acute inflammation Flashcards
List the causes of acute inflammation.
1- Pathogens
2-Mechanical trauma e.g. surgery
3-Dead tissues-necrosis: inflames adjacent tissue
4-chemical changes e.g. PH
5-Physical changes e.g. extreme heat,cold
6-hypersensitivity
Recognise the benefits of acute inflammation.
1- Rapid response
2- Neutrophils remove cause of inflammation
3- Protection of inflammed area via cardinal signs:
4-Plasma proteins localise problem.
Describe the sequence of microvascular change.
-INCREASE IN BLOOD FLOW
1- constriction of transient arterioles
2-dilation of local arterioles
3-Relaxation of smooth muscle
This leads to increase of blood flow due to poiseulle’s law which states that blood flow is proportional to change in radius to the power of 4.
-INCREASE IN PERMEABILITY
-MOVEMENT OF NEUTROPHILS TO EXTRACELLULAR SPACE
1-Margination: neutrophils move towards endothelium of plasma from centre where they usually reside
2-Pavementation: neutrophils adhere to endothelium
3-Emigration: neutrophils move out into extracellular space
stimulating agent is destroyed microphages destroy debris epithelial surface regenerated exudate drained vascular changes returned to normal
Describe the sequence of events in exudate formation.
- Increased permeability of blood vessels leads to movement of plasma from the capillaries to the extracellular tissue =EXUDATION
- Exudate contains plasma proteins, particularly immunoglobulin and fibrinogen.
- The build up of exudate causes Oedema= swelling and pain.
- This increases viscosity which in turn causes the movement of neutrophils into the extracellular space
List the local effects of acute inflammation.
dolor calor tumor-swelling rubor-redness loss of function
Summarise the mediators of acute in ammation and describe their overall function
-Plasma proteins:
-Cell surface mediators: allow adhesion of neutrophils
-Released from cells
They are involved in vasodilation, permeability, chemotaxis, itchiness and pain, neutrophil adhesion
List the systemic effects of acute in ammation.
Immediate Pyrexia- increased body temp. Feeling unwell- nausea, abdominal pain Neutrophilia- increased WBC Long term Lymphadenopathy- increased regional lymph node Weight loss anaemia
Describe the complications of acute in ammation.
A. Suppuration: build up of pus under pressure- Abscess.
can be multi locate when the pus abscess breaks through the pyogenic membrane.
Pus: exudate, debris, RBCs, dead tissue, organisms
Pyogenic membrane: walls off pus- neutrophils, fibroblasts, capillary sprouts
Emphaema- pus in hollow viscus e.g. gall bladder or pleural cavity
pyaemia- pus discharge into blood stream
B. Organisation: granulated tissue- repair and heal process.
Leads to fibrosis ( formation of XS fibrous tissue) and formation of a scar.
New patch which contains:
angiogenesis- new capillary formation
macrophage formation
new fibroblast and collagen
C. Septic shock: CO=HRXSV BP=COXSVR
when inflammation occurs:
-release of mediators-vasodilation-SV falls:
release of catecholamines e.g. adrenaline
HR increases-tachycardia
when this doesn’t happen-BP falls
-activation of coagulation-vasodilation-haemoragic skin rash
-bacteria endotoxins- pyrexia
D. Dissemination: septic patients- when the bacteria/toxins move into the bloodstream.
bacteriemia- bacteria move into blood stream
toxaemia- toxins move into blood stream
septicemia- bacteria grow in blood stream
pneumonia vs pneumonitis
Pleurisy
Pneumonia- infection in the air spaces
Pneumonitis- lung tissue
pleurisy- pleural cavity
what Is present in pus?
fluid, endogenous protein, organisms, dead cells
summarise the plasma mediators involved in acute inflammation
a. kinin-involved in pain
b. complement cascade- links inflammation to immune system
c. fibrinolysis-products are vasoactive, help maintain blood supply
d. blood coagulation
summarise the cell released mediators
a. histamine: vasodilation, increases perm, local injury. released from mast cells
b-5-HDT: vasoconstriction, decreased perm. preformed in platelets. released when platelets degranulate in coagulation
c.prostaglandins: both
d.leukotrienes: vasoactive
e.NO: relaxes smooth muscle, anti-platelet- vasodilation
f. free radicals
g. cytokines
h. omega-3 FA
i.platelet activating factor: decreases perm
Main cells, proteins involved in acute inflammation
Neutrophils
- most abundant WBC
- Phagocyte- moves towards pathogen by chemotaxis and ingests it
- contains enzymes and oxidants e.g. H2O2
- involved in formation of Pus
Plasma proteins:
- fibrinogen: forms fibrin-coagulating factor- localises inflammation
- Immunoglobulin: humoral response
what is the meaning of vasoactive?
Acts on vessels
Increases permeability
Constricts smooth muscle- prevents inflammation from spreading
