Inflammation And The Three I’s Flashcards
Outline the bodies three lines of defence
1st - skin and mucous membranes. Epidermis ( outer layer ) - primary barrier
Mucous membranes try to stop it getting any further if skin is breached
2nd - inflammation. Non-specific, natural, innate and rapid response
3rd - immunity - specific, aquired immunity, adaptive and slow response.
Describe and explain inflammation and the five cardinal signs -
Inflammation is the bodies no-specific protective response to tissue disease injury in attempt to destroy/dilute or wall off both the injurious agent and injured tissue.
Result - cardinal signs
Redness - increased blood flow ( rubor )
Swelling - more fluid to area ( tumor )
Warmth - specific/non ( calor )
Pain - due to compression of nerve endings ( function laesa)
What is the purpose of inflammation ?
Prevent minor infections becoming overwhelming
Prepare damaged tissue for repair.
Factors that cause inflammation -
Injury/trauma - physical sport, an accident, radiation, electrical or chemical ( burn )
Infection - viruses/ bacteria, fungi /worms
Infarction - lack of o2 to an area
Immune reactions - foreign protein hypersensitivity eg allergies and autoimmunity eg gluten interolerence
Nutrient deprivation - high fatty processed diet trigger inflammatory response.
What suffix helps to identify when referring to inflammation ?
ITIS
Conjunctivitis - eyes
Appendicitis - appendix
Pericarditis - pericardium
Osteoarthritis - joint
Mechanism of inflammation
1) vascular response
Changes with blood flow - vasoconstriction, short time period. Blood vessels near affected area constrict allowing blood to clot and localise harmful agents.
Prologned vasodilation - they re-open therefore increasing blood flow and increase hydrostatic
Opening of capillary beds and increased vascular permeability.
Bradykini ( protein ) released and causes capillary endothelium to retract ( crenellation )
This creates gaps so plasma can leak
Oedema formation
Therefore heamoconcentration -> statis - slowing of blood in an area.
Mechanism of inflammation
2) cellular response -
Neutrophils are first ( not long lasting, smaller and quicker ) to emigrate to injury site followed by monocytes then macrophages. They squeeze through endothelial gaps by diapedesis.
Mechanisms of inflammation
2) cellar response - diapedesis stages:
Margination - chemical mediators attract WBC’s and their movement
Not smooth - WBC’s roll and get stuck ( adhesion ) towards endothelial cells.
They flatten out across blood vessels ( pavementing ) and move along as best they can and move through gaps in blood vessel - only some of cell will get through ( pseudopod formation )
Amoebiod action - try move itself through so it can emigrate outside blood vessel.
Diapedesis - ‘cell walking’ from inside blood vessel to outside
Happens due to chemotaxis response to injury.
Mechanism of inflammation
3) phagocytosis -
4) lymphatic drainage -
3) Process of ingestion of forgein material or particular matter
4) lymphatic system assists in tissue fluid drainage. Inflammation means lymphatic vessels open up therefore aiding drainage of excess fluid and any antigens not dealt with by inflammatory processes.
APC’s present to immune system, triggers. 3rd line of defence - specific immune system.
Common blood tests used to detect acute inflammation:
WBC count -
WBC differential -
WBC count - reference value: 5,000 - 10,000/mm^3
With inflammation value increases way above reference.
WBC differential - neutrophils higher than 75% suggest bacterial infection
Lymphocytes higher than 46% suggests viral infection
Eosinphils higher than 8% suggests worms
This test helps break down into type of WBC and therefore helps guide treatment.
Common blood tests used to detect acute inflammation
Erythrocyte sedimentation rate -
This is how long it takes RBC’s to fall to bottom of test tube
0-17mm/hr for men
1-25mm/hr for women
Common blood tests used to detect acute inflammation
Erythrocyte sedimentation rate -
This is how long it takes RBC’s to fall to bottom of test tube
0-17mm/hr for men
1-25mm/hr for women
Characteristics of acute inflammation:
Usually a known cause eg trauma
Onset is rapid
Deterioration is rapid
Full resolution and follows a definite course
Neutrophils involved first, followed by monocytes to macrophages
Involves active phagocytosis
Beneficial outcome, prevents invasion and restoration of full function.
Characteristics of chronic inflammation-
Often cause is unknown eg unresolved acute inflammation/ complications of it.
Slow insidious onset
Slower deterioration as lack of an acute response
Fails to resolve and follows a slow, self perpetuation course.
Macrophages and fibroblasts are cells involved
Persistent irritants therefore resistant to phagocytosis
Results in destructive scar tissue formation and loss of function.
Examples of medication used for inflammation:
Aspirin
Non-steroidal anti-inflammatory drugs ( NSAIDs )
- ibuprofen
- naproxen
Corticosteroids
- predinsolone ( often used for chronic )
Immunosuppressants also used but are non- specific therefore leads patients prone to other infections
