PED1003/L21 Anti-Inflammatories Flashcards

1
Q

Define acute inflammation.

A

Local accumulation of fluid containing plasma proteins and white blood cells

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2
Q

Give 3 features of acute inflammation.

A

Non-specific
Very dynamic
Local physiological response to injury
Responds to infection and cell death

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3
Q

What is the aim of immediate inflammatory response? (3)

A

Restrict damage or infection to a localised area
Remove causative agent and damaged tissue
Promote immune cell (and molecules) access to the shite to initiate repair of damaged tissue

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4
Q

Give 3 cardinal signs of acute inflammation.

A

Heat
Erythema
Oedema
Pain

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5
Q

What are the innate responses to induce acute inflammation? (3)

A

bacteria trigger macrophages to release cytokines and chemokines
Vasodilation and increased vascular permeability cause redness, heat and swelling
Inflammatory cells migrate into tissue, releasing inflammatory mediators that cause pain

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6
Q

Give 4 key cells recruited during acute inflammation.

A

Macrophage
Dendritic cell
Neutrophil
Eosinophil
Basophil
Mast cell

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7
Q

What are the 4 main stages of inflammation?

A

Tissue damage
Vasodilation
Cell recruitment
Tissue repair

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8
Q

Describe the process of inflammation. (3)

A

Damage -> activation of sentinal cells via complement or phagocytosis, releasing cytokines, chemokines, histamine and prostaglandins
Vasodilation and vascular permeability -> exudate of complement and cells
Extravasation and chemotaxis -> further cell recruitment and swelling

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9
Q

What are eicosanoids? (2)

A

Group of physiologically active lipid compounds
Signalling molecules made by enzymatic or non-enzymatic oxidation of arachidonic acid

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10
Q

Give the 2 groups of eicosanoids.

A

Prostanoids
Leukotrienes

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11
Q

Describe how prostanoids are made. (3)

A

Membrane phospholipids -> arachidonic acid via phospholipase A2
Arachidonic acid -> intermediate prostaglandin via cyclo-oxygenase (COX)
I-prostaglandin (PGH2) -> prostacyclin (PGI2), prostaglandins (PGE2) or thromboxane (TXA2)

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12
Q

Give 3 functions of prostacyclin (PGI2).

A

Vasodilation
Stops platelet activation
Increased blood flow

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13
Q

Give 3 functions of prostaglandins (PGE2).

A

Fever
Pain
Vascular permeability

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14
Q

Give 2 functions of thromboxane (TXA2).

A

Vasoconstriction
Activates platelets

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15
Q

Describe leukotriene synthesis.

A

Phospholipid -> arachidonic acid via phospholipase A2
Arachidonic acid -> 5-HPETE via lipooxygenase (LOX)
5-HPETE -> leukotrienes

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16
Q

Give 2 functions of leukotrienes.

A

Inflammation
Chemotactic effect on neutrophils

17
Q

How does aspirin work?

A

Acetylates COX enzyme irreversibly

18
Q

How does celecoxib work?

A

Specific COX-2 inhibitor

19
Q

Describe synthesis of NSAIDs. (2)

A

Phospholipid -> Arachidonic acid via phospholipase A2
Arachidonic acid -> COX-1 or COX-2

20
Q

What is the function of COX-1?

A

Housekeeper

21
Q

What is the function of COX-2? (2)

A

Induced upon inflammatory cell activation
In kidney and CNS

22
Q

What is the function of tyrosine aminotransferase?

A

Immunosuppressive

23
Q

What is the function of lipocortin?

A

Inhibition of eicosanoid generation

24
Q

What is the role of NFkB regulated genes?

A

Involved in transcription

25
Q

What is the role of activator protein 1 regulated genes? (3)

A

Wound healing
Collagenase
Vitamin C & D metabolism

26
Q

Give 4 glucocorticoid gene targets.

A

Increased tyrosine aminotranferase & lipocortin
Decreased NFkB regulated genes & activator protein 1 regulated genes

27
Q

Adrenocorticotrophic hormone (ACTH) stimulates production of natural glucocorticoid steroid hormones in response to what? (2)

A

Stress
Increased production of cortisol

28
Q

Give an example of a manufactured glucocorticoid.

A

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

29
Q

Give 2 roles of cortisol in inflammation.

A

Prevents release of inflammatory mediators
Inhibits TNF-a and TH1 cells
Switches towards TH2 immune response to prevent over-inflammation

30
Q

Cushing’s syndrome is a result of build up on which hormone?

A

Cortisol

31
Q

Describe the difference between latrogenic and endogenous Cushing’s syndrome.

A

Latrogenic - due to long-term high dose corticosteroid use
Endogenous - due to ACTH over-production in body