Acute Inflammation Flashcards
characteristics of acute inflamation
immediate short duration innate stereotyped limits damage
causes
microbial infections hypersensitivity reactions physical agents chemicals tissue necrosis
clinical signs
Rubor-Redness
Tumor- Swelling
Calor- Heat
Dolor-Pain
what changes occur in the vessels
vasoconstriction few seconds vasodilations few minutes permeability increased due to increased capillary hydrostatic pressure oedema formation red cell stasis
what pressures do we need for optimum flow into the interstitium
we need high capillary hydrostatic pressure and high interstitial oncotic pressure
what is stasis, why is it good
reduced flow through the vessel
important because allows more time for exudate + transudate formation
what is exudate
type of interstitial fluid - protein rich to areas of injury
increased vascular permeability
what is transudate
type of tissue fluid when actually being moved out of the vessel into the interstitium
no change in vascular permeability
heart/renal/hepatic failure
mechanisms of increased vascular permeability
endothelial contraction (gaps between the endothelial cells)
direct injury - toxins damage the wall
endothelial cytoskeleton reorganisation
leucocyte dependant injury (enzymes and toxic ROCs)
why does blood increase viscosity
fluid moves out of vessel
increased concentration of proteins in blood
increased viscosity
reduced flow
stages of neutrophil emigration into the interstitium
Margination- stick to the endothelial cell layer
Rolling-roll along the endothelium
Adhesion-stick more avidly to the cell layer
Emigration-through the blood vessel wall
how do the clinical signs relate
increased vascular permeability, transudate and exudate formation- TUMOR
increased concentration of RBC in vascular system- RUBOR
reduced flow due to RBC stasis-CALOR
adhesion molecules
SELECTINS-on endothelial cell surface, unregulated by chemical mediators
INTEGRINS- on neutrophil surface, bind to receptors on the endothelial surface
functions of the neutrophils
chemotaxis- process of entering the interstitium
phagocytosis-immune response
killing of micro-organisms- lysosome contains hydrolytic enzymes
pls explain the chemotaxis process in more detail
movement along a chemical gradient of chemoattractants
- pseudopod
- neutrophil cytoskeleton rearrangement
- bacterial peptides
why is inflammation an effective response
delivery of nutrients, oxygen, cells, plasma proteins
dilution of toxins
stimulation of immune response
destruction of dead and foreign material
pain and loss of enforcing rest (malaise)
Chemical mediators
Important in up regulation of adhesion molecules (selectins)
examples: amines, peptides, cytokines and chemokines, exogenous mediators, phospholipid derivatives
local complications of inflammation
reduced blood supply to normal tissues
swelling causes obstruction of tubes and structures
loss of fluid (exudate and transudate)- blood is left highly viscous
Pain causes by stasis
systemic complications of inflammation
fever-pyrogens affecting thermoregulatory centre
leucocytosis-WBC production increased
acute phase response- CRP release and malaise
shock- septic overwhelming infection, widespread vasodilation, leads to rapid death
what happens after acute inflammation
complete resolution
chronic inflammations with some fibrous repair
continued acute inflammation with chronic inflammation
death
what happens in complete resolution
drainage of the exudate neutrophils phagocytosed fibrous repair if architecture preserved mediators are inhibited no margination, vessel calibre return to normal
how does oedema formation reduce damage
dilutes the toxins delivers exudate (proteins) to the site of injury- such as immunoglobulins increased lymphatic draining delivers antigens to the lymph nodes
appendicitis
blocken lumen, accumulation of bacteria, increased pressure and reduced blood flow
pneumonia
streptococcus pneumonia, smoking and COPD riskfactors, shortness breath, fever cough, chest pain
