,

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• type II reactive• necrotic

the homogeneous red necroses of glomerular vessels and arteries

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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).

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

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

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•

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

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•

•

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). 

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Morphological markers of specific granulomaes

Syphilis

Gigantic cells of Pirohov’ &

Langans’

Multitude plasmocytes

Vasculites

Necrosis

Epitelioidcells

Lymphocytes

Tuberculosis

Necrosis

Epitelioid cells

Lymphocytes

Solitary plasmocytes

Gigantic cells of

Pirohov’ & Langans’

Leprosy

Fibroblastes

Plasmocytes

Virkhov;s cells

Lymphocytes

Epitelioid cells

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Morphological markers of specific granulomaes

Rinoscleroma

Epitelioidcells

Plasmocytes

Leucocytes

Mikulch’ cells

Hyaline globes

Glanders

Granulation tissue

Neutrophyles

necrosis with kariorexis

Microabscesses

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AIDS(acquired immune deficiency

syndrome).

Periods:• incubate (asymptomatic carrier)• limphadenopathic syndrome

(LAS)•pre – AIDS (syndrome which is

associative with AIDS)•acquired immune deficiency

syndrome (AIDS).38

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AIDS Syndromes:• lymphatic nodes defeat

• injury, which formed at opportunistic infections

• development of malignant tumors.

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AIDS stages•Follicular hyperplasia

•Diffuse hyperplasia by angioimmunoblastic lymphadenopatic type

•Lymphoid emaciation (виснаження).

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AIDS finishes by death

always!!!

and there is

the end…

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Thank you for attentio

n!