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Pharmacology Drugs > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is the mechanism of action of Corticosteroids?

A
  • Prevent interleukin 1 and IL-6 production by macrophages

- Inhibits all stages of T-cell activation

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2
Q

When are Corticosteroids used?

A
  • Malignancy
  • Psoriasis/Psoriatic arthritis
  • Crohn’s disease
  • Vasculitis
  • Maintenance therapy in vasculitis
  • Steroid sparing agent in asthma
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3
Q

What is the mechanism of action of Methotrexate?

A
  • Competitively and reversibly inhibits dihydrofolate reductase
  • Inhibits purine and thymidine synthesis so therefore inhibits DNA, RNA and proteins
  • Cytotoxic in the S-phase of the cell and has a greater toxic effect on rapidly dividing cells.
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4
Q

When is methotrexate used?

A
  • Cancer
  • Non-malignant disease such a R.A psoriasis. Mechanism is not via anti-folate action

Well tolerated and 50% of patients continue drug for more than 5 years. Improved QOL. Retardation of joint damage

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5
Q

What are the side effects of Methotrexate?

A
  • Mucositis (response to folic acid supplementation)
  • Marrow suppression (respond to folic acid supplementation)
  • Hepatitis
  • Cirrhosis
  • Pneumonitis
  • Infection Risk
  • High tetragenic and abortifacient
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6
Q

What are the pharmacokinetics of Methotrexate?

A
  • Oral bioavailability is 33% and intramuscular is 76%
  • Administered PO, IM or S/C
  • Weekly dosing.
  • 50% protein bound so NSAIDs can displace
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7
Q

What is the mechanism of action of Sulfasalazine?

A
  • Inhibition of T cell proliferation
  • T cell apoptosis
  • Inhibition of IL-2 production
  • Reduced chemotaxis of neutrophil
  • Reduced degranulation of neutrophils
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8
Q

What are the uses of Sulfasalazine?

A
  • Relief of pain and stiffness in RA and to finght infection
  • Used for Inflammatory arthritis
  • Effective in IBD (activity in intestine)
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9
Q

What are the side effects of Sulfasalazine?

A

Mainly due to sulfapyridine moiety

  • Myelosuppression
  • Hepatitis
  • Rash

Other

  • Nausea
  • Abdominal pain/vomiting
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10
Q

What are the features of Sulfasalazie in practice?

A
  • Effective and favorable toxicity
  • Very few interactions
  • Long term blood monitoring not always needed
  • No carcinogenic potential and safe in pregnancy
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11
Q

What is the mechanism of action of Azathioprine?

A

Cleaved to 6-mercatopurine

Anti-metabolite decreases DNA and RNA synthesis

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12
Q

What are the use of Azathioprine?

A
  • SLE & Vasculitis - as maintenance
  • Rheumatoid arthritis
  • Inflammatory bowel disease
  • Atopic dermatitis
  • Bullous skin disease
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13
Q

What are the side effects of Azathioprine?

A
  • Bone marrow suppression (monitor FBC)
  • Increased risk of malignancy (Esp transplanted patients)
  • Increased risk of infection
  • Hepatitis (monitor LFT)
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14
Q

What are the features of the metabolism of Azathioprine?

A
  • Metabolised by thiopurine methyltransferase
  • TPMT gene is highly polymorphic
  • Individuals vary markedly in TPMT activity
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15
Q

What can result from low/absent TPMT level?

A
  • Risk of myelosuppression

- Test TPMT activity before prescribing

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16
Q

What is the mechanism of action of Mycophenolate mofetil?

A
  • Inhibits inosine monophosphate dehydrogenanse
  • Impairs B- and T-cell proliferation
  • Spares other rapidly dividing cells
17
Q

When is Mycophenolate mofetil used?

A
  • Primary in transplantation. Induction and maintenance therapy
  • Lupus nephritis
18
Q

What are the side effects of Mycophenolate mofetil?

A
  • Nausea
  • Vomiting
  • Diarrhoea
  • Myelosuppression
19
Q

What is the mechanism of action of Cyclophosphamide?

A
  • Alkylating agent - cross links DNA so that it cannot replicate
  • May immunological effects
  • Suppresses T cell activity
  • Suppresses B cell activity
20
Q

When is Cyclophosphamide used?

A
  • Lymphoma
  • Leukaemia
  • Solid cancers
  • Lupus nephritis
  • Wegener’s granulomatosis
21
Q

How is Cyclophosphamide activated in the body?

A
  • Pro drug converted in the liver to active form.
  • Main active metabolite is 4-hydroxycyclophosphamide.
  • This exist in equilibrium with it tautomer, aldophosphosphamide.
22
Q

What are the possible routes of damage during the excretion of cyclophosphamide?

A
  • Excreted by the kidney
  • Acrolein, another metabolite is toxic to the bladder epithelium and can lead to haemorrhagic cystitis.
  • This is prevented through the use of aggressive hydration and/or mensa
23
Q

What is the mechanism of action of Anti-TNF?

A
  • Decreased inflammation by affecting the cytokine cascade.
  • Decrease recruitment of leukocytes to join and elaboration of adhesion molecules and production of chemokines
  • Decrease angiogenesis and VEGF levels
  • Decrease Joint destruction MMPs and other destructive enzymes.
  • Decrease in bone resorption and erosion and cartilage breakdown.
24
Q

What is the risk of Anti-TNF use?

A
  • TB reactivation is a risk

- TNF-alpha is released by macrophages in response of a TB infection

25
Q

What is the mechanism of action of Rituximab?

A
  • Binds specifically to unique cell-surface marker CD20 which is found on subset of B cells but not on stem cell, pro-B cells, plasma cells any other cell type.
  • Causes B cell apoptosis
26
Q

When is Rituximab used?

A

-Effective in RA (stops B cells presenting antigen to T cells, to prevent cytokines releasing and antibodies)

27
Q

What is the mechanism of action of Calcinerium inhibitors?

A

-Active against helper T cells, preventing production of IL-2 calcineurin inhibition

28
Q

What are the examples of calcinerium inhibitors?

A
  • Ciclosporin

- Tacrolimus

29
Q

What are examples of corticosteroids?

A
  • Fludrocortisone
  • Hydrocortisone
  • Betamethasone
  • Prednisolone
  • Dexamethasone

Pharmacology Drugs (22 decks)

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