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pharm exam 3 summer > Rheumatologic Pharmacology > Flashcards

Rheumatologic Pharmacology Flashcards

1
Q

Goal of therapy in Rhematology treatment

A

-control inflammatory process -> disease remission

1) pain relief
2) maintain function
3) improve QOL

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2
Q

5 Markers of treamtmen

A

1) reduction of number of joints involved
2) pain releif
3) decrease morning stiffness
4) reduce serologic markers
5) improve QOL

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3
Q

4 groups of drugs

A

1) anti finflamatories
2) Anti-imflamtory/ imunomodulators (steroids)
3) DMARDS
4) Gout drugs

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4
Q

3 subgroups of DMARDS

A

1) immunomodulators
2) immunosupressives
3) biologic agents

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5
Q

What is the primary frunction of NSAIDS?

A

reduce inflamation and pain

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6
Q

Do NSAIDS alter disease progression?

A

NO

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7
Q

How long does it take NSAIDs to reduce inflamation?

A

1-2 weeks

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8
Q

When does the analgesic effect of NSAIDS begin?

A

immediately

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9
Q

Which drug slows the appearance of bone errosions?

A

Glucocorticosteroids

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10
Q

At what dose do gluccosteroids supress inflamtion?

A

-low doses

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11
Q

What dose to gluccosteroids supress immune system?

A

high doses >40mg

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12
Q

How are gluccosteroids often used?

A

As a bridge therapy between NSAIDs and DMARDS for inflamtions

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13
Q

What is the first line DMARD?

A

methotrexate

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14
Q

What do biologic DMARDS target?

A
  • the inhibit TNF alpha and IL
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15
Q

Do DMARDS slow down the disease or stop it?

A

slow it down

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16
Q

How long does it take to see the effects of DMARDs?

A

3 months

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17
Q

What are the three principles of Immunomodulating drugs?

A

1) don’t increase risk of infections
2) not immunosupressive
3) not as powerful as other DMARDS

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18
Q

What are the two immunomodulating RXs?

A

Hydroxychloroquine

Sulfalazine

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19
Q

Hydroxychloroquine

A
  • anti-malarial drug

- Most MILD DMARD

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20
Q

What is the proposed MOA of hydrocychloroquine?

How long does it take it to work?

A

suppress T-lymphocyte responses to mitogens, inhibit DNA & RNA synthesis, and trap free radicals

-3-6 months

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21
Q

What skin disorder my hydroxychloroquine cause?

A

SEVERE PSORIASIS

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22
Q

What serious ADRS dor hydroxychloroqine have?

A
  • torsades
  • agranulocytosis
  • aplastic anemia
  • leukopenia
  • thrombocytopenia
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23
Q

What serious opthalmic ADR does hydroxychlorquine have?

A

Retinopathy

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24
Q

How often should pts. on hydroxychloquine have an eye exam?

A

every 2 months

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25
Q

What two conditions is hydroxychloroquine used in?

A

RA: slows errosions
SLE: fatique, malise, skine

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26
Q

How does sulfalazine compare to hydroxychloroquine?

A

a little more agressive/effective in treatment

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27
Q

What two conditions is sulfalzine known for treating?

A

chrons and UC

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28
Q

What does sulfalazine inhibit?

A

prostaglandins & the release of inflammatory cytokines (IL 2,6,12 thnf alpha)

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29
Q

When does sulfalazine cause hemolytic anemia?

A

in G6PD pts

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30
Q

What is the serious ADR of Sulfalzine (it is also the drug “known” to cause this)?

A

SJS

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31
Q

How often should CBC/ hepatic be done for pts. on sufalazine?

A

-prior to treatment
-everory other week - 3 mo
- 1/mo - 3 mo
1 every other 3 mo

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32
Q

What conditions is sulfalazine used in?

A

RA, IBS, Arthritis, psoriatic arthritis

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33
Q

What is the onset for sulfalazine?

A

1-3 months

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34
Q

What weird thing may sulfalazine cause?

A

urine and skin turn orange

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35
Q

Why is it important to hydrate while on sulfalazine?

A

renal stones

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36
Q

How do you take sulfalazine

A

with food

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37
Q

4 characteristics of Immunosupressing Rheumatic Drugs

A

1) suplress inflamation and autoimunity
2) take long time to work
3) work better than other DMARDS
4) increase infection risk

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38
Q

Immunosupressive RXs MOA: Methotrexate and Leflunomide

A
  • Antimetabolites: interferes with DNA synthesis, repair, and cellular replication
  • They inhibit enzymes needed to make amino acids - > decrease immune cell numbers
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39
Q

Meth trexate onset

A

3-6 weeks

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40
Q

Doseing of Methotrexate

A

ONCE A WEEK!!!!!
-Give 1 mg folate daily
extremly toxic if taken daily

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41
Q

Methotrexate contraindications

A
  • pregnancy
  • blood dyscrasias
  • renal/hepatic imparitment
42
Q

What are the 5 BLACK BOX warnings of Methotrexate?

A

1) fatal hepatotoxicity
2) renal failure
3) pneumonias
4) marrow supression
5) malignant lymphoma

43
Q

Monitoring of methotrexate

A

CBC 1/ 4-8 wks

44
Q

What can patients not consume while on methotrexate?

A

ETOH

45
Q

What is the gold standard treatment for RA?

A

methotrexate

46
Q

Immunosupressent MOA: Leflunomide

A

inhibits pyrimidine synthesis, resulting in anti-proliferative and anti-inflammatory effects

47
Q

half life of Leflunomide

A

19 days

48
Q

Dosage of Luflunomide

A

loading dose

49
Q

How long does it take to see effect from luflunomide

A

months

50
Q

How is luflunomide eliminated?

A

bile

51
Q

What drige can you take to increase elimination of lufluminde because it increases bile secretion?

A

Chloestyramine

52
Q

How is luflunomide monitored?

A

CBC monthly for 6 months, then q6-8 wks

53
Q

Cyclophosphamide

A

MOST POWERFUL IMMUNOSUPRESSANT

54
Q

What major complications do pts w/ cyclophosphamide have

A

bladder CA, myelosupresion, infection

55
Q

Immunosupressor : Cyclosporine

A

used for organ trns

-IRREVERSIBLY DECREASES KIDNEY FUNCTION

56
Q

immunsupressor: Azathioprine

A

used for chemo and organ trn

57
Q

Immunosupressor Mycophenolate

A

used for organ trn

58
Q

4 Principals of Biologic Agnets

A

1) made from living organisms or its profucts
2) copies effects a natural substance in imune system
3) engineered
4) decrease inflamation

59
Q

Biologics include these 3 things

A
  • interlukins
  • antibodies
  • vaccines
60
Q

3 types of Biologics

A

1) intravenous immunogloculins
2) monoclonoal imunoglobulins
3) JAK inhibitor

61
Q

Intravenous Immunoglobulin

A

used in rheumatologic DZ

62
Q

Monoclonal Antibodies

A
  • against human cell or human profuct

- used in Rheumatologic Dz and chemo

63
Q

PROS of Biologics against DMARDS

A
  • it’s effects on immune system is finer tuned

- fewer side effects

64
Q

CONS of Biologics

A

SUPER EXPENSIVE

65
Q

what do Monoclonal Antibodies primarily work on?

A

cytokines

66
Q

Can monoclonal antibodies be given oraly?

A

NO

-IM, SQ, IV

67
Q

What is increased with use of monoclonal antibodies?

A

-infection

68
Q

Can two different biologics be combined?

A

No

69
Q

can biologics be combined with DMARDs?

A

Yes

70
Q

Biologic monoclonalantibody agents that target TNF alpha

A

Etanercept (Enbrel)
infliximab (Remicade), adalimumab (Humira) Golimumab (Simponi),
Certolizumab pegol (Cimzia)

71
Q

Biologic monoclonalantibody agents that target T cell

A

Abatacept

72
Q

Biologic monoclonalantibody agents that target 20CD+ Bcell

A

Rituximab

73
Q

Biologic monoclonalantibody agents that target IL 1

A

Anakinra

74
Q

Biologic monoclonalantibody agents that target IL- 6

A

Tocilizumab

75
Q

TNF alpha inhibitory monoclonal antibodies used and onset

A
  • RA, psoriatic arthritis, IBD, Spnydloarathyropathy

- days- 3 months

76
Q

Serious ADRS of TNF monoclonal antibodies

A
  • opportunistic infections- TB

- aplastic anemia

77
Q

What needs to be done before starting TNF monoclonal antibodies?

A

TB testing

78
Q

JAK Inhibitor MOA: Tofacitinib

A
  • JAK are enzymes that influence immune cell fucntion from cytokine
  • JAK inhibors reduce cytokine signaling- slow down Dz progession
79
Q

What 2 DMARDS can JAK NOT BE USED WITH?

A

AZOTHIOPRINE

CYCLOSPRINE

80
Q

What RX is used in systemic complaints or skin DZ?

A

Hydroxychloroquine

81
Q

What RX is used in mild joint DZ?

A
  • hydroxychloroquine

- sulfalazine

82
Q

What RX is used in moderate of severe joint DZ?

A
  • METHOTREXATE

- methotrexate + TNF agent

83
Q

Does gout involve the immune system?

A

NO just inflammatory aspect

84
Q

Colchicine MOA

A
  • used for gout

- interrupts urate deposition, WBC can migrate to crystals

85
Q

Serious ADR of Cholchisine

A
  • myopathy

- myelopsurpression

86
Q

gout prophylaxis colchicine dose

A

.6 mg once or twice/ day

87
Q

prophylatic colchicine MAX

A

1.2 mg/day

88
Q

Colchasine dosage in acute attack

A

1.2 oraly, 6 1 hr later, MAX 1.8/hr, then to prophylaxic dose

89
Q

NSAIDS used in Gout

A
  • indomethcin
  • naproxen
  • sulindac
90
Q

Probenecid MOA

A
  • uricosuric- increases uric acid in urine
  • need to drink lots of water
  • not really used anymore
  • many drug interactions
91
Q

Allopurinol MOA and onset

A
  • xanthine oxidase inhibitor- precents uric acid formation

- 2-3 month onset

92
Q

ADR for Allopurinol

A

increased gout attack when initiated

93
Q

Febuxostat MOA

A
  • xanthine oxidase inhibitor

- chornic gout

94
Q

What is more effective, allopurinol or febuxostat?

A

Febuxostat

95
Q

Pegloticase - when do you use it

A

-use only in refractory gout or when other med have not worked

96
Q

What meds need to be discontinued when starting a pt. on pegloticase?

A

any other uric acid lowering meds

97
Q

What prohylaxic meds need to be given before pegloticase?

A

antihistmaines

corticosteroids

98
Q

3 phases of gout treatment

A

1) acute inflamtion
2) prevent acute inflamation
3) lower uric acid

99
Q

1st phase acute inflamtion gout trt mild

A

no RX preference

100
Q

1st phase acute inflamtion gout trt sever

A
  • cholchisine + NSAID

- steroids + colchasine

101
Q

2nd phase trt gout- preventing acute inflamation

A

colchasine low dose + NSAIDS

102
Q

3rd phase lowering Urich acid levels

A
  • allopurinol

- febuxostat

pharm exam 3 summer (4 decks)

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