inflammation Flashcards

1
Q

What are the four main signs of acute inflammation?

A

Colour
heat
pain
swelling

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2
Q

four factors of inflammation being a universal process

A

immunity and infection
genetic
cell biology
hameatology

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3
Q

What is inflammation

A

a rapid non specific response to cellular injury

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4
Q

what three things occur during acute inflammation

A

change in blood flow
structural changes in the microvasculature (capillaries, venules and arterioles)
recruitment/accumulation of immune cells and proteins

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5
Q

what cells are typically found in the interstitium?

A

mast cells

macrophages

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6
Q

what cells are typically found in the vascular endothelium?

A

.leukocytes

.neutrophils

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7
Q

inflammatory signals results in …

A

. non apoptotic cell death

.detection of foreign material

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8
Q

what are the 2 vasodilators released during infection?

A

histamine

Nitric oxide

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9
Q

what vascular changes are observed during inflammation?

A

Increased permeability
. dilation
.reduced flow
.plasma leakage

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10
Q

Give 3 sources of histamines

A

source: Mast cells, basophils, platelets

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11
Q

Give 2 sources of prostaglandins

A

mast cells, leukocytes

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12
Q

Give three sources of cytokines (TNF, IL-1)

A

.Macrophages
.endothelial cells
mast cells

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13
Q

give two sources of chemokines

A

leukocytes

activated macrophages

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14
Q

Give a source of Complement. (C5a, C3a, C4a)

A

plasma

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15
Q

what does histamine do?

A

Vasodilation, increased vascular permeability, endothelial activation

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16
Q

actions of prostaglandins

A

vasodilation, pain, fever

17
Q

action of cytokines

A

endothelial activation, fever

18
Q

action of chemokines

A

chemotaxis, leukocyte activation

19
Q

action of Complement (C5a, C3a, C4a)

A

LEUKOCYTE chemotaxis and activation, vasodilation, Oponisation (attach opsins for phagocytosis)

20
Q

what is exudate

A

Fluid, proteins and cells that have seeped out of a blood vessel

21
Q

Give an example of immune cell recruitment

A

Chemokine: CXCL8 otherwise known as IL-8

Receptors: CXCR1 and CXCR2, g-coupled 7-transmembrane proteins

Cell type: Neutrophils. Often the first cell type recruited to the site of inflammation

22
Q

what are the four stages of neutrophile extravasition

A

1) Chemo attraction, cytokines lead to endothelial upregulation of adhesion molecules e.g selectin
2) rolling adhesion: carbohydrate low affinity ligand binds e.g PSGL binds P and E selectin
3) Tight adhesion: Chemokines promote higfh affinity switch in integrins e.g ICAM 1/2
4) TRANSMIGRATIO- cytoskeletal rearranges and pseudopodia occurs ( temp entension of cytoplasm)- mediated BY PECAM.

23
Q

how to neutrophils work at sight of infection

A

. use of TLR4 and CD14 to identify lipopolysaccharides (LPS) present in gram-negative bacteria
Pathogen clearance via phagocytosis+netosis
.Cytokine secretion: recruit and activates other immune cells

Phagocytosis
Large particles engulfed into membrane bound vesicles (phagosomes)
Phagosome fuses with lysosome (vesicles containing enzymes e.g. elastase and lysozyme) -> phagolysosome
Ractive oxygen species (ROS) – phagocyte NADPH oxidase
Antimicrobial peptides – e.g. defensins.

24
Q

define antigen

A

A molecule or molecular structure that can be recognised by an antibody
any substance to which your immune system can mount an antibody or adaptive immune response

25
Q

what are the 4 types of antigen

A

Antigen types:
Foreign antigen: an antigen derived from molecules not found in the body
Self antigen: an antigen derived from molecules produced by our bodies
Immunogen: an antigen independently capable of driving an immune response in the absence of additional substances
Hapten: a small molecule that alone does not act as an antigen but when bound to a larger molecule can create an antigen

26
Q

give some chronic diseseases

A
Asthma
Hepatisis
Inflammatory bowel disease
Multiple sclerosis
Rheumatoid arthritis
Glomerulonephritis
Psoriasis
27
Q

give some dieases assoicated with granulomatous inflammation

A
Examples: Tuburculosis
Leprosy
Foreign body granuloma
Tumor reactions
Sarcoidosis
Crohns disease ( a specific type of IBD)
28
Q

chronic inflammation charactersitics:

A

. perisistent infection e.g hep B/c
unclearable particulates
autoimmunity

29
Q

positives of macrophages

A

Phagocytic
cytotoxic
anti-inflammatory (e.g IL-10, TGF-beta)
Wound repair

30
Q

Negatives of macrophages

A

cytotoxic
inflammatory
pro-fibrotic

31
Q

T cells in inflammation:

A

.pro inflammatory e.g TNF, IFN-gamma)
Cytotoxic e.g granzymes, perforin
regulatory e.g TNF-beta

32
Q

differences between acute and chronic inflammation

A
Acute:
Immediate
vasodilation
neutrophils
histamine release
prominent necrosis
complete resolution or progresses to chronic
Chronic:
Delayed onset
persistent inflammation
Monocytes/macrophages
cytokine release
prominent scarring
scarring/loss of function of tissues occurs
33
Q

What are 3 advantages to acute and chronic inflammation?

A

. Clear inflammatory agent
.removes damaged cells
.restores normal tissue function

34
Q

What are three negatives to chronic/acute inflammation

A

.Excess tissue damage
.scarring
.loss of organ function leading to organ failure

35
Q

What causes scarring and excess tissue damage

A

excessive extracellular matrix deposition

36
Q

give a consequence of inflammation

A

Bronco-pneumonia