A1 Inflammation Flashcards
When does inflammation occur
Secondary induced innate responses when phagocytes etc are active
Does inflammatiok stay thebsame
No can change in amount and time eg acute or chronic
What are the functions of inflammation
Restrict damage or infection to site
Remove damage tissue or the pathogen
Promotes immune cell migration to site
What are the 3 causes / etiology
Physical damage eg hammer
Biological eg pathogen
Chemical eg toxins
What other biological etiology does inflammation have
Necrotic tissue
What are the 5 cardinal signs of inflammation
Heat Erytherma (redness) Oedema swelling Pain Loss of function eg if physical damage
Explain the 4 stages of inflammation
Tissue damage/infection
Vascular dilation/permeability by mediators
Cell recruitment and exudation of eg plasma proteins/salts/water
Tissue repair - constriction, scarring
What happens to endothelial cells in the second stage
Swell and cell retention forming holes for exudation etc
What is it called when cells adhere to endothelium before emigration
Margination
If bacteria present what is the first thing that triggers things like dilation , cell recruitment
Gets phagocytosed/recognised eg by prr and phagocytes release cytokines and chemokines
What types of cells are involved
Mast, basophils, eosino, neutrophils, dendritic cells,monocytes(macrophages in tissue)
What does inflammation do to toxins which is advantageous
Dilutes them
Why is exudation in inflammation advantageous
Provides nutrients and o2 to cells and tissue
What plasma protein helps impede movement of bacteria in inflammation
Fibrin
How does inflammation link innate to adaptive
Immune cells like DC then leave via lympatic drainage and cause t cell etc activation
What type of non specific antibodies are involved in inflammation
Ab from b1 cells
What type of enyzmes increases in inflammation which is bad
Mmp/ proteolytic enzymes
Why is inflammation due to haemophilus influenzae dangerous
It causes swelling of the epiglottis which stops breathing in airways
What jappens with meningitis inflammation
Blood supply to brain stops
When is inflammation unecessary to harmless things like pollen
Allergies/ type 1 hypersensitivity causes the inflammatory response
What 2 things activate mast cells to secrete granules etc
Prr recognising damps or pamps
Or
Ige binding to fcr e on the mast cell surface
Give examples of pamps
Lps, fimH adhesin on ecoli
Which lipid mediators does mast cells produce
Pgd2 (prostaglandin)
And
LTB4 and LTC4 (leukotrienes)
Give exmaples of inflammatory cytokines produced by mast cells
Tnf a, il-1b, il 6
What types of cutokines are pro inflammatory released by mast cells
Tnf a, il 6 , il 1b
What are some examples of pre formed granules in mast cells that are inflammatory mediators
Histamine, seratonin , tryptase
Give examples of vasodilators for inflammayion
Histamine , prostaglandin, c3a, c5a
Give examples of permeability mediators
Histamine, pg, kinins
Which types of molecules help migration of immune cells in inflammation
C3a,5a, chemokines eg il8, leukotrienes
What proteins in neuotrophils helps attract other immune cells
Cationic proteins
What kind of osmotic pressure xauses fluid retention back into capillaries
Colloid osmotic pressure (plasma protein presence)
In oedema which end of blood vessels / capillaries does fluid enter in exudation etc
Arterial end (leaves venule end)
Other than inflammatory oedema what others are there
Pulmonary eg when at high altitude fluid fills alveoli
Lympoedema from lymphatic drainage obstruction
What mediator helps vasodilate in inflammation via cgmp increase
NO via NOS
What types of cells produce histamine
Mast, baso, eosinophils, platelets
Histamine aswell as dilation causes permebaility of what
Venules
What is the primary cause of permeability
Histamine
What happens when histamine binds h1 receptors
Activates phospholipase a and c which breakdown phospholipids into arachidonic acid
Arachidonic acid is released when theres an increase in what
Histamine or through neutrophil/monocyte interaction with tissue
What is the cox pathway of arachidonic catabolism
Into pgh2
This is a precursor for pgd2, pge2 which produces to pgf2
Also produces TXa2 (thromboxane a2)
And PGI2 (prostacyclin)
Which prostaglandin produces pain
Pge2
What is main goal of PG
Vascular permeability
What does PGI2 do prostacyclin
Stops platelet aggregation ane cuases dilation
What does thromboxane a2 cause
Platelet aggregation and constriction
What is the lipooxygenase pathway
Into 5h pete
Converts to LTB4 or LTC4
LTC4 then can produce D4 and E4
What do LTC4,D and E do
Cause airway constriction and mucus build
Also vascular permeability
What foes LTB4 do
Chemotaxis and stimulates neutrophils margination on endothelial cells
Whcih cox is upregulated in inflammation
Cox 2
PAF is made by most cells in inflammation. What is it’s purpose
Dilation Platelet aggregation for repair Phagocytosis upregulated Increases arachidonic catabolism Chemotaxis
How do cytokines have effect
Through receptors eg chemokine gpcr
What is the major inflammatory cytokine
Tnf A (mainly from macrophages)
How does tnf a allow margination similar to ltb4
Upregulates selectins on endothelial cells which allow cells to stick before emigration
What chemicals are ipregulated due to tnfa
Il1 and chemokines like il8
What syndrome is caused by tnf a
Toxic shock
How does tnf a cause fever
Srimulates hypothalmic cells to secrete prostaglandins which cause fever
How does tnf a affect liver
Causes uprefulatuon of serum proteins from liver hepatocytes
Does il1 cause fever
Yes
How does il1 impact liver
Increases synthesis of acute phase proteins
What cell is chemokine il8 specific to
Neutrophils
What is the movemnet of immune cells in called
Diapedesis
