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OV3017 Eye Disease > 9 - Pathogenesis of inflammatory disease > Flashcards

9 - Pathogenesis of inflammatory disease Flashcards

1
Q

what is inflammation

A
  • response of living tissue to damaging stimuli
  • directs immune components to site of damage

function is to containd damage and initiate repair processes to restore normal function

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2
Q

what are some causes on inflammation

A
  • infection
  • hypersensitivity reactions
  • auto immunity
  • trauma
  • chemical/toxic
  • radiation
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3
Q

classification of inflammation

A

acute (minutes or days)

  • chronic (weeks or months)
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4
Q

signs of acute inflammation

A
  • redness
  • wamth
  • pain
  • swelling
  • loss of function
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5
Q

what are the major features of acute inflammation

A
  • vascular events
  • cellular events
  • triggered by inflammatory mediators which also perpetuate the inflammatory process
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6
Q

acute inflammation. major events VASCULAR

A
  1. Vasodilation (redness)
  2. increased blood flow (increased heat)
  3. increased vascular permeability ( contributes to oedema)

movement of inflammatory cells from blood vessels to site of injury - they minimise damage + initiate repair

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7
Q

extravasation of leukocytes(neutrophils) into tissues steps

A

neutrophils = phagocytes

  1. margination
  2. rolling.
  3. diapedesis
  4. chemotaxis
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8
Q
  1. margination
A

cell moves from centre of blood column to endothelial wall of blood vessels

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9
Q
  1. rolling
A

these white blood cells start rolling along the inner surface of the blood vessel.
endothelium has adhesion molecules, allowing inflamm. cell to attach

rolls along vessel wall before coming to rest

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10
Q
  1. diapedesis
A

cell squeezes through vessel wall - towards site of injury

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11
Q
  1. chemotaxis
A

once cell leaves vessel, able to move along conc. gradient of inflam. chemicals that are released from the site of inflammation

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12
Q

what is the role of phagocytes

A

to eliminate potential pathogens/ damaged tissues

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13
Q

phagocytosis

A
  1. phagocytes arrive at site of infammaton by chemotxcis
  2. attach to micro-organisms/cell deprsis of surface receptors
  3. material internalized + destroyed
  4. opsonization
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14
Q

inflammatory mediators

A
  • vasoactive amines
  • plasma proteases
  • arachidonic acid metabolites
  • cytokines
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15
Q

arachidonic acid pathway

A

this metabollic pathway generates a series of inflammatory mediators known as eicosanoids

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16
Q

process of eicasanoid synthesis

A

too long to write

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17
Q

what are mast cell mediators

A
  • include pre formed and newly formed mediators
  • pre formed incude: histamine, heparin, and neutral protease
    newly formed: leukotrienes, prostoglandn
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18
Q

what do mast cell mediators have a role in

A

type 1 hypersensitivity reaction

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19
Q

where do MSM lie

A

close proximity to blood vessels

20
Q

what do mast cells contain

A

granules containing pre formed mediators such as histamine and heparin

21
Q

what happens when mast cells release the granules (degranulation)

A

histamine release - causes vasodilation and increases vascular permeability

22
Q

what happens after degranulation

A

delayed second phase response (swelling/itching)

23
Q

what are the outcomes of acute inflammation

A

1) complete resolution
2) scar formation
3) progress to chronic inflammation, mediated by lymphocytes and macrophages

24
Q

what is the ocular response to inflammation

A
  1. redness
    - could be consequence to heamorrhage. more likely vasodilation

redness varies in locaiton: diffused or localised

25
Q

another ocular response to inflammation

A

oedema

26
Q

what is oedema a consequence of

A
  • ## increased vascular permeability #
27
Q

exudates

A

another ocular response to inflammation
- increased vascular permeability
- rich in protein
- rich in inflammatory cells

28
Q

cellular infiltration

A
  • ocular response to inflammation
  • sterile or non sterile
  • acute (neutrophils)
  • chronic )lymphocytes/macrophages)
29
Q

what else can corneal infiltrates occur in response to

A

bacterial toxins e.g stappholococci

30
Q

discharge

A
  • ocular response
  • serous (watery)
  • mucopurolent
  • plurulent
31
Q

conjunctival papillae and follicles

A
  • ocular response
  • papillae common in allergic eye disease: each papilllae consists of dilated blood vessel at the centre with surrounding lymphocytes
  • covered by hypotrophic endothelium
  • follicles charecteristics of viral infection or toxic reaction
32
Q

inflammation of the posterior segment

A

often chronic conditions
- anterior ischaemic optic neuropath
- sarcoidosis

33
Q

ocular autoimmune diseases in the absence of systemic involvement

A
  • moorens ulcer: causes a progressing thinning of peripheral cornea
  • sympathetic ophtalmia - occurs due to penetrating injury to one eye followed by inflammation in other eye
34
Q

ocular autoimmune disease with systemic involbement

A

-Reiter’s disease

-Ankylosing spondylitis

-Rheumatoid arthritis

-Behçet’ disease

-SLE

-Sjögren’s syndrome

-Sarcoidosis

-Cicatricial pemphigoid

35
Q

what is the pathogensis of autoimmunity

A
  • autoreactive T helper cells (CD4) often responsible for initiating tissue damage via production of cytokines

*autoreactive cytotoxic T cells (CD8) can also cause tissue damage

*antibodies cause tissue damage via a type II mechanism

36
Q

pathogensis of allergic eye disease

A
  • caused by type 1 or type IV hypersensitivity reaction
37
Q

what type of reaction is acute allergic conjunctivitis and seasonal allergic conjunc.

A

type 1 hypersenitivity reaction

38
Q

what reaction is atopic allergic conj. and giant papillary conjunc.

A

type IV

39
Q

type 1 hypersenitivtiy is also referred to as?

A

atropy

40
Q

what is type 1 hypersensitivity caused by

A

overproduction of igE

41
Q

how is type 1 hypersensitivity triggered

A
  • in minutes
  • exposure to environmental antigens e.g pollen/dust mites

strong genetic link

42
Q

type 1 mechanism

A
  • mast cells have high affinity receptor for igE
  • igE synthesised in response to certain allergens (antigens)
  • allergens land on mucous membranes, then picked up by antigen presenting cells
  • allergen is presented to TH2 cells which provide cytokine signals to B cells to produce more igE
  • igE binds to mast cells
  • if exposed to same allergen again, it binds to igE on the mast cell
  • this causes degranulation
43
Q

what happens in type 1 mechanism AFTER mast cell degranulation

A
  • degrnaulation: mast cell release histamines/heparin

These cause itching, mucus secretion, vasodilation and oedema

44
Q

type II hypersensitivity

A
  • antibody directed against membrane and cell surface antigens
  • antigen + antibody reactions activate complement producing membrane damage
45
Q

type IV hypersensitivty - basics

A
  • delayed type hypersensitivity
  • takes more than 12 hours to develop after antigenic challenge
  • T cell mediated mechanism
46
Q

type 4 mechanism

A
  • antigen presenting cells in conjunctiva pick up an antigen
  • go to lymph nodes & activate T cells
  • T cells go back to conjunctiva and produce cytokines + attract macrophages
  • cause tissue damage
47
Q
A

OV3017 Eye Disease (19 decks)

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