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Pharm: Psych > 3.2: Rheumatoid > Flashcards

3.2: Rheumatoid Flashcards

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1
Q

What is RA?

A
  • Chronic inflammatory disease of the joints that is autoimmune in nature
  • Leads to pain and destruction of the joints
  • Etiology is unknown
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2
Q

Important mediators of RA?

A
  1. IL6 / 1
  2. TNF alpha
  3. T and B cells
  4. Prostaglandins
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3
Q

2 categories of RA drugs?

A
  1. To decrease joint pain
    a. NSAIDs
    b. Analgesics: acetaminophen
    c. Glucocorticoids: dexamethasone
  2. To control joint damage:
    a. DMARDs: “Disease modifying antirheumatic agents”
    b. BRM: Biologic response modifiers”
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4
Q

What is dexamethasone?

A

Glucocorticoid that can be used in symptomatic treatment of RA

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5
Q

Which are the DMARDs?

A
  1. Methotrexate
  2. Sulfasalazine
  3. Hydroxychloroquine
  4. Leflunomide
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6
Q

Characteristics of DMARDs?

A
  • Prevent joint damage and reduce pain
  • Take weeks - months to be efficacious
  • Course is months - years
  • Thought to inhibit the immune system
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7
Q

2 indications of Hydroxychloroquine?

A
  1. Mild RA: often with other DMARDs

2. Malaria

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8
Q

Mechanisms of Hydroxychloroquine?

A
  1. Inhibits TLR signalling in B cells

2. Inhibits APC to T cells

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9
Q

Onset of Hydroxychloroquine?

A

3 - 6 monthsq

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10
Q

Side effects of Hydroxychloroquine?

A
  1. Blindness: higher with LT treatment, high dose, age

* **Safe during pregnancy and lactation

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11
Q

Which DMARD safe for pregnancy / lactation?

A

1 Hydroxychloroquine

2. Sulfasalazine

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12
Q

Relative efficacy and toxicity of Sulfasalazine?

A
  • Similar efficacy to Methotrexate

- More toxic than Hydroxychloroquine

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13
Q

MOA of Sulfasalazine?

A
  • Thought to inhibit T an B cell responses: NFKB
  • Prodrug converted by gut bacteria into sulfapyridine
  • Sulfapyridine is the active component
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14
Q

Onset of Sulfasalazine?

A

1 - 3 months

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15
Q

Side effects of Sulfasalazine?

A
  1. Agranulocytosis: fully reversible, monitor
  2. Hepatotoxicity
    * ***Safe in pregnancy
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16
Q

Drug of choice for active, severe RA?

A

Methotrexate

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17
Q

Other indication for Methotrexate?

A

Cancer: used at 1/100 - 1/1000 dose less for RA

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18
Q

Onset of Methotrexate?

A

4 - 6 weeks

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19
Q

MOA of Methotrexate?

A
  • Increases adenosine which slows immune system

- Shown to decrease appearance of new bone erosions

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20
Q

Drug shown to decrease appearance of new bone erosions?

A

Methotrexate

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21
Q

Side effects of Methotrexate?

A
  1. Hepatotoxicity: no alcohol
  2. Pulmonary toxicity
  3. Renal toxicity
  4. Marrow suppression
  5. Increased risk of lymphoma
  6. Teratogen
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22
Q

Metabolism of methotrexate?

A

90% renal excretion

- DO NOT USE IN PTN WITH COMPROMISED RENAL

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23
Q

Who is Methotrexate contraindicated in?

A
  1. Pregnancy/breast feeding: abortive agent
  2. Liver disease
  3. Renal disease
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24
Q

Indication of Leflunomide?

A
  • Alternative to those who are unable to take or are unresponsive to methotrexate
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25
Q

Onset of Leflunomide?

A

1-2 months

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26
Q

What is Leflunomide a low cost alternative to?

A
  • The TNF inhibitors

- Also is taken oral rather than IV which is added benefit

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27
Q

MOA of Leflunomide?

A
  • Inhibits dihydroorotate dehydrogenase responsible for synthesis of Uridine
  • Arrests cell in G1
    1. Inhibits T cell proliferation
    2. Inhibits B cell production of Ig
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28
Q

Side effects of Leflunomide?

A
  1. Htn: increased if using NSAIDS
  2. GI / Rash
  3. Hepatotoxicity: Increased with methotrexate
    - Monitor LFTs
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29
Q

What should not be taken with methotrexate?

A

Leflunomide: High rate of liver toxicity

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30
Q

Contraindications of Leflunomide?

A
  1. Pregnancy

2. Liver disease

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31
Q

Which drugs should not be taken in pregnancy?

A
  1. Leflunomide

2. Methotrexate

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32
Q

Importance of TNF alpha?

A
  • Cytokine regulating inflammatory response
  • Made by CD4 T cells, macs, and masts
  • **Signals for the following pathways:
    1. Bone resorption: osteoclasts
    2. Cartilage breakdown: chondrocytes/synoviocytes
    3. Joint inflammation: Leukocytes
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33
Q

What are the anti TNF alpha?

A
  1. Adalimumab
  2. Etanercept
  3. Infliximab
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34
Q

MOA of anti TNFs?

A
  • Bind to TNF alpha preventing it from binding to its receptor
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35
Q

Route of Anti TNFs?

A
  • Subcutaneous or IV
  • ## Given weekly or b weekly
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36
Q

Efficaciousness of anti TNFs?

A

As effective as methotrexate

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37
Q

Onset of AntiTNFs

A
  • 1-4 weeks
38
Q

Impact of Anti TNFs?

A
  1. Decreased swelling and pain
  2. Decrease new erosions
  3. Decreased progression of structural damage
39
Q

What are anti TNFs often used with?

A

Methotrexate if not responding to metho

40
Q

Side effects of TNFs?

A
  1. Increased opportunistic infections
  2. Reactivate latent TB and HBV
  3. Exacerbation of CHF
  4. MS
  5. Lymphoma
  6. Sepsis: in acute / chronic infection
41
Q

What to screen for before anti TNFs?

A
  1. Latent TB infection

2. Latent Hep B

42
Q

What type of drugs is Adalimumab?

A

TNF alpha inhibitor

43
Q

What type of drugs is Etanercept?

A

TNF alpha inhibitor

44
Q

What type of drugs is Infliximab?

A

TNF alpha inhibitor

45
Q

Which drug is a T cell inhibitor?

A

Abatacept

46
Q

Which drug is a B cell inhibitor?

A

Rituximab

47
Q

Which drug is an IL6 inhibitor?

A

Tocilizumab

48
Q

Which drug is an IL1 inhibitor?

A

Anakinra

49
Q

What type of drug is Abatacept?

A

T cell inhibitor

50
Q

What type of drug is Rituximab?

A

B cell inhibitor

51
Q

What type of drug is Tocilizumab?

A

IL 6 inhibitor

52
Q

What type of drug is Anakinra?

A

IL 1 Inhibitor

53
Q

MOA of Abatacept?

A

T cell inhibition via blocking CD28 stimulation

54
Q

Who is Abatacept particularly effective in?

A

Patients unresponsive to TNF alpha inhibitors

55
Q

Adverse effects of Abatacept? What to not give with?

A
  1. Reactivation of TB / HBV

* ***Do not give with TNF alpha blockers

56
Q

MOA of Rituximab?

A

Binds to CD20 on B cells depleting them from body

57
Q

Onset of Rituximab?

A

3 months but 1 injection can last 6 - 24 months

58
Q

Which drug has longest course of action after it is administered?

A

Rituximab

59
Q

Adverse effects of Rituximab?

A
  1. PML: “Progressive multifocal leukoencephalopathy”
    - fatal demyelination
  2. Increased infection
  3. Reactivation of latent infections
60
Q

Drug known to cause PML?

A

Rituximab

61
Q

MOA of Anakinra?

A

IL 1 Receptor antagonist

62
Q

Route of anakinra?

A

Sub q once daily: 4 - 6 hour half life

63
Q

Adverse effect of anakinra?

A
  1. Neutropenia

2. Same as others

64
Q

Drug causing neutropenia?

A

Anakinra

65
Q

What should not be combined with biologiques?

A
  • Other Biologiques

- Can be used with DMARDs, however

66
Q

Side effects of Tocilizumab?

A
  1. Bone marrow suppression
  2. Hepatotoxicity: Monitor LFTs
  3. Increased cholesterol
  4. Cancer
  5. Infections
67
Q

Which drug inhibits cytokine signalling?

A

Tofacitinib: Inhibits JAK tyrosine kinases

68
Q

MOA of Tofacitinib?

A

Inhibits cytokine signalling via JAKs

69
Q

Toxicity of Tofacitinib?

A
  1. Marrow suppression
  2. Hepatotoxicity: increased cholesterol
  3. Increased infections
70
Q

Alternative to methotrexate as disease progresses?

A

Leflunomide, progressing to biologique

71
Q

What is gout linked to?

A
  1. Purine rich diet: meat, booze
  2. Metabolic syndromes
  3. Overproduction or decreased excretion of uric acid
    * **Usually decreased excretion
72
Q

Where does gout usually first present?

A

In the big toe

73
Q

What are tophi?

A

Urate crystal deposits around joint promoting inflammation and joint destruction

74
Q

Drugs used for acute gout?

A
  1. Chclocicine
  2. NSAIDs
    * ***Also use during chronic treatment to prevent acute attack
75
Q

Which drugs promote uric acid excretion

A
  1. Uricosuric agents: probenecid
76
Q

Which drugs inhibit uric acid synthesis?

A
  1. Allopurinol

2. Febuxostat

77
Q

Which drugs directly degrade uric acid?

A
  1. Pegloticase
78
Q

Which pain relievers should not be used for gout?

A
  1. Aspirin
  2. Salicylates
    * *Will induce gout at low doses but not at high
79
Q

What is Chclocicine?

A
  • Plant alkaloid preventing tubulin polymerization
  • Decreases leukocyte migration and phagocytosis
  • Anti Inflammatory with NO analgesics
  • Give in first 24 - 48 hours of attack
80
Q

Side effects of Colchicine?

A
  1. Nausea, vomiting, diarrhea

Therapeutic window is narrow and overlaps with side effects

81
Q

MOA of probenecid?

A
  • Inhibits anion transport in prox tubule

- Increased uric acid excretion

82
Q

When do give chronic gout drugs?

A
  • Not within 3 weeks of actual attack
  • Can initiate or prolong symptoms
  • **Prophylaxis with NSAID to decrease this risk
83
Q

Contraindications of probenecid?

A
  1. Uric acid overproduction: kidney stones
  2. Renal insufficiency
  3. Kidney stones
84
Q

MAO of allopurinol and febuxostat?

A
  • Inhibition of xanthine oxidase

- Xanthine oxidase catalyzes final two steps in purine degradation

85
Q

Who are allopurinol and febuxostat best in?

A
  1. High level of endogenous level of uric acid
  2. Recurrent kidney stones
  3. Presence of tophi
86
Q

Side effects of allopurinol and febuxostat?

A
  1. Allopurinol hypersensitivity: deadly
    - Renal disease, high dose, asians more likely
    * **Febuxostat does not cause this
  2. Thrombocytopenia
87
Q

DDI of allopurinol and febuxostat?

A

6-mercaptopurine and azathioprine (prodrug)

88
Q

Treatment goal of gout?

A

Serum uric acid

89
Q

Drug to use in overproduction?

A

Allopurinol

90
Q

Drug to use in undersecretion?

A

Probenecid

91
Q

Allopurinol indications?

A
  1. Tophi
  2. Renal failure
  3. Kidnestones
92
Q

Administration of Pegloticase?

A
  • IV infusion every 2 weeks

- Effective more rapidly than others

Pharm: Psych (7 decks)

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