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S2 Case 1 - IBD > Physiology + Pharmacology of Inflammation + Autoimmunity > Flashcards

Physiology + Pharmacology of Inflammation + Autoimmunity Flashcards

1
Q

Describe inflammation

A

Protective response
Response of blood vessels + leukocytes

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2
Q

Describe acute inflammation

A

Rapid
Presence of leukocytes
Exudation of fluids + plasma proteins

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3
Q

Describe chronic inflammation

A

Longer
Presence of lymphocytes + macrophages
Fibrosis + tissue disruption

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4
Q

What happens in acute inflammation?

A

Vasodilation = mediators - eg. histamine binds
Increased blood flow
Increases permeability of microvasculature
Increase viscosity of blood
Stasis = slows moving RBCs = fluid leaves capillary
Neutrophil accumulation

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5
Q

What are the stimuli for acute inflammation?

A

Infections
Tissue necrosis
Foreign bodies
Immune reactions

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6
Q

How do leukocytes adhere to endothelium?

A

Leukocytes redistribute along endothelium
Detach + adhere = mediated by selectins
Firmly adhered = mediated by integrins
Transmigration
Emigrate to site of tissue, followed by chemoattractant

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7
Q

How do leukocytes respond?
(Phagocytosis)

A

Particle bound to phagocyte receptor
Plasma membrane form vesicle
Phagosome fuses with lysosomal granule
ROS + NO + lysosomal enzymes = kill + degrade

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8
Q

Describe cell-derived mediators

A

Produced locally
Pre-accumulated or synthesised de novo

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9
Q

Describe plasma protein-derived mediators

A

Produced in liver
Circulate in plasma as inactive precursors

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10
Q

What mediators does anti-inflammatories target?

A

Prostaglandins
Leukotrienes

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11
Q

Describe prostaglandin + leukotrienes

A

Phospholipase release arachidonic acid COX-1 + COX-2 convert AA in prostaglandin
OPTION 1: Thromboxane synthetase convert PGH2 to thromboxane
OPTION 2: prostacyclin synthetase convert PGH2 to prostacyclin

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12
Q

What are COX-1/2 inhibitors?

A

Aspirin
Ibuprofen
Paracetamol

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13
Q

What is the anti-inflammatory effect of COX-1/2 inhibitors?

A

Block PGs production = reduce vasodilation

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14
Q

What is analgesic effect of COX-1/2 inhibitors?

A

Reduce pain by inhibiting PGs production

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15
Q

What is anti-pyretic effect COX-1/2 inhibitors?

A

Lower higher temperature

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16
Q

Describe COX-2 specific inhibitors

A

More selective for inflammation
Less GI toxicity
eg. celecoxib

17
Q

Describe 5-lipoxygenase

A

Present in neutrophils
Convert AA to 5-HPETE
Precursor to leukotrienes
Cause vasoconstriction

18
Q

How do lipoxygenase reduce inflammation?

A

Inhibit LTs production
Or block leukotriene receptors

19
Q

Describe glucocorticoids

A

Reduce transcription of genes encoding phospholipase A2
eg. cortisone

20
Q

Describe NF-kB transcription factor

A

Activated by huge number of stimuli
Master regulator of inflammation
Regulates expression of cytokines

21
Q

What is the outcome of acute inflammation for short-lived injury?

A

Damaged tissue can regenerate
Complete removal of debris by macrophages
Complete resolution

22
Q

What is the outcome of acute inflammation for extended injury?

A

Damaged tissue cannot regenerate
Connective tissue grows in area of damage
Fibrosis

23
Q

What is the outcome of acute inflammation for persistence injury?

A

Damage interferes with repair process
Persistent inflammation
Chronic inflammation

24
Q

What is chronic inflammation?

A

Prolonged duration

25
Q

What are the causes of chronic inflammation?

A

Persistent infections
Immune-mediated inflammatory diseases

26
Q

What are the features of chronic inflammation?

A

Infiltration with mononuclear cells
Tissue destruction
Attempts at healing

27
Q

What are the cells involved in chronic inflammation?

A

Macrophages
Lymphocytes
Plasma cells

28
Q

What is autoimmunity?

A

Genetic susceptibility, breakdown in natural tolerance + environmental triggers

29
Q

What are examples of autoimmunity diseases?

A

Pathogenic effects of autoantibodies
T cell-mediated autoimmunity

30
Q

Describe pathogenic effects of autoantibodies

A

Affect molecular function (type 2 hypersensitivity) = antibodies bind to antigens on top of cell

a) ABs to Ach receptor in myasthenia gravis = receptor internalisation + remove muscle surface

b) ABs to TSH receptor in Grave’s disease = mimics effect of TSH = excess thyroid hormone secretion

31
Q

Describe T cell-mediated autoimmunity

A

Insulin dependent diabetes
= cells of pancreas destroyed by CD8 T cells

32
Q

How do you develop chronic autoimmune disease?

A

Self-antigen cannot be eliminated
Constant presence = chronic inflammation
Tissue damage = release of more self-antigens
Leukocytes attracted by cytokines (released by damaged tissue)
Self-destructive process continues

S2 Case 1 - IBD (18 decks)

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