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AAI: Pharmacology + Biology > Arthritis > Flashcards

Arthritis Flashcards

(40 cards)

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1
Q

Is Rheumatoid arthritis organ specific?

A

It’s Non-organ specific

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2
Q

What is osteoarthritis?

A

Caused by wear and tear of joints causing inflammation

Non-inflammatory disorder (use of synovial joints)

Characterised by cartilage loss

Affects knees, hips + small hand joints

Link to obesity

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3
Q

Describe the pain in osteoarthritis

A

Worsened by movement

Eased by rest

Worse at the end of the day

Commonly affects:

  • hands
  • knees
  • spine
  • hips

Unilateral (affect only one joint e.g. left hand only)

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4
Q

What are the treatment options for OA?

A

Steroid injections

NSAIDs / Cox-2 inhibitors

Surgery - knee replacement

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5
Q

Mechanism of NSAIDs

A

NSAIDs inhibit COX enzyme

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6
Q

NSAID use in Osteoarthritis treatment

A

In Arthritis, NSAIDs block cyclooxygenase enzymes (particularly COX-2) which reduces inflammation, pain + stiffness

COX enzymes convert arachidonic acid to prostaglandins

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7
Q

How + when do we take corticosteroids injections + what drugs are used

A

Intra-articular (into joints)

When pain is moderate to severe

Drugs:

  • triamcinolone
  • methylprednisolone

Can cause cartilage injury + loss

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8
Q

What is Rheumatoid Arthritis?

A

Autoimmune disease in which the body’s immune system attacks the joints causing chronic inflammation.

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9
Q

Signs of RA

A

Joint damage

Muscle wastage

Deformity

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10
Q

Symptoms of RA

A

Pain

Stiffness

Joint swelling

Joint deformity

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11
Q

Blood lab tests for RA

A

WBCs = INCREASED

Erythrocyte sedimentation rate (speed at which your red blood cells clump and fall together to the bottom of a glass tube within an hour) = INCREASED

Anaemia

Rheumatoid factor (group of proteins your body creates when your immune system attacks healthy tissue - Antibodies to IgG) = INCREASED

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12
Q

Risk factors of RA

A

Age

Gender - women developing premenopausal

Post-partum

Stress

Genetics - if one twin has, the other is 20% likely

Smoking

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13
Q

Describe the pain in Rhematoid Arthritis

A

Improves movement

Worse on waking

Affects small joints

Affects bilateral joints

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14
Q

What is Rheumatoid disease?

A

Systemic disease (affects many organs or body as a whole) that affects:

  • Especially at the joints
  • Eyes inflammed (50%)
  • Skin
  • Vasculitis - destroy group of blood vessels
  • Lungs
  • Salivary glands (reduced)
  • Pericarditis (inflammation of pericardium)
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15
Q

What are the type of treatment options for RA?

A

Symptomatic relief

  • Analgesia to reduce need for NSAIDs
  • NSAIDs (+ PPI)

Slow progression

  • DMARDs
  • Steroids
  • Biologicals

Monitor effectiveness

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16
Q

Function of DMARDs

(Disease modifying anti-rheumatic drugs)

A

Directly inhibits cell proliferation

(inhibit wide variety of cytokines including interleukins, interferons + TNFalpha)

Slow-acting (may take months for benefits to become apparent)

No analgesic activity

Used for rheumatic disorders + where inflammation does not respond to COX enzyme inhibitors

Slows course of disease

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17
Q

Treatment lines of DMARDs

Study These Flashcards
A

1st LINE - Start w/ combination therapy (MTX + 1 other DMARD)

2nd LINE - Mono therapy w/ rapid dose titration

Slow onset of action - take up to 3 months

Used with glucocorticoids until effective (shouldn’t be used long term)

18
Q

Counselling points when using DMARDS

Study These Flashcards
A

Dose increased gradually

Improvement takes a few months

Monitoring is necessary

Nausea

Signs of:

  • Blood dyscrasias (formed elements in blood) = sore throat, tiredness
  • liver toxicity = jaundice
  • lung toxicity

Bone toxicity

Perform LFTS, FBC + U+E before + during treatment

19
Q

What are the drugs in DMARDs?

Study These Flashcards
A

Methotrexate = 1st choice

Sulfasalazine

Leflunomide

IM gold

20
Q

Function of Methotrexate

Study These Flashcards
A

Dihydrofolate reductase inhibitor

(pyrimidine synthesis = inhibits DNA/RNA synthesis)

Immunosuppressant

Commonly used

Dose - 7.5-25 micrograms

Weekly dosing

21
Q

What causes autoimmune diseases

Study These Flashcards
A

Autoimmune diseases is when your immune system attacks its own cells

Leads to tissue damage

Genetic factors can influence it

Can be influenced by pregnancy, infection, diet + environment

22
Q

When do you start on DMARDs?

Study These Flashcards
A

Within 3 months

23
Q

When do we reduce dose of DMARDs?

Study These Flashcards
A

Reduce to a dose when symptom control has been achieved

24
Q

What do patients need to take with Methotrexate

Study These Flashcards
A

Folic acid

To prevent side effects

Folic acid does not prevent inflammatory effects of methotrexate

25
Name other mechanisms of methotrexate in rheumatoid arthritis
Folic acid antagonism Cytokine alteration Adenosine signalling Generation of reactive oxygen species Effects of eiocosanoids + matrix metalloproteases Effects of methyl donors
26
Counselling points of MTX
**WEEKLY DOSE** Take **folic acid** as directed = **ONCE WEEKLY** but **not** on the **same day** as **MTX** **Regular** blood tests Recognise + **report** signs of serious side effects **Contraception** = **avoid pregnancy** due to birth defects Patients given **patient information book** about MTX Injectable methotrexate - cytotoxic, sharps bin, disposal etc
27
ADME of Methotrexate
Absorption **unaffected** w/ age **Decreased** metabolism + excretion w/ age **Increased risk** of toxic effects NSAIDs interaction - avoid OTC - renal toxicity - reduced excretion of MTX
28
What is Sulfasalazine (SFZ)?
**Immunosuppressant** 500mg OD **Increased weekly** - max. 2-3 grams per day in divided doses Onset of action is 6 weeks
29
What are the side effects of Sulfasalazine?
GI intolerance - nausea + vomiting Blood disorders - bruising + unexplained bleeding Discolouration of urine + contact lenses (happen in the first 3-6 months)
30
Function of Leflunomide
**Immunosuppressant** Metabolised to **teriflunomide** Inhibits **dihydroorotate dehydrogenase** (involved in pyrimidine synthesis, inhibiting DNA synthesis)
31
What are the adverse effects of Leflunomide?
Diarrhoea Nausea, rash, alopecia Abnormal LFT Teratogen * contraception including male treatment * additional 2 years post stopping treatment * present in breast milk
32
Function of Hydroxychloroquine
Used in mild/moderate cases Alternative 1st line drug **Inhibit lymphocyte function** Long half life
33
Function of Gold
**Immunosuppressant** e. g. **sodium aurothiomalate** (deep intramuscular) e. g. **auranofin** (oral) **2nd/3rd** line treatment Weekly until response Rashes, blood disorders
34
Other types of DMARDs
Pencillamine - penicillin metabolite Cyclosporine - T-cell function (severe RA) Azathioprine - inhibit purine synthesis Only relieve symptoms - do not modify disease progression so less used
35
Describe the use of Steroids in RA
Used orally for flare/exacerbations of RA Bridging therapy = between starting/switching to reduce symptoms (rapid symptom control) IM, IA, IV (IV can be toxic)
36
What are the oral steroids used in RA?
**Prednisolone** Can't be used long term Side effects: * osteoporosis = bone protection * PPI`(for long-term therapy)
37
Anti-TNFalpha therapy in RA
**Block TNFα which reduce inflammation and joint damage** Licensed for moderate-severe RA where response to other DMARDs is inadequate Alone/w/MTX MONOCLONAL ANTIBODIES Adalimumab - 40mg SC alternate weeks Infliximab - 3/mg/kg IV @2,6 then 8 weeks Etanercepts - 25mg SC TWICE WEEKLY
38
Name a interleukin-1 inhibitor used for RA
**Anakinra** = IL-1RI antagonist IL-1 = pro-inflammatory cytokine which mediates many cellular responses including synovial inflammation (joints) **Injection** site reactions **NICE rejected due to weak efficacy**
39
Name a new drug for use in RA
**Tofacitinib** **Janus Kinase inhibitor** Janus kinase involved in cytokine signalling + gene transcription **NICE accepts if price reduces**
40
What is Abatacept?
Drug used to treat autoimmune diseases e.g. rheumatoid arthritis This is by blocking B7 binding to CD28 NICE not recommended due to cost

AAI: Pharmacology + Biology (11 decks)

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