Anti-inflammatories Flashcards

1
Q

What is COPD treated with?

A

β2 agonists
muscarinic antagonists
Corticosteroids

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2
Q

How is asthma characterised?

A

Shortness of breath, wheezing
Inflammation of airways
Bronchial hyper-reactivity
Reversible airway obstruction
Associated with over-active Th2 cells which activate interleukins and IgE which activate eosinophils and mast cells
Polymorphisms in β2 adrenoreceptors

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3
Q

What are some common asthma treatments?

A

Salbutamol
Steroids
Beta blockers

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4
Q

How is early phase allergic asthma characterised?

A

Reversible airway obstruction and inflammation

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5
Q

How is late phase allergic asthma characterised?

A

Mast cells in the lower respiratory tract being activated, releasing cytokines. This leads to leukocyte infiltration, causing inflammation

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6
Q

How is allergic rhinitis characterised?

A

Allergen activates mast cells in nasal mucosa
Nasal congestion

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7
Q

Where are histamine and prostaglandins released from?

A

Mast cells

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8
Q

What physiological effects do mast cell activation have?

A

Bronchoconstriction and increased vascular permeability from prostaglandins
Nerve endings stimulated for coughing
Decreased lung elasticity from mucus and increased collagen

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9
Q

What mechanism do NSAIDs have?

A

Cyclo-oxygenase inhibitors. Prevents prostaglandin and thromboxane production

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10
Q

What effects do NSAIDs have?

A

Decreases vasodilation and therefore odema
Analgesic and antipyretic
Inhibits prostaglandins and thromboxanes (these are very lipophilic)

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11
Q

What is the active ingredient of aspirin?

A

Acetyl salicilic acid

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12
Q

What side effects can aspirin have?

A

Gut irritation, leading to internal bleeding and diarrhea

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13
Q

What is COX1 responsible for?

A

Normal functioning. Constituitively expressed in most tissue. Responsible for platelet aggregation, renal blood flow and prostaglandins protecting the GI tract

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14
Q

How is COX2 characterised?

A

inducible and is used in inflammatory cytokines (IL-1 and tumour necrosis factor (TNFα)). Plays a role in renal homeostasis and the CNS

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15
Q

Where is COX3 found?

A

Brain and kidneys
Least well understood

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16
Q

What is the COX enzyme structure like?

A

2 identical subunits forming and dimer
Two catalytic sites:
Peroxidase site
Cyclo-oxygenase site

17
Q

How do the COX1 and COX2 binding sites differ?

A

COX-1 has Iso523
COX-2 has Val523 which makes a wider channel. This increases its specificity

18
Q

How does aspirin bind to COX enzymes?

A

Its acetyl group forms a bond with serine on the cyclo-oxygenase site. This permanently binds to COX, making it a suicide inhibitor.
Aracodonic acid can no longer enter the COX site

19
Q

What side effects can COX inhibitors have?

A

Gastric bleeding due to inhibition of prostagladins not secreting stomach acid
Disruption of renal flow due to prostaglandins being inhibited
Liver damage due to phase 1 of metabolism on paracetamol forming a cytotoxic intermediate

20
Q

How can inhibition of prostaglandins be treated?

A

Misoprostol (PG analogue)

21
Q

What are DMARDs used for?

A

Reducing joint damage, pain and inflammation in individuals with rheumatoid arthritis

22
Q

How does cyclosporin work as an immunosuppressant?

A

Decreases T cell proliferation by inhibiting IL-2 synthesis and IL-2 receptor expression

23
Q

What are the main side effects of cyclosporin?

A

Most serious side effect is nephrotoxicity
Hepatotoxicity and hypertension can also occur

24
Q

What is a syndrome developed from chronic prednisolone use?

A

Cushing’s syndrome

25
Q

What characterises Cushing’s syndrome?

A

Hypertension
Cataracts
Poor wound healing
Increased abdominal fat
muscle wasting

26
Q

How can monoclonal antibodies be used to treat inflammation?

A

Recognises TNFα and prevents it binding to its receptors
Humanised so that the antibody isn’t rejected
High affinity and selectivity for the target

27
Q

How does methotrexate treat rheumatoid arthritis?

A

folic acid antagonist with cytotoxic and immunosuppresant activity.

28
Q

Which rheumatoid arthritis drug is also used to treat chronic inflammatory bowel disease?

A

Sulfasulazin

29
Q

What does cyclosporine bind to in cytokine inhibition?

A

Calcineurin (dephosphorylates NFKB)

30
Q

What does glucocorticoid do in cytokine inhibition?

A

Inhibits NFKB transcription of cytokines