Gout and Rheumatoid Drugs Flashcards

1
Q

What is Podagra

A

1st MTP joint becomes red and painful

textbook sign of gout

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2
Q

What is gout

A

build up of uric acid crystals in the kidneys and joints

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3
Q

What type of immune response causes gout

A

type 3 immune mediated

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4
Q

What can cause gout

A

Purine-rich diet

Alcohol (beer especially)

Kidney disease

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5
Q

Why is gout treated therapeutically

A

To lower uric acid levels (<6mg/dl)

To prevent deposition of uric acid crystals

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6
Q

What are the ways to prevent uric acid build up

A

interfere with uric acid synthesis

Increase uric acid secretion

Inhibit immune cells entry into the joint

decrease inflammation

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7
Q

What is the gold standard for preventing future gout attacks

A

Allopurinol and febuxostat

WILL NOT TREAT

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8
Q

What can be used for acute gout attacks

A

Indomethacin and NSAIDs (Naproxen)

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9
Q

What drug can be used for both acute attacks and prevention

A

Colchicine

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10
Q

What are the two stages of gout

A

Acute and chronic

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11
Q

What stage of gout is indomethacin used in and what does it do

A

Acute attacks

Decreases granulocytes in the area which prevents inflammation

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12
Q

What stage of gout are NSAIDs used in and what does it do

A

Acute attacks

For pain control (DO NOT USE ASA)

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13
Q

What stage of gout is colchicine used in and what does it do

A

Acute mostly but can be both

Decreases immune cell chemotaxis

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14
Q

What stage of gout is allopurinol used in and what does it do

A

Chronic
purine analog that inhibits uric acid synthesis

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15
Q

What stage of gout is probenecid used in and what does it do

A

Chronic
Promotes uric acid excretion and inhibits the secretion of NSAIDs

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16
Q

What can cause an acute gout flare

A

A quick decrease in serum rate concentration

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17
Q

Why does a rapid decrease in serum rate concentration cause gout flares

A

Urate lowering disrupts the physical state and or surface chemical composition of preformed crystal deposits-> component crystals interact with local cells = inflammation

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18
Q

Which class of DMARDs is often used first and why

A

Non-biologics because they are safer and cheaper

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19
Q

What are DMARDs used for

A

RA and other inflammatory arthritis

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20
Q

At what point are DMARDs introduced to RA treatment

A

When intrinsic autoimmune response is going crazy and normal drug options have been exhausted

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21
Q

How to DMARDs help in the treatment of RA

A

Slow the course of disease
induce remission
Prevent further joint damage

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22
Q

When is the best time to initiate DMARD treatment

A

Within 3 months of diagnosis for best possible results

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23
Q

What does folate help with in the body

A

Maintains purine and thymidine synthesis in oral dividing cells

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24
Q

What does methotrexate interfere with

A

folate metabolism

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25
Q

How does methotrexate work

A

Acts as a competitive inhibitor for the enzyme dihydrofolate reductase = inhibition of lymphocyte proliferation in RA

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26
Q

What needs to be supplemented when taking methotrexate

A

folic acid

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27
Q

What’s a benefit of prescribing methotrexate

A

It can be combined with other DMARDs

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28
Q

How long does it take the body to respond to methotrexate

A

3-6 weeks

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29
Q

Common side effects of methotrexate

A

Mucosal ulceration and nausea
myelosuppression (Cytopenia)
Hepatotoxicity
hypersensitivity pneumonitis

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30
Q

What are common CNS side effects from methotrexate

A

Headache
fatigue
malaise
impaired ability to concentrate

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31
Q

What test needs to be preformed on methotrexate and why

A

Blood work (LFT & CBC) to monitor bone marrow

32
Q

When is hydroxychloroquine used

A

In early and mild RA and also in lupus

33
Q

Can hydroxychloroquine be prescribed as a monotherapy

A

No, needs methotrexate otherwise joint damage will not be slowed

34
Q

What is the mechanism of action for hydroxycholroquine

A

inhibition of phosolipase
antagonism for prostaglandins
decreased platelet aggregation
Inhibition of endosomal activation
suppressed antioxidant activity

35
Q

When should hydroxychloroquine dose be reduced

A

When patients have renal insufficiency

36
Q

Possible side effects of hydroxychloroquine

A

Headache
nausea/vomiting (Most common)
skin rash/pruritis
Occular toxicity

37
Q

What happens with ocular toxicity

A

Visual changes and retinopathy

Need routine eye exam, including right before starting

38
Q

What drugs could hydroxychloroquine effect

A

Digoxin
telbivudine
penicillamine

39
Q

How does Leflunomide help with RA

A

Causes cell arrest of autoimmune lymphocytes

inhibits pyrimidine synthesis which interferes with DNA that is needed for proliferation

40
Q

What are common side effects of Leflunomide

A

Headache, nausea, diarrhea

higher risk for opportunistic infection

41
Q

What type of inhibitor is Leflunomide and what does it interact with

A

Reversible inhibitor of dihydrooroate dehydrogenase (DHODH)

42
Q

What is DHODH

A

Enzyme necessary for pyrimidine synthesis

43
Q

When is Leflunomide contraindicated

A

in pregnancy

44
Q

What is sulfasalazine and when is it used

A

Been used for decades to treat IBD but can also treat RA

45
Q

How is sulfasalazine metabolized

A

By gut bacteria into 5-ASA and sulfapyridine

46
Q

What does 5-ASA do

A

Reduces inflammation by suppressing prostaglandin synthesis

47
Q

What does sulfapyridine do

A

Causes adverse side effects

48
Q

What are common reactions to sulfasalazine

A

N/V
Diarrhea
abdominal pain
dermatologic reaction

49
Q

What is it important to monitor while on sulfasalazine

A

Liver function and bone marrow

At higher risk for hepatitis and myelosuppression

50
Q

What are common biologic DMARDs

A

Anakinra, Etanercept, Infliximab, adalimumab, rituximab

51
Q

What is the brand name of etanercept

A

Enbrel

52
Q

How does Enbrel work

A

Genetically engineered fusion protein that binds to TNF-a

53
Q

When is etanercept most effective

A

When combined with methotrexate

54
Q

How is etanercept administered

A

SQ 2x/week

55
Q

What is a common reaction of enbrel

A

Local inflammatory reaction

56
Q

What is the brand name of infliximab

A

Remicade

57
Q

How does infliximab work

A

Chimeric IgG antibody that binds TNF-a

58
Q

How is infliximab administered

A

As a combination therapy with methotrexate and as a infusion over 2 hours every few months

59
Q

Why is infliximab not recommended as a monotherapy

A

Anti-infliximab antibodies may develop

60
Q

What are the adverse effects of infliximab

A

Infusion reaction (Fever, chills, urticaria)

Increased risk of infection

61
Q

What is the brand name of adalimumab

A

Humira

62
Q

How does adalimumab work

A

Human recombinant antibody that binds to TNF-a

63
Q

Is Humira and mono therapy or combination therapy

A

Can be either

64
Q

How is Adalimumab administered

A

SQ injection either weekly or bi-weekly

65
Q

What are adverse effects of humira

A

Headaches or nausea

Local inflammatory reaction at infusion site

Increased risk of infection

66
Q

What is the brand name of rituximab

A

Rituxam

67
Q

How does rituximab work

A

Genetically engineered chimeric murine/human monoclonal antibody directed against CD20 antigen on B-cell surface

68
Q

What is the cellular result of taking rituximab

A

B cell apoptosis through complement activation and antibody dependent cell-mediated cytotoxicity

69
Q

When is rituximab indicated

A

Patients who have had inadequate response to anti-TNF therapies

70
Q

What is given prior to rituximab infusion and why

A

Methylpredisolone
30min prior
Reduce severity of infusion reaction

71
Q

When is Anakinra indicated

A

Only when you have run out of all other treatment options

72
Q

How does Anakinra work

A

IL-1 receptor antagonist

73
Q

What can’t Anakinra be combined with

A

TNF inhibitors

74
Q

How is Anakinra administered

A

SQ injection daily or every other day

75
Q

What are the adverse side effect of Anakinra

A

Neutropenia and increased risk of infection