Part 7 DMARDs & Part 8 GLUCOCORTICOIDS

Proverbs 16:3

a. Disease-modifying antirheumatic drugs

DMARDs stands for:
a. Disease-modifying antirheumatic drugs
b. Direct metabolic anti-rheumatic drugs
c. Disease-mediated analgesic response drugs
d. Delayed musculoskeletal anti-inflammatory drugs

a. Chemically diverse agents

DMARDs are best described as:
a. Chemically diverse agents
b. Antibiotics only
c. Opioid analgesics
d. Anticoagulants

b. Alter or reverse disease progression

The primary role of DMARDs is to:
a. Provide immediate pain relief
b. Alter or reverse disease progression
c. Increase platelet aggregation
d. Treat fever and inflammation

b. SAARDs (Slow-acting antirheumatic drugs)

Another term for DMARDs is:
a. NSAIDs
b. SAARDs
c. COX inhibitors
d. Opioid agonists

d. Slow-acting antirheumatic drugs

[DMARDs ]

SAARDs refers to:
a. Strong-acting antirheumatic drugs
b. Selective anti-inflammatory receptor drugs
c. Steroid-acting analgesic response drugs
d. Slow-acting antirheumatic drugs

c. 6–12 months

DMARDs generally achieve full therapeutic effect within:
a. 24–48 hours
b. 1–2 weeks
c. 6–12 months
d. 1–2 days

DMARDs Classification

Gold Compounds =Nonbiologic Agents

Methotrexate =Nonbiologic Agents

Abatacept =Biologic Agents

Tocilizumab =Biologic Agents

TNF-a blockers =Biologic Agents

Anakinra =Biologic Agents

Rituximab =Biologic Agents

Antimalarials =Nonbiologic Agents

Leflunomide =Nonbiologic Agents

Sulfasalazine =Nonbiologic Agents

[DMARDs]

Nonbiologic Agents or Biologic Agents

Gold Compounds =______

Methotrexate =______

Abatacept =______

Tocilizumab =______

TNF-a blockers =______

Anakinra =______

Rituximab =______

Antimalarials =______

Leflunomide =______

Sulfasalazine =______

c. Methotrexate

[DMARDs: Nonbiologic Agents]

Which drug is considered the first-line DMARD?
a. Sulfasalazine
b. Leflunomide
c. Methotrexate
d. Hydroxychloroquine

a. AICAR transformylase and thymidylate synthetase

• ↑ AMP → enhance release of Adenosine

[DMARDs: Nonbiologic Agents]

Methotrexate exerts its anti-inflammatory effect by blocking:

a. AICAR transformylase and thymidylate synthetase
b. T lymphocyte responses to mitogens
c. dihydroorotate dehydrogenase
d. inhibits chemotaxis and inhibits DNA & RNA synthesis

d. Adenosine

[DMARDs: Nonbiologic Agents]

Methotrexate enhances release of:
a. Histamine
b. Serotonin
c. Leukotrienes
d. Adenosine

b. Enhanced adenosine release leading to inhibition of inflammation

[DMARDs: Nonbiologic Agents]

The anti-inflammatory action of methotrexate is mainly due to:
a. Increased thromboxane production leading to inhibition of inflammation
b. Enhanced adenosine release leading to inhibition of inflammation
c. Decreased prostaglandin formation leading to inhibition of inflammation
d. Direct opioid receptor stimulation leading to inhibition of inflammation

a. Chemotaxis

[DMARDs: Nonbiologic Agents]

Methotrexate inhibits inflammation partly by blocking:
a. Chemotaxis
b. Platelet aggregation
c. Cholesterol synthesis
d. Histamine release

b. Anticancer effect

[DMARDs: Nonbiologic Agents]

Higher doses of methotrexate are used for:
a. Antitussive therapy
b. Anticancer effect
c. Antidiarrheal therapy
d. Antipyretic therapy

a. Antimalarials

[DMARDs: Nonbiologic Agents]

Which drug is considered the second-line DMARD?
a. Antimalarials
b. Antivirals
c. Antibiotics
d. Anticancer

a. Hydroxychloroquine and Chloroquine

[DMARDs: Nonbiologic Agents]

Antimalarials used as second-line DMARDs include:
a. Hydroxychloroquine and Chloroquine
b. Ibuprofen and Naproxen
c. Morphine and Codeine
d. Aspirin and Diclofenac

a. Blocking T-lymphocyte responses to mitogens

[DMARDs: Nonbiologic Agents]

Hydroxychloroquine and chloroquine act by:
a. Blocking T-lymphocyte responses to mitogens
b. Blocking of AICAR transformylase and thymidilate synthetase
c. Activating dopamine receptors
d. Increasing uric acid excretion

b. Inhibiting chemotaxis

[DMARDs: Nonbiologic Agents]

Hydroxychloroquine and chloroquine act by:
a. Blocking of AICAR transformylase and thymidilate synthetase
b. Inhibiting chemotaxis
c. Activating dopamine receptors
d. Increasing uric acid excretion

a. DNA and RNA

[DMARDs: Nonbiologic Agents]

Antimalarials inhibit synthesis of:
a. DNA and RNA
b. DNA only
c. RNA only
d. Nucleic Acid

a. Optic neuritis

[DMARDs: Nonbiologic Agents]

A toxic effect of antimalarials is:
a. Optic neuritis
b. Respiratory depression
c. GI bleeding only
d. Hyperglycemia

a. Tinnitus, headache, dizziness

[DMARDs: Nonbiologic Agents]

Cinchonism associated with antimalarials includes:
a. Tinnitus, headache, dizziness
b. Fever, rash, edema
c. Cough, dyspnea, wheezing
d. Tremors, seizures, paralysis

a. Aurothiomalate and Aurothioglucose

[DMARDs: Nonbiologic Agents]

Parenteral gold compounds
a. Aurothiomalate and Aurothioglucose
b. Auranofin
c. Hydroxychloroquine and Chloroquine
d. Leflunomide

b. Auranofin

[DMARDs: Nonbiologic Agents]

Gold compound is given orally
a. Aurothiomalate
b. Aurothioglucose
c. Auranofin
d. Sulfapyridine

a. Sulfapyridine

[DMARDs: Nonbiologic Agents]

Sulfasalazine is metabolized into:
a. Sulfapyridine
b. Morphine and codeine
c. Allantoin and urate
d. Adenosine and AMP

c. 5-aminosalicylate (mesalamine)

[DMARDs: Nonbiologic Agents]

Sulfasalazine is metabolized into:
a. Allantoin
b. A77-1726
c. 5-aminosalicylate (mesalamine)
d. Adenosine

b. Inflammatory bowel disease (IBD)

[DMARDs: Nonbiologic Agents]

Mesalamine (5-aminosalicylate) is commonly used in:
a. Parkinsonism
b. Inflammatory bowel disease (IBD)
c. Acute pulmonary edema
d. Hypercholesterolemia

I. nausea and vomiting

IV. skin rashes and discoloration

VI. hematotoxicities

[DMARDs: Nonbiologic Agents]

Sulfasalazine adverse effects:

I. nausea and vomiting

II. respiratory depression

III. coma

IV. skin rashes and discoloration

V. bronchodilation

VI. hematotoxicities

a. A77-1726

[DMARDs: Nonbiologic Agents]

Leflunomide is metabolized into:
a. A77-1726
b. Sulfapyridine
c. Allantoin
d. 5-aminosalicylate (mesalamine)

b. Dihydroorotate dehydrogenase

[DMARDs: Nonbiologic Agents]

Leflunomide MOA
a. COX-2 only
b. Dihydroorotate dehydrogenase
c. Inhibits chemotaxis and inhibits DNA & RNA synthesis
d. Xanthine oxidase

b. Ribonucleotide synthesis

[DMARDs: Nonbiologic Agents]

Leflunomide decreases inflammation by inhibiting:
a. Inhibits chemotaxis and inhibits DNA & RNA synthesis
b. Ribonucleotide synthesis
c. T lymphocyte responses to mitogens
d. AICAR transformylase

b. T-cell modulating biologic

[DMARDs: Biologic Agents]

Abatacept is classified as a:
a. B-cell depleting biologic
b. T-cell modulating biologic
c. TNF-α blocker
d. IL-1 neutralizing agent

a. Inhibit activation of T cells

[DMARDs: Biologic Agents]

The mechanism of abatacept is to:
a. Inhibit activation of T cells
b. Block xanthine oxidase
c. Neutralize IL-1 directly
d. Deplete CD20 B lymphocytes

a. As monotherapy or combined with methotrexate

[DMARDs: Biologic Agents]

Abatacept may be used:
a. As monotherapy or combined with methotrexate
b. For moderate or severe RA
c. Approved for use in RA (not very effective)
d. Only for pain control

d. B-cell depleting agent

[DMARDs: Biologic Agents]

Rituximab is best described as a:
a. T-cell modulating biologic
b. TNF-α blocker
c. IL-6 inhibitor
d. B-cell depleting agent

c. CD20 B lymphocytes = reduced inflammation

[DMARDs: Biologic Agents]

Rituximab targets which cell marker?
a. CD4 B lymphocytes
b. CD8 B lymphocytes
c. CD20 B lymphocytes
d. COX-2

b. Reducing B lymphocytes and inflammation

[DMARDs: Biologic Agents]

The anti-inflammatory effect of rituximab occurs by:
a. Increasing prostaglandins
b. Reducing B lymphocytes and inflammation
c. Blocking uric acid formation
d. Increasing histamine release

b. Methotrexate

[DMARDs: Biologic Agents]

Rituximab is commonly combined with:
a. Aspirin
b. Methotrexate
c. Ibuprofen
d. Prednisone only

b. Inhibiting IL-6 mediated signaling

[DMARDs: Biologic Agents]

Tocilizumab works by:
a. Neutralizing IL-1
b. Inhibiting IL-6 mediated signaling
c. Blocking TNF-α only
d. Depleting B cells

b. Moderate or severe RA

[DMARDs: Biologic Agents]

Tocilizumab is commonly used for:
a. Mild OA
b. Moderate or severe RA
c. Mild RA
d. Moderate or severe OA

a. IL-1 neutralizing agent

[DMARDs: Biologic Agents]

Anakinra is classified as an:
a. IL-1 neutralizing agent
b. TNF-α blocker
c. Opioid agonist
d. COX inhibitor

a. Rheumatoid arthritis (not very effective)

[DMARDs: Biologic Agents]

Anakinra is approved for use in:
a. Rheumatoid arthritis
b. Acute MI
c. Gout nephropathy
d. Hyperlipidemia

b. It is approved for RA but not very effective

[DMARDs: Biologic Agents]

Which statement about anakinra is true?
a. It is highly effective in RA
b. It is approved for RA but not very effective
c. It blocks IL-6 signaling
d. It depletes B cells

a. Severe injection-site irritation

[DMARDs: Biologic Agents]

A common adverse effect of anakinra is:
a. Severe injection-site irritation
b. Respiratory depression
c. GI bleeding
d. Renal stone formation

a. Adalimumab and Infliximab

[DMARDs: Biologic Agents]

TNF-α blockers
a. Adalimumab and Infliximab
b. Hydroxychloroquine and Methotrexate
c. Rituximab, Tocilizumab, Anakinra
d. Sulfasalazine, Leflunomide, Auranofin

d. Certolizumab and Golimumab

[DMARDs: Biologic Agents]

Which of the following are TNF-α blockers?
a. Leflunomide and Auranofin
b. Hydroxychloroquine and Methotrexate
c. Rituximab and Tocilizumab
d. Certolizumab and Golimumab

d. Etanercept

[DMARDs: Biologic Agents]

Which of the following are TNF-α blockers?
a. Tocilizumab
b. Rituximab
c. Anakinra
d. Etanercept

a. Severe infection

[DMARDs: Biologic Agents]

A major adverse effect of TNF-α blockers is:
a. Severe infection
b. Hyperglycemia
c. Respiratory depression
d. Uric acid stones

a. Local
b. Systemic

[GLUCOCORTICOIDS]

2 ways to administered glucocorticoids
a. Local
b. Systemic
c. Topical
d. Intramuscular

b. PO or IV

[GLUCOCORTICOIDS]

A systemic route of glucocorticoid administration?
a. Intrasynovial only
b. PO or IV
c. Topical cream
d. Subcutaneous

a. Intrasynovial only

[GLUCOCORTICOIDS]

A local route of glucocorticoid administration?
a. Intrasynovial only
b. PO or IV
c. Topical cream
d. Subcutaneous

a. RA and SLE

[GLUCOCORTICOIDS]

Systemic glucocorticoids are commonly used in the management of:
a. RA and SLE
b. Hypercholesterolemia
c. Acute diarrhea
d. Gout nephropathy

b. Systemic lupus erythematosus (SLE)

[GLUCOCORTICOIDS]

Which rheumatologic disease may require life-threatening emergency glucocorticoid therapy?
a. Osteoarthritis
b. Systemic lupus erythematosus (SLE)
c. RA
d. Hyperlipidemia

c. Methylprednisolone

[GLUCOCORTICOIDS]

Pulse therapy with glucocorticoids in severe SLE commonly uses:
a. Prednisone
b. Hydrocortisone
c. Methylprednisolone
d. Dexamethasone only

c. 1000 mg IV for 3 days

[GLUCOCORTICOIDS]

The dose used in pulse therapy for life-threatening SLE is:
a. 100 mg IV for 1 day
b. 500 mg PO for 5 days
c. 1000 mg IV for 3 days
d. 50 mg IM weekly

c. 4–6 months

[GLUCOCORTICOIDS]

Intrasynovial glucocorticoids are commonly given every:
a. Daily
b. Weekly
c. 4–6 months
d. Once yearly only

a. Osteoarthritis unrelieved by NSAIDs or analgesics

[GLUCOCORTICOIDS]

Local (intrasynovial) glucocorticoids are used for:
a. Osteoarthritis unrelieved by NSAIDs or analgesics
b. Hyperuricemia
c. Acute pulmonary edema
d. Anticoagulation