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Applied Pharmacology bs > Arthritis Treatments > Flashcards

Arthritis Treatments Flashcards

1
Q

When seeing itis what does it refer to?

A

Inflammation

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2
Q

which type of arthritis most commonly effects small joints first (such as hands and feet)?

A

rheumatoid arthritis

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3
Q

Osteoarthritis is a disease affecting which kind of joints?

Give an example of these.

A

synovial joints

eg. Wrist, elbow, shoulder, knee, fingers, feet, spine

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4
Q

What is osteoarthritis is characterised by?

A

loss of cartilage and bone from articulating surfaces

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5
Q

What type of arthritis does cartilage get worn away and there are changes in protein structure of the cartilage?
What happens as a result of this?

A

osteoarthritis

  • cartilage layer becomes thin
  • bone underneath grows to fill where cartilage was
  • results in bones spurs
  • bones rub together and changes the shape of the joint …making deformities
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6
Q

What are the risk factor groups for osteoarthritis?

A
  • obesity
  • over 40 years old
  • females more prone
  • genetics eg. Collagen gene mutation
  • previous joint injury/disease
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7
Q

What are the negative effects of histamine and bradykinin?

A
  • Increased permeability of venules = oedema

- Increased sensitivity to c fibres (PAIN)

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8
Q

Name 5 examples of NSAIDs.

A 
Aspirin
Ibuprofen
Diclofenac
Meloxicam
Indomethacin
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9
Q

What are the effects of NSAIDs?

A

Antipyretic (prevent or reduce fever)
- inhibits actions on PG’s on hypothalamus
Analgesic
- reduce sensitivity of neurones to bradykinins
- effective against pain of muscular/skeletal origins
Anti-inflammatory
- reduce vasodilation and decrease permeability of venules
-May scavenge oxygen radicals - decrease tissue damage
-

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10
Q

How do NSAIDs reduce pain?

A

Blocking COX - 1 and COX-2. Stops your body producing as many prostaglandins

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11
Q

What is a specific action of aspirin?

A

Aspirin – inhibits NFκB expression → ↓ transcription of genes for inflammatory mediators

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12
Q

What are the side effects of NSAIDs?

A

Risk of gastric ulcers
Impair coagulation
Use with caution in elderly (GI bleeding can be serious/ fatal)
Risk of CV events in patients with cardiac disease/ hypertension
May induce asthma attack, angioedema, urticaria or rhinitis

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13
Q

Why is their a risk of gastric ulcers and CV events when using NSAIDs?

A
  • NSAIDs may block COX 1 as well as COX 2
  • PGs produced by COX1 are involved in many beneficial processes:
  • Production of GI mucus (protective)
  • Blocking ↑ risk of ulcer
  • Cardiovascular function : PGs (e.g. PGI2) inhibit platelet aggregation
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14
Q

What are examples of NSAIDs that are believed to be specific to blocking COX 2 only?

A

E.g.
- meloxicam
- But rofecoxib (early COX-2 inhibitor) withdrawn, as some patients died from CV complications (↓ PGI2 → platelet aggregation?)
- celecoxib
- etoricoxib
Used mainly in patients at high risk of serious GI side effects (but with little CV risk*)

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15
Q

What are some of the common side effects of celecoxib and etoricoxib?

A

headaches,
dizziness
skin rash
peripheral oedema

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16
Q

Misoprostol is a synthetic prostaglandins what is it used for?

A

Used alongside NSAIDs
preserves mucous lining of GI tract
protects against ulceration
also used to induce abortion

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17
Q

What are the side effects of misoprostol?

A
  • diarrhoea (can be severe),
  • vaginal bleeding
  • Precautions in women of childbearing age!
  • Proton Pump Inhibitors (e.g. omeprazole) as reduces acid secretion
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18
Q

What are the actions of misoprostol?

A

Inhibits gastric acid secretion and may stimulate increased mucus production.

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19
Q

Why should aspirin be used with caution with warfarin?

A
  • its rapidly absorbed in stomach
  • displaces warfarin bound to plasma proteins
    ie. increase plasma warfarin and potentiates warfarin’s anti-coagulation activity as warfarin is not active until free from plasma proteins.
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20
Q

What is the difference between paracetamol and NSAIDs ?

A
  • paracetamol has no anti-inflammatory effect

- actions may involve COX but in CNS (COX3?)

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21
Q

What are the side effects of paracetamol ?

A
  • Few side-effects
  • Chronic use of large doses → kidney damage
  • Toxic doses (10 – 15g) → potentially fatal liver damage (occurs 24 – 48hr after O.D.)
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22
Q

What are the treatment options for osteoarthritis ?

A
  • weight loss
  • exercise - strengthens core muscles/ improves aerobic fitness
  • suitable footwear and pacing
  • joint supports or braces
  • thermotherapy/ TENs device
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23
Q

What drugs are used to treat osteoarthritis?

A
  • Paracetamol – regular dosing ± oral NSAID (with PPI*)
  • Topical NSAID or capsaicin (esp knee/ hand)
  • Opioid analgesic – for further relief
  • Intra-articular corticosteroid injection → temporary benefit
  • Joint replacement surgery (hip, knee, ankle)
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24
Q

What are the actions of strontium ranelate used to treat osteoarthritis?

A
  • promotes osteoblast differentiation/ inhibits osteoclast activity*
  • reduces pain*
  • Indicated for prevention of fractures in severe osteoporosis (OP)
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25
What are the side effects of strontium ranelate used to treat osteoarthritis?
- Found to increase risk of MI and thrombotic events so only used to treat server osteoarthritis
26
What are the actions and negatives of glucosamine sulphate?
- major constituent of ECM - Present in cartilage + synovial fluid - Demonstrated positive effects both in vitro + in vivo (animal models) - Differing results from clinical trials – measured pain and structural improvement - Overall no sig benefit but poss long-term side effects - Not recommended by NICE!
27
Rheumatoid arthritis causes ... | this leads to?
``` - Causes joint inflammation, especially: Synovial membrane Tendon sheaths Bursae* - Leads to proliferation of synovial membrane + erosion of cartilage/ bone ```
28
Which type of arthritis is an autoimmune disease?
rheumatoid arthritis
29
What are the symptoms of rheumatoid arthritis?
Symptoms presented – - usually a throbbing and aching sort of pain. Often worse in the mornings and after resting, not after activity. - Stiffness - especially in the morning. Rheumatoid arthritis morning stiffness usually lasts longer than half an hour (i.e. longer than O.A.) - Warmth and redness – affected joint hot, tender to touch and painful + inflammation around the joints, such as tear glands and salivary glands.
30
What are the treatment options in rheumatoid arthritis?
``` Treatment of pain: - NSAIDs - opioid analgesics Limitation of joint damage: - Glucocorticoids - Immunosuppressants - Disease Modifying Antirheumatic Drugs (DMARDS) - Anticytokines ```
31
Where are Glucocorticoids naturally found in the body?
made by your adrenal glands
32
Why are glucocorticoids used for short term treatment in rheumatoid arthritis?
- manage flare-ups | - as they rapidly reduce inflammation
33
Why are glucocorticoids used for long term treatment in rheumatoid arthritis?
if other treatment options failed - must discuss complications
34
What are the actions of glucocorticoids?
- metabolic effects - Increase breakdown of protein and fat to release glucose - anti-inflammatory - inhibit production of inflammatory mediators - immunosuppressive - inhibit NF-B which is necessary for activation of immune cells (B cells) and synthesis of cytokines.
35
What are the actions of Mineralocorticoids?
water & electrolyte balance - Aldosterone – increased reabsorption of Na and H2O in collecting duct/ DCT – inc bp.
36
A short acting steroid lasts between 1-12 hours. Give examples of these.
Cortisone/ hydrocortisone | Twice daily cream or intra-articular injection
37
An intermediate acting steroid lasts between 12 - 36 hours. Give examples of these.
Prednisolone | Daily oral or intra-articular injection
38
Long acting steroids last between 36-55 hours. Give an example of these.
Dexamethasone | Intra-articular injection every 3 - 21 days
39
What are the actions of glucocorticoids in rheumatoid arthritis?
anti-inflammatory, immunosuppressant actions: ↓ transcription of pro-inflammatory cytokines (e.g. IL-2) ↓ circulating lymphocytes inhibit phospholipase A2 → ↓ release of arachidonic acid……………. ↑ synthesis of anti-inflammatory proteins (e.g. protease inhibitors)
40
What are the unwanted side effects of corticosteroids?
- moon face - increased abdominal fat - Thinning of skin - increased risk of infection - poor wound healing - muscle wasting - osteoporosis - hypertension - buffalo hump
41
How can you reduce the side effects of corticosteroids?
- lower plasma concentration | - choose specific route of administration to achieve this
42
What are the dangers of stopping steroids abruptly?
Cause suppression of normal steroid synthesis - due to excessive negative feedback - may precipitate acute adrenal failure - Patients should carry steroid card
43
Name examples of Disease Modifying Antirheumatoid Drugs (DMARDs)
Sulfasalazine, gold compounds, penicillamine, immunosuppressants (e.g. methotrexate, ciclosporin, azathioprine, leflunomide), anticytokines
44
Why are DMARDs used?
- to slow onset of rheumatoid arthritis | -
45
What is the first choice of DMARDs drug used in the UK?
Sulfasalazine
46
What is sulfasalazine a mixture of ?
Complex of salicylate (NSAID) + sulphonamide (antibiotic)
47
How is sulfasalazine thought to act?
- by scavenging free radicals produced by neutrophils | - Causes remission in ‘active’ R.A.
48
What are the side effects of sulfasalazine?
GI upset, headache, skin reactions, leukopenia
49
Penicillamine is produced by
hydrolysis of penicillin
50
What are the actions of penicillamine?
Thought to ↓ IL-1 generation + ↓ fibroblast proliferation → ↓ immune response
51
How is sulfasalazine administered?
Given as enteric-coated tablets (poorly absorbed orally)
52
How is penicillamine administered?
orally
53
What are the side effects of penicillamine ?
rashes, stomatitis (40% patients); anorexia, taste disturbance, fever, n & v
54
What should penicillamine not be given with?
Should not be given with gold compds – metal chelator!
55
What are the actions of Gold compounds (sodium aurothiomalate/ auranofin)?
Auranofin (oral) → inhibits induction of IL-1 + TNF-α → ↓ pain + joint swelling
56
how is sodium auranofin administered?
IM injection
57
What are the side effects of gold compounds?
Side-effects: skin rashes, flu-like symptoms, mouth ulcers, blood disorders (33%) Serious side-effects: encephalopathy, peripheral neuropathy + hepatitis (10%)
58
How long does the effects of gold compounds develop?
3-4 months
59
What are the actions of Anti-malarials (chloroquine/ hydroxychloroquine)?
- ↑pH of intracellular vacuoles → interferes with antigen-presenting - Induces apoptosis in T-lymphocytes
60
how long do the therapeutic effect of Anti-malarials (chloroquine/ hydroxychloroquine) take ?
1 month
61
What are the side effects of Anti-malarials (chloroquine/ hydroxychloroquine)?
Side-effects: n+v, dizziness, blurring of vision – requires screening
62
Name examples of Anticytokine Drugs and what their target action is?
adalimumab, etenercept, infliximab – target TNF; rituximab, abatacept, natalizumab – target leukocyte Rs; tocilizumab - blocks IL-6 Rs → disrupt immune signaling
63
Anticytokine drugs are used when patients do not repond well to other DMARDs. What other drug can be used as well as these?
methotrexate
64
how are anticytokine drugs administered?
S.C or I.V injection
65
What are the side effects of anticytokine drugs?
Side-effects: - may develop latent disease (e.g. TB, hep B, herpes zoster, etc) + opportunistic infection - nausea, - abdominal pain, - worsening heart failure, - hypersensitivity
66
What type of drug is Ciclosporin?
Immune suppressant
67
What are the actions of Ciclosporin?
Inhibits IL-2 gene transcription → ↓ T cell proliferation
68
How is ciclosporin administered?
Poorly absorbed orally – special formulations (capsules/ oral solutions)
69
What are the side effects of ciclosporin the immunosuppressant?
Nephrotoxicity* Hepatotoxicity Hypertension Also: nausea/ vomiting, gum hypertrophy, GI problems Accumulates in high concentration in tissues (i.e. remains for some time) *is a poisonous effect of some substances, both toxic chemicals and medication, on the kidneys. There are various forms of toxicity.
70
What are the actions of the immunosuppressant Azathioprine?
- Cytotoxic: interferes with purine metabolism → ↓ DNA synthesis - Depresses cell-mediated + antibody-mediated immune reactions i. e. targets cells in induction phase of immune response - Main specific effect: suppression of bone marrow
71
What are the actions of the immunosuppressant Methotrexate?
- Folic acid antagonist → inhibits DNA synthesis - Blocks growth and differentiation of rapidly dividing cells - Inhibits T cell activation
72
What is one of the benefits of using methotrexate?
it is faster acting than other drugs
73
What are the side effects of the immunosuppressant methotrexate?
Side-effects: possibility of blood dyscrasias (abnormalities) + liver cirrhosis (requires monitoring), folate deficiency
74
What are the actions of the immunosuppressant Leflunomide?
Specific inhibitor of activated T cells
75
What are the side effects of leflunomide?
diarrhoea, alopecia, ↑ liver enzymes → risk of hepatotoxicity
76
What are the general problems when using immunosuppressant's?
Glucocorticoids + other IS drugs: Increase risk of infection Increase risk of cancer

Applied Pharmacology bs (10 decks)

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