Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Rheumatology > Rheumatology Pharm > Flashcards

Rheumatology Pharm Flashcards

1
Q

Bind and block promoter sites of proinflammatory genes IL-1 alpha and IL-2 beta. Decreased production of tumor necrosis factor alpha

A

glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do glucocorticoids make us more susceptible to infection?

A

decreases adherence of leukocytes to vascular endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What cells that are part of the immune system do glucocorticoids increase the production of from the bone marrow?

A

neutrophils (decreases eosinohils, monocytes, lymphocytes, APCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What vaccines are contraindicated in a patient receiving chronic glucocorticoid therapy?

A

live vaccines (MMR, varicella, small pox)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do you periodically need to monitor for in a patient receiving glucocorticoids?

A

BP, glucose, lipids, eye exam, bone density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Do steroids need dose adjustments in patients who have renal impairment?

A

nope!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What severity level of RA would a patient who has < 5 inflamed joints, no extraarticular dz, negative RF and anti-CCP antibody, and no evidence of erosions on xray?

A

mildly active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Initial treatment recommendations for mild RA and negative RF with good prognostic signs

A

hydroxycholoraquine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In terms of general drug classes, what can be used in addition to DMARDs for short term symptom management of RA?

A

NSAIDs or steroids until DMARDs have taken effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What severity level of RA would a patient who has at least 5 inflamed joints, elevated ESR/CRP, positive RF and ACCP antibody, and radiographic evidence of disease be?

A

moderate to severly active RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Initial treatment choice for a patient who has moderate to severely active RA

A

methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment options for a patient who has moderate to severely active RA who is unable to tolerate methotrexate

A

TNF inhibitors such as Etanercept (Enbrel) or Adalimumab (Humira)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How long does it take for maximal results of RA therapy take effect?

A

3-6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the role of narcotic analgesics in RA?

A

no role unless end stage disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Antimalarial agent that is used as a single agent with mild RA and no evidence of joint destruction and no inflammatory/autoimmune markers on labs. Usually used as add-on to methotrexate tx.

A

Hydroxychloroquine (Plaquenil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Toxicity associated with Hydroxychloroquine (Plaquenil)

A

macular damage. Need eye exam every 6-12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Drug class that Hydroxychloroquine (Plaquenil) decreases the metabolism of (ie increases half-life making it more potent)

A

beta blockers (except atenolol and nadolol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Drug that inhibits angiogenesis and decreases inflammatory cytokines and IgM RF production

A

sulfasalazine (Azulfidine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Needed to break down sulfasalazine into sulfapyridine and 5-aminosalicylic acid

A

coliform bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Toxicity associated with sulfasalazine

A

myelosuppression. Monitor with CBC every 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Most commonly used drug for RA. Reduces neutrophil adhesion. Suppression of cell mediated immunity. Inhibitis IL-1, 6, and 8

A

methotrexate

22
Q

What is methotrexate a structural analog of and needs to be supplemented when patients are on this drug?

A

folic acid

23
Q

What are the toxicities associated with methotrexate?

A

myelosuppression, hepatotoxicity, and pulmonary toxicity

24
Q

Name the TNF inhibitors

A

etanercept (enbrel), infliximab (remicade), adalimumab (humira)

25
Q

bind to tumor necrosis factor-alpha making it inactive interfering with inflammatory activity by decreasing production of IL-6 and CRP

A

TNF inhibitors

26
Q

TNF factor associated with infusion reactions

A

Infliximab (Remicade)

27
Q

Block box warning of TNF inhibitors

A

latent TB infection activation

28
Q

What is used in conjunction with infliximab (remicade) to decrease the development of infliximab antibodies

A

methotrexate

29
Q

Very expensive TNF inhibitor

A

Etanercept (Enbrel)

30
Q

Decreases progression of joint erosions and joint space narrowing. Similar to methotrexate (inhibitor of dihydrofolate reductase) that leads to decreased B and T cell proliferation

A

Leflunomide (Avara)

31
Q

What can reduce the extensive half-life of Leflunomide (Avara) to 1 day?

A

activated charcoal and cholestyramine

32
Q

Blocks IL-1 receptor to decrease degree of joint destruction and inflammation. No known pharmacokinetic drug interactions

A

Anakinra (Kineret)

33
Q

What should you not use in combination with Anakinra (Kineret)?

A

TNF inhibitors

34
Q

Chelating agent used for treatment of

Wilson’s disease, arsenic poisoning, copper, lead and mercury poisoning. Depresses T cell activity

A

D-Penicillamine (Depen, Cuprimine)

35
Q

Inhibits enzymatic activity required for DNA synthesis

Decrease production of T and B cells. Carcinogenic

A

Azithroprine (Imuran)

36
Q

Blocks activation of T cells and IL-2. Many drug interactions that increase it’s concentration. Renal toxicity

A

Cyclosporine A (Sandimmune, Neoral)

37
Q

Black box warning “Only physicians experienced in immunosuppressive therapy…”

A

Cyclosporine A (Sandimmune, Neoral)

38
Q

Has similar efficacy but greater toxicity compared to traditional DMARDs. decreases prostaglandin production

A

gold compounds- Auranofin (Ridaura)

Gold Sodium Thimate (Myochrysine)

39
Q

Meds to avoid with SLE that may cause an exacerbation

A

sulf containing abx, minocyclie, oral contracepties

40
Q

work for both cutaneous and MSK involvement in SLE. may prevent renal and CNS damage

A

Hydroxychloroquine (Plaquenil)

41
Q

Used in SLE for significant organ involvement

A

glucocorticoids

42
Q

What should be include in pharm treatement if a patient with SLE is antiphophlipid antibody positive?

A

Warfarin. antiphospholipid antibody causes a hypercoaguable state

43
Q

First line treatment for acute gout attack

A

NSAIDs- naproxen or indomethacin

44
Q

Second line treatment for acute gout attack

A

colchicine

45
Q

Pharm treatment used to prevent acute gout attacks, but are NOT initiated during an acute attack

A

allopurinol, febuxostat, or probenecid

46
Q

Medications that cause fluid retention and exacerbate CHF

A

NSAIDs and glucocorticoids

47
Q

NSAID that at higher doses doesn’t inrease CV risks

A

Naproxen

48
Q

NSAID that cannot be given to patients with sulfa allergies

A

Celecoxib (Celebrex)

49
Q

What should you give a patient having an acute gout attack who is already on chronic colchicine?

A

give a loading dose

50
Q

Medications that increase uric acid or inhibit renal excretion of uric acid

A

thiazide/loop diuretics, niacin, aspirin

Rheumatology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions