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PED2006 - Systems Pharmacology > Inflamm & Immune [21-22] > Flashcards

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

A

Hay fever

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
Q

APC to cell cycle replication pathway

A

MHCII on APC binds TCR
Activates calcineurin pathway
IL-2 gene releases IL-2
Binds IL-2 receptor
mTOR pathway
Cell cycle

26
Q

Glucocorticoid immunosuppression effect

A

GR binds p65 subunit of NF-kB
Prevents activation of inflammatory genes
Also promotes IkBa synthesis (inhibitor)
Suppresses T cell activation

27
Q

Calcineurin inhibitor example and how it works

A

Cyclosporine
Binds cyclophilins
Inhibits Calcineurin phosphatase
Prevents IL-2 formation

28
Q

What are immunosuppressive drugs needed for

A

Transplantation
The require life long immuno suppression
Needs narrow therapeutic window

29
Q

Side effects of immunosuppressants

A

Poor wound healing
Coagulation disorders

30
Q

How do many auto immune diseases and cancers arise

A

Over expression of PDL
PDL tells PD1 on T cells to deactivate themselves
Evades immune system by not being recognised

PED2006 - Systems Pharmacology (19 decks)

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