inflammations
DESCRIPTION
Inflammations. assistant-professor Volodymyr Voloshyn. (in accordance with Ya.Ya. Bodnar et al., Rubin & Farber, Serov et al.; Frank Netter’s illustrations). - PowerPoint PPT PresentationTRANSCRIPT
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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!