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
page-73
can inflammation occure in avascular tissue ??
cornea
=keratitis
Bad effect of inflammation ?
- hypersensitivity
- allergy
- autoimmune disease
- rheumatoid arthritis
- atherosclerosis
74
Cardinal signs of inflammation ?
- rubor=Redness
- tumor=swelling
- calor =heat
- dolor =pain
- functio laesa /loss of function
76
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
76
Inflammation classification ?
1.Acute inflammation
=serous i
=fibrinous i
=purulent i
=ulcer
2.Chronic inflmmation
=chronic specific
=chronic non-specific
76
Acute inflammation definiton ?
the initial rapid response to infection & tissue damage is AI
77
Causes of Acute inflammation ?
- Infection
- Immune response
- Ischemia
- Trauma
- tissue necrosis
- foreign bodies
77
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
77
Cells of AI?
- Polymorphoneuclear leokocyte-Neutrophil
- Macrophage
- Eosinophil
- Leukocyte
77-78
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
78
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
80
Whicha acute inflammation is more complicated ?
Fibrinous inflammation
80
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
80-81
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 ?
87
C5a
IL-8
LTB4
Vasodilators chemical mediators ?
Prostaglandin
\histamine
nitric oxide 92
pain mediators > 92
prostaglandin
bradykinin
fever mediators ?
IL-1
TNF
prostaglandin
Inc vascular permeability?? 92
C5a
C3a
leukotrienes -C4 D4 E4
PAD
bradykinin
physiological giant cells
113
megakaryocytes of bone marrow
osteoclastic giant cell in bone
syncytotrophoblast of the placneta
pathological giant cells ?
lagnhans
osteoclastic giant cell
aschoff giant cells
reed sternberg giant cell
multinucleate giant cell
fate of granuloma ?
cold abscess
dystrophic calcification
formation of sinus tract
soft vs hard tubercle ? 110
soft tiubelce— central caseartion necrosis
hallmark of TB ?
soft tubercle
key features of granuloma ?
modified activated macrophages
= epithelioid cells
langerhans cell ?
APC
Morphology of granuloma ?
107
granuloma def ?
microscopic aggregation
of epithelioid cell / epithelial like cells
surrounded by collar of lymphpocytes
which stain for granuloma ??
H & E
granulomatous I ?
106
form of chronic I characterized by collections of activated Macrophages + t lymphocytes + necrosis
exudate vs transudate ?
101
exudate cause ?
inc vascular permeability
transudate cause ?
inc hydrostatic pressure
dec plasma colloidsl osmotic pressure
character of exudate ?
high -== protein + specific gravity
exudate defiantion ?
99
acute phase protein name ? 114
C-reactive protein
serum amyloid A = SAA
fibronogen
pathogenesis of TB ?
109
which giant cell in TB ?
langhans giant cell
cat scratch disease agent ?
bartonella henselae
frustrated phagocytosis ?
90
phagocytosis def ?
88
phagocytosis M/A ?
88+89
why ESR rise in acute phase response ?
rise fibrinogen
form rouleaux - stack that sediment rapidly
what is epithelioid cells ?
108
activated M vs Epithelioid cell ?
108
which mediator is must for necrosis in TB ?
TNF
Ecosanoids fucntion ?
96
