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Inflammations

assistant-professor Volodymyr
Voloshyn

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

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.

Etiology.
exogenous:
biological
physical
chemical

endogenous:
- the structures of own tissue
and cells
- the metabolisms 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

Inflammation Indications
(markers)
Clinical:

temperature;
tumor;
hyperaemia;
pain;
function lose.

Morphological:
Alterations (A):
(primary, secondary);

Exudation (B);
Proliferation (C).

A
B

Pathogeny of
inflammation
Exudation
Alteration

Dystrophy

Microcirculati
on changes

Spasm
Paresis
Marginal
leucocells
placing

Mitosis

Plasma
infiltration

Endoteliocells
activation
Plasmorrhagy

Proliferation

Necrosis

Blood cells
immigration

Leucodiapedesis

Phagocytosis

Completed
Uncompleted

Erythrodiapedesis

Amitosis

Endocytobiosis
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A
B

Pathogeny of
inflammation
Alteration

Dystrophy

Necrosis

Exudation

Microcirculation
changes

Spasm
Paresis
Marginal
leucocells
placing

Mitosis

Plasma
infiltration

Endoteliocells
activation
Plasmorrhagy
Proliferation

Blood cells
emigration

Leucodiapedesis

Phagocytosis

Completed
Uncompleted

Erythrodiapedesis

Amitosis

Endocytobiosis
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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.

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.
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A
B

Pathogeny of
inflammation
Alteration

Dystrophy

Necrosis

Exudation

Microcirculati
on changes

Spasm
Paresis
Marginal
leucocells
placing

Mitosis

Plasma
infiltration

Blood cells
emigration

Endoteliocells
activation
Plasmorrhagy
Proliferation

Leucodiapedesis

Phagocytosis

Completed
Uncompleted

Erythrodiapedesis

Amitosis

Endocytobiosis
10

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

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Infiltration types

(and signs)

by polymorphonuclear leucocytes
roundcells
macrophage
(pale-gray infiltration)
eosinofilic

hemorrhagic

(gray-green tint)

(erythrocytes infiltration)

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A
B

Pathogeny of
inflammation
Alteration

Dystrophy

Necrosis

Exudation

Microcirculati
on changes

Spasm
Paresis
Marginal
leucocells
placing

Mitosis

Plasma
infiltration

Endoteliocells
activation
Plasmorrhagy
Proliferation

Blood cells
immigration

Leucodiapedesis

Phagocytosis
Completed
Uncompleted

Erythrodiapedesis

Amitosis

Endocytobiosis
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Stages of phagocytosis:
approaching
adhesion
absorption
digestion

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A
B

Pathogeny of
inflammation
Alteration

Dystrophy

Necrosis

Exudation

Microcirculati
on changes

Spasm
Paresis
Marginal
leucocells
placing

Mitosis

Plasma
infiltration

Endoteliocells
activation
Plasmorrhagy
Proliferation

Blood cells
immigration

Leucodiapedesis

Phagocytosis

Completed
Uncompleted

Erythrodiapedesis

Amitosis

Endocytobiosis
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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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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.

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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).

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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
granulomes
organizing:
Accumulation young
mononuclear;
their transformation into
macrophages;
formation of mature
granulomaes.
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Granulamatosis inflammation
Unspecific

Specific

Acute

Chronic

Tuberculosis

Syphilis (Luis)

Rheumatism

Syphilis (Luis)

Brucellosis

Leprosy

Tularemia

Rinoscleroma

Sarcoidosis

Glanders

Typhus, spotted fever


Typhoid (fever)
Hydrophobia

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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

microscopic (right) with fungal


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

Severe chronic fibrosing


pneumonitis ("carnification"),
gross appearance

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

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).

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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
(caseous) necrosis (arrow).
central

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Morphological markers of specific granulomaes


Tuberculosis

Syphilis

Leprosy

Necrosis

Vasculites

Epitelioid
cells

Necrosis

Epitelioid
cells

Lymphocytes
Solitary
plasmocytes
Gigantic
cells of
Pirohov &
Langans

Epitelioid
cells

Virkhov;s
cells
Fibroblastes

Lymphocytes
Plasmocytes
Multitude
plasmocytes
Gigantic cells
of Pirohov &
Langans

Lymphocytes

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Morphological markers of specific granulomaes


Rinoscleroma

Glanders

Epitelioid
cells

Granulation
tissue

Plasmocytes
Neutrophyles
Leucocytes
Mikulch
cells

necrosis with
kariorexis

Hyaline
globes

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).
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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

()

.
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and
there is
the
end
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Thank you
for
attention!
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