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Pharmacology > Drugs for Arthritis > Flashcards

Drugs for Arthritis Flashcards

1
Q

NSAIDs work by blocking _____ synthesis, which is why they make ____ drugs less effective.

A

Block PROSTAGLANDIN synthesis

Diuretics (induce renal PG synthesis)

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2
Q

What is a prostaglandin?

A

Derived from arachidonic acid (AA), a fatty acid that is ingested in the diet and stored as a phospholipid

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3
Q

List 3 prostaglandins responsible for producing vasodilation.

A
  1. PGAs
  2. PGEs
  3. Prostacyclin (PGI2)
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4
Q

List 2 prostaglandins that produce vasoconstriction, make platelets sticky, and produce pain.

A
  1. PGF

2. Thromboxane

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5
Q

List 2 important functions of prostaglandins.

A
  1. Stabilizing gastric mucosal lining

2. Maintaining renal artery vasodilation

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6
Q

REFER TO SLIDE 4

A

DIAGRAM OF ENZYME BREAKDOWN (IMPORTANT)

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7
Q

List the 3 isoforms of cyclooxygenase enzyme and where they are found.

A
  1. Cox-1: platelets, kidneys and stomach
  2. Cox- 2: induced in inflammation, infection or activated by inflammatory cytokines (IL-1 and tumor necrosis factor); found in synoviocytes, endothelial cells and macrophages
  3. Cox-3: human brain, spinal cord and heart
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8
Q

Cox-3 Is inhibited by _____ but insensitive to _____.

A

Inhibited by ACETAMINOPHEN

Insensitive to ASPIRIN

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9
Q

What is the MOA of aspirin?

A

Inhibits cyclooxygenase and therefore blocks production of prostaglandins and thromboxanes

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10
Q

What are 5 indications for the use of aspirin?

A
  1. Decrease pain
  2. Decrease Fever
  3. Decrease inflammation
  4. Prevents thrombus formation
  5. Reduce risk of colon cancer (reduce opioid dose)
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11
Q

How does aspirin produce analgesic effects, anti-inflammatory responses, and antiplatelet actions?

A
  1. Analgesic effect: decreased production of prostaglandins that sensitize nociceptors
  2. Anti-inflammatory response: blockade of prostaglandin-induced increased vascular permeability
  3. Anti-platelet action: arises from irreversibly binding to platelet
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12
Q

List 5 ADRs associated with the use of aspirin.

A
  1. GI problems ranging from minor stomach discomfort to hemorrhage and ulceration 2. Renal dysfunction
  2. Anemia secondary to blood loss
  3. Thrombocytopenia
  4. Bronchospasm (5%)
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13
Q

Even normal doses of aspirin can cause between __ and __ mL of blood loss in the feces/day.

A

3 and 8mL

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14
Q

List 6 signs associated with aspirin overdose.

A
  1. Headache
  2. Tinnitus
  3. Confusion
  4. Respiratory hyperventilation
  5. Later respiratory depression
  6. Metabolic acidosis
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15
Q

What is the MOA of NSAIDs?

A

Reversibly inhibits the Cox enzyme with varying effects on Cox-1 versus Cox-2

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16
Q

_____ are more potent than aspirin at equal doses and have almost identical beneficial and adverse effects with the exception that they are not used for _____.

A

Cardiac protection

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17
Q

List 4 ADRs affecting the CNS relative to NSAID use.

A
  1. Cognitive dysfunction
  2. Confusion
  3. Behavioral disturbances
  4. Dizziness
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18
Q

NSAIDs can ______ blood pressure by inhibiting vasodilating prostaglandins.

A

INCREASE

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19
Q

How do NSAIDs negatively affect muscle?

A

Negatively affect satellite cells crucial for muscle hypertrophy and strengthening

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20
Q

NSAIDs decrease the effectiveness of what 3 drugs?

A
  1. Diuretics
  2. Beta Blockers
  3. ACE inhibitors
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21
Q

What is the MOA of Cox 2 inhibitors?

A

Block the action of COX-2 enzyme

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22
Q

List 3 indications for the use of Cox 2 inhibitors.

A
  1. Musculoskeletal pain reduction
  2. Prevent aspirin and NSAID GI complications (hypertensive affect remains)
  3. Do not inhibit platelet aggregation but inhibit post op pain
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23
Q

Cox 2 inhibitors are linked to increased _____ events due to possible inhibition of ______ formation and lack of a positive effect on ______.

A
  1. Cardiovascular events
  2. Prostacyclin (PCI2)
  3. Platelet aggregation
24
Q

What is the MOA of acetaminophen?

A

Inhibits cyclooxygenase enzyme in CNS

25
Q

List 3 indications for the use of acetaminophen.

A
  1. Pain
  2. Fever
  3. NOT inflammation unless at 4g/day
26
Q

True or False: Acetaminophen interfere with the cardioprotective effects of aspirin.

A

FALSE

Acetaminophen does not interference with cardioprotective effects of aspirin

27
Q

List 2 ADRs associated with acetaminophen use.

A
  1. Increased BP

2. Liver toxicity at 10-15g

28
Q

What are 2 sxs associated with liver toxicity? How is this treated?

A
  1. Nausea/Vomitting
  2. Hepatotoxicity 24 hours later

Treatment with acetylcysteine if caught early

29
Q

Significant effect on arterial properties is seen at an aspirin dose of ____ mg/day but not at ___ mg/day

A

325 mg/day

100mg/day

30
Q

What is rheumatoid arthritis? What pro-inflammatory cytokine is released by the inflamed synovium?

A
  1. Inflamed synovium secretes large amounts of proinflammatory cytokines specifically Tumor Necrosis Factor-a (TNF-a).
  2. Inflammation and joint destruction.
31
Q

_____ induces c-reactive proteins (CRP) which is a predictor of _____ risk and severe RA.

A

IL-6 (interleukin 6)

Cardiovascular risk

32
Q

What is the MOA of corticosteroids? (4)

A
  1. Activates a protein that inhibits phospholipase A2
  2. Interferes with inflammation cell adhesion and migration through vascular endothelium
  3. Impairs leukotriene and prostaglandin synthesis
  4. Impairs transport of immune complexes
33
Q

What is an indication for the use of corticosteroids in patients with RA?

A

Bridge between acute flare up and DMARDs (Disease Modifying Anti-Rheumatoid Drugs)

DMARDs take long time to activate so provide corticosteroid until DMARD kicks in

34
Q

What is the dosing of corticosteroids? What is the dosing if the corticosteroid is injected directly into the joint?

A
  1. May be given 1X/day or several times/day in split doses

2. If injected directly into joint: rule is not to exceed more than four injections in one year

35
Q

_____ is given to prevent bone lose with corticosteroid use.

A

Alendronate

36
Q

List 10 ADRs associated with corticosteroid use.

A
  1. catabolic effect on all types of supportive tissue
  2. Osteoporosis
  3. Muscle wasting
  4. Hypertension
  5. Aggravation of diabetes
  6. Glaucoma
  7. Cataracts
  8. Obesity
  9. Cushings
  10. Hypothalmic-pit-adrenal suppression
37
Q

_______ can occur if a patient abruptly discontinues corticosteroids.

A

Hypothalmic-pit-adrenal suppression (adrenal crisis)

38
Q

Why should you never abruptly withdraw steroids?

A

Creates an adrenal crisis

Need to withdraw slowly to allow body to begin to produce cortisol again.

39
Q

_____ is a conventional synthetic DMARD.

A

Methotrexate

40
Q

List 4 MOAs of methotrexate,

A
  1. Folic acid antagonist that impairs DNA synthesis,
  2. Dec cytokines ( IL-1, TNFa, IL-6 and IL-8)
  3. Inhibits proliferation of rapidly replicating monocytes & lymphocytes- Immunosuppressant
  4. Inhibits leukotriene synthesis
41
Q

List 5 ADRs associated with methotrexate.

A
  1. GI problems
  2. Bone marrow suppression
  3. Liver dysfunction
  4. Hair loss
  5. Mucosal ulcers
42
Q

______ is a targeted synthetic DMARD.

A

Tofacitinib (Janus Kinase Inhibitor)

43
Q

What is the MOA of Tofacitinib?

A

Inhibits enzyme responsible for activating IL-2, IL-4, IL-5, and IL-21 these are responsible for triggering inflammation

44
Q

List 2 ADRs associated with the use of Tofacitinib.

A
  1. Neutropenia

2. Increased cholesterol

45
Q

______ is a biologic DMARD.

A

TNF-A inhibitor (tumor necrosis factor alpha)

46
Q

What is the MOA of TNF-A inhibitors?

A

Formed by two TNF receptors fused to a human immunoglobulin so it binds to TNF-a to prevent its binding to its true receptor-a TNF decoy

47
Q

List 5 ADRs associated with TNF-A inhibitors.

A
  1. Infections
  2. Lupus-like syndrome
  3. Upper respiratory tract infection
  4. Reactivation of TB
  5. Postmarketing reports: HF, anemia
48
Q

TNF-A inhibitors are given either by ____ or _____.

A

Subcutaneous injection

Intravenous infusion

49
Q

TNF-A inhibitors are all given with _____ for improved effectiveness.

A

Methotrexate

50
Q

List 2 biologic DMARDs that are non-TNF inhibitors.

A
  1. Interleukin-6 Inhibitor: Tocilizumab (Actemra); ADRs high rates of infection & high LDL
  2. Abatacept (Orencia): prevents activation of lymphocytes
51
Q

When should a patient start taking DMARDs for RA? How long can it take for visible improvement to be present?

A
  1. Take as soon as diagnosis is made
  2. May take weeks to months for visible improvement
  3. Maximal efficacy may take up to 6 months but some improvement not seen in 3 months then tx must be modified
52
Q

____ should be part of the initial DMARD treatment, along with low dose _____ <7.5 mg/day.

A

Methotrexate (MTX)

Prednisone

53
Q

What drug should be taken when initial treatment with traditional DMARDs is not effective?

A

Biologic DMARDs

54
Q

List 3 ADRs associated with biologic DMARDs.

A
  1. Tuberculosis reactivation
  2. Greater risk of contracting viral infections including herpes and even hepatitis B and C
  3. TNF inhibitors may have an increased risk of developing cancer
55
Q

List 5 rehab concerns to be aware of in patients with RA.

A
  1. monitor for fatigue and bone marrow depression
  2. Monitor for infection
  3. Check for skin rashes
  4. Allow for adequate hydration
  5. Consider catabolic effects of steroids during ROM and strengthening procedures
56
Q

_____ and _____ are used to treat OA.

A

NSAIDs

Acetaminophen

Pharmacology (12 decks)

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