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Pharmacology > Year 2 Arthritis drugs > Flashcards

Year 2 Arthritis drugs Flashcards

1
Q

How does aspirin work?

A

Inhibits NFkB expression -> reducing inflammatory mediator gene transcription

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2
Q

How do celecoxib, diclofenac and ibuprofen work?

A

Reduce IL-6 and TNF-a in SF

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3
Q

Which drug has some COX2 selectivity?

A

Meloxicam

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4
Q

Name COX2 inhibitors?

A

Celecoxib Etoricoxib

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5
Q

When are celecoxib or etoricoxib given?

A

To patients with ^ risk of GI problems but little CV risk

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6
Q

Common side effects of celecoxib and etoricoxib?

A

Headache, dizziness, skin rash, peripheral oedema

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7
Q

How does paracetamol work?

A

-Supresses PG production - Involve COX3 in CNS

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8
Q

How does strontium ranelate?

A

-^ osteoblack and decrease osteoclast -reduce pain - prevents fractures

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9
Q

Strontium ranelate problems?

A

^ MI risk & thrombotic events

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10
Q

What do glucocorticoid drugs do?

A
  • metabolic effects - anti-inflammatory -immunosuppressive
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11
Q

Which natural steroids show both MC&GC activities?

A

Hydrocortisone Corticosterone

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12
Q

Which natural steroid shows only MC activities

A

Aldosterone

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13
Q

Which synthetic steroids show both MC&GC activites?

A

Prednisolone Prednisone

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14
Q

Which synthetic steroids show only GC activites?

A

Dexamethasone Betamethasone Beclomethasone Budesonide

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15
Q

Which synthetic steroids show mainly MC activites?

A

Fludrocortisone

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16
Q

What is fludrocortisone used for?

A

Addison’s disease (adrenal insufficiency)

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17
Q

What is the most common 1st choice DMARD?

A

Sulfasalazine

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18
Q

How does Sulfasalazine work? How is it given?

A

Collects free radicals. Enteric-coated tablet

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19
Q

Side effects of Sulfasalazine?

A

GI upset, headache, skin reactions, leukopenia.

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20
Q

How does penicillamine work? How is it given?

A

Reduce IL-1 generation & fibroblast proliferation. Orally.

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21
Q

Side effects of penicillamine?

A

Rashes, stomatitis, anorexia, taste disturbance.

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22
Q

How does gold compounds (sodium auronofin) work? Given?

A

Inhibits IL-1 + TNF-a. Reducing pain and swelling. Deep IM injection

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23
Q

Side effects of gold compounds (sodium auronofin)?

A

Skin rashes, flu-like, mouth ulcers, blood disorders, encephalopathy, peripheral neuropathy& hepatitis..

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24
Q

How do anti-malarials work?

A

^intracellular vacuoles interfering with antigen presenting. Apoptosis in T-lymphs.

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25
Q

Side effects of anti-malarials?

A

N+V, dizziness, vision blurring.

26
Q

How do anticytokine drugs work?

A

-Engineered recombinant antibodies.

27
Q

What are these drugs, adalimumab, etenercept, infliximab? Targets?

A

Anticytokine drugs, TNF.

28
Q

What are these drugs Rituximab, Abatacept, Natalizumab? Targets?

A

Anticytokine drugs. Leukocyte Rs.

29
Q

What type of drug is tocilizumab? Target?

A

Anticytokine drug. Blocks IL-6 Rs.

30
Q

Side effects of anticytokine drugs?

A

Develop latent disease (TB, hep b). Infections, nausea, pain, worsening heart failure.

31
Q

What are the immunosuppressant’s?

A

Ciclosporin Azathioprine Methotraxate Leflunomide Cyclophosphamide

32
Q

How does ciclosporin work?

A

Immunosuppressant but no effect on inflammation. Inhibits IL-2 gene transcription

33
Q

Side effects of ciclosporin?

A

Nephrotoxicity, hepatotoxicity, hypertension, n&v, gum hypertrophy, GI problems.

34
Q

How does azathioprine work?

A

Cytotoxic: interferes with purine metabolism, targets cells in induction phase of immune response. Suppresses bone marrow.

35
Q

How does methotrexate work?

A

Faster than others. Folic acid antagonist ->inhibits DNA synthesis& T cell activation.

36
Q

Side effects of methotrexate?

A

Blood dyscrasias, liver cirrhosis, folate deficiency.

37
Q

How does leflunomide work?

A

Inhibits activated T cells. Orally.

38
Q

Leflunomide side effects?

A

Diarrhoea, alopecia, ^ liver enzymes.

39
Q

How does cyclophosphamide work?

A

Only used when others failed. Activated to phosphoramide mustard+acrolein.

40
Q

Misoprostol? When given? Effects? Side effects?

A

Synthetic PG. Given with NSAIDs. Protected GI tract, Diarrhoea. Abortions.

41
Q

Omeprazole

A

Proton pump inhibitor, reduce acid secretion.

42
Q

Gold compounds examples

A

Sodium autothiomalate, auranofin

43
Q

Anti-malarials examples

A

Chloroquine, hydroxychloroquine.

44
Q

What is glucosamine sulphate?

A

?benefit. Major constituent of ECM. No overall sig dif. X Nice.

45
Q

Matrix metalloproteinases degrade?

A

Type II collagen

46
Q

Cathepsin-B splits?

A

Aggrecan

47
Q

Blocking COX -> Blocks … & what result?

A

PGI2 increasing platelet aggregation.

48
Q

Prostaglandins cause?

A

Vasodilation

49
Q

Prostaglandins potentate effects of?

A

Histamine and bradykinin

50
Q

How are NSAIDs analgesic?

A

Reduce neuron sensitivity to bradykinin

51
Q

How are NSAIDs anti-inflam?

A

↓bradykinin -> ↓ vasodilation -> ↓venule permeability

52
Q

What (4) prevent further joint damage?

A

Glucocorticoids, immunosuppressants, DMARDs, anticytokines.

53
Q

What pro-inflam cytokines are expressed with joint destruction?

A

TNF, IL-1B, IL-6.

54
Q

What do macrophages secrete?

A

Cytokines (TNF and IL-1)

55
Q

What does TNF stimulate?

A

Fibroblasts

56
Q

What does IL-1 stimulate?

A

Osteoclasts

57
Q

What do fibroblasts do?

A

release matrix-degrading metalloproteinases

58
Q

Two ways anti-inflam/immune suppressants work

A

X phospholipase A2 -> ↓arachidonic acid. & ↓pro-inflam cytokine transcript

59
Q

Card on steroids

A

>1 month. Suppression of normal steroid synthesis, excessive neg feedback.

60
Q
A
61
Q
A

Pharmacology (6 decks)

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