Year 2 Arthritis drugs Flashcards

(61 cards)

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
Side effects of anti-malarials?
N+V, dizziness, vision blurring.
26
How do anticytokine drugs work?
-Engineered recombinant antibodies.
27
What are these drugs, adalimumab, etenercept, infliximab? Targets?
Anticytokine drugs, TNF.
28
What are these drugs Rituximab, Abatacept, Natalizumab? Targets?
Anticytokine drugs. Leukocyte Rs.
29
What type of drug is tocilizumab? Target?
Anticytokine drug. Blocks IL-6 Rs.
30
Side effects of anticytokine drugs?
Develop latent disease (TB, hep b). Infections, nausea, pain, worsening heart failure.
31
What are the immunosuppressant's?
Ciclosporin Azathioprine Methotraxate Leflunomide Cyclophosphamide
32
How does ciclosporin work?
Immunosuppressant but no effect on inflammation. Inhibits IL-2 gene transcription
33
Side effects of ciclosporin?
Nephrotoxicity, hepatotoxicity, hypertension, n&v, gum hypertrophy, GI problems.
34
How does azathioprine work?
Cytotoxic: interferes with purine metabolism, targets cells in induction phase of immune response. Suppresses bone marrow.
35
How does methotrexate work?
Faster than others. Folic acid antagonist -\>inhibits DNA synthesis& T cell activation.
36
Side effects of methotrexate?
Blood dyscrasias, liver cirrhosis, folate deficiency.
37
How does leflunomide work?
Inhibits activated T cells. Orally.
38
Leflunomide side effects?
Diarrhoea, alopecia, ^ liver enzymes.
39
How does cyclophosphamide work?
Only used when others failed. Activated to phosphoramide mustard+acrolein.
40
Misoprostol? When given? Effects? Side effects?
Synthetic PG. Given with NSAIDs. Protected GI tract, Diarrhoea. Abortions.
41
Omeprazole
Proton pump inhibitor, reduce acid secretion.
42
Gold compounds examples
Sodium autothiomalate, auranofin
43
Anti-malarials examples
Chloroquine, hydroxychloroquine.
44
What is glucosamine sulphate?
?benefit. Major constituent of ECM. No overall sig dif. X Nice.
45
Matrix metalloproteinases degrade?
Type II collagen
46
Cathepsin-B splits?
Aggrecan
47
Blocking COX -\> Blocks ... & what result?
PGI2 increasing platelet aggregation.
48
Prostaglandins cause?
Vasodilation
49
Prostaglandins potentate effects of?
Histamine and bradykinin
50
How are NSAIDs analgesic?
Reduce neuron sensitivity to bradykinin
51
How are NSAIDs anti-inflam?
↓bradykinin -\> ↓ vasodilation -\> ↓venule permeability
52
What (4) prevent further joint damage?
Glucocorticoids, immunosuppressants, DMARDs, anticytokines.
53
What pro-inflam cytokines are expressed with joint destruction?
TNF, IL-1B, IL-6.
54
What do macrophages secrete?
Cytokines (TNF and IL-1)
55
What does TNF stimulate?
Fibroblasts
56
What does IL-1 stimulate?
Osteoclasts
57
What do fibroblasts do?
release matrix-degrading metalloproteinases
58
Two ways anti-inflam/immune suppressants work
X phospholipase A2 -\> ↓arachidonic acid. & ↓pro-inflam cytokine transcript
59
Card on steroids
\>1 month. Suppression of normal steroid synthesis, excessive neg feedback.
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