inflammation in organs without blood vessels. the inflammation … 56... · 2018-12-13 · pannus...
TRANSCRIPT
Inflammation in organs without blood vessels.
The inflammation-organism relationship (beneficial and
harmful effects of inflammation; outcome of the acute inflammation, systemic sings of acute
inflammation)
Special type of inflammation
• Organs without blood vessels
• Examples:
– cornea, cartilage, heart valves
• No real circulatory response
• Only regressive changes
• Reflex action of the surrounding
tissue
Cornea
• From the neighboring conjuctiva
– Circulatory response
• blood plasma flows into tissue spaces
– Exudative and infiltrative processes
• granulocytes migrate into the cornea
(Recognition: difficult - elongated shape)
• Persistent stimulus
– vascularisation opacity of the cornea
Intact cornea
Cornea
H.-E.; 100x
Epithelium Corneal connective tissue (substantia propria)
Fibroblast cells
Collagen fibers
H.-E.; 200x
Epithelium
Corneal connective tissue (substantia propria)
Fibroblast cells
Collagen fibers
H.-E.; 400x
Cornea
• From the neighboring conjuctiva
– Circulatory response
• Blood plasma flows into tissue spaces
– Exudative and infiltrative processes
• Neutrophil granulocytes migrate into the
cornea
(Recognition: difficult - elongated shape)
• Persistent stimulus
– Vascularisation (neoangiogenesis) opacity of the
cornea Pannus
Keratitis/Pannus
http://davidlwilliams.org.uk/wp-content/uploads/archivesite/pic441.jpg
https://www.google.hu/search?q=keratitis+pannus&client=firefox-
b&dcr=0&tbm=isch&tbo=u&source=univ&sa=X&ved=0ahUKEwiw8Nz_n7HXAhVBGxQKHaK8CnMQsAQIJA&biw=1920&bi
h=916#imgrc=fNLcr08yDo3gwM::
Keratitis, elongated neutrophil
granulocytes
Pannus
Pannus
In ophtalmology, pannus is a progressive change occurs
where blood vessels and scar tissue invade the cornea.
In normal individuals, the cornea is avascular.
Chronic inflammation or local hypoxia may lead to
corneal vascularization, or pannus.
H.-E.; 40x
Pannus
H.-E.; 100x
Pannus
H.-E.; 200x
Pannus
H.-E.; 400x
Pannus
Chronic Superficial Keratitis (Pannus) is a disease seen
most commonly in the German Shepherd, but does occur
in other breeds.
Cartilage
• Chondritis
• Monochodritis
• Polychondritis
• Feline auricular chondritis
Feline auricular chondritis
Pinna: Marked multifocal, chronic lymphoplasmacytic
and neutrophilic chondritis and dermatitis with
degeneration splitting and necrosis of auricular cartilage.
• Auricular chondritis has been reported in rats, mice,
cats, dogs, in a horse and very rarely in cattle.
• It has been classified among the immune-mediated
diseases due to similarities to rheumatoid arthritis
and lupus erythematosus as well as its favorable
response to immunomodulatory therapy.
• Clinical signs include pain, swelling, erythema and
deformation of the pinnae.
• Other organs such as joints, eyes and heart may be
present as well.
• Histologically, lesions consist of lymphoplasmacytic
infiltrates and loss or necrosis of cartilage.
Valves
• neutrophil migration is missing
• proliferative processes
– proliferation of the basic cells
– endothels
– fibrin
• vascularisation from the neighboring
tissues
– blood vessels from the heart muscles
Valves/Endocarditis
• Endocarditis
– Mostly bacterial: E. rhusiopathiae, streptococci, staphylococci, klebsiella, C. pyogenes (rarely parasital, fungal)
– valvular - parietal endocarditis
– acute - chronic (vegetative - verrucosus)
– mitral > aortic > tricuspid > pulmonary
• Consequences of endocarditis
– acute cardiac failure
– chronic cardiac failure
– septic thromboembolism
Inflammation
The inflammation-organism relationship
(1) Complex pathological process.
(2) Congenital non-specific protective mechanism.
(3) Aim: elimination of different exogenous and endogenous non-infective physical, chemical and infective biological (viral, bacterial infections) agents + necrotic tissues and cells. Keep the integrity of the organism, minimisation of the destruction of the tissues and cells.
(4) Rapid protection until effective immune response (in the fibrovasculare tissues; duration: few hours-days).
The inflammation-organism relationship
(4) Rapid protection until effective immune response.
- Few seconds after injury!
The inflammation-organism
relationship
(4) Rapid protection until effective immune
response.
- Effective immune response: acquired, specific
protective mechanism based on lymphocyte
proliferation.
- Specific for the inflammatory agents (antigens).
- Specific clonal proliferation (expansion) of the
T- and/or B-lymphocytes (cellular and/or
humoral immune response => 3-5 days after
inflammatory injury!).
Effective immune response
= Subacute inflammation Lymphocytes
The inflammation-organism
relationship
(5) This protective
inflammatory reaction
tries to restrict
(localize) the
destructive, cytotoxic
effect of the infective,
and non-infective
inflammatory stimuli to
the site of entry.
The inflammation-organism
relationship
(6) Diluting, inactivating biologic
and chemical toxins.
(7) Killing and sequestrating
microbes and neoplastic cells.
(8) Degrading foreign body.
(9) Providing wound healing
(growth) factors to ulcerated
surfaces and traumatised tissue.
Aulus Cornelius Celsus
- Clinical features of acute
inflammation were
described by Celsus (dated
around 2000 BC)
- Four cardinal signs of acute
inflammation: rubor, tumor,
calore and dolore, redness,
swelling, heat, and pain.
Rudolf Virchow
-A fifth clinical sign, loss
of function (functio
laesa) was later added
by Rudolf Virchow
(1858).
The inflammation-organism relationship
• beneficial and harmful effects of inflammation
• outcome of the acute inflammation
• The systemic sings of acute inflammation
• rubor (redness)
• tumor (swelling)
• calor (warming up)
• dolor (pain)
1st century AD Celsus
• functio lesa (decreased function)
Galenus
Cytokines
Cytokines are a broad and loose category of small
proteins (~5–20 kDa) that are important in cell
signaling.
Cytokines are produced by a broad range of cells,
including immune cells like macrophages, B-
lymphocytes, T- lymphocytes and mast cells, as well as
endothelial cells, fibroblasts, and various stromal cells.
Cytokines include chemokines, interferons, interleukins,
lymphokines, and tumour necrosis factors but generally
not hormones or growth factors.
Cytokines
They act through receptors, and are especially important in the
immune system.
They are important in health and disease, specifically in host
responses to infection, immune responses, inflammation,
trauma, sepsis, cancer, and reproduction.
Virtually all nucleated cells, but especially endo/epithelial cells
and resident macrophages are potent producers of IL-1, IL-6,
and TNF-α.
The action of cytokines may be autocrine or paracrine in
chemotaxis or chemokinesis and endocrine as a pyrogen.
Cytokines
Cytokines have been classed as lymphokines,
interleukins, and chemokines, based on their presumed
function, cell of secretion, or target of action.
The term interleukin was initially used by researchers
for those cytokines whose presumed targets are
principally leukocytes. Lymphokines, produced by
lymphocytes
Monokines, produced exclusively by monocytes.
Interferons, involved in antiviral responses.
Chemokines mediate chemoattraction (chemotaxis)
between cells.
Macrophages
Proinflammatory
cytokine
Proinflammatory cytokines are cytokines that are important
in cell signaling and promote systemic inflammation.
They are produced predominantly by activated macrophages
and are involved in the upregulation of inflammatory
reactions.
IL-1, TNF-alpha, and chemokines are examples of
proinflammatory cytokines.
Proinflammatory cytokines are used to activate neutrophils.
Pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α
function to be a part of pathological pain.
Hypercytokinemia
„Cytokine storm”
- When the immune system is fighting pathogens, cytokines
signal immune cells such as T-cells and macrophages to
travel to the site of infection.
- In addition, cytokines activate those cells, stimulating them to
produce more cytokines.
- Normally, this feedback loop is kept in check by the body.
However, in some instances, the reaction becomes
uncontrolled, and too many immune cells are activated in a
single place.
- Uncontrolled release of more than 150 known inflammatory
mediators (IL-1, IL-6, TNF-alpha).
Clinical signs of inflammation
• the pathopysiologic background of the lesions were described at the end of the 19th century by Cohnheim
• Inflammation is not an independent, isolated process
– Although it develops on circumscribed parts of the body
• in an organ or on a part of an organ
– in regional lymph nodes
– it can have distant effect in the body
• fever, lack of appetite, depression
Clinical signs of inflammation
• in regional lymph nodes always similar lesions to the primary process
– circulatory disturbance: active hyperaemia
– exudation: leakage of serum to the sinusoids
– infiltration: detached endothelial cells, granulocytes, lymphocytes in the sinusoids
– proliferative process: proliferation of the reticular cells and lymphocytes
– alterative process : necrosis occurs too
Organism - inflammation
• 1. CNS
– coordination
• 2. Endocrine system
– Mineralo- and glycocorticoids
• 3. Immunological state
– Allergic reaction
• 4. Others (condition)
General condition and inflammation
• hormonal factors (inhibitory, stimulatory)
- anterior pituitary (adenohypophysis): ACTH
- cortex of the adrenal gland : glyco corticoids
(hydrocortizone, cortizone)
- anterior pituitary (adenohypophysis): STH
- cortex of the adrenal gland: mineralo corticoids
(dezoxy-corticosterone)
General condition and inflammation
• hormonal factors (inhibitory, stimulatory)
• STH - increases cell proliferation
– glyco corticoids from the adrenal gland:
• decrease
– the permeability of the cell membrane and the wall of the capillary
– the exudation
– the proliferation of the fibroblasts
– the increased permeability effect of the hyaluronidase
– the tissue antigen-antibody reaction
• inhibit the migration of the granulocytes
Effects of the antigens
• Normergia
– the organism did not meet the antigen yet
• Hyperergia
– the organism did meet the antigen already
(seroconversion)
– sudden severe inflammatory reaction
• severe hyperaemia, exudation, fibrinoid degeneration
• eosinophil cellular infiltration, proliferative processes
– Immunity (antibodies)