Inflammation Flashcards
1
Q
What are the body’s defence mechanisms
A
- Skin & Mucous membranes - prevent entry of harmful substances (via blink reflex/eyelashes/tears/enzymes/skin etc.)
- Inflammation - rapid, non-specific response
- Immunity - slow, specific response
2
Q
Signs of Inflammation
A
- Redness (rubor) - caused by vasodilation
- Swelling (tumor) - via increased vascular permeability
- Heat (calor) - vasodilation
- Pain (dolor) - nerve endings = compressed or sensitised by swelling/chemicals
- Loss of function - due to tissue damage/pain/swelling
3
Q
Purpose of inflammation
A
- Destroy/ dilute/ isolate injurous agent and damaged tissue
- Prevents minor infection from becoming major
- Prepares the tissue for repair process.
4
Q
Causes of Inflammation
A
- Injury/Trauma - physical/thermal/chemical etc.
- Infection - virus/bacteria/fungi etc.
- Infarction - lack of o2
- Immune reactions - allergies/ protein insensitivity/ auto-immune responses
- Nutrient deprivation
5
Q
Vascular Response of Inflammation
A
- Transient Vasoconstriction- automatic short term narrowing of the blood vessels - contains pathogen/foreign material
- Prolonged Vasodilation - allows more cells to arrive and fight infection & dilutes pathogen (causes rubor and calor)
- Increased Vascular Permeability - increased blood pressure in area pushes capillary cell wall open
- Crenallation - bradykinin causes endothelial retraction so gaps in capillary cell wall get larger.
- Plasma Leakage - leave capillary via bigger gaps (tumor)
- Haemoconcentration - blood is thicker due to loss of proteins causing stasis - slowing of blood flow.
6
Q
Cellular Response in Inflammation
A
- leukocytes emigrate to area (neutrophils 1st then monocytes).
- Margination - move to outside of blood flow (caused by chemical attraction and + charge of damaged tissue)
- Rolling - more resistance on edge - move slower
- Adhesion - stick to edge
- Pavementing - Flatten out
- Chemotaxis - endothelial gaps get larger
- Pseudopod - projection pushes through gap
- Amoeboid action - “wriggles” through
- Emigration via diapedesis - “Cell Walking” leaves blood vessel
- Chemotaxis - releases chemicals that attract other leukocytes.
7
Q
4 stages of inflammation
A
- Vascular response
- Cellular response
- Phagocytosis - monocytes become macrophages after diapedesis; engulf pathogens/foreign material/ damaged material
- Lymphatic drainage - lymph vessels open + drain excessive fluid/products of inflammation/remaining antigens (presented to immune cells - may trigger immune respomnse)
8
Q
Acute vs Chronic inflammation
A
ACUTE
- rapid onset and deterioration
- usually known cause
- resolves
- mainly involves neutrophils and monocytes
- full function is restored
CHRONIC
- Slow onset and deterioration
- Doesn’t resolve
- Macrophages and fibroblasts
- Scar tissue formation - function is reduced
9
Q
Blood tests for acute inflammation
A
- White Blood Cell count - increased
- Erythrocyte sedimentation rate - increased fibrinogen levels - faster RBC clumping
- C-reactive protein levels - increased but may settle down in chronic cases.
10
Q
Treatments for Inflammation
A
- Aspirin - reduces lipids released by damaged tissue
- NSAIDs - “ “
- Corticosteroids - Interrupt inflammatory process by stopping chemotaxis and phagocytosis
- Immunosuppressants - stops out of proportion white blood cell activity (non-specific so can leave vulnerable to other pathogens)