Part 6.3.3 - Drugs for Rheumatologic Disorder - DMARDs, Glucocorticoids

f. None

DMARDS except:

a. Disease-modifying Antirheumatic Drugs

b. Slow-acting Antirheumatic Drugs

c.Chemically diverse agents

d. Do not just take away the pain, they can instead alter or even reverse disease progression

e. Full effects: 6-12 months

f. None

c. Both

DMARDs can be

a. Nonbiologic or the small molecule drugs

b. Biologic or the large molecule drugs

c. Both

d. None

b. Biologic

Recombinant DMARDs.

a. Nonbiologic

b. Biologic

c. Both

d. None

f. None

Nonbiologic DMARDs except:

a. Methotrexate

b. Antimalarials

c. Gold Compounds

d. Sulfasazaline

e. Leflunomide

f. None

a. Methotrexate

Nonbiologic DMARD:

1st line DMARD

a. Methotrexate

b. Antimalarials

c. Gold Compounds

d. Sulfasazaline

e. Leflunomide

f. None

True about Methotrexate except:

a. Inhibition of AICAR transformylase = ↑ AMP = ↑ release of Adenosine

b. Inhibition of Thymidylate synthetase = ↑ AMP = ↑ release of Adenosine

c. ↑ release of Adenosine: Inhibition of Inflammation

d. Only low dose must be administered.

e. Higher doses induce anti-cancer effect and hepatotoxic

f. None

b. Antimalarials

Nonbiologic DMARD:

2nd line DMARDs.

a. Methotrexate

b. Antimalarials

c. Gold Compounds

d. Sulfasazaline

e. Leflunomide

f. All

MOA of antimalarials such as Hydroxychloroquine & Chloroquine.

a. Inhibit T-lymphocytes responses to mitogens

b. Inhibit movement of inflammatory cells (Chemotaxis)

c. Inhibit DNA & RNA synthesis

d. a and b

e. b and c

f. All

c. Both

Toxic effect/s of antimalarials.

a. Optic neuritis

b. Cinchonism

c. Both

d. None

c. Gold Compounds

Nonbiologic DMARD:

No longer recommended due to significant toxicities as well as questionable efficacy.

a. Methotrexate

b. Antimalarials

c. Gold Compounds

d. Sulfasazaline

e. Leflunomide

f. All

Gold Compounds.

a. Aurothiomalate

b. Aurothioglucose

c. Auranofin

d. a and b

e. b and c

f. All

d. a and b

Parenteral Gold Compounds.

a. Aurothiomalate

b. Aurothioglucose

c. Auranofin

d. a and b

e. b and c

f. All

c. Auranofin

Oral Gold Compounds.

a. Aurothiomalate

b. Aurothioglucose

c. Auranofin

d. a and b

e. b and c

f. All

Gold compounds toxicity

a. Nephrotic syndrome

b. Hypersensitivity

c. Both

d. None

c. Both

Metabolite/s of Sulfasazaline.

a. Sulfapyridine

b. 5-aminosalicylate

c. Both

d. None

a. Sulfapyridine

Metabolite of Sulfasazaline postulated to be active as a DMARD.

a. Sulfapyridine

b. 5-aminosalicylate

c. Both

d. None

b. 5-aminosalicylate

Also known as mesalamine which is applicable to patients with inflammatory bowel disease.

a. Sulfapyridine

b. 5-aminosalicylate

c. Both

d. None

f. All

Toxicities of sulfasalazine.

a. Nausea & Vomiting

b. Skin rashes and discoloration

c. Hemolytic anemia

d. a and b

e. a and c

f. All

e. Leflunomide

Nonbiologic DMARD:

Prodrug metabolized to A77-1726.

a. Methotrexate

b. Antimalarials

c. Gold Compounds

d. Sulfasazaline

e. Leflunomide

e. Leflunomide

Nonbiologic DMARD:

Inhibits dihydroorotate dehydrogenase inhibiting ribonucleotide synthesis resulting to arrest of cell cycle.

a. Methotrexate

b. Antimalarials

c. Gold Compounds

d. Sulfasazaline

e. Leflunomide

c. Both

Biologic DMARD

a. Large molecule drugs

b. Recombinant DNA technology

c. Both

d. None

f. None

Biologic DMARDS except:

a. Abatacept

b. Rituximab

c. Tocilizumab

d. Anakinra

e. TNF-alpha Blockers

f. None

a. Abatacept

Biologic DMARDS:

T-cell modulating biologic; Inhibits activation of T-cells

a. Abatacept

b. Rituximab

c. Tocilizumab

d. Anakinra

e. TNF-alpha Blockers

a. Abatacept

Biologic DMARDS:

Used as monotherapy or in combination with methotrexate in patient with rheumatoid arthritis.

a. Abatacept

b. Rituximab

c. Tocilizumab

d. Anakinra

e. TNF-alpha Blockers

b. Rituximab

Biologic DMARDS:

1) B-cell depleting agent; targets CD20 B-lymphocytes = reduced inflammation

2) Combined with Methotrexate

a. Abatacept

b. Rituximab

c. Tocilizumab

d. Anakinra

e. TNF-alpha Blockers

c. Tocilizumab

Biologic DMARDS:

Inhibits IL-6-mediated signalling.

a. Abatacept

b. Rituximab

c. Tocilizumab

d. Anakinra

e. TNF-alpha Blockers

c. Tocilizumab

Biologic DMARDS:

Used for moderate or severe rheumatoid arthritis (RA).

a. Abatacept

b. Rituximab

c. Tocilizumab

d. Anakinra

e. TNF-alpha Blockers

d. Anakinra

Biologic DMARDS:

1) IL-1 Neutralizing Agent

2) Recommended for RA, but less effective compared to other biologics

a. Abatacept

b. Rituximab

c. Tocilizumab

d. Anakinra

e. TNF-alpha Blockers

a. SC

Route of Anakinra

a. SC

b. ID

c. IV

d. IM

c. Both

Adverse effects of anakinra.

a. Severe infection

b. Irritation at the site of injection

c. Both

d. None

f. None

TNF-alpha Blockers except:

a. Infliximab

b. Certolizumab

c. Adalimumab

d. Golimumab

e. Etanercept

f. None

e. TNF-alpha Blockers

Biologic DMARDS:

1) Inhibit 5-TNF-alpha → Inhibit inflammation → Inhibits symptoms associated with different rheumatologic diseases like RA

2) Adverse effect is severe infection

a. Abatacept

b. Rituximab

c. Tocilizumab

d. Anakinra

e. TNF-alpha Blockers

f. All

Glucocorticoids can be used for.

a. Respiratory disease

b. Rheumatologic disease

c. Endocrine disorder

d. a and b

e. b and c

f. All

f. All

Glucocorticoids.

a. Administered PO (Systemic)

b. Administered IV (Systemic)

c. Administered Intrasynovial (Local)

d. a and b

e. b and c

f. All

d. a and b

Used in management of Rheumatoid Arthritis and Systemic Lupus Erythematosus

a. Glucocorticoids administered PO (Systemic)

b. Glucocorticoids administered IV (Systemic)

c. Glucocorticoids administered Intrasynovial (Local)

d. a and b

e. b and c

f. All

b. Pulse therapy of Methylprednisolone (1000mg IV for 3 days)

Particular for patients who have Life-threatening SLE.

a. Pulse therapy of Methylprednisolone (500mg IV for 5 days) - Intermittently

b. Pulse therapy of Methylprednisolone (1000mg IV for 3 days) - Intermittently

c. Pulse therapy of Methylprednisolone (300mg IV for 3 days) - Intermittently

d. Pulse therapy of Methylprednisolone (1000mg IV for 10 days) - Intermittently

c. Glucocorticoids administered Intrasynovial (Local)

Glucocorticoids.

Used in management of osteoarthritis (OA) that is unrelieved with 1 st line agents like NSAIDs or analgesics.

a. Glucocorticoids administered PO (Systemic)

b. Glucocorticoids administered IV (Systemic)

c. Glucocorticoids administered Intrasynovial (Local)

d. a and b

e. b and c

f. All

c. Glucocorticoids administered Intrasynovial (Local)

Given every 4-6 months only, to prevent joint destruction.

a. Glucocorticoids administered PO (Systemic)

b. Glucocorticoids administered IV (Systemic)

c. Glucocorticoids administered Intrasynovial (Local)

d. a and b

e. b and c

f. All

D. Needle-shaped, negatively birefringent crystals

What crystal shape and birefringence pattern are diagnostic for Gout on synovial fluid analysis?

A. Rhomboid-shaped, positively birefringent crystals

B. Envelope-shaped, non-birefringent crystals

C. Spherical, isotropic crystals

D. Needle-shaped, negatively birefringent crystals

B. Inhibits microtubule formation

What is the mechanism of action of Colchicine in acute gout treatment?

A. Inhibits xanthine oxidase

B. Inhibits microtubule formation

C. Enhances renal excretion of uric acid

D. Converts uric acid into allantoin

C. Diarrhea

What is the chief side effect / watch-out feature of Colchicine?

A. Hypertension

B. Constipation

C. Diarrhea

D. Visual disturbances

A. Purine-based xanthine oxidase inhibitor

What is the mechanism of action of Allopurinol?

A. Purine-based xanthine oxidase inhibitor

B. Non-purine selective xanthine oxidase inhibitor

C. Recombinant uricase enzyme

D. Uricosuric transport inhibitor

B. Non-purine selective xanthine oxidase inhibitor

What is the mechanism of action of Febuxostat?

A. Purine-based xanthine oxidase inhibitor

B. Non-purine selective xanthine oxidase inhibitor

C. Recombinant uricase enzyme

D. Uricosuric transport inhibitor

B. Increased risk of Tuberculosis reactivation

What is the major watch-out risk when using TNF-alpha inhibitors like Adalimumab, Infliximab, or Etanercept?

A. Severe acute pancreatitis

B. Increased risk of Tuberculosis reactivation

C. Irreversible ototoxicity

D. Hyperuricemia

B. Induction of Lipocortin-1, which inhibits Phospholipase A2

What mechanism allows Glucocorticoids (e.g., Methylprednisolone) to reduce inflammation during RA flares?

A. Direct inhibition of COX-2 enzymes

B. Induction of Lipocortin-1, which inhibits Phospholipase A2

C. Blockade of Interleukin-1 receptors

D. Inhibition of Xanthine Oxidase