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PR3154 finals > IC13 drugs for gout, OA, RA > Flashcards

IC13 drugs for gout, OA, RA Flashcards

1
Q

normal plasma urate concentration?

A

2-7mg/dL

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2
Q

drug induced hyperuricaemia?

A

thiazide or loop diuretics
low dose aspirin
ciclosporin

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3
Q

MOA of colchicine

A

use for acute attacks
reduces leukocyte migration into the joint

1) binds to tubulin (cytoskeleton)
2) prevents tubulin polymerisation into microtubules
3) inhibits leukocyte migration and phagocytosis
4) inhibits leukotriene B4 (LTB4) and prostaglandin (PG) production.

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4
Q

what NSAIDs are contraindicated for gout?

A

aspirin and salicylates

induce kidney retention of uric acid [23-27]. However, low-dose aspirin used for cardiovascular prophylaxis should be continued during the treatment of a gout flare despite this effect

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5
Q

which gc recommended for gout

A

prednisolone

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6
Q

SE of colchicine

A

gi side effects (due to effects on proliferation of gi wall): n/v, diarrhoea, abdo pain
muscle weakness
pale lips
change in amount of urine.

risk of myopathy, neuropathy, pancytopenia (blood dyscrasia related to bleeding) esp in renal or hepatic impairment

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7
Q

caution for colchicine

A

renal impairment
esp crcl<30 or for prolonged duration increases toxicity

drug drug interaction w pgp cyp3a4 inhibitors and inducers.
- macorlides, azoles, antiarrhythmic (verapamil, diltiazem…)§, rifampin, atorvastatin

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8
Q

onset of colchicine

A

relief pain in 24 to 36 hours

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9
Q

MOA of allopurinol and febuxostat and use

A

uric acid synthesis inhibitors

used to prevent recurrence
DO NOT USE during acute attacks

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10
Q

allopurinol (and xanthine oxidase inhibitor) warning

A

allopurinol hypersensitivity syndrome (AHS)

severe cutaneous adverse reaction (SCAR) warning (allopurinol > febuxostat)

febuxostat = MACE warning

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11
Q

risk factors for SCAR

A

renal impariment;: crcl <60, thiazide therapy, hlab5801 genotype (common in han Chinese)

reduce dose if renally impaired

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12
Q

side effect of xanthine oxidase inhibitors

A

maculopapular rash (related to hypersensitivity),
n/v, diarrhoea, stomach pain
fever, sore throat
dark urine
jaundice

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13
Q

probenecid use?

A

uricosuric agent
increases uric acid excretion

used to prevent recurrence
DO NOT USE during acute attacks, may increase risk of uric acid kidney stone formation

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14
Q

moa of uricosuric agents

A

inhibit proximal tubule anion transport
inhibit uric acid re-absorption
increase uric acid excretion

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15
Q

when to start probenecid

A

2-3 weeks after flare

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16
Q

probenecid pracutions and C/I

A

1) take plenty of fluid (≥2L of water) to minimise renal stone formation (CONTRAINDICATED in PMH urolithiasis)

2) keep urine pH > 6 by administration of alkaline (eg potassium citrate)

risk of hemolytic anaemia in patients w g6pd deficiency

not recommended if crcl<50

17
Q

SE of probenecid

A

n/v
painful urination
lower back pain
allergic reaction
rash

proBACK(pain)neACID(urine = pain)

18
Q

another drug for oa other than nsaids

include MOA

A

intra articular hyaluronic acid (slow-acting)

moa: shock absorption, traumatic energy dissipation, protective coating of cartilage, lubrication, reduces pain and stiffness

induces biosynthesis of HA (in the synovial fluid) and extracellular matrix

19
Q

methotrexate mechanism of action

A

major: increase adenosine levels due to AICAR and/or ATIC inhibition

minor: inhibits (i) dihydrofolate reductase and (ii) thymidylate synthetase.

overall effects: increased extracellular adenosine level and activation of adenosine A2a receptor =
(i) antiproliferative effects on T cells
(ii) inhibition of macrophage functions,
(iii) decrease in pro-inflammatory cytokines, adhesion molecules, chemotaxis, phagocytosis.

20
Q

side effects of methotrexate (related to mechanism)

A

inhibition of dihydrofolate reductase reduces the proliferation of other cell types (due to reduced purine and therefore DNA synthesis), more specifically those that are rapidly proliferating: skin and GI

  • n/V
  • mouth and GI ulcers
  • hair thinning
21
Q

management of potential side effects of methotrexate

A

administration of folic or folinic acid or folate 12-24 hours after mtx to decrease toxicity.

22
Q

differences between management of mtx toxicity with folate vs folinic acid

A

folate = cheaper but require high doses due to depletion of n5, n10 methylene FH4

vs

folinic acid = rapidly converted to n5,n10 methylene FH4 = more efficient at rescuing toxicity s dihydrofolate reductase activity is bypassed

23
Q

sulfasalazine mechanism of action

A

metabolised by sulfapyridine and 5aminosalicylic acid
= effect on gut flora = decrease IgA, IgM rheumatoid factors, suppression of T and B cells, macrophages, decrease in inflammatory cytokines (eg IL1beta, TNF, IL6)

24
Q

side effects of sulfasalazine

A

GI: nausea, dyspepsia
CNS: headache, dizzy

Derm: rash

Haem: agranulocytosis, neutropenia, hemolytic anaemia

Genitourinary: oligospermia (reversible infertility in men),
urine discolouration

Infection

25
Q

MOA of leflunomide

A

converted to teriflunomide
= inhibit dihydroorotate dehydrogenase
=
(i) decrease pyrimidine synthesis and arrest G1 phase
(ii) (decrease t cell, b cell) inhibit T cell proliferation, B cell autoantibody production
(iii) inhibit NF-KB activation of pro-inflammatory pathway

26
Q

caution and management for leflunomide

A

very long half life (years)

can manage with colestyramine (bile salt binding resin) to wash out (eg before pregnancy)

TERATOGENIC

27
Q

side effects of leflunomide

A

GI: diarrhoea, nausea
CNS: headache,

liver: increase transaminases

derm: alopecia, rash

heme: myelosuppression

Infection

28
Q

moa of hydroxychloroquine

A

reduced MHC class II expression and antigen presentation

reduced TNF, IL1 and cartilage resorption

antioxidant activity

29
Q

SE of hydroxychloroquine

A

gi: n/v, stomach pain

ophth: retinopathy

derm: photosx, hyperpigmentation, hairloss

cvs: qtc prolongation

metabolic: hypoglycaemia

cns: headache, dizziness, neuropsychiatric smx

30
Q

ADR of tofacitinib

A

cytopenia of neutrophils, lymphocytes, platelets, NK cells
= immunosuppression = opportunistic infections (eg herpes zoster)

anemia (affect jak2 activation by erythropoietin)

hyperlipidemia

TO(lesterol)fA(nemia)ci(topenia)tinib

31
Q

MOA of tofacitinib

A

JAK janus kinase pathway inhibitor
- blocks cytokine production by blocking JAK/STAT activation of gene transcription

32
Q

what are the bDMARDS

A

TNF: infliximab, adalimumab, etanercept, (GOLIMUMAB)

IL1: anakinra

IL6: tocilizumab

CD20 rituximab
CD28 abatacept

33
Q

side effects of TNF blockers

A

infection: resp and skin

autoimmune: multiple sclerosis

malignancy: increased risk of lymphoma

ophth: optic neuritis

heme: leukopenia, aplastic anemia

34
Q

C/I for TNF blockers

A

live vaccination
hep B

35
Q

monitoring for TNF blockers

A

screen for latent or active TB

36
Q

side effect of anakinra

A

infections

injection site reactions

37
Q

side effect of tocilizumab

A

stomatitis
skin eruptions
increase ALT/AST (transaminases)
fever, infections,neutropenia

sTOmach ci(skin) li(ver) zu mab (neutropenia, fever, infection)

38
Q

tocilizumab interactions

A

cyp450:
1A2, 2C9, 3A4

PR3154 finals (13 decks)

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