Inflammation Flashcards
Inflammation definiton ?
response of vascularized tissues that delivers leukocytes and molecules of host defence from the circulation to the sites of infection and cell damage in order to eliminate the offending agents
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can inflammation occure in avascular tissue ??
cornea
=keratitis
Bad effect of inflammation ?
- hypersensitivity
- allergy
- autoimmune disease
- rheumatoid arthritis
- atherosclerosis
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Cardinal signs of inflammation ?
- rubor=Redness
- tumor=swelling
- calor =heat
- dolor =pain
- functio laesa /loss of function
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Pathogenesis of cardinal features ?
- Rubor=Vasodilation=Histamine & NO=Redness=Hyperamia
2.Tumor=Swelling=Exudation =Edema=Extravascular accumulation of fluid=inc granulation tissue
3.Calor=Heat=Inc blood flow
4.Dolor=Pain=sweeling & edema=compress nerve ending
5.Function laesa =pain & tissue destruction =fibroplasia & metaplasia
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Inflammation classification ?
1.Acute inflammation
=serous i
=fibrinous i
=purulent i
=ulcer
2.Chronic inflmmation
=chronic specific
=chronic non-specific
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Acute inflammation definiton ?
the initial rapid response to infection & tissue damage is AI
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Causes of Acute inflammation ?
- Infection
- Immune response
- Ischemia
- Trauma
- tissue necrosis
- foreign bodies
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Componenets of Acute inflammation ?
- Dilatation of blood vessels
- inc blood flow
- inc permeability of microvasculature
- plasma protein and leukocyte leave the circulation
- Emigration of leukocyte from the microcirculation
- Leukocytes accumulate in the focus of injury
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Cells of AI?
- Polymorphoneuclear leokocyte-Neutrophil
- Macrophage
- Eosinophil
- Leukocyte
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Fates/Outcome of Acute Inflammation ??
- Complete resolution
=removal of cellular debris & microbs by macrophage
=resorption of edema fluid by lymphatics
2.Healing by connective tissue replacement
=Scarring & Fibrosis
3.Progression to chronic inflammtion
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Morphological types of AI ?
- Serous Inflamamtion
=pleural & pericardial effusion , ascites
=exudation of cell poor fluid into spaces created by cell injury /body cavities
2.Fibrinous inflammation
=Pricarditis,Meningitis
=vascular leaks are large to pass Large molecules
3.Purulent inflammation
=Abscess,Boil
=Production of pus/purulent exudates
=Abscess —- localized collections of pus
4.Ulcers
=local defect/excavation of the surface of an organ/tissue that is produced by sloughing /shedding of inflammed necrotic tissue
=Peptic ,stomach,duodenum
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Whicha acute inflammation is more complicated ?
Fibrinous inflammation
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Events of ACute inflammtion ??
- Vascular events
- Cellular events
Vascular events of Acute Inflammation ?
- Transient vasoconstriction
- Persistent vasodilation of arterioles
=vasodilation
=Histamine + NO
=inc blood flow
=Rubor & Calor
3.Inc vascular permeability of the microvasculature
4.Slowing of blood flow -Stasis
=Combined Vasodilation +Inc vascular permeability
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Inc vascular permeability-Mechanism ?
- Contraction of endothelial cells
=inc gap between endothelial cells
=most common & rapidly/immediatley
=Histamine+Bradykinin+Leukotriens
2.Endothelial injury
=direct damage to endothelium
=burn-toxin-mirobes
=necrosis and detachement
3.Leukocyte mediated endothelial injury-
=Leukocyte adhere to the endothelium and release proteolytic enzyems
4.Transcytosis
=Transport of fluid and proteins through the endothelial cells
=Vascular endothelial growth factor-VEGF
5.leakage from new blood vessels
Cells of acute inflammation?
neutrophils
chronic inflammation where neutrophil is the inflammaotry cells ?
- chronic pyogenic osteomyelitis
- chronic irritation & damage in the lungs
chronic inflmmation cells ?
lymphpocytes
acute I where lymphocytes are cells ?
acute viral infection
exogenous chemotactic substances ?
bacterial products
endogenous chemotactic substances ?
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C5a
IL-8
LTB4
Vasodilators chemical mediators ?
Prostaglandin
\histamine
nitric oxide 92
pain mediators > 92
prostaglandin
bradykinin
