Inflamm & Immune [21-22] Flashcards

1
Q

Signs of acute inflammation

A

Redness
Swelling
Heat
Pain

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2
Q

What cells are involved in acute inflammation

A

Neutrophils

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3
Q

What causes redness and heat

A

Vasodilation in inflammation
Increases blood flow to tissues

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4
Q

What causes swelling

A

Increased vascular permeability
Endothelial retraction
Gaps for WBC

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5
Q

What is the cellular component to acute inflammation

A

Emigration of leukocytes to tissue

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6
Q

What cells are involved in chronic inflammation

A

Macrophages
Activate lymphocytes via APC
Activate cytokines and antibodies

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7
Q

Drugs classes to reduce inflammation

A

NSAIDs
Steroidal anti inflammatory
Anti-histamines

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8
Q

What do steroidal anti inflammatories do and example

A

Block phospholipids A2 using GR agonist (lipocortin)
Can’t make arachidonic acid
Can’t make leukotrienes, prostaglandins, thromboxanes (inflammatory mediators)

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9
Q

NSAIDs MOA

A

Inhibit cyclooxygenase and also a leukotriene inhibitors
(After arachidonic acid production)

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10
Q

What is COX1

A

Housekeeper
Side effects exerted through COX1 inhibition
Makes thromboxane

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11
Q

When is COX2 induced

A

Upon inflammatory cell activation
NSAIDS exert their effect on COX2

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12
Q

Process of inflammation from pathogen

A

PAMP on pathogen / DAMP from damaged cell binds toll like receptor on macrophage
Activates NF-kB
Cytokine secretion
Inflammation

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13
Q

Adverse effects of NSAIDS

A

Rashes
Bronchospasm

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14
Q

What does inhibiting COX2 do

A

Causes COX1 pathway to increase
Makes more thromboxanes
Blot clots

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15
Q

Allergy pathway

A

Allergen
APC
T helper 2
B cells
Ab class switch to IgE
Sensitisation (binding to mast cell)
Degranulation (release histamine)

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16
Q

What is type 1 hypersensitivity

17
Q

How is hay fever mediated by H receptors

A

H1 receptors stimulant phospholipase C to convert PIP2 into IP3
Increases Ca2+ conc
Bronchoconstriction

18
Q

Difference between first gen and second gen anti histamines

A

First gen cross BBB
Second gen don’t so are non drowsy (Loratidine)

19
Q

What is anaphylaxis and how is it treated

A

Systemic release of histamine from mast cells
- low bp
- swelling
- sustained bronchoconstriction
Treated with B2 agonist - adrenaline

20
Q

What are most antihistamines

A

Inverse agonists instead of neutral antagonist (reverses activity rather than stops it)

21
Q

Immunosuppressive drugs

A

Glucocorticoids
Calcineurin inhibitors
mTOR inhibitors
IL-2 receptors antagonists
Nucleic acid synthesis antagonists

22
Q

How to immunosuppressant exhibit their effect

A

Block expression and activity of T cell growth factor and activate IL-2

23
Q

3 processes after plasma cell releases antibodies in immune response

A

Opsonisation (binding)
Agglutination (clumping)
Neutralisation (killing)

24
Q

4 functions of antibodies

A

Enhance phagocytosis (agglutination, chemoattraction)
Neutralisation
NK cell activation
Classical complement cascade activation (C3b MAC)

25
APC to cell cycle replication pathway
MHCII on APC binds TCR Activates calcineurin pathway IL-2 gene releases IL-2 Binds IL-2 receptor mTOR pathway Cell cycle
26
Glucocorticoid immunosuppression effect
GR binds p65 subunit of NF-kB Prevents activation of inflammatory genes Also promotes IkBa synthesis (inhibitor) Suppresses T cell activation
27
Calcineurin inhibitor example and how it works
Cyclosporine Binds cyclophilins Inhibits Calcineurin phosphatase Prevents IL-2 formation
28
What are immunosuppressive drugs needed for
Transplantation The require life long immuno suppression Needs narrow therapeutic window
29
Side effects of immunosuppressants
Poor wound healing Coagulation disorders
30
How do many auto immune diseases and cancers arise
Over expression of PDL PDL tells PD1 on T cells to deactivate themselves Evades immune system by not being recognised