assistant-professor Volodymyr Voloshyn
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Transcript of assistant-professor Volodymyr Voloshyn
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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!