Acute Inflammation Flashcards
Some causes of inflammation:
- Infection
- Hypersensitivity
- Trauma
- Chemicals
- Necrosis
Hypersensitivity:
Excess immune response due to altered state of immunological responsiveness
Cardinal signals of acute inflammation
Redness - dial action of vessels
Heat - increased blood flow
Swelling - accumulation of fluid
Pain - due to distortion of tissue (chemical mediators released e.g. prostaglandins)
Loss of function
6 stages of inflammation:
• Release of chemical mediators
•Vasodilatation
•Increased vascular permeability
•Fluid accumulation
•Cellular recruitment
•Phagocytosis
Functions of neutrophils:
They can move via:
• Contracting microtubules
• Chemotaxis
They can stick to opsonised microorganisms:
• When bacteria encounter immunoglobulins or complement components, neutrophils can bind to them
They are Phagocytes
What allows neutrophils to marginate?
- Loss of intravascular fluid
- Slowing of flow to the site
Adhesion
Neutrophils adhere to vascular endothelium
Caused by interaction between paired adhesion molecules on the neutrophil and endothelial surfaces
Emigration
When neutrophils pass between endothelial cells through basal lamina and into adventitia
Chemical agents in acute inflammation (4)
Cytokines
Complement
Histamine
Prostaglandins
Role of PAF:
Docks with corresponding receptor on neutrophil and promotes expression molecules allowing firm neutrophil adhesion to endothelial surface
Function of histamine
Causes vascular dilation and permeability
What do prostaglandins cause?
Some cause increased vacular permeability, some cause platelet aggregation
Chemokines
Family of chemicals which attract more white blood cells to site of inflammation
Eg IL-8 attracts neutrophils
Benefits of inflammation:
•Dilution of toxins
•Entry of antibodies
•Stimulation of immune response
Harmful effects of inflammation
Digestion of normal tissue
Swelling
Inappropriate inflammatory response
What is resolution?
Everything is back to normal
Ideal conditions include:
•Good regenerative capacity
•Minimal tissue damage/cell death
•Quick elimination of the causative agent
•Good vascular drainage to remove fluid and debris
What makes up the organisation state after acute inflammation?
Formation of granulation tissue
Can occur with substantial amounts of tissue loss, or large amounts of fibrin
New capillaries, leading to more macrophages, leading to proliferation of fibroblasts, leading to fibrosis and/or scarring
What is suppuration?
Formation of pus:
- Mix of neutrophils, debris, bacteria etc
If it gets walled off, can form abscess
Difference in healing outcomes in different tissue types:
Bone - Replaced by stronger lamellar bone
Liver - Can get complete healing unless architecture is damaged then there is scarring
Kidney - Epithelium can regenerate, architecture can’t
Smooth muscle - Only vascular smooth muscle can regenerate other smooth muscle is replaced by scar tissue
Neural tissue - Does not repair well, peripheral nerves may regrow but recovery is variable
What predisposes progression from acute to chronic inflammation?
If causative agent is not removed
The cellular exudate starts to change:
• Neutrophils are replaced with lymphocytes, plasma cells, macrophages
When might you get primary chronic inflammation?
Acute inflammation fails to resolve
Collection of pus, abscess formation and walling off with granulation and fibrous tissue
Presence of foreign material:
Recurring cycles of acute inflammation then healing
What cells are involved in chronic inflammation?
Lymphocytes (Small purple dots):
Plasma cells (Fried eggs):
Macrophages (Bigger blobby ones)
Sometimes eosinophils (Tomatoes with sunglasses)
What is granulomatous inflammation?
A collection of histiocytes
Examples of conditions:
•Tuberculosis
•Sarcoidosis
•Crohn’s disease
Primary and Secondary healing (skin):
Primary intention:
•Two edges of the wound can be brought together
•Fibrin joins the edges together weakly
•Over time, epidermal regrowth and collagen synthesis makes a stronger join
Secondary intention:
•Tissue defect filled in by granulation tissue
•Epithelial regrowth over the surface
•Fibrous scar forms and contracts over time
Role of lymphocytes in chronic inflammation:
B cells turn into plasma cells and produce immunoglobins/antibodies
T killer cells are cytotoxic and recruit other cells
Helper T cells activate killer T cells and plasma cells
