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Pharmacology > Overview of drug treatments of RA > Flashcards

Overview of drug treatments of RA Flashcards

1
Q

What are the 3 therapeutic targets of drugs for inflammatory arthritis?

A

Relieve symptoms

Avoid permanent joint damage

Reduce systemic complications of chronic inflammation

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2
Q

Give 4 symptoms of inflammatory arthritis?

A

Pain, swelling, fatigue, EMS

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3
Q

Give 2 systemic complications of chronic inflammation?

A

Anemia: lack of healthy RBCs

Amyloidosis: excess antibody buildup in form of amyloid (protein)

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4
Q

Why should physiotherapy be considered for systemic pain relief of RA?

A

Best to stay as active as possible, especially if there is severe joint damage

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5
Q

Why should occupational therapy be considered for systemic pain relief of RA?

A

Modifications can help when patient suffers from EMS, severe joint damage

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6
Q

What are the 2 main medications used when there is localised joint problems caused by RA?

A

NSAIDs, paracetamol

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7
Q

Give 3 organs that can suffer from harmful long-term side effects of NSAIDs?

A

Heart, kidney, GI tract

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8
Q

When can a local corticosteroid injection be administered for RA?

A

For one large joint only

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9
Q

Is local corticosteroid injection suitable for repeated use?

A

No, as this can cause toxicity

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10
Q

When is surgery appropriate for localised joint problems due to RA?

A

Very severe joint damage to extent that joint replacement is needed

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11
Q

What is the therapeutic effect of NSAIDs?

A

Decreases prostaglandin E2 and prostacylins

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12
Q

What is the analgesic effect of NSAIDs?

A

Decrease of prostaglandins makes nerves less sensitive to inflammatory mediators

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13
Q

What is the anti-pyretic effect of NSAIDs?

A

Decrease of IL-1

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14
Q

Why are NSAIDs described as imprecise targets?

A

They block COX enzymes which reduces too many prostaglandins, so causes ‘off-target’ bystander damage (side effects) as well as ‘on-target’ pain relief

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15
Q

How is decreased clotting a side effect of NSAIDs?

A

Platelet activity is decreased

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16
Q

How are peptic ulcers a side effect of NSAIDs?

A

Peptic ulcers form due to direct erosion of stomach lining and less protective mucus is produced due to decreased prostaglandins

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17
Q

How long does it take for local corticosteroids to start therapeutic effects after injection?

A

Few days

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18
Q

What is the condition caused as a side effect of long-term use of corticosteroids?

A

Osteoporosis

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19
Q

What are DMARDs?

A

Disease Modifying Anti Rheumatic Drugs

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20
Q

What is the main therapeutic effect of DMARDs?

A

Immunosuppressant drugs that suppress inflammation to prevent permanent joint damage and cartilage erosion

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21
Q

Why is bridging therapy used for DMARDs?

A

Bridging therapy provides rapid, effective inflammation suppression whilst waiting for administered DMARDs to take effect

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22
Q

Give one example of a bridging therapy used for DMARDs?

A

Corticosteroids

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23
Q

What DMARD are patients usually started on until RA progresses?

A

Methotrexate with steroids

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24
Q

Why is methotrexate the first-line drug for RA?

A

Very good efficacy and is the most established DMARD

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25
Q

What 4 factors are can be affected by methotrexate when considering drug safety?

A

Increased infection susceptibility
Liver toxicity
Folic acid antagonist
Lung damage

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26
Q

What bridging therapy is used for methotrexate?

A

Folic acid

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27
Q

When are folic acid and methotrexate administered?

A

Different days

28
Q

Does the patient need to be monitored regularly when they are taking methotrexate?

A

Yes, need to regularly do full blood count, test renal and liver function

29
Q

What makes patients suitable to take methotrexate?

A

No susceptibility/current/past liver or renal problems

30
Q

What drug does methotrexate interact with?

A

Trimethoprim

31
Q

Why can’t methotrexate be used with trimethoprim?

A

They both act on folic acid pathway and cause folate deficiency

32
Q

How can trimethoprim and methotrexate affect bone marrow when they are used at the same time?

A

Folate deficiency anaemia: Folate deficiency causes bone marrow to produce abnormally large RBCs, which are too big to enter bloodstream and those that do enter aren’t healthy

33
Q

What are the usual starting doses for methotrexate and folic acid, and when should they be administered?

A

Methotrexate: 7.5 mg on monday orally/subcutaneous injection

Folic acid: 5 mg on friday

34
Q

If the starting dose of methotrexate doesn’t provide adequate health benefits, how can the dosage be adjusted?

A

Titrate up to 20 mg over months

35
Q

What is the guideline for when to start use of TNF-alpha blocker agents?

A

At least 2 DMARDs (including methotrexate) were tried and ineffective for more than 6 months

36
Q

What drug is TNF-alpha blocker agent usually administered with for active RA?

A

Methotrexate

37
Q

How efficacious are TNF-alpha blocker agents?

A

Very good efficacy

38
Q

What 2 effects of TNF-alpha blocker agents should be considered in terms of safety?

A

Causes immunosuppression, reaction to injections

39
Q

What patients are suitable to take TNF-alpha blocker agents?

A

Patients who don’t have reactions to injections or infusions

It is also an expensive treatment

40
Q

What is the mechanism of infliximab?

A

Human-mouse monoclonal antibody that targets TNF-alpha, inhibiting inflammation

41
Q

Other than RA, what can infliximab be used to treat?

A

Psoriatic arthritis

42
Q

What is etanercept, and what is its mechanism of action?

A

Recombinant human TNF-alpha p75 Fc region fusion protein (produced from recombinant DNA)

Binds to TNF-alpha and inhibits it

43
Q

What 3 conditions can etanercept be used to treat, other than RA?

A

Ankylosing spondylitis
Juvenile idiopathic arthritis
Psoriatic arthritis

44
Q

What is the mechanism of action of adalimumab?

A

Human monoclonal antibody that binds to TNF-alpha

45
Q

What 2 conditions are treated with adalimumab, other than RA?

A

Ankylosing spondylitis
Psoriatic arthritis

46
Q

What type of drugs are used if TNF-alpha blocker agents fail?

A

Drugs that have other targets

47
Q

Give 5 examples of drugs used to treat RA after TNF-alpha blocker agents fail?

A

rituximab: acts on CD20

tocilizumab: acts on IL-6

golimumab

belimumab: inhibits B-cell activating factor

Janus Kinase (JAK) inhibitors: tofacitinib, baricitinib

48
Q

What does rituximab act on to treat RA?

A

CD20

49
Q

What does tocilizumab act on to treat RA?

A

IL-6

50
Q

What 2 drugs do patients usually try before taking belimumab?

A

Hydroquinone, corticosteroids

51
Q

What other condition is belimumab used to treat, other than RA?

A

SLE

52
Q

Give 2 examples of JAK inhibitors that are used to treat RA?

A

Tofacitinib, baricitinib

53
Q

Why are JAK inhibitors more convenient than other biologics in terms of administration?

A

Most biologics are administered by IV or IM, but JAK inhibitors can be given orally

54
Q

Why are corticosteroids very good and efficacious immunosuppressants?

A

They have multiple target sites

55
Q

How does Cushing’s disease occur?

A

Cortisol excess due to very slow tapering/withdrawal of corticosteroids

56
Q

What are the symptoms of Cushing’s disease?

A

Osteoporosis, obesity, moon face, buffalo hump, hypertension, hyperglycemia, striae, myopathy, psychiatric, hypokalemia

57
Q

What is the buffalo hump, seen in Cushing’s disease?

A

Excess fat buildup behind neck, which is the dorsal cervical fat pad

58
Q

What is the moon face, seen in Cushing’s disease?

A

Extra fat buildup on sides of face so that face looks round

59
Q

In Cushing’s disease, where does obesity typically present in the body?

A

Truncal obesity (concentrated in center of body rather than extremities)

60
Q

How does Addison’s disease occur?

A

Cortisol deficiency due to very fast tapering/withdrawal of corticosteroids

61
Q

What are the symptoms of Addison’s disease?

A

Nausea, vomiting, headache, joint pain, fever, hypoglycemia, hypotension, hyperkalemia

62
Q

Which 2 corticosteroids are injected into a single painful joint?

A

Triamcinolone, methylprednisolone

63
Q

Which corticosteroid is given orally in acute flare ups, and what is the dosage and duration?

A

30mg prednisolone given orally daily for 2 weeks

64
Q

What 2 corticosteroids are given in severe flare ups, and what is the route of administration?

A

Hydrocortisone, methylprednisolone given intravenously

65
Q

Can corticosteroids be administered as topical formulations?

A

Yes, different formulations have different strengths

Pharmacology (11 decks)

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