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Pharmacology PED1003 > Inflammation and anti-inflammatories > Flashcards

Inflammation and anti-inflammatories Flashcards

1
Q

The local accumulation of fluid containing plasma proteins and white blood cells (WBCs)

A

Often non-specific (innate response)
Very dynamic (changing and different)
Local physiological response to injury
Responds to infection and cell death

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2
Q

An immediate response aims to…

A

Restrict damage or infection to a localised area.
Remove the causative agent and damaged tissue.
Promote immune cells (and molecules) access to the site to innate repair of damage tissue.

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3
Q

Innate: Non-specific defence mechanism - First line of defence

A

Skin
Mucous membrane
Secretions of the skin and mucous membranes

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4
Q

Innate: Non-specific mechanism - Second line of defence

A

Phagocytic white blood cells.
Antimicrobial proteins.
The inflammatory response.

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5
Q

Adaptive: Specific defence mechanism - Third line if defence

A

Lymphocytes

Antibodies

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6
Q

Cardinal signs of acute inflammation

A 
Heat (Calor)
Erythema (Rubor)
Oedema (Tumour)
Pain (Dalor)
Loss of function
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7
Q

Innate responses that induce actute inflammation

A
  1. Bacteria trigger macrophages to release cytokines and chemokines.
  2. Vasodilation and increased vascular permeability cause redness, heat and swelling.
  3. Inflammatory calls migrate into tissue, releasing inflammatory mediators that cause pain.
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8
Q

Key cells recruited during acute inflammation

A

Macrophage
Dendritic cells
Mast cells
Mostly neutrophils

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9
Q

4 stages of inflammation

A
  1. Tissue damage
  2. Vasodilation
  3. Cell recruitment (phagocyte migration and margination)
  4. Tissue repair - Clotting, annexin (lipocortin) and fibrin release. Fibrin lays down collagen (scars)
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10
Q

Overview of inflammation

A
  1. Damage leads to activation of sentinel cells (via complement or phagocytosis), releasing cytokines (TNF-α, IL-1β), chemokines (IL-8), histamine and prostaglandins.
  2. Vasodilation and vascular permeability (histamine). Exudate of complement and cells.
  3. Extravasation and chemotaxis (IL-8), further cell recruitment = swelling
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11
Q

Eicosanoids

A

Group of physiologically active lipid compounds.
Signalling molecules made by the enzymatic or non-enzymatic oxidation of arachidonic acid.
20 carbons in length
Prostanoids (prostaglandins and thromboxane)
Leukotrienes

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12
Q

Prostanoids formation

A

Membrane phospholipids + Phospholipase A2 ->
Arachidonic acid + Cyclo-oxygenase (COX) ->
Intermediate prostaglandin (PGH2) ->
Prostacyclin (PGI2) / Thromboxane (TXA2) / Prostaglandins(PGE2)

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13
Q

Prostacyclin (PGI2) induces…

A
  1. Vasodilation

2. Stops platelet activation

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14
Q

Thromboxane (TXA2) induces…

A
  1. Vasoconstriction

2. Activates platelets

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15
Q

Prostaglandins (PGE2) induces…

A
  1. Fever
  2. Pain
  3. Vascular permeability
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16
Q

Leukotrienes formation

A

Membrane phospholipids + Phospholipase A2 ->
Arachidonic acid + Lipooxygenase (LOX) ->
5-HPETE ->
Leukotrienes

17
Q

Leukotrienes induce…

A
  1. Inflammation

2. Chemotactic effect on neutrophils

18
Q

Dyspepsia meaning

A

Indigestion

19
Q

Eicosanoids formation

A

1

Membrane phospholipids + Phospholipase A2 ->
Arachidonic acid + cyclo-oxygenase (COX) ->
Intermediate prostaglandin (PGH2) ->
PGI2/PGE2/TXA2
#2
Membrane phospholids + Phospholipae A2 ->
Arachidonic acid + Lipooxygenase (LOX) ->
5-HPETE ->
Leukotrienes

20
Q

Drugs used to combat pain and inflammation

A

Antihistamines - Antagonists of the histamine receptors
NSAIDs - Non-steroidal anti-inflammatory drugs
Glucocorticoids - Steroidal anti-inflammatory drugs
Immuno-suppressants - Reduction of immune cell activation or response

21
Q

NSAIDs and non-opioid analgesics: Paracetamol

A

Analgesic and antipyretic activity.
No anti-inflammatory action
Liver damage on overdose

22
Q

NSAIDs and non-opioid analgesics: Ibroprofen

A

Short term analgesic and anti-inflammatory action.
Gastric irritation, increased rick of ulceration
FDA Cat. D drug

23
Q

NSAIDs and non-opioid analgesics: Aspirin

A 
Acetylates COX
Irreversible inhibitor
Anti-platelet activity
Increased risk of gastrointestinal bleeding and irritation
Bad for asthma patients
24
Q

NSAIDs and non-opioid analgesics: Celecoxib

A

Specific COX-2 inhibitor
Fewer side effects
Suggested increased risk of stroke and heart attack following use FDA Cat. D drug

25
Q

What do NSAIDs block? pg111

A

Cox-1 and Cox-2

26
Q

Cox-1

A

‘Housekeeper’
Performs many roles
Expressed widely
Unwanted responses (side effects) thought to be exerted mainly through Cox-1 isoform inhibition.

27
Q

Cox-2

A

Induced upon inflammation cell activation
Also in kidney and CNS
Anti-inflammatory, analgesic and antipyretic activity of NSAIDs thought to be exerted mainly by Cox-2 isoform inhibition.

28
Q

Glucocorticoid gene targets

A

Tyrosine aminotransferase immunosupressive.
Lipocortin, inhibition of eicosanoid generation.
NFkB regulated genes (including COX).
AP1 regulated genes - Wound healing, collagenase, vitamin c and d metabolism

29
Q

Natural glucocorticoids

A

Adrenocorticotrophic hormone (ACTH) stimulates production of natural glucocorticoid steroid hormones.
Increase in response to stress.
Increased production of cortisol.

30
Q

Synthetic glucocorticoids

A

Beclometasone (asthma inhaler)
Hydrocortisone cream
Prednisolone (allergies, skin infections)

31
Q

Cortisol (hydrocortisone)

A

Cortisol is a glucocorticoid
Prevents the release of inflammatory mediators
Inhibits TNF-α and Th1 cells
Switches towards Th2 immune response rather than general immunosuppression
Believed to be a protective mechanism which prevents an over-activation of inflammatory response

32
Q

Adverse effects of glucocorticoids

A

Cushings syndrome - build up of cortisol.
Latrogenic Cushings syndrome due to long-term high dose corticosteroid use.
Endogenous Cushings syndrome due to ACTH over-production in the body (rare).
Easy bruising, muscle wasting and atherosclerosis, euphoria, depression, psychosis, thinning skin, poor wound healing and hyperglycaemia.

33
Q

Analgesic meaning

A

A drug acting to relieve pain

Pharmacology PED1003 (18 decks)

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