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Pharmacology > 19 - Inflammation & Anti-Inflammatories > Flashcards

19 - Inflammation & Anti-Inflammatories Flashcards

1
Q

Macrophages release what in response to bacteria…

A

Cytokines and chemokines

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2
Q

Cytokines and chemokines released by macrophages lead to…

A

Vasodilation and increased vascular permeability

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3
Q

After vascular permeability has increased, inflammatory cells…

A

Migrate into tissues leading to further release of inflammatory mediators than cause pain

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4
Q

Outline the timeframe of inflammatory response

  1. 0-12 hrs
  2. 6hrs-5 days
  3. 12hrs-4 days
  4. 5-7 days
A

Outline the timeframe of inflammatory response

  1. 0-12 hrs - microvascular events
  2. 6hrs-5 days - accumulation of inflammatory cells
  3. 12hrs-4 days - systemic effects
  4. 5-7 days - healing

(Inflammatory mediators are relased throughout)

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5
Q

Which cell type is involved in local inflammation?

A

Mast cells

When activated granules are released containing inflammatory mediators

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6
Q

The process of inflammatory inititation comprises two paths…

A

One mediated by vasoactive mediators, the other by chemotactic factors (both are inflammatory mediators)

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7
Q

Outline the path of inflammatory initiation via vasoactive mediators…

A
  1. Vasoactive mediators
  2. ↑ vascular permiability + arteriole dilation ⍟ + venule constriction ⌾
  3. Oedma
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8
Q

Outline the path of inflammatory initiation mediated by chemotactic factors…

A
  1. Recruitment and stimulation of inflamatory cells
  2. Chronic and acute inflammation
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9
Q

The characteristics of inflammed tissue can be remembered using the phrase ‘Calor, dolor, rubor, tumor’ which translates as…

A

Heat, pain, redness and swelling

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10
Q

Resolution of inflammation

Step 1

In response to inflammation which four ‘clean up’ proccesses intially occur?

A
  • Pathogen clearence
  • Wound sealing (clotting, fibrin)
  • Irritant removal
  • Liportin (Annexin A1) release
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11
Q

Annexin A1 triggers removal of _____ _____ and the replacement of lost _____ __________.

A

Annexin A1 triggers removal of nercrotic debris and the replacement of lost healthy tissue.

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12
Q

If fibrin can’t be removed the result is…

A

Scarring

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13
Q

Eicosonoids are signalling molecules with an ___________ structure

A

Eicosonoids are signalling molecules with an icosohedral (20 sided/ 20 carbon) structure

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14
Q

Eicosonoids are __ carbon fatty acids derived from ________ ____

A

Eicosonoids are 20 carbon fatty acids derived from arachidonic acid

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15
Q

PAF (platelet activating factor) is derived from:

a) Prostanoids
b) Phospholipids
c) 20 carbon fatty acids
d) Leukotriene

A

PAF (platelet activating factor) is derived from:

a) Prostanoids

b) Phospholipids

c) 20 carbon fatty acids
d) Leukotriene

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16
Q

Which 20 carbon fatty acid is the precursor for inflammatory molecules (eicosonoids)?

A

Arachidonic acid

17
Q

COX converts PGH2 into…

A

Prostacyclin and thromboxase

18
Q

Cyclic endoperoxidases make a good…

A

Upstream drug target against inflammation (as it is responsible for production of prostacyclin and thromboxane)

19
Q

State 4 approaches to reducing inflammation…

A
  • Immunosuppresion (prevent the response)
  • Antipyretic (reduce local temperature)
  • Analgesic (reduce local pain)
  • Reduce fenestration of blood vessels
20
Q

Name the 4 main classes of anti-inflammatory drugs…

A
  1. Antihistamines
  2. NSAIDs
  3. Glucocoritcoids
  4. Immunosuppresants
21
Q

Give 4 examples of analgesics and state any other relevant properties (such as anti-inflammatory) that they may have…

A
  • Ibruprofen* - anti-inflammatory
  • Paracetamol - antipyretic
  • Aspirin* - irreversible COX inhibitor, anti-platelet activity
  • Celecoxib* - specific COX2 inhibitor

*NSAIDs

22
Q

The two main known cyclooxegenase (COX) enzymes are…

A

COX1 and COX2

23
Q

COX1 is…

a) found mainly in the kidney and heart
b) thought to be the source of NSAID activity
c) found mainly in the liver and the GI tract
d) Thought to be the source of NSAID side effects

A

COX1 is…

a) found mainly in the kidney and heart
b) thought to be the source of NSAID activity
c) found mainly in the liver and the GI tract

d) Thought to be the source of NSAID side effects

(as it is widely expressed)

24
Q

Rofecoxib is a…

A

Specific COX2 inhibitor which was taken off the market due to evidence of increased (x2) risk of heart attack and stroke

25
Q

COX 2 is induceable and found mainly in the…

A

Kidney and heart

26
Q

Inhibiting COX enzymes inhibits the production of…

A

Prostacyclin and thromboxase

27
Q

5-lipoxygenase is a good drug target as it…

A

Preceeds many downstream targets

28
Q

The exact mechanism of NSAIDs is unknown, however it is thought that inhibition of _______ is the source of their activity.

A

The exact mechanism of NSAIDs is unknown, however it is thought that inhibition of COX 2 is the source of their activity.

29
Q

Glucocorticoids exhibit a direct effect on:

a) G-Proteins
b) Gene expression
c) Ionotropic receptors
d) Post-translational modification of proteins

A

Glucocorticoids exhibit a direct effect on:

a) G-Proteins

b) Gene expression

c) Ionotropic receptors
d) Post-translational modification of proteins

30
Q

Glucocorticoids exhibit two overall effects…

A

Immunosuppression and anti-inflammatory

**(Immunosuppressive effects lead to reduced eicosanoid production, which reduces inflammation)

31
Q

Outline how the immunosuppresive effects of glucocorticoids lead to its anti-inflammatory properties…

A
  • Immunosuppresive effect
    • reduces phospholipids & increases lipocortin synthesis = reduced phospholipase activity
    • reduces COX transcription
  • These factors reduce eicosanoid production, which reduces inflammation
32
Q

Glucocorticoids enter cells and bind to intracellular glucocorticoid (GR) receptors. This results in repression or increase in transcription of specific genes.

Outline the typical changes which occur…

A
  • Increases in tyrosine aminotransferase and lipocortin (annexin)
  • Decreases in AP1 genes (wound healing, collegenase) and NFkB genes (including COX)
33
Q

Adverse effects of glucocorticoid therapy include Cushing’s Syndrome. Describe some of the symptoms…

A
  • Moon face
  • Purple striae
  • Buffalo hump
  • Mood changes (euphoria, depression, psychosis)
  • Poor wound healing, bruising
  • Hyperglycaemia

Pharmacology (23 decks)

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