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pharmacology 3 > drug management for rhuematoid arthritis > Flashcards

drug management for rhuematoid arthritis Flashcards

1
Q

therpeutic goals in RA

A

prserve function - disease modification

prevent pain

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2
Q

burden of inflammation in RA lies in

A

the synovium
becomes infiltrated with macrophages, T and B lymphocytes, vessels, fibroblasts, other inflammatory cells
cause destruction of the normal joint cartilage and bone

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3
Q

RA pathogenesis

A

T-lymphocyte becomes reactive to a self antigen
T cells are reactive to normal tissue - proliferation and activation
macrophage activation
antibody production and joint tissue damage

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4
Q

drugs targetting T-cell proliferation and function

A

methootrexate
leflunomide
glucocorticoids

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5
Q

drugs targeting macrophage function

A

TNF-a inhibitors

glucocorticoids

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6
Q

drugs targeting uncertain mode of action

A

sulfasalazine

hydroxychloroquine

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7
Q

TNF-a is secreted by

A

macrophages and acts through TNF-receptors

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8
Q

macrophages secrete TNFa when

A

tiggered by activated T lymphocyte

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9
Q

what does TNFa do

A

engages on receptors

cells populatng the synovium are activated to facilitate inflammation

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10
Q

synovium cells and their response to TNFa

A 
endothelial cells - adhesion receptors for leukocytes 
lymphocytes - activation, proliferation 
macrophages - activation 
APC - maturation and migration 
some tumour cells - apoptosis
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11
Q

two engineered anti-TNFa antibodies

A

infliximab

adalimumab

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12
Q

infliximab

A

human sequences and mouse sequences, modified to minimise human antigenicity

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13
Q

adalimumab

A

comletely humanised Fab sequence

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14
Q

adverse effects of TNFa inhibition

A

immune supression

  • increased nfection rate, including some infections only seen in immunosuppression
  • particular risk in people with dormant tuberculosis
  • increased rate of some malgnancies
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15
Q

3 glucocorticoids

A

hydrocortisone
prednisolone
dexamethasone

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16
Q

how glucocorticoids interact with the cell

A

GC binds to circulating corticosteroid binding globulin
steroid binds cytosolic glucocorticoid receptor, which translocated to nucleus
steroid receptor complex binds recognition sequences on promoter of responsive genes, stimulating transcription

17
Q

effects of glucocorticoids

A

macrophages - decrease of cytokines including TNFa ans decrease of other proinflammatory functions
t lymphocytes - decrease in recruitment and proliferation
b lymphocytes - decreasse in antibody production

18
Q

GCs are used in

A

systemic - autoimmune disease, allograft (transplant) tolerance
local - asthma, dermatitis, ulcerative colitis, inflammatory arthritis and others

19
Q

adervse effects of GC when used systemically

A

metabolic and mineralocorticoid adverse effects
commonly used systemically early in treatment
avoid or minimise, to prevent adverse effects

20
Q

dihydrofolate reductase

A

turns folic acid into tetrahydrofolate by adding 4 hydrogens

21
Q

tetrahydrofolate

A

essential for asssembling purines and pyrimidines

22
Q

action of methotrexate

A

antagonist fr dihydrofolate reductase - stops production of dihydrofolate which causes prevention of T cell proliferation

23
Q

mathotrexate toxicity

A

antiprolferative actions

  • bone marrow
  • gut (mouth ulcers, GI upset)

tetragonicity risk (high doses embryotoxic

hepatotoxicity and pulmonary fibrosis

24
Q

excretion of methotretaxe

A

mostly renally excreted - check renal function

25
Q

leflunomide

A

blocks dihydroorotate dehydrogenase, which is in the pathway for pyrimidine synthesis
- also antiproliferative
- also teratogenic
has a long half life
avoid n young women, or reliable contraception
causes hepatotoxicity

26
Q

prostaglandins and prostaglandin inhibition in RA

A

for pain
non-opoiod analgesics
prostaglandins are products of macrophages - sensitise pain receptors and pro-inflammation

27
Q

inhibiting prostagladnin production

A
  • suppresses sign of inflamation, including pain

- does NOT prevent disease progression

28
Q

typical drug prescription for RA

A
  • MTX or leflunomide
  • add hydrocychloroquine, sulfasalazine
  • add biological agent, usually anti-TNFa
  • los dose systemic glocucorticoids commonly used in early phase, when pursuing remission
  • cyclooxygenase inhibitors (NSAIDs) for analgesia and acute anti-inflammatory action
29
Q

non-pharmacological management

A

protection of joints (splints)
management of CV risk
general functional support, to compensate for disability
psychological support

pharmacology 3 (8 decks)

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