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MCD - Cell Pathology > Inflammation > Flashcards

Flashcards in Inflammation Deck (24)
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Definition of inflammation

Reaction of vascularised tissue to sub-lethal cell injury


Cardinal signs of acute inflammation

Rubor - Redness
Calor - Heat
Tumor - Swelling
Dolor - Pain
Loss of function


Role of histamine in acute inflammation

- Vasoactive amine
- Produced by mast cells
- Preformed and released cell degranulates
- Leads to vasodilation and increased blood vessel permeability
- Dysregulation = allergy


List other mediators involved in acute inflammation and their functions

Prostaglandins - Vasodilation
Chemokines - Activate neutrophil chemotaxis to inflammation site
Complement - Stimulate mast cell degranulation, neutrophil chemotaxis and opsonisation.
Cytokines - Pro and anti-inflammatory signalling


Examples of prostaglandins

Macrophages, endothelial cells, platelets


Examples of chemokines

Leukocytes, endothelial cells


What are complement?

Circulating proteins synthesised in the liver and released during acute inflammation


Examples of cytokines and cytokine-releasing cells

Macrophages, monocytes, dendritic cells, endothelial cells


Targeting inflammatory mediators

- Histamine
- Prostaglandins
- Interleukin-1 and Tumour Necrosis Factor


What is exudate and what is its function?

Comprises what comes out of leaky capillaries - Fluid, cells, proteins (importantly fibrin), antibodies
Fluid dilutes pathogen, allows soluble mediators to spread.
Fibrin walls off pathogen, stops it spreading, gives inflammatory cells substrate to hold onto/migrate through.


Process of cellular events

1) Neutrophils enter tissue
2) Migrate to site of injury
3) Become activated
4) Carry out designated role
5) Interact with other cell types (e.g. release of soluble mediators)


Histological features of acute inflammation

- High levels of neutrophils
- Eosinophils
- Mast cells
- Presence of thin fibrin proteins, exudate present.


Causes of chronic inflammation

- Persistent damage
- Persistent infection
- Prolonged exposure to toxic agent
- Autoimmunity
- Foreign body


Histological features of chronic inflammation

- High levels monocytes/macrophages
- Lymphocytes present
- Plasma cells present
- Granulation tissue (much darker staining)
- Often all three of active inflammation (inflammatory cells), tissue destruction, and attempts at repair visible at once


Summarise granulomatous inflammation

Particular form of chronic inflammation showing granuloma formation
- Cluster of macrophages
- Involves specific immune reaction T-cells


Causes of granulomatous inflammation

Foreign material
Reaction to tumours
Immune diseases


Histological features of granulomatous inflammation

Granulomas - mass of granulation tissue
Densely dotted tissue
ENTIRELY granulated


Outline differences between acute and chronic inflammation

Neutrophils(A), Monocytes/Macrophages (C)
Histamine (A), Cytokines (C)
Prominent necrosis (A), prominent scar tissue (C)
Immediate onset and lasts a few days (A), delayed onset and last weeks/months (C)
Outcomes include complete resolution or progression to chronic inflammation (A), outcomes include scar tissue formation and/or disability (C)


Positive long term progression of inflammation

- Removal of causative agent
- Cessation of inflammatory reaction
- Healing of tissue damage to preserve integrity and function


Negative long term progressions of inflammation

Unwanted effects
- Possible excess local tissue damage and scarring
- Secondary effects on nearby tissue
- Can evolve into systemic inflammatory reaction and multi-organ failure
- E.g. septic shock or amyloidosis


Explain the two outcomes of wound healing

- Tissue returns to normal
- Tissue containing cells that can regenerate replace lost cells
- Little structural damage done, cells need framework to build on
Repair (scarring)
- Tissue loss too great, cells unable to regenerate
- Scar tissue formed


Explain process of scar formation

Fibroblasts produce large amounts of collagen. The collagen is then remodelled to maximise tensile strength to best replace the function of the lost tissue.


Summarise steps in cellular egress (movement of cells from blood vessels to tissue)

Margination - Cells pushed to edges of vessel.
Rolling and Adhesion - White blood cell 'rolls' along wall of vessel. Selectins on endothelial cells (wall of vessel) and leukocytes then bind white blood cells to endothelial cells.
Transmigration - Neutrophils dissolve basement membrane, enter interstitium.
Chemotaxis - Following chemical gradient and signalling molecules to site of inflammation.
Phagocytosis - Engulfing of target cells


Explain process of phagocytosis

Opsonisation - Opsonins (various protein/chemical mediators) attach to bacteria. Enhances neutrophil recognition and attachment.
Ingestion - Phagocytosis and entrapment of bacteria in vacuoles.
Killing - Destruction in vacuoles by free radicals, lysozyme, lactoferrin, major basic protein.