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Biomedical Science 2 > Imflammation > Flashcards

Imflammation Flashcards

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Biology 101 flashcards
1
Q

Inflammation is the

A

host response to injury

It can occur due to infection, trauma, exposure to noxious chemicals or allergens

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2
Q

Inflammation can occur due to certain conditions

A

meningitis, arthritis,

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3
Q

Inducers of inflammation can include:

A

cell lysis during viral replication, virulence factors - LPS (endotoxin), exotoxins, helminth-derived proteases, PAMP’S,
Cellular necrosis and release of intracellular contents, degredation of basement membrane, loss of epithelial or endothelial integrity - leakage of plasma proteins

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4
Q

Point of inflammation

A
  1. Deliver effector molecules, drugs and cells to the site of infection or injury
  2. Induce local blood clotting
  3. Stimulate adaptive immune response
  4. Promote repair of injured tissue
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5
Q

Outcome of acute inflammation

A

when stitches are applied due to surgery, by 6 months for example, the signs of any inflammation can clear

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6
Q

Outcome of inflammation

A

Complete elimination of pathogen (in the case of acute inflammation)

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7
Q

Inflammatory disease

A

Infections where inflammation causes damage: hepatitis c, Sepsis, tuberculosis,

Post inflammatory fibrosis: Hepatic Cirrhosis, chronic rejection

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8
Q

Cardinal signs of inflammation

A

Redness, swelling, heat, pain, loss of function, lethargy, apathy, loss of appetite, increased sensitivity to pain

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9
Q

Characteristic features

:

A

Vasodilation, vascular permeability, leukocyte extravasation,
Stimulation of immune response - drainage to lymph nodes,

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10
Q

Extravasation,

A

selectin mediated adhesion to leukocyte is weak, and allows leukocytes to roll along the vascular endothelial surface. During extravasation, the number of binding molecules increases

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11
Q

Main components of inflammatory response

A

Mast cells, granulocytes (neutrophils and eosinophils), mononuclear phagocytes (monocytes and macrophages), T lymphocytes, platelets, NK cells, Fibroblasts,

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12
Q

Vasoactive mediators include

A

histamine and kinins,

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13
Q

Lipid mediators include

A

eicosinoids

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14
Q

Different cells produce different

A

cytokines and mediators

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15
Q

Histamine

A

Causes degranulation also through c3a and c5a, cytokines, mechanical damage, has receptors H1 TO H4, on vascular smooth muscle it causes vasodilation, binds to endothelial cell receptors,

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16
Q

Kinins

A

activate cascades (|clotting),

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17
Q

Prostaglandins and Leukotrienes

A

prostaglandins generated from cox 1 and 2,

these are powerful vasodilators, potentiate vasoactive mediators, pryogenic, short half life.

Leukotrienes are generated from arachidonic acid by 5- lipoxygenase,

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18
Q

TNF

A

cytokine which induces chemokine production, and adhesion of molecules on endothelial cells, activates phagocytes, increases proteins triggering local clotting,

19
Q

Development of Inflammation

A

dilation of small blood vessels (via histamine, prostaglandins e.t.c.)

Increased vascular permeability - passage of fluid and small proteins endothelial cell activation, repair and resolution

20
Q

Pain and fever

A

Pain can be caused by inflammatory mediators, badykinin causes pain, Exudation of plasma increases tissue pressure

Fever causes an increase in temperature, defences work better, faster lymphocyte division, increases cell migration,
stimulated macrophages release IL-1 stimulating PGE2 synthesis. Acts on Hypothalamus.

21
Q

When inflammation occurs,

A

activity of edema rises, then of neutrophils (pmn), the macrophages

22
Q

Neutrophils are

A

phagocytes, they engulf pathogenic material. They can phagocytose a bacteria for example. If the pathogen is too big, they can release materials to degranulate the pathogen,

23
Q

People who lack neutrophils would be

A

immunodeficient

24
Q

The neutrophil response has to be turned off after it is not necessary

A

for the resolution of inflammation. The neutrophils are programmed to die via apoptosis, and certain changes to the neutrophil promote the uptake via phagocytosis.

25
Q

Regulation of Acute inflammation

A

Happens via:

  1. mediators - strict temporal and spatial synthesis
  2. macrophages - different phenotyopes - pro inflammatory role (M1)
26
Q

Necrosis

A

loss of intracellular contents - inflammatory response.
Primary necrosis - direct damage
Secondary necrosis - apoptotic cells not cleared

27
Q

Efferocytosis

A

clearance of apoptotic signals by phagocytes

28
Q

Neutrophils exhibit various signals

A

find me (attract phagocytes) , keep out, eat me/ do not eat me

29
Q

Pro resolution/ repair mediators - lipoxins and resolvins

A

Secreted by macrophages, neutrophils, and structural cells
Derived from arachidonic acid
They reduce
1. endothelial migration
2. Neutrophil chemotaxis
3. Production of pro- inflammatory cytokines
4. vascular permeability

Initiate phagocytosis of apoptotic neutrophils

30
Q

TGF - Beta (repair mediator)

A

Potent inhibitor of pro inflammatory macrophage activation

Mediates wound healing
angiogenesis,
fibroblast proliferation
Collagen synthesis and deposition

31
Q

Inflammation could be potentially modulated

A

if you wanted to:

Promote apoptosis, cell recruitment, control the inflammatory response, delay apoptosis and efferocytosis,

32
Q

Partial resolution of inflammation can occur

A

TB is an example of this. When this happens, a granuloma can form and inside, macrophages with the pathogen are contained

33
Q

Ulcerative collitis

A

Chronic inflammatory state – partial but never complete
resolution
• Response to commensal bacteria results in immune cell activation in the lamina propria which damages
epithelium – continuing self-destructive process.

34
Q

Treating U.C.

A

Periods of remission and flare ups

damp down the inflammatory response

35
Q

Rheumatoid arthritis

A

is a chronic inflammation. It can be treated via NSAID’s and disease modifying anti-rheumatic drugs.

36
Q

Detrimental effects of Inflammation

A

digestion of normal tissue

37
Q

IgE Mediated allergic reaction

A

peanut allergy, leading cause of fatal and near fatal symptoms.

Type 1 hypersensitivity or immediate reaction - atopy- igE against inoccuous substance.

Early introduction to peanuts reduces risk of being allergic

38
Q

Silicosis

A

inhalation of silica dust - stone cutting, ceramics, concrete manufacture.

39
Q

steroidal anti- inflammatory drugs

A

glucocorticoids are an example. Complex modification of gene expression.

Decrease T cell activation, fibroblast function, expression of cox2, decrease release of inflammatory mediators

40
Q

Clinical use of steroidal anti-inflammatory drugs

A

asthma, inflammatory conditions of skin, ear, nose,

hypersensitivity states

autoimmune diseases,

graft vs. host disease

41
Q

Side effect of steroidal anti inflammatory drugs

A

suppression of endogenous corticosteroids. stress on sudden stoppage.

increased risk of infection, osteoprosis, slow wound healing.

42
Q

antihistamines are used for

A

insect bits, hay fever cases,
they can be oral or topical

side effects can include antiemetic, sedation

43
Q

Peanut allergy

A

some must strictly avoid
epi-pen (epinephrine)
hospital treatment may be needed
oral immunotherapy - desensitisation or sustained unresponsiveness
However meta analysis showed immunotherapy associated with…

44
Q

Treating sepsis

A

1 in 5 deaths worldwide attributed to sepsis

early recognition

Biomedical Science 2 (4 decks)

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