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MM Test 1 > B6.005 Pharmacotherapy of RA and Joint Pain > Flashcards

B6.005 Pharmacotherapy of RA and Joint Pain Flashcards

1
Q

typical clinical presentation of gout

A

pain, erythema, and swelling in joint (often toe)
acute pain
middle aged male
overweight

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2
Q

what is gout

A

metabolic disease characterized by recurrent episodes of acute arthritis due to depositions of monosodium urate in joint and cartilage

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3
Q

therapeutic goals of gout treatment

A

terminating attacks
providing control of pain and inflammation
preventing future attacks
preventing complications such as renal stones, tophi, and destructive arthropathy

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4
Q

drug classes used for acute gout treatment

A 
NSAIDs
corticosteroids
intra-articular steroid injection
APAP
colchicine
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5
Q

NSAIDs in acute gout treatment

A

most commonly used treatment
inhibit urate crystal phagocytosis
replaced colchicine as drug of choice

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6
Q

corticosteroids in acute gout treatment

A

used in patients who cannot tolerate NSAID or failed NSAID/colchicine therapy

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7
Q

intra-articular steroid injection in acute gout treatment

A

beneficial in patients with just one or two large joint affected
good option for elderly patients with other illnesses

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8
Q

types of NSAIDs

A 
nonselective:
-aspirin
-ibuprofen
-indomethacin
COX2 selective:
-celecoxib
-meloxicam
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9
Q

features of COX1

A

enzymes in GI tract
constitutive
protective

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10
Q

features of COX2

A

inducible

inflammatory

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11
Q

anti inflammatory mechanism of aspirin

A

nonselective COX inhibitor

irreversibly inhibits COX and platelet aggregation

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12
Q

analgesic effects of aspirin

A

most effective in reducing pain through reducing inflammation

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13
Q

antipyretic effects of aspirin

A

mediated by COX inhibition in CNS and inhibition of IL-1

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14
Q

aspirin adverse effects

A

gastric upset
gastric and duodenal ulcers
less frequently: hepatotoxicity, asthma, rashes, renal toxicity

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15
Q

features of ibuprofen

A

nonselective COX inhibitor
prescribed in lower doses than aspirin
analgesic but not anti-inflammatory efficacy

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16
Q

features of indomethacin

A

popular for gout and ankylosing spondylitis

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17
Q

mechanism of COX2 selective inhibitors

A

inhibit PGE synthesis by COX2 induced at sites of inflammation without affecting actions of constitutively active housekeeping COX1 found in GI tract, kidneys, and platelets
binds active site of COX2 more effectively than COX1

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18
Q

effects of COX2 selective inhibitors

A

analgesic, antipyretic, and anti inflamm effects similar to nonselective NSAIDs but with less GI adverse effects
no impact on platelet aggregation (mediated by COX1) thus, can have increased incidence of cardiovascular thrombotic events

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19
Q

features of APAP

A

weak inhibitor of COX enzymes
central, direct analgesic effects (not well understood)
NOT an anti-inflammatory
antipyretic

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20
Q

side effects of APAP

A

fewer GI sides effects than NSAIDs, generally well tolerated

danger of liver damage at doses > 4g/day

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21
Q

mechanism of colchicine

A

inhibits microtubule aggregation which disrupts leukocyte chemotaxis and phagocytosis
inhibits crystal induced production of chemotactic factors

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22
Q

side effects of colchicine

A

diarrhea and other GI effects

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23
Q

2 classes of gout prophylaxis

A

urate concentration-lowering drugs

uricosuric drugs

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24
Q

what are the urate concentration lowering drugs

A

xanthine oxidase inhibitors- allopurinol and febuxostat

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25
Q

mechanism of allopurinol

A

blocks conversion of xanthine to uric acid

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26
Q

mechanism of febuxostat

A

xanthine oxidase inhibitor
more selective than allopurinol
little dependence on renal excretion

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27
Q

what are the uricosuric drugs?

A

probenecid
sulfinpyrazone
lesinurad (zurampic)

28
Q

mechanism of probenecid/sulfinpyrazone

A

increases renal clearance of uric acid by inhibiting tubular absorption
GI and kidney stone side effects may limit use

29
Q

mechanism of lesinurad

A

inhibits urate transporter URAT1

responsible for the majority of the renal reabsorption of uric acid

30
Q

what does DMARD stand for

A

disease modifying anti rheumatic drugs

31
Q

what is the difference between using DMARDs and NSAIDs in RA

A

NSAIDs offer mainly symptomatic relief but have little effect on disease progression
DMARDs can be more expensive, but can improve prognosis
DMARDs are slower acting than NSAIDs

32
Q

examples of DMARDs

A 
methotrexate*
chlorambucil
cyclophosphamide*
cyclosporine*
azathioprine*
mycophenolate mofetil
chloroquine/ hydroxychloroquine
gold compounds
sulfalazine*
33
Q

methotrexate mechanism

A

inhibition of AICAR transformylase and thymidylate synthetase (by inhibiting dihydrofolate reductase)
secondary effects of polymorphonuclear chemotaxis

34
Q

cyclophosphamide mechanism

A

cross links DNA to prevent cell replication

35
Q

cyclosporine mechanism

A

inhibits IL-1 and IL-2 receptor production

36
Q

azathioprine mechanism

A

suppresses B cell and T cell function, immunoglobulin production, and IL-2 secretion

37
Q

mycophenolate mofetil mechanism

A

inhibits cytosine monophosphate dehydrogenase and T cell lymphocyte proliferation

38
Q

chloroquine/ hydroxychloroquine mechanism

A

unclear

39
Q

gold compounds mechanism

A

alter morphology and functional capabilities of human macrophages

40
Q

sulfasalazine mechanism

A

IgA and IgM rheumatoid factor production are decreased

41
Q

what are biologic therapies

A

organic compounds made by living cells that modify biologic responses:

  • Ab-Ag interactions
  • cytokine-receptor interactions
  • cell signaling protein, inhibitors, or ligands
42
Q

classes of biologic therapies

A 
anti-TNF agents
B cell depleting agents
T cell costimulation inhibitors
cell growth arrestors
IL-1 inhibitors
IL-17A inhibitors
43
Q

etanercept

A

anti-TNF agent

cytokine receptor fusion protein

44
Q

infliximab

A

anti-TNF agent

chimeric monoclonal antibody

45
Q

adalimumab

A

anti-TNF monoclonal antibody

46
Q

rituximab

A

B cell depleting monoclonal antibody

47
Q

abatacept

A

T-cell co-stimulation inhibitor

receptor-ligand

48
Q

leflunomide

A

cell growth arrestor (G1 phase)

49
Q

anakinra

A

IL-1 inhibitor

cytokine receptor decoy

50
Q

secukinumab

A

anti-IL-17A monoclonal antibody

51
Q

ixekizumab

A

IL-17A receptor antagonist

used in moderate to severe plaque psoriasis

52
Q

mechanisms of steroidal anti-inflammatory therapy

A

molecular mechanism inhibits transcription of genes that encode inflammatory proteins (cytokines, chemokines, adhesion molecules, inflamm enzymes)

  • inhibition of NFkB and AP-1 transcription factors
  • recruitment of histone deacetylase 2, reversing histone acetylation
53
Q

net result of steroids

A

decreased lymphocytes (T and B), monocytes, eosinophils, and basophils

54
Q

short to medium duration corticosteroids

A 
hydrocortisone (cortisol)*
cortisone*
prednisone*
prednisolone
methylprednisolone
meprednisone
55
Q

intermediate duration corticosteroids

A

triamcinolone*
paramethasone
fluprednisolon

56
Q

long acting corticosteroids

A

bethamethasone

dexamethasone*

57
Q

use of corticosteroids in RA

A

widely used
effects are prompt and dramatic
slows the appearance of new bone erosions
applicable in other rheumatic diseases (SLE, sarcoid, gout)
pronounced side effects w long term use

58
Q

side effects of steroid treatment

A 
weight gain (puffy face, truncal obesity)
acne
hypokalemia
hypertension, diabetes
peptic ulcer
osteoporosis
glaucoma
muscle wasting
acute psychosis
59
Q

why can progressive RA lead to neuropathic pain?

A

erosion of bone and cartilage in vertebral column can lead to flattened discs and compressed spinal nerves

60
Q

what types of drugs are useful for neuropathic pain?

A

non-opioid analgesics

61
Q

classes of non-opioid analgesics

A

drugs that modify 5-HT (serotonin) or NE uptake
alpha-2 adrenergic agonists
anticonvulsants
NMDA receptor antagonists

62
Q

drugs that modify 5-HT (serotonin) or NE uptake

A

amitriptyline*
duloxetine*
desipramine

63
Q

alpha-2 adrenergic agonists

A

tizanidine

clonidine

64
Q

anticonvulsants

A

gabapentin*
carbamazepine*
pregabalin
clonazepam

65
Q

NMDA receptor antagonists

A

dextromethorphan
ketamine
amantadine

66
Q

example opioid analgesics

A

fentanyl
hydromorphone
oxycodone
morphine

MM Test 1 (20 decks)

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