Download Acute inflammation

Inflammation
• Local response of living mammalian
tissues to injury do to:
• Physical agens
• Chemical agents
• Infective agens
• Immunological agents
Signs of Inflammation
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Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)
Functio laesa
Types of inflammation
• Acute inflammation: short duration, early
body reaction, followed by repair
• Chronic inflammation: longer duration,
occur when• healing of acute inflammation is incomplet
• Stimulus induces chronic inflammation
from the begining
Acute inflammation
• Acute inflammatory process involves:
• Vascular events- vasodilatation
increased permeability
• Cellular events- influx of inflammatory cells
phagocytosis
release of inflammatory
enzymes
Morphologic types of acute
Inflammation
1. Alterative
2. Exudative – appearance of escaped
plasma determinates the morphological
type
3. Proliferative
Alterative inflammation
• viral hepatitis
• diphteric endocarditis
• lyssa
Diphteric myocarditis
Exudative inflammation
Type of exudation
• Serous
• Catarrhal
• Purulent (pyogenic, suppurative)
• Fibrinous
Serous inflammation
• watery, low protein
content
• Skin blisters
• 2nd degree thermal
burns
• Viral meningitis
• Effusions
Catarrhal Inflammation
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mucinous secretion
Rhinitis
Nasopharyngitis
Bronchitis
Bronchitis
Purulent inflammation
• necrotic and viable
neutrophils,necrotic
tissue
On serous membranes
On mucous membranes
Intersticial inflammation
• Involvement of stroma
• Abscesscircumscribed
• Phlegmon- diffuse
Abscess
Phlegmon
Fibrinous inflammation
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great vascular permeability – fibrinogen
On serous membranes
On mucous membranes
Crupous
Pseudomembranous
Necrotizing
Ulcerative
Intesticial type
On serous membranes
On mucous membranes: Crupous
Lobar pneumony
Pseudomembranous inflammation
Necrotizing (escharotic)
• Flue tracheitis
• burns
Ulcerative
Ulcerophlegmonous inflammation
Intersticial fibrinous inflammation
Intersticial fibrinous inflammation
Rheumatic fever
Proliferative inflammation
• productive polyserositis,
• palmar fasciitis
Chronic Inflammation
• Granulomatous
• Nonspecific
Immunopathology
• Abnormally amplified mechanisms
• Hypersensitivity reactions
• Gill and Coombs- 4 types
on the basis of the immunological
mechanisms that mediate disease
Type I reaction
(immediate hypersensitivity)
• Occur in minutes
• Reexposure to an
antigen to whisch the
host has been
previously sensitised
1. exposure to the A
which stimulate IgE
2. reexposure
3. rapid release of
preformed potent
chemicals from mast
cells
Type I reaction
• Local (depends on the portal of entry)
symptoms- swelling, erythema,
edema, pruritus
Alergic rhinitis
Atopic dermatitis
Allergic conjunctivitis
Extrinsic allergic asthma
Food allergies
Type I reaction
• Generalized
Symptomes: nausea, vomiting,
bronchoconstriction, hypotension,
urticaria, circullatory collaps, shockAnaphylactic shock
Type II reaction
(Antibody-mediated cytotoxicity)
• The circulating
cytotoxic antibody
reacts with a normal
or damaged cell
surface
•Complement-mediated cytotoxicity:
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binding of antibody with cell surface antigen causes
activation of complement and MAC directly lyses
cell membrane
Immune hemolytic anemia
hemolytic anemia of newborn
autoimmune hemalytic anemia
incompatibile blood transfusion
Antibody induced thrombocytopenic purpura
Rheumatic fever
Pemphigus and pemphigoid group
Goodpasture syndroma
Wegener granulomatosis
Pulmo-renal syndroma
•Antibody dependent cell-mediated
cytotoxicity:
• Antibody caused cell death
defense against parasites
Hashimoto thyreoiditis
Autoimmune gastritis
Hyperacute graft rejection og a renal
transplant
Antibody dependent cell-mediated
cytotoxicity:
• Antibody caused
dysfunction:
Basedow disease
Myastenia gravis
Type III reaction
Type III reaction
(immunocomplex disease)
• Circulating immunocomplexes
• In situ immunocomplex formation
• Antigens: exogenous- bacteria, viry,
protozoa, drugs (heroin)
autoantigens: tumour cells,
DNA, RNA, ribosomes,
immunoglobulins
Type III reaction
• Acute: postinfectious GN, membranous
GN, polyarteritis nodosa
• Chronic: Cryoglobulinemia type II and III,
SLE, dermatomyositis,
rheumatoide arthritis, autoimmune
hepatitis
Diffuse membranous GN
Type IV reaction
(cell mediated hypersensitivity)
• Not require the presence of antibody
• Is delayd anywhere from 24 h to 2 weeks
• Iniciated by specifically sensitized T
lymphocytes
• 2 subtypes
Type IV reaction
1. Delayed type hypersensitivity
• Persistent antigen in macrophages
• Infections with intracellular bacteria:
Mycobacterium, Spirochets,Brucella,
Yersinie, Fungi, some parasits
• Tuberculin-type:
• Granulomatous type:
Sarcoidosis
2. Cell mediated cytotoxicity
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CD 8+ T cells or NK cells
Chronic rejection – GVHD
Polymyositis
Sclerodermia
Spontaneous regression of tumours
Kontaktalergie
Non-organ-specific autoimmune
disease
Morphological patterns of
glomerular reaction on injury
1. Endocapillary proliferation
• Postinfectious GN
• SLE
Postinfectious GN
Postinfectious GN- humps
2. Mesangial proliferation
• IgA nephropathy
• Non IgA nephropathy
IgA nephropathy
IgA nephropathy
3. Membranoproliferative change
• Membranoproliferative
GN
• Primary
• Secondary
Membranoproliferative GN
4. Thickening of GBM
• Immunocomplexes
• Pathological substancies
- amyloid
- glycosylated
Diffuse membranous GN
Diffuse membranous GN
Amyloidosis
Diabetic glomerulosclerosis
5. Changes of podocytes
• Minimal change
disease
• FSGS
Minimal change disease
Focal segmental
glomerulosclerosis
Case report
• abcd