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Pharmacology > Anti-inflammatories > Flashcards

Anti-inflammatories Flashcards

1
Q

What are NSAIDs?

A

Non-steroidal anti-inflammatory drugs

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2
Q

How do NSAIDs work?

A

Inhibiting the production of inflammatory mediators such as prostaglandins and thromboxanes

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3
Q

What are inflammatory mediators?

A

Paracrine mediators made by one cell and locally effect another
Lipophillic so easily diffuse out of cells and bind to receptors on the cell surface

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4
Q

What are the receptors on cell surfaces that inflammtory mediators bind to?

A

Cyclo-oxygenases (COX)

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5
Q

What is the pathway that NSAIDs inhibit?

A

Phospholipase A2 generates precursor needed for everything
Arachidonic binds with COX which forms prostaglandins and thromboxanes

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6
Q

What do prostaglandin antagonists do?

A

Reduces swelling and redness as it is a vasodilator

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7
Q

What are thromboxanes?

A

Lead to blood clotting and vasoconstriction
Attract immune cells to the affected areas

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8
Q

What are the anti-inflammatory effects?

A

Decreasing vasodilation and therefore oedema

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9
Q

What are NSAIDs ineffective against?

A

Mediators that contribute to tissue damage associated with chronic inflammatory conditions

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10
Q

How are NSAIDs antipyretic? Why is this needed?

A

Lower raised temperatures
Thermostat in the hypothalamus is activated by IL-1 induced COX2 production of PGE

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11
Q

How are NSAIDs anagelsic?

A

Reducing certain sorts of pain by decreasing the production of prostaglandins in damaged and inflamed tissue which sensitises nociceptors

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12
Q

COX1

A

Enzyme repsonsible for the production of prostaglandins which have normal homeostatic functions- consitutive expression

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12
Q

COX2

A

Enzyme responsible for the protective and immune functions that cause inflammation- inducible expression

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13
Q

COX3

A

Variant of COX1 found in the brain and the kidneys, isn’t as widespread but is thought to be a target for paracetamol

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14
Q

COX structure

A

Made up of two identical subunits each with two catalytic sites
Only very small differences between the 3 isoforms

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15
Q

What is the difference in structure between COX1 and COX2?

A

Isoleucine in COX1 is replaced by valeine in COX2
As they are different sizes drugs can be made to be selective to one or the other

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16
Q

WHy can NSAIDs cause gastric disturbances?

A

Prostaglandins play a key role in maintaining the mucus layer of the mucus layer of the stomach so can cause stomach ulcers

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17
Q

How does aspirin work?

A

Binds covalently to Serine residue in COX which prevents arachidonic acid from reaching the COX site

18
Q

What gut side effects are caused by NSAIDs?

A

Dyspepsia, diarrhoea, nausea, vomiting, gastric bleeding, ulceration

19
Q

How can renal function be effected by NSAIDs?

A

Renal failure as prostaglandins maintain renal blood flow

20
Q

Aspirin

A

Anti-platelet action (anit-thrombotic) and a weak acid
Reduced risk of colonic and rectal cancer, alzeimhers
Rapid and efficient absoprtion in the ileum
Suicide inhibitor so is irrversible

21
Q

Paracetamol

A

Analgesic, antipyretic, in the CNS but a weak anti-inflammatory
COX3/1 selective
Well absorbed and metabolised in the liver
Less side effects than aspirin with long term use but large doses increases kidney damage
Competitive inhibitor

22
Q

Other side effects of NSAIDs

A

Liver damage, bronchospasm and asthma attacks and skin rashes

23
Q

What does rhematoid athritis effect?

A

Joints, inflammation of synovium, erosion of cartilage and bone
Increases mortality by an increased risk of cardiovascular disease such as heart attacks and strokes

24
Q

Symptoms of rheumatoid athritis

A

Joint swelling, pain, morning joint stiffness, poor sleep, fatigue, loss of weight, flu like symptoms

25
Q

What are the most common drugs used to treat RA?

A

DMARDs halt or reverse disease
NSAIDs only treat symptoms

26
Q

What are DMARDs?

A

Disease modifying anti-rheumatic drugs
Mixed group of drugs with different mechanisms of action but are slow in clinical onset

27
Q

What is penicillamine?

A

(D isoform only) Metabolite of penicillin that may decrease generation or synthesis of collagen and is also used as a heavy metal chelator in poisoning

28
Q

Drugs used to treat rhematoid arthritis

A

Low doses of methotrexate
Sulfasalizine
Penicillamine
Immunosuppressant drugs

29
Q

What drugs are immunosuppressant? How do they work?

A

Cyclosporin and Glucocorticoids
Inhibit the induction phase of the inflammatory response by inhibiting transcription of proinflammatory cytokines

30
Q

How does cyclosporin prevent transplant rejection?

A

Inhibits IL-2 synthesis and decreases proliferation of T cells
Binds to cyclophillin immunophillin which then binds to calcineurin to prevent activation/signalling via transcription factors

31
Q

What are biopharmaceuticals?

A

New anti-cytokine or anti-inflammatory drugs that work via humanized monoclonal antibodies
High affinity and selectivity for their target, and long half life

32
Q

How do biopharmaceuticals work as anti-inflammatories?

A

By neutralising the action of either soluble or membrane bound proinflammatory cytokines

33
Q

What is used to treat COPD?

A

B2 agonists, muscarinic antagonists and corticosteroids

34
Q

What is associated with reduced efficacy of bronchodilators?

A

Polynorphisms in B2-adrenoceptors

35
Q

What is used to treat asthma?

A

Bronchodilators such as salbutamol
Anti-inflammatory agents such as prednisolone and omalizumab

36
Q

What is allergic rhinits/ respiratory allergy?

A

When an allergen activates mast cells in nasal mucosa and conjunctivae
Nasal conjestion, sneezing and allergic conjunctivitis

37
Q

What is allergic asthma?

A

When an allergen activates mast cells in the lower respiratory tract causing early/immediate phase reactions and late phase reactions

38
Q

What are late phase reactions in allergic asthma?

A

Occur in 50% of patients
When cytokines cause leukocyte infiltration which leads to inflammation
Some develop chronic asthma due to chronic inflammation causing tissue damage

39
Q

What are early/immediate phase reactions in allergic asthma?

A

Reversible airway obstruction and inflammation

40
Q

Overactivity in what cells is also associated with asthma?

A

Th2 cells

41
Q

How are mast cells key mediators of type 1 hypersensitivity reactions?

A

Smooth muscle contraction, increased vascular permeability, mucous secretion, platelet activation, stimulation of nerve endings, and recruitment and activation of eosinophils

42
Q

What pathophysiology is associated with chronic inflammation of the airways?

A

Dilated blood vessels, thickened basement membranes, mucus plug with eosinophils and desquamated epithelial cells, oedema, hypertrophied smooth muscle and infiltration of inflammatory cells

43
Q

Salbutamol

A

B2 agonist
Dilates airways

Pharmacology (5 decks)

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