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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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histion:• 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 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

Mitosis Amitosis

Alteration Dystrophy Necrosis

III

III Proliferation

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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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Serosal inflammation

(acute motion)

Fibrinous inflammation

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."

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).

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.

CROUPOUS (LOBAR) PNEUMONIA

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.

Types of purulent inflammation

• There are two types: phlegmon & abscess.

• Specific forms: empyema & cold abscess

Catarrhal inflammation

acute: serosal, mucus, festering, putrid, hemorrhagic;

chronic: atrophic, hypertrophic;

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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 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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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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Virus pneumonia (hemorrhagic defeat of Lung)

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Virus pneumonia (defeat of Kidney)

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Virus pneumonia (hemorrhagic defeat of Liver)

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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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Productive InflammationMiocarditis

Interstitial Granulematic

Around animal parasites

kondilomes Hyperplastic growthing

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.

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Phases of granulomesorganizing:

• Accumulation young mononuclear;

• their transformation into macrophages;

• formation of mature granulomaes.

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.

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.

Tuberculosis granulomas

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Granulamatosis inflammation

Specific

Tuberculosis

Syphilis (Luis)

Leprosy

Glanders

Rinoscleroma

Unspecific

Acute

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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•

•

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). 

Tuberculosis

Syphilis

Rinoscleroma

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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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Thank you for attentio

n!