inflammation and autoimmunity Flashcards

1
Q

what cells are associated with acute inflammation?

A

leukocytes (neutrophils)

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2
Q

what cells are associated with chronic inflammation?

A

lymphocytes and macrophages

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3
Q

5 step process of inflammation?

A

1- vasodilation
2 - increased vascular permeability
3- increased viscosity of bleed
4- stasis
5- accumulation of neutrophils

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4
Q

3 steps of acute inflammation?

A

vasodilation - increased blood flow
increased permeability - permits oedema
leukocyte migration

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5
Q

what is margination of leukocytes?

A

they redistribute along endothelium

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6
Q

what is rolling of leukocytes?

A

when they adhere transiently to vascular surfaces due to selectins

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7
Q

what happens in adhesion of leukocytes?

A

firmly adhere to surface due to integrins

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8
Q

how do leukocytes migrate through endothelium?

A
  • interaction mediated by adhesion molecules PECAM-1/ CD81
  • release collagenases to pierce basement membrane
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9
Q

what is chemotaxis of leukocytes?

A

emigrate towards injury, following chemo attractants
exogenous - bacterial products
endogenous - chemical mediators (chemokines)

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10
Q

what happens after recruitment of leukocytes to injury site?

A

phagocytosis
- engulfment, killing and degradation

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11
Q

effect on body temp of acute inflammation?

A

increased COX and prostaglandin release from hypothalamus increase body temperature

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12
Q

what classifies a fever?

A

body temp elevation of 1-4 degrees

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13
Q

what is NF-kB transcription factor?

A

master regulator of inflammation
regulates expression of cytokines, chemokines, adhesion molecules and enzymes

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14
Q

drugs developing to target NF-kB?

A

IKK inhibitors
Proteasome inhibitors
inhibitors to block translocation
inhibitors of DNA-binding activity

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15
Q

2 causes of chronic inflammation?

A

1) persistent infections = microorganisms difficult to eradicate
2) immune-mediated inflammatory diseases = inappropriate activation

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16
Q

3 features of chronic inflammation?

A

infiltration with mononuclear cells
tissue destruction
attempts at healing

17
Q

role of macrophages, lymphocytes, plasma cells in chronic inflammation?

A

macrophages - products eliminate injury agents to initiate repair
lymphocytes - release of cytokines make reaction chronic and severe
plasma cells - produce antibodies

18
Q

how do cell-derived mediators help inflammation?

A

produced locally, pre-accumulated and released rapidly

19
Q

how do plasma protein derived mediators help inflammation?

A

circulate in plasma and activated at site

20
Q

how are prostaglandins and leukotrienes made?

A

generated by several enzymes

21
Q

what does phospholipase A2 do?

A

releases arachidonic acid (AA) from phospholipids

22
Q

what does COX1/2 do?

A

converts AA into prostaglandins PGG2 PHG2

23
Q

what does thromboxane synthesase do?

A

covert PGH2 into thromboxane

24
Q

what does prostacyclin synthetase do?

A

convert PGH2 into prostacyclin PGI2

25
difference between cox 1/2 inhibitors and specific cox 2 inhibitors?
cox2 are selective and cause less GI toxicity
26
3 properties of NSAIDs to help inflammation?
anti inflammatory - block prostaglandins analgesic - reduce pain anti-pyretic - lower temperature
27
how do lipoxygenase inhibitors work?
block 5-lipoxygenase that produce precursors to leukotrienes
28
how do glucocorticoids work?
reduce transcription of genes encoding phospholipase A2 reduce cytokines
29
2 type of autoimmune diseases?
- pathogenic effects of autoantibodies - T cell-mediated autoimmunity
30
how does myasthenia gravis cause weakness of skeletal muscle?
antibodies bind to Ach receptor and cause internalisation and removal of muscle surface
31
how does graves disease cause hyperthyroidism?
antibodies mimic effect of TSH hormone causing excessive secretion
32
what happens in autoimmune haemolytic anaemia?
autoantibodies damage red blood cells
33
what do autoantibodies do in lupus?
bind to soluble fragments of DNA which get deposited at susceptible sites
34
how does insulin-dependent diabetes occur?
cells of pancreas destroyed by CD8 T cells