Anti Inflammatory And Corticoids Flashcards

1
Q

3 goals of RA therapy?

A

Stop inflammation, relieve symptoms, and prevent joint and organ damage

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2
Q

7 non drug therapies for RA?

A

Rest, exercise, PT, OT, nutrition and diet, bone protection, lower CV risk.

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3
Q

What is drug of choice for additional pain relief? What is the first drug of choice for RA and why?

A

Acetaminophen

NSAIDS because of anti inflammatory action and pain relief

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4
Q

3 mechanism of actions for prednisone?

A

Through GR
GR complexing with NFKB and AP1
Lipocortin, an inhibitor of PLA2

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5
Q

What is the clinical application for using prednisone?

A

Autoimmune diseases like RA
Relieve pain and inflammation while waiting for DMARD effects
Flare ups

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6
Q

How is prednisone converted to its active form?

A

The liver converts prednisone, which is a pro drug, to prednisone

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7
Q

What is the idea in mind when using prednisone for active RA?

A

Use it for a short time to quickly minimize disease activity while waiting for DMARDs to kick in. Not a great idea to use chronic, but if you are, use it with DMARDs and less than 5mg a day.

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8
Q

How many joints are involved in mild RA and what is the initial treatment for it?

A

5 and under

DMARD monotherapy and consider giving glucos for flare ups

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9
Q

How many joints involved in moderate RA, what are two big differences between mild and moderate as far as labs, what would be initial treatment for moderate?

A

Greater than 5
Rheumatoid factor and antibodies against CCP
Combination DMARDS with glucos for flare ups or
TNF inhibitor with glucos for flare ups, maybe MTX
Non TNF maybe MTX glucos for flare ups

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10
Q

What is the mechanism of action of methotrexate, 3 things?

A

Becomes MTX PG which leads to blocking thymidine synthesis, blocks purine synthesis, and adenosine activating purinergic G protein receptors for ani inflammatory effect.

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11
Q

What is unique to methotrexate effect and what is the most significant clinical application?

A

Quickest acting of DMARDs 3-6 weeks

First line drug of choice for RA

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12
Q

2 most common adverse effects of Methotrexate and what 3 adverse effects with chronic administration?

A

Mucosal ulcers and nausea

Cytopenias (particularly WBC), cirrhosis, and pneumonia

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13
Q

How is sulfasalazine metabolized and what is the clinical application for it?

A

It is metabolized to 5 ASA (active agent in IBD) and sulfapyridine (active agent in RA)
Early mild RA with methotrexate and/or hydroxy. This is the triple therapy.

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14
Q

2 most common adverse effects of sulfasalazine?

A

GI and leukopenia

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15
Q

MOA of leflunomide and its clinical application?

A

Inhibition of DHODH to block synthesis of rUMP that causes cell arrest in autoimmune lymphocytes (particular T cells).
Alternative nonbiological DMARD to methotrexate, so second choice drug.
Can be used in combination with DMARDs as well.

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16
Q

5 most common adverse effects for leflunomide?

A

Diarrhea, respiratory infections, alopecia, rash and nausea

17
Q

What is the MOA and effect of hydroxychloroquine?

A

Increases pH in lysosomes of antigen presenting cells (auto antigens is key here) and limits association with peptides from MHC.

18
Q

3 clinical applications of hydroxy and what is the 1 adverse effect to know?

A

First choice for RA by itself or with methotrexate.
Lupus
Malaria

retinal damage

19
Q

Two DMARDs Ok for pregnancy?

A

Hydroxy and sulfa

20
Q

What is the general rules of biologic DMARDs?

A

Can combine with non biological DMARDs but never with another biologic DMARD.

Typically faster onset and high rate of response
More expensive and increased risk for severe adverse effects

21
Q

4 anti inflammatory cytokines to know?

A

6, 10, 23 and TGFbeta.

22
Q

MOA of TNF antagonists, 2 effects, clinical application, 2 adverse effects?

A

Neutralize TNF
Reduce RA symptoms and disease progression
Moderate to severe RA
Serious infections and severe allergic reactions

23
Q

MOA, clinical pplciaiton and administration of etanercept?

A

Protein that has 2 receptors for 2 TNF molecules
RA, psoriasis, and AS
Subq once or twice a week

24
Q

MOA of infliximab, clinical application and administration?

A

Monoclonal antibody to TNF
RA with methotrexate, IBD and other inflammatory conditions
IV every 6-8 weeks

25
Q

MOA of adalimumab, clinical application and administration?

A

Full human monoclonal antibody against TNF
RA, psoriasis, AS, and Crohns
Sub q every week or two.

26
Q

MOA of Rituximab, clinical application, 1 adverse effect to know?

A

Anti cd20
Moderate to severe RA in combo with methotrexate in pts who have not responded to TNF blockers
Infusion hypersensitivity reactions

27
Q

Once rituximab binds the B cell, what are the 3 ways it can destroy the B cell?

A

Complement, direct lysis via NK, and phagocytosis

28
Q

MOA of abatacept, clinical application, 1 adverse effect?

A

Block CD80/86 on B cell from activating T cells
Moderate to severe RA in patients who haven’t responded to DMARDs or TNF blockers
Serious infections

29
Q

MOA of tocilizumab, clinical application, 1 adverse effect?

A

Antibody against IL6
Moderate to severe RA when DMARDs and TNF blockers don’t work
Upper respiratory infections

30
Q

MOA of tofacitinib, clinical application, 2 adverse effects?

A

Jak3 blocker
Moderate to severe RA in patients who don’t response to methotrexate
Secondary malignancies and opportunistic infections

31
Q

MOA for anakinra, clinical application and 2 adverse effects?

A

IL1 receptor blocker
Moderate to severe RA
Infections and hypersensitivity reactions