4 Inflammation Flashcards
*Q: What is inflammation a reaction to? Development?
A: Reactions of living vascularised tissue to sub-lethal cellular injury
Evolutionary development to protect against infection and trauma
*Q: Describe acute inflammation. Length? Involves release of? Typical of which 2 responses?
A: = Transient and early response to injury
Hours/few days
Involves release of chemical mediators
Typical vascular and leucocyte response
*Q: Describe chronic inflammation. Length? Usually due to? What does it not contain? Compared to acute, what is not as prominent?
A: Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair occur simultaneously
Weeks/months/years
=Usually due to persistent injury causing agent
no exudate
Necrosis is not as prominent as in acute inflammation
*Q: What is a Granuloma. What does granulation tissue contain?
A: = collection of immune cells known as histiocytes (macrophages) that form when the immune system attempts to wall off substances it perceives as foreign but is unable to eliminate
lots of fibroblasts producing granulomatous tissue
Q: What are the 4 components of inflammatory responses and healing?
A: -cells
- extra cellular matrix
- soluble factors
- vessels
Q: Which cells are involved in inflammatory responses and healing? (5)
A: -neutrophils
- macrophages
- lymphocytes
- eosinophils
- mast cells
Q: What forms of extra cellular matrix are involved in inflammatory responses and healing? (3)
A: -collagen
- proteoglycans
- fibroblasts
Q: Which soluble factors are involved in inflammatory responses and healing? (4)
A: -antibodies
- cytokines
- complement system
- coagulation system
Q: What are the 5 cardinal signs of a inflammation/vascular event? Include what causes them.
A: CALOR: Caused by histamine mediated vasodilation
TUMOR (Oedema - increased fluid in interstitial fluid): Caused by histamine mediated increase in permeability of vessels
dolor=pain
RUBOR: Blood flow isn’t as fast so you get redness
Loss of Function: Due to swelling and pain
Q: What is histamine? Produced by? Packaged into?
A: Vasoactive amine
Produced by mast cells
Packaged into granules inside mast cells - when antigen binds to IgE on the surface of mast cells - causes cross-linking and degranulation
Q: What can histamines lead to? Dysregulation leads to?
A: Vasodilation and Increased Vascular Permeability
allergy (Type 1 Hypersensitivity)
Q: What is a ‘complement’? released when? Stimulate? (3)
A: circulating proteins that are synthesises in the liver and released during acute inflammation
- mast cell degranulation
- neutrophil chemotaxis
- opsonisation
Q: What are cytokines
A: broad range of chemicals that modulate function of other cells
Q: Name drugs/chemicals that target these Inflammatory Mediators:
- Histamine
- Prostaglandins
- IL-1 and TNF
A: = Anti-histamines
= Aspirin
= Anti-TNF antibodies
Q: What is hydrostatic pressure?
A: the pressure exerted by a fluid at equilibrium at a given point within the fluid, due to the force of gravity
Q: What is colloid osmotic pressure?
A: form of osmotic pressure exerted by proteins in a blood vessel’s plasma that usually tends to pull water into the circulatory system
Q: What’s the relationship between hydrostatic and colloid osmotic pressure?
A: oppose eachother
Q: What is exudate? Specific gravity? Cause?
A: fluid with a high content of protein and cellular debris which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces WITH high specific gravity
usually as a result of inflammation
Q: What is transudate? Specific gravity? Cause?
A: fluid that remains in the vessels which has low protein and few cells with low specific gravity
usually result of disturbances in hydrostatic and colloid osmotic pressure, NOT CAUSED BY INFLAMMATION
Q: What is specific gravity?
A: ratio of the density of a substance to the density of a reference substance
Q: What does exudate consist of? (4) Describe 2 in terms of pathogen.
A: fluid, cells, proteins including fibrin, antibodies
Fluid - dilutes pathogen and allows soluble mediators to spread
Fibrin - walls off pathogen to stop it spreading. Gives inflammatory cells substrate to hold on to/migrate through
Q: What are the 3 types of exudate? Give an example for each.
Which has lowest protein content?
Which is more due to traumatic injury?
Describe the content of one. (4)
A: Serous = fluid filled
- EXAMPLE: Blister
- Lower protein content of all the exudates
Fibrinous = High fibrin content
- More due to traumatic injury
- EXAMPLE: Viral Pericarditis
Purulent = pus filled
- Combination of fibrin, inflammatory cells, debris and fluid
- EXAMPLE: peritonitis following bowel perforation
Q: Describe the pathway of neutrophil action in acute inflammation. (5)
A: 1. Enter tissue
- Migrate to site of cell injury - chemotaxis
- Become activated
- Carry out their designated role - e.g. phagocytosis
- Interact with other cell types - release of soluble mediators
Q: Why are neutrophils described as key players in inflammation? Main role? (3)
A: FIRST CELLS to the damaged area
- Kill bacteria and recruit more cells
- Phagocytosis
- Degranulation
Q: What is involved in cellular egress? (4)
A: -margination
- rolling and adhesion
- transmigration (diapedesis)
- chemotaxis
Q: What is margination in cellular egress?
A: cells being pushed to the edges of vessels
Q: Describe rolling and adhesion in cellular egress. (3)
A: Once at the margin they can bind to endothelial cells through selectins on the neutrophil and endothelial cells
The selectin bonds are loose - the neutrophil rolls along the side of the blood vessel and is slowed down
As it slows down more permanent bonds are formed which fixes the neutrophil to the vessel wall
Q: Describe transmigration in cellular egress. (2)
A: Neutrophil dissolves basement
Enters interstitium
Q: What is ‘killing’ in phagocytosis? By? (4)
A: Destruction of phagocytosed material in vacuole
By free radicals, lysozyme, lactoferrin (binds iron and stops bacteria reproducing), major basic protein (produced by eosinophils - cytotoxic to helminth parasites)
Q: What’s the importance of eosinophils? (2)
A: Important in allergic and parasitic causes of inflammation
Q: What’s the importance of mast cells?
A: Important in allergic diseases
Q: What are the 4 ways inflammatory responses are controlled?
A: -Mediators and neutrophils have short half life
- Stimulus (e.g. bacteria) removed
- Mast cells and lymphocytes release anti-inflammatory products (lipoxins)
- Macrophages release anti-inflammatory products
Q: How does an acute inflammatory response evolve into a chronic one? (3)
A: -Breakdown of myofibres
- Fewer neutrophils in chronic inflammation
- Other cell types involved
Q: What is the cause of chronic inflammation? 4 examples. Which 3 cells are involved? Abundance?
A: Persistent Damage
- Persistent infection
- Prolonged exposure to toxic agent
- Autoimmunity
- Foreign body (e.g. splinter)
-Macrophages
-Lymphocytes
-Plasma Cells
(high)
Q: Do monocytes/ macrophages live for less or more time than neutrophils? What’s the role of M? (2) When are they more abundant? (2)
A: -M live longer
- phagocytosis
- Control many other inflammatory cells - by releasing cytokines
Increased in viral and atypical bacterial infections
Q: What is granulomatous inflammation? What does it involve? 4 causes?
A: FORM OF CHRONIC INFLAMMATION - shows granuloma formation
-Involves specific immune reaction T cells
- Infection
- Foreign Material
- Reaction to Tumours
- Immune Diseases (e.g. Crohn’s, sarcoid)
Q: Describe the histological features of granulomatous inflammation. (2)
A: -Macrophages in the middle and lymphocytes around the outside
-Horseshoe shaped nuclei - fused macrophages - seen at latter stages of granulomatous inflammation
Q: How do acute and chronic inflammation differ in terms of:
main cell involved?
main soluble factor involved?
prominent feature?
onset?
A: neutrophils, M
histamines, cytokines
necrosis, scar tissue
immediate, delayed
Q: 2 outcomes of acute inflammation? 2 for chronic?
A: -complete resolution
-progression to chronic inflammation
- scar tissue formation
- disability
Q: What are positive outcomes of inflammation? (3)
A: Remove causative agent
Cessation of inflammatory reaction
Healing of tissue damage to preserve integrity and function (resolution)
Q: What are the negative effects of inflammation? (2- 2,2) Examples? (2)
A: LOCAL:
- Excess local tissue damage/scarring
- Secondary effects on nearby tissue - e.g. bronchoconstriction in asthma
SYSTEMIC:
- Systemic inflammatory reaction
- Secondary multi-organ failure
EXAMPLE: Septic Shock, Amyloid (in response to inflammatory reaction, the liver produces amyloid proteins which can deposit in various organs)
Q: What are the 2 parts to wound healing?
A: RESOLUTION = regeneration of normal functional parenchymal cells
REPAIR = connective tissue and SCAR TISSUE formation
Q: What occurs during ‘resolution’? What are the 2 conditions for it to occur? Give an example.
A: Tissue architecture returns to normal
- Tissue contains cells that are capable of regeneration to replace lost cells
- Little structural damage done as cells need a framework to build on (basement membrane)
Pneumococcal pneumonia
Q: When does the ‘repair’ part of wound healing occur? What occurs? Process? (3)
A: Tissue loss is too great and cells are unable to regenerate
Replace normal tissue with fibrous scar tissue
Process:
- Fibroblasts - produce collagen
- Collagen - strong scar type collagen
- Remodelling - reorganisation of collagen fibres for maximal tensile strength
Q: Describe what hinders repair? (7) Include 2 subheadings.
A: General
- Poor nutrition (protein needed for collagen production)
- Vitamin Deficiency (C needed by fibroblasts to make collagen, A needed for epithelial regeneration)
- Mineral Deficiency
- Suppressed Inflammation
Local
- Poor blood supply
- Persistent foreign body (e.g. splinter)
- Movement (e.g. broken bones need casts to hold the bones in place)
*Q: What are the 3 complications of repair?
A: -keloid formation
- contractures
- impaired organ function
Q: How do you get keloid formation? Where?
A: Excess collagen deposition
You can get scar tissue formation other than at the site of original injury
Q: Describe contractures as a complication of repair. What happens if it occurs across a joint?
A: Fibrous scar tissue contracts as part of its maturing process
If this happens across a joint, you can get reduced joint mobility
Q: How can complications of repair cause impaired organ function?
A: Fibrous scars forming in organs will cause loss of functional tissue which affects organ function
Q: Where are neutrophils produced? Where do they abide?
Q: bone marrow
circulate in blood and migrate into damaged tissue
Q: What is neutrophil degranulation?
A: release contents of cytoplasmic granules including enzymes, free radicals and soluble mediators
Q: Where do monocytes/macrophages originate? Difference?
Q: bone marrow
circulate in small numbers as monocytes in blood
once in tissue they’re called macrophages
