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63 Cards in this Set

  • Front
  • Back
What are the four stimuli of inflammation?
1. Physicsl (cut, burn)
2. Chemical (acids, chemicals)
3. Microbial (bacterial toxin, parasite, viral)
4. Immunological (normal immune response, hypersensitivity)
What are the cardinal signs of acute inflammation?
Redness (Erythema)
Loss of function
What is the "triple response"?
This is the term for the 3 of the cardinal signs - heat, redness and swelling
What is the vascular response to acute inflammation?
Hyperaemia (more blood in them!)
Sludging of RBCs
Blood clotting
Margination of leukocytes
High endothelial venule (HEV) formation
Thickened and raised
Exudation (more permeable and dilated)
Why is exudate formed?
There is an altered balance between osmotic pressure and hydrostatic pressure, meaning more fluid and plasma proteins in tissues.
What causes pain?
Tissue tension and action of soluble mediators on sensory neurones
Explain the half lives of inflammatory mediators.
They have short half lives and are rapidly inactivated
Give some examples of preformed mediators.
Histamine (mast cells, basophils)
Serotonin (platelets)
Give some examples of newly synthesized mediators.
Prostaglandins (all leukocytes)
Leukotrienes (all leukocytes)
PAF (all leuk)
NO (macrophages)
Cytokines (all leuk)
Give some examples of blood clotting mediators.
Thrombin (liver)
Fibrinolysin (aka Plasmin, from liver)
Kinins (liver)
Which mediators induce VASODILATION?
Which mediators induce VASCULAR PERMEABILITY?
Which mediators induce PAIN?
How many phases of the TRIPLE RESPONSE are there?
2 - Immediate Phase and Delayed Phase
Explain what the IMMEDIATE PHASE of the triple response is due to.
Histamine in mast cells
Serotonin in granules of platelets
Blood clotting factors
Explain what the DELAYED PHASE of the triple response is due to.

NOTE: This phase may not be visible, due to extent
What is the relationship between prostaglandin and paired mediators?
Prostaglandin LOWERS THE THRESHOLD of sensory pain fibres to other mediators

EX. Bradykinin gives a small pain degree, but added with PGE gives LARGE degree. Same with oedema and itch!
What is the definition of a prostaglandin?
Fatty acids produced from phospholipids in cell membranes
How is prostaglandin LIKE a hormone and UNLIKE one?
Produced in response to stimuli
Act via G-protein linked receptors
Rapidly destroyed

No stored form
Locally acting (paracrine)
Can be synthesized by most cells
What does PGE stimulate?
Vasodilation and vascular permeability as well as promoting the sensation of pain
What is the relationship between PGE and neutrophils?
PGE recruits neutrophils to damaged areas
What is PGE produced from?
Arachidonic Acid is acted on by CYCLOOXYGENASE (COX) to produce PGH2, the parent prostaglandin
How is Arachadonic acid produced?
When insult occurs, PHOSPHOLIPASE A2 (PLA2) acts on membrrane phopholipids to split PHOSPHATIDYLCHOLINE (PC) into ARACHIDONATE and PAF

What are the different PGEs that can be made?
PGI2, PGF2, PGE2, PGD2 and Thromboxine A2

NOTE: All cells can make these, except ONLY platelets can make Throm-A2
Explain COX
There are 2 isoforms.

COX1 is constituitive and involved in 'housekeeping' like maintaining the gut

COX2 is inducible and is involved in inflammatory response
Serous exudate
Watery (ex. blister)
Fibrinous exudate
Rich in fibrinogen protein (precursor to fibrin); has fluid too
Catarrhal exudate
Mucin (ex. mucus membranes)
Haemorrhagic exudate
Frank bleeding into tissues
Suppurative/Purulent exudate
"Pus", often localized inside an abscess
Necrotizing exudate
Cell death, ischaemia, acute venous congestion
What are the functions of exudate?
1. Dilute toxins
2. Distribute clotting factors and mediators
3. Opsonization of pathogens by antibodies and complement
4. Continuously drains to lymph vessels
What are the three steps of leukocyte adherence?
Tethering and rolling
What molecules are involved in leukocyte adherence?
1. Selectin on endothelium aligns with mucin-like molecule on leukocyte
2. Chemoattractant from ednothelium attracted to chemoreceptor on leukocyte
3. Integrin on cell allows compliance with Ig family member on endo
What are the two types of Selectin and when are they seen?
P selectin is seen in the immediate pathway and E selectin is seen in the delayed
What are the functions of neutrophils in inflammation?
1. Phagocytosis of pathogens via Ag/Ab complexes, TLR and C3bR
2. Liquification of surrounding tissue by lysosomal enzymes following degranulation
3. Amplification of inflammation by synthesis of PGE, LT and PAF
4. Amplification of inflamm by secreted factors
How is monocyte migration different from neutrophil?
It is much slower, delayed 1-3 days
What are the functions of macrophages in inflammation?
1. Phagocytosis of pathogens
2. Secrete toxic factors (NO, H2O2)
3. Secrete IL1, TNFalpha, IL6, which promote leuko adherence, induce acute phase response and fever
4. Secrete colony stimulating factors (CSF) to promote differentiation of immature granulocytes and monocytes
What is leukocytosis?
An increase in concentration of white blood cells in blood
What is meant by a neutrophil 'shift to the left'?
Where there is neutropaenia, more neutrophils are released from marrow resulting in neutrophilia...as more and more are seeded to tissues, immature cells start to be released from marrow to keep up with demand.
This is the shift, and the neutrophils are immature and are called 'band neutrophils'
How is fever induced? (Pyrexia)
Il1 and TNF act as endogenous pyrogens (generate heat).
Could also be induced via microbial products acting through TLRs
How is fever beneficial?
1. Decreases microbial replication because of temp
2. Increases phagocytosis and killing by neutrophils and macrophages
3. Increases antigen presentation efficiency
What is the acute phase response?
It occurs in most forms of inflammation, infection and tissue injury.
It is the increased production of several plasma proteins after injury and in disease states by the liver
What is anaemia of inflammation?
The transient reduction of erythrocytes in blood as a result of inflammatory mediators on the liver.
Goal is to reduce the iron in blood that is available for bacteria and microbes
What is septic shock?
Infection-induced syndrome characterized by a generalised inflammatory state.
Characteristics are fever, acute phase response, hypoglycaemia, exudation or haemorrhage, metabolic acidosis and organ dysfunction

NOTE: Permeability of gut intestinal flora increases...bad news bears
The return to normal is the inflammatory rxn is mild and the cause is eliminated
What is REPAIR?
The formation of scar tissue if rxn is extensive
In resolution, what makes up the built-in termination programme?
In resolution, what makes up the 'return to normal' sequence?
Fibrinolysis - plasmin digests fibrin clots
Phagocytosis - macrophages get dead cells, debris, fibrin in DEMOLITION PHASE
Regeneration of tissue
What is the DEMOLITION PHASE of resolution?
When macrophages phagocytose dead cells, debris, fibrin products, etc
In resolution regeneration, what cells grow?
The lost tissue is replaced by proliferation of cells of the same type to keep original architecture
What is resolution regeneration mediated by?
Wound cytokines secreted from macrophages, including TGFbeta and PDGF

These act as growth factors for endothelials, epithelials, smooth musclem cells and fibroblasts
What type of tissue is formed in repair ('organization')?
Granulation tissue
What is the original tissue architecture replaced with in REPAIR?
Avascular fibrous scar tissue with a loss of function
What is a repair ADHESION?
Connective tissue between two organs
What gives rise to suppuration?
Pyogenic bacteria that resist uptake or destruction
Why does an abscess cavity form in suppuration?
Because of the alterations in tissue osmotic pressure induced by exudation and cell death.

Water is drawn into area of pus, enlarging the cavity
What is pus?
Dead and dying neutrophils and bacteria
Describe formation of granulation tissue in suppuration?
Tissue forms around abcess cavity and brings in a large number of neutrophils and secretes new connective tissue components.

Also, fibroblast proliferation and formation of new blood vessels
What is a pyogenic membrane?
This forms initially as a thin layer of granulation tissue around an area of suppuration, forming a walled abscess.
This grows to form an abscess capsule.
What is the fate of abscesses?
1. Rupture
2. Healing initiated by granulation tissue - resolution or repair
3. Chronic abscess - cyst or inspissated
What aids in progression of acute to chronic inflammation?
1. Persistent suppuration - failure to kill all microorganisms
2. Foreign body response
What does persistent, non-resolving acute inflammation lead to?
Fibrous scarring or fibrosis...ie, LOSS OF FUNCTION