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Pharm exam module 2 > Gout and Rheumatoid Drugs > Flashcards

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
How does methotrexate work
Acts as a competitive inhibitor for the enzyme dihydrofolate reductase = inhibition of lymphocyte proliferation in RA
26
What needs to be supplemented when taking methotrexate
folic acid
27
What's a benefit of prescribing methotrexate
It can be combined with other DMARDs
28
How long does it take the body to respond to methotrexate
3-6 weeks
29
Common side effects of methotrexate
Mucosal ulceration and nausea myelosuppression (Cytopenia) Hepatotoxicity hypersensitivity pneumonitis
30
What are common CNS side effects from methotrexate
Headache fatigue malaise impaired ability to concentrate
31
What test needs to be preformed on methotrexate and why
Blood work (LFT & CBC) to monitor bone marrow
32
When is hydroxychloroquine used
In early and mild RA and also in lupus
33
Can hydroxychloroquine be prescribed as a monotherapy
No, needs methotrexate otherwise joint damage will not be slowed
34
What is the mechanism of action for hydroxycholroquine
inhibition of phosolipase antagonism for prostaglandins decreased platelet aggregation Inhibition of endosomal activation suppressed antioxidant activity
35
When should hydroxychloroquine dose be reduced
When patients have renal insufficiency
36
Possible side effects of hydroxychloroquine
Headache nausea/vomiting (Most common) skin rash/pruritis Occular toxicity
37
What happens with ocular toxicity
Visual changes and retinopathy Need routine eye exam, including right before starting
38
What drugs could hydroxychloroquine effect
Digoxin telbivudine penicillamine
39
How does Leflunomide help with RA
Causes cell arrest of autoimmune lymphocytes inhibits pyrimidine synthesis which interferes with DNA that is needed for proliferation
40
What are common side effects of Leflunomide
Headache, nausea, diarrhea higher risk for opportunistic infection
41
What type of inhibitor is Leflunomide and what does it interact with
Reversible inhibitor of dihydrooroate dehydrogenase (DHODH)
42
What is DHODH
Enzyme necessary for pyrimidine synthesis
43
When is Leflunomide contraindicated
in pregnancy
44
What is sulfasalazine and when is it used
Been used for decades to treat IBD but can also treat RA
45
How is sulfasalazine metabolized
By gut bacteria into 5-ASA and sulfapyridine
46
What does 5-ASA do
Reduces inflammation by suppressing prostaglandin synthesis
47
What does sulfapyridine do
Causes adverse side effects
48
What are common reactions to sulfasalazine
N/V Diarrhea abdominal pain dermatologic reaction
49
What is it important to monitor while on sulfasalazine
Liver function and bone marrow At higher risk for hepatitis and myelosuppression
50
What are common biologic DMARDs
Anakinra, Etanercept, Infliximab, adalimumab, rituximab
51
What is the brand name of etanercept
Enbrel
52
How does Enbrel work
Genetically engineered fusion protein that binds to TNF-a
53
When is etanercept most effective
When combined with methotrexate
54
How is etanercept administered
SQ 2x/week
55
What is a common reaction of enbrel
Local inflammatory reaction
56
What is the brand name of infliximab
Remicade
57
How does infliximab work
Chimeric IgG antibody that binds TNF-a
58
How is infliximab administered
As a combination therapy with methotrexate and as a infusion over 2 hours every few months
59
Why is infliximab not recommended as a monotherapy
Anti-infliximab antibodies may develop
60
What are the adverse effects of infliximab
Infusion reaction (Fever, chills, urticaria) Increased risk of infection
61
What is the brand name of adalimumab
Humira
62
How does adalimumab work
Human recombinant antibody that binds to TNF-a
63
Is Humira and mono therapy or combination therapy
Can be either
64
How is Adalimumab administered
SQ injection either weekly or bi-weekly
65
What are adverse effects of humira
Headaches or nausea Local inflammatory reaction at infusion site Increased risk of infection
66
What is the brand name of rituximab
Rituxam
67
How does rituximab work
Genetically engineered chimeric murine/human monoclonal antibody directed against CD20 antigen on B-cell surface
68
What is the cellular result of taking rituximab
B cell apoptosis through complement activation and antibody dependent cell-mediated cytotoxicity
69
When is rituximab indicated
Patients who have had inadequate response to anti-TNF therapies
70
What is given prior to rituximab infusion and why
Methylpredisolone 30min prior Reduce severity of infusion reaction
71
When is Anakinra indicated
Only when you have run out of all other treatment options
72
How does Anakinra work
IL-1 receptor antagonist
73
What can't Anakinra be combined with
TNF inhibitors
74
How is Anakinra administered
SQ injection daily or every other day
75
What are the adverse side effect of Anakinra
Neutropenia and increased risk of infection

Pharm exam module 2 (2 decks)

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