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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
Q

What are the side effects of strontium ranelate used to treat osteoarthritis?

A
  • Found to increase risk of MI and thrombotic events so only used to treat server osteoarthritis
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26
Q

What are the actions and negatives of glucosamine sulphate?

A
  • 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!
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27
Q

Rheumatoid arthritis causes …

this leads to?

A 
- Causes joint inflammation, especially:
Synovial membrane
Tendon sheaths
Bursae*
- Leads to proliferation of synovial membrane + erosion of cartilage/ bone
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28
Q

Which type of arthritis is an autoimmune disease?

A

rheumatoid arthritis

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29
Q

What are the symptoms of rheumatoid arthritis?

A

Symptoms presented –

  • usually a throbbing andaching 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.
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30
Q

What are the treatment options in rheumatoid arthritis?

A 
Treatment of pain:
- NSAIDs
- opioid analgesics 
Limitation of joint damage:
- Glucocorticoids
- Immunosuppressants
- Disease Modifying Antirheumatic Drugs (DMARDS)
- Anticytokines
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31
Q

Where are Glucocorticoids naturally found in the body?

A

made by your adrenal glands

32
Q

Why are glucocorticoids used for short term treatment in rheumatoid arthritis?

A
  • manage flare-ups

- as they rapidly reduce inflammation

33
Q

Why are glucocorticoids used for long term treatment in rheumatoid arthritis?

A

if other treatment options failed - must discuss complications

34
Q

What are the actions of glucocorticoids?

A
  • 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
Q

What are the actions of Mineralocorticoids?

A

water & electrolyte balance - Aldosterone – increased reabsorption of Na and H2O in collecting duct/ DCT – inc bp.

36
Q

A short acting steroid lasts between 1-12 hours. Give examples of these.

A

Cortisone/ hydrocortisone

Twice daily cream or intra-articular injection

37
Q

An intermediate acting steroid lasts between 12 - 36 hours. Give examples of these.

A

Prednisolone

Daily oral or intra-articular injection

38
Q

Long acting steroids last between 36-55 hours. Give an example of these.

A

Dexamethasone

Intra-articular injection every 3 - 21 days

39
Q

What are the actions of glucocorticoids in rheumatoid arthritis?

A

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
Q

What are the unwanted side effects of corticosteroids?

A
  • moon face
  • increased abdominal fat
  • Thinning of skin
  • increased risk of infection
  • poor wound healing
  • muscle wasting
  • osteoporosis
  • hypertension
  • buffalo hump
41
Q

How can you reduce the side effects of corticosteroids?

A
  • lower plasma concentration

- choose specific route of administration to achieve this

42
Q

What are the dangers of stopping steroids abruptly?

A

Cause suppression of normal steroid synthesis

  • due to excessive negative feedback
  • may precipitate acute adrenal failure
  • Patients should carry steroid card
43
Q

Name examples of Disease Modifying Antirheumatoid Drugs (DMARDs)

A

Sulfasalazine,
gold compounds,
penicillamine,
immunosuppressants (e.g. methotrexate, ciclosporin, azathioprine, leflunomide), anticytokines

44
Q

Why are DMARDs used?

A
  • to slow onset of rheumatoid arthritis

-

45
Q

What is the first choice of DMARDs drug used in the UK?

A

Sulfasalazine

46
Q

What is sulfasalazine a mixture of ?

A

Complex of salicylate (NSAID) + sulphonamide (antibiotic)

47
Q

How is sulfasalazine thought to act?

A
  • by scavenging free radicals produced by neutrophils

- Causes remission in ‘active’ R.A.

48
Q

What are the side effects of sulfasalazine?

A

GI upset, headache, skin reactions, leukopenia

49
Q

Penicillamine is produced by

A

hydrolysis of penicillin

50
Q

What are the actions of penicillamine?

A

Thought to ↓ IL-1 generation + ↓ fibroblast proliferation → ↓ immune response

51
Q

How is sulfasalazine administered?

A

Given as enteric-coated tablets (poorly absorbed orally)

52
Q

How is penicillamine administered?

A

orally

53
Q

What are the side effects of penicillamine ?

A

rashes, stomatitis (40% patients); anorexia, taste disturbance, fever, n & v

54
Q

What should penicillamine not be given with?

A

Should not be given with gold compds – metal chelator!

55
Q

What are the actions of Gold compounds (sodium aurothiomalate/ auranofin)?

A

Auranofin (oral) → inhibits induction of IL-1 + TNF-α → ↓ pain + joint swelling

56
Q

how is sodium auranofin administered?

A

IM injection

57
Q

What are the side effects of gold compounds?

A

Side-effects: skin rashes, flu-like symptoms, mouth ulcers, blood disorders (33%)
Serious side-effects: encephalopathy, peripheral neuropathy + hepatitis (10%)

58
Q

How long does the effects of gold compounds develop?

A

3-4 months

59
Q

What are the actions of Anti-malarials (chloroquine/ hydroxychloroquine)?

A
  • ↑pH of intracellular vacuoles → interferes with antigen-presenting
  • Induces apoptosis in T-lymphocytes
60
Q

how long do the therapeutic effect of Anti-malarials (chloroquine/ hydroxychloroquine) take ?

A

1 month

61
Q

What are the side effects of Anti-malarials (chloroquine/ hydroxychloroquine)?

A

Side-effects: n+v, dizziness, blurring of vision – requires screening

62
Q

Name examples of Anticytokine Drugs and what their target action is?

A

adalimumab, etenercept, infliximab – target TNF;

rituximab, abatacept, natalizumab – target leukocyte Rs;

tocilizumab - blocks IL-6 Rs → disrupt immune signaling

63
Q

Anticytokine drugs are used when patients do not repond well to other DMARDs. What other drug can be used as well as these?

A

methotrexate

64
Q

how are anticytokine drugs administered?

A

S.C or I.V injection

65
Q

What are the side effects of anticytokine drugs?

A

Side-effects:

  • may develop latent disease (e.g. TB, hep B, herpes zoster, etc) + opportunistic infection
  • nausea,
  • abdominal pain,
  • worsening heart failure,
  • hypersensitivity
66
Q

What type of drug is Ciclosporin?

A

Immune suppressant

67
Q

What are the actions of Ciclosporin?

A

Inhibits IL-2 gene transcription → ↓ T cell proliferation

68
Q

How is ciclosporin administered?

A

Poorly absorbed orally – special formulations (capsules/ oral solutions)

69
Q

What are the side effects of ciclosporin the immunosuppressant?

A

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
Q

What are the actions of the immunosuppressant Azathioprine?

A
  • 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
Q

What are the actions of the immunosuppressant Methotrexate?

A
  • Folic acid antagonist → inhibits DNA synthesis
  • Blocks growth and differentiation of rapidly dividing cells
  • Inhibits T cell activation
72
Q

What is one of the benefits of using methotrexate?

A

it is faster acting than other drugs

73
Q

What are the side effects of the immunosuppressant methotrexate?

A

Side-effects: possibility of blood dyscrasias (abnormalities) + liver cirrhosis (requires monitoring), folate deficiency

74
Q

What are the actions of the immunosuppressant Leflunomide?

A

Specific inhibitor of activated T cells

75
Q

What are the side effects of leflunomide?

A

diarrhoea,
alopecia,
↑ liver enzymes → risk of hepatotoxicity

76
Q

What are the general problems when using immunosuppressant’s?

A

Glucocorticoids + other IS drugs:
Increase risk of infection
Increase risk of cancer

Applied Pharmacology bs (10 decks)

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