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Pharmacology > Drugs used in Treatment of Gout and Rheumatoid Arthritis > Flashcards

Drugs used in Treatment of Gout and Rheumatoid Arthritis Flashcards

1
Q

Recurrent acute inflammatory arthritis with red, tender, hot and swollen
joints
?

A

Gout

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2
Q

Uric acid, a product of purine metabolism, has low water solubility, especially at low pH. When blood levels are high, it precipitates and deposits in joints, especially the big toe, kidney and subcutaneous tissue called?

A

tophy

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3
Q

Types of gout ?

A
  1. Primary or hereditary gout :
    - to genetic error in purine metabolism
  2. Secondary gout:
    due to drugs that
    - Inhibit uric acid excretion
    - Increase urate production by increasing rate of cell death (cancer chemotherapy)
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4
Q

Stages of Gout?

A
  • Asymptomatic hyper-uricemia (serum uric acid higher than 6 mg/dl)
  • Acute intermittent gout (attacks of gout or flares)
  • Inter-critical stage (in between attacks)
  • Chronic gout (deformities)
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5
Q

Non-pharmacological treatment of gout: ?

A

 Try to lose weight and do physical exercises
 Drink a lot of water (2-3 liters/day)
 Avoid alcohol and smoking
 Avoid drugs as salicylate and diuretics
 Low purine diet (avoid red meat, sea products, dried fruits, beans,…)

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6
Q

Pharmacological treatment of gout ?

A
  1. Uricostatics (drugs that interfere with uric acid synthesis):
    - Allopurinol
    - Febuxostat
  2. Uricosurics (drugs that increase uric acid excretion)
    - Probenecid
  3. Uricases (enzyme that breakdown uric acid):
    - Pegloticase
  4. Tubulin inhibitors
    - Colchicine
  5. Anti-inflammatory drugs
    - Non-steroidal anti-inflammatory drugs (NSAIDs) except salicylate
    - Corticosteroids
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7
Q

Interfere with uric acid synthesis by inhibiting xanthine oxidase enzyme.
xanthine and hypoxanthine are more soluble, have a higher renal clearance
than that of uric acid

Type of drug?

A

Uricostatic drugs: Allopurinol

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8
Q

Uricostatic drugs: Allopurinol

Pharmacokinetics?

A

Converted by the liver to active metabolite alloxanthine (oxypurine)

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9
Q

Uricostatic drugs: Allopurinol

Uses?

A
  1. first choice drug in chronic gout:
    (With long-term allopurinol therapy, tophi gradually disappear and nephropathy is halted, even reversed.)
  2. Secondary hyperuricaemia : due to cancer chemotherapy/
    radiation/thiazides or other drugs
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10
Q

Adverse effects of Uricostatic drugs: Allopurinol

A

uncommon.

- May induce acute attack of gout, Fever, rash, toxic epidermal necrolysis

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11
Q

Interfere with uric acid synthesis by inhibiting xanthine oxidase
enzyme.

Drug?

A

Uricostatic drugs: Febuxostat

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12
Q

Uricostatic drugs: Febuxostat

Uses?

A
  1. alternative drug for treating symptomatic gout only in patients intolerant to allopurinol, or in those with some contraindications.
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13
Q

Adverse effects Of Uricostatic drugs Febuxostat?

A

Liver damage: liver function needs to be monitored during
febuxostat therapy.

Like other drugs used to treat hyperuricaemia, NSAID/colchicine
cover should be provided for 1–2 months while initiating febuxostat therapy.

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14
Q

Inhibit Urate Transporters (URAT1) of renal proximal tubule,
preventing urate reabsorption

Drug?

A

Uricosurics: Probenecid

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15
Q

Uses of Uricosurics: Probenecid

A
  1. Chronic gout and hyperuricaemia: Probenecid is a second line/adjuvant drug to allopurinol.
  2. prolong penicillin or ampicillin action by
    enhancing and sustaining their blood levels, e.g. in gonorrhoea.
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16
Q

Adverse effects of Uricosurics: Probenecid?

A
  • May induce acute attack of gout
  • Uric acid kidney stones
  • Gastric irritation
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17
Q

Contraindications of Uricosurics: Probenecid?

A
  • Acute gout
  • Previous kidney stones or existing renal disease
  • Elderly patients Caution in peptic ulcer disease
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18
Q

Recombinant mammalian uricase enzyme that convert urate to allantoin,
which is more soluble and easily excreted in urine

Drug?

A

Uricase enzyme: Pegloticase

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19
Q

Uricase enzyme: Pegloticase

Uses?

A

Chronic gout in patients refractory to conventional therapy, given by I.V.
infusion given every 2 weeks

20
Q

Adverse effects of Uricase enzyme: Pegloticase?

A

 May induce acute attack of gout
 Kidney stones
 I.V. Infusion reactions and anaphylaxis- due to presence of
antipegloticase antibodies

21
Q

Inhibition of microtubule assembly decreases macrophage migration into the inflamed joint and phagocytosis of urate crystals.

Drug?

A

Tubulin inhibitor: Colchicine

22
Q

Treatment of acute attacks of gout

Drug?

A

Tubulin inhibitor: Colchicine

23
Q

Tubulin inhibitor: Colchicine

Adverse effects?

A

Severe diarrhea, nausea, vomiting, abdominal cramps
 Bone marrow depression
 Cardiac toxicity, arrhythmia
 Hepatotoxicity
 Alopecia (hair loss)
Because of higher toxicity, it is used only when NSAIDs are ineffective or
cannot be used

24
Q

First line of treatment of acute attack of gout- in high and quickly repeated
doses.
?

A

Anti-inflammatory drugs

 Non-steroidal anti-inflammatory drugs: naproxen, piroxicam, diclofenac

25
Q

Anti-inflammatory drugs

Avoided in case of?

A

 Gastric ulcer  Renal insufficiency  Heart failure

26
Q

contraindicated in gout ?

A

Salicylate

27
Q

Used in acute gout attacks only in cases resistant to NSAIDs and colchicine, ?

A

Corticosteroids

28
Q

Preferred route of administration is intra-articularly

?

A

Corticosteroids

29
Q

Chronic autoimmune disorder in which the normal immune response is
directed against an individual’s own tissue, especially joints ?

A

Rheumatoid Arthritis

30
Q

Rheumatoid Arthritis lead to?

A
  • Damage in joints:
    = Synovial inflammation and hyperplasia
    = Cartilage and bone destruction (“deformity”)
  • Systemic effects as:
    = Anemia, weight loss, osteoporosis
    = Cardiovascular, renal and central nervous system problems
31
Q

Pharmacological treatment of rheumatoid arthritis

?

A
  1. Non-steroidal anti-inflammatory drugs (NSAIDs)
  2. Disease modifying anti-rheumatic drugs (DMARDs)
    - DMARDs are chemically diverse drugs aiming at slowing tissue-damaging process
    - Has no effect on relieving pain, but slow deformity after months of starting treatment
32
Q

DMARD

Onset? Stop progress of disease ? Prevent formation of new deformities ? Uses?

A
  • slow
  • yes
  • yes
  • moderate to serve chronic cases to arrest the disease
33
Q

NSAID

Onset? Stop progress of disease ? Prevent formation of new deformities ? Uses?

A
  • rapid
  • no
  • no
  • mild/early cases : afford symptomatic relief in pain, swelling , morning stiffness , immobility
34
Q

Disease modifying antirheumatic drugs (DMARDs)?

A

A. Nonbiological drugs :

  1. Immunosuppressants: Methotrexate
  2. Sulfasalazine
  3. Chloroquine or Hydroxychloroquine
  4. Leflunomide

B. Biological agents

  1. TNFα inhibitors: Etanercept, Infliximab
  2. IL-1 antagonist: Anakinra
35
Q

Inhibits dihydrofolate reductase, thus inhibit production of
inflammatory cytokines, as TNF-α, chemotaxis and cell-mediated
immune reaction
Drug ?

A

Methotrexate

36
Q

Methotrexate
Adverse effects
?

A

 At low-dose: nausea, diarrhea, rash, headache

 Severe toxicity: hepatotoxicity, bone marrow depression (treated by folic acid)

37
Q

Onset of symptom relief is relatively rapid (4–6 weeks), therefore
preferred for initial treatment. Oral low-dose weekly Mtx regimen has
improved acceptability
?

A

Methotrexate

38
Q

is now the DMARD of first choice and the standard treatment for
most patients. Combination regimens of 2 or 3 DMARDs include Mtx.
?

A

Methotrexate

39
Q

Anti-malarial drug, Reduce monocyte IL–I, consequently inhibiting B
lymphocytes, and inhibit them to produce inflammatory cytokines.

Drug?

A

Hydroxychloroquine

40
Q

Induce remission in upto 50% patients of RA, but take 3–6 months
?

A

Hydroxychloroquine

41
Q
  1. Fastest onset of action (4 weeks)
  2. Inhibits T-cell proliferation by blocking pyrimidine synthesis
    Drug?
A

Leflunomide

42
Q

TNF-α blocking agents (Infliximab)

?

A

Biologic disease modifier

43
Q

monoclonal antibody?

A

Biologic disease modifier

Example: TNF-α blocking agents (Infliximab)

44
Q

Binds TNF-α preventing its interaction with cell surface receptors
decreasing macrophage and T-cell function
?

A

TNF-α blocking agents (Infliximab)

45
Q

Quicker response than nonbiologic DMARDs .

?

A

Biologic disease modifier

46
Q

Though effective as monotherapy, they are generally added to Mtx when
response to the latter is not adequate or in rapidly progressing cases,
?

A

Biologic disease modifier

Example: TNF-α blocking agents (Infliximab)

47
Q

Adverse effects:
Of Biologic disease modifier
Example: TNF-α blocking agents (Infliximab)
?

A

Infections, especially upper respiratory tract infections, cough

Pharmacology (4 decks)

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