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Pharmacology II > Exam 3: Autoimmune diseases > Flashcards

Exam 3: Autoimmune diseases Flashcards

1
Q

What occurs during immune system dysfunction

A

Self-tolerance and Immune tolerance fail, activated T lymphocytes and antibodies attack the individual’s own cells.

  • RESULTS:
    • tissue damage and altered physiologic function
    • causes release of a greater quantity of self antigen
    • initiates adaptive immune response via activated T lymphocytes or antibodies
  • ** THESE REACTIONS = AUTOIMMUNITY
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2
Q

What genes predispose to autoimmune disease

A

Major histocompatibility complex (MHC) genes

  • Encode cytokines and are recognized by T lymphocytes for antigen processing
  • many autoimmune diseases are linked to specific MHC alleles
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3
Q

List diseases classified as familial autoimmunity:

A
  1. Thyroid disease
  2. Systemic Lupus Erythematosus
  3. Rheumatoid arthritis
  4. Multiple sclerosis
  5. type 1 diabetes mellitus
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4
Q

Autoimmune diseases are often preceded by what? (See slides 13&14 to study more..

A

Infection

- triggers local immune response
- produces immune attack against self-antigens * - Cytokines and other chemical messengers released locally from foreign antigens activate antigen-specific T lymphocytes and self-reactive T lymphocytes * - Antigens released from injured tissues that have been damaged due to infection may also initiate an autoimmune reaction
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5
Q

How do autoantibodies initiate disease and give example of each

A
  1. Alter/inhibit receptor function (no tissue damage)
    * *Myasthenia graves = acetylcholine receptors are inhibited; neurotransmission fails, resulting in paralysis
  2. Stimulate receptors that would normally be stimulated by a hormone
    * *Hyperthyroidism = antibodies against the thyroid-stimulating receptor stimulate thyroid cells directly
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6
Q

Organ specific autoimmune disease is mediated by what cells?

A

Mediated by T lymphocytes

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7
Q

Treatment for oran specific autoimmune disease

A

reduce inflammation
= corticosteroids, anticytokine therapies

  • Effects reduce the severity of tissue reactions that promote inflammation
  • Large dosages produce significant atrophy of the lymphoid tissues throughout the body
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8
Q

Why are steroids considered for Organ Specific autoimmune diseases?

A
  1. suppress the growth of lymph tissues

2. decrease T lymphocytes and antibodies produced from B lymphocytes

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9
Q

Why does steroid treatment for organ specific autoimmune disease increase susceptibility to infection?

A

Large dosages produce significant atrophy of lymphoid tissues throughout the body.
- This decreases the production of T lymphocytes and antibodies from the lymph tissues, which decreases immunity and increases susceptibility to infection

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10
Q

Main ideas for autoimmune disease treatment

A

Reduce inflammation (steroids)
Antagonists (blockers) to cytokines
-**Immunosuppressvie drugs are used to inhibit T cell responses

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11
Q

T or F, Goals of therapy for autoimmune disease RA are curative

A

False, therapy goals are palliative

  • Reduce joint inflammation and swelling
  • relieve pain and stiffness
  • encourage normal function
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12
Q

Which two drugs are cornerstones of treatment for the autoimmune disease RA

A

Aspirin and NSAIDS are cornerstones

- reduce inflammation (swelling), pain and fever

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13
Q

List the adverse effects of aspirin on autoimmune disease

A
  1. Adverse gastrointestinal effect
  2. Effects on kidney
    • retention of sodium and water
    • may cause hyperkalemia
  3. Special senses adverse effects
    • *Tinnitus is sign of toxicity to aspirin
  4. Respiratory system
    • Toxic levels may cause central respiratory paralysis = respiratory acidosis
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14
Q

What is the sign of toxicity to aspirin

A

Tinnitus

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15
Q

Name some oral complications of aspirin and NSAIDS

A

Prolonged bleeding

Oral aphthous ulceration/Aphthous stomatitis

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16
Q

Action of sulfasalazine (Azulfidine)

A

Interferes with prostaglandin synthesis

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17
Q

Indication of sulfasalazine (Azulfidine)

A

Used for treatment of RA in patients with inadequate response to aspirin and NSAIDS

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18
Q

Side effects of sulfasalazine (Azulfidine)

A

headache, photosensitivity, GI distress, anorexia

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19
Q

Is it ok to use celebrex with aspirin?

A

Yes, OK to use with low dose aspirin

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20
Q

List the adverse cardiovascular risks of celebrex

A
  1. increased risk for stroke
  2. Monitor patient’s blood pressure when used with antihypertensives = decrease effectiveness of BP meds
  3. Increased risk for heart attack
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21
Q

Celebrex is contraindicated in what patients

A
  1. Aspirin/NSAID allergic patients

2. Allergic to sulfonamides

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22
Q

Define DMARDS

A

Disease-modifying anti-rheumatic drugs

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23
Q

In what patients are DMARDS used

A

Used for treatment of RA and OA

Patients who do not respond to COX-2 inhibitors

24
Q

How quickly do DMARDS act?

A

Slow onset of action

- May take 3-4 months to see effects

25
Q

Name the 4 preparations of DMARDS

A
  1. Immune modulator
  2. Antimalarials
  3. Penicillamine
  4. Gold compounds
26
Q

List the immune modulator drug names

A
  1. methotrexate

2. leflunomide (Arava)

27
Q

How long does a response occur to methotrexate after starting treatment?

A

Response within 3-6 weeks

- faster than other DMARDS

28
Q

What are the two indications for methotrexate?

A
  1. High dose = chemotherapy

2. Low dose = immune modulator for autoimmune diseases

29
Q

List the adverse effects of methotrexate

A
  • Most common = mucosal ulcerations, nausea
  • Chronic use =
    • Cytopenias - depression of WBC count
    • Cirrhosis of liver
    • Acute pneumonia-like syndrome
30
Q

Mechanism of leflunomide (Arava)

A

Inhibits pyrimidine synthesis, resulting in anti-proliferative and anti-inflammatory effects

31
Q

Effects of leflunomide (Arava)

A
  • reduces pain and inflammation

- Slows progression of structural damage

32
Q

What is the drug of choice for severe RA or psoriatic arthritis (unresponsive to NSAIDS)

A

methotrexate

33
Q

Most common side effects of leflunomide (Arava)

A

headache
diarrhea
nausea

34
Q

Describe the purpose for anticytokine therapies and why the would be effective

A

IL-1b and TNF-a are “pro inflammatory cytokines” involved in pathogenesis of RA.

  • When secreted by macrophages, the cytokines stimulate synovial cells to proliferate and produce collagenous, which degrees cartilage, stimulates bone resorption and inhibits proteoglycan synthesis
  • *Drug antagonists to these cytokines are effective in treating RA
35
Q

Name the anticytokine therapy drugs

A
  1. etanercept (Enbrel)
    - TNF alpha blocker
  2. infliximab (Remicade)
    - TNF alpha blocker
  3. adalimumab (Humira)
    - TNF alpha blocker
  4. anakinra (Kineret)
    - Interleukin-1 receptor antagonist
36
Q

Indication of etanercept (Enbrel)

A

Moderate to severe RA

37
Q

Side effects and risks of Enbrel

A

Risk: risk for activation of hepatitis and tuberculosis in carriers
Side effects:
- headache, injection site reaction, upper respiratory tract infections

38
Q

Mechanism of action for infliximab (Remicade)

A

Inhibits progression of structural damage and improves physical function in patients with moderate to severe disease

39
Q

What occurs with long-term use of infliximab?

A

associated with developing antibodies against the drug, unless the drug is combine with methotrexate

40
Q

Side effects of infliximab

A

infections leading to pneumonia, cellulitis; blood dyscrasias

41
Q

Indication for Humira

A

Treatment of moderate to severe RA in patients with inadequate response to one or more DMARDS

42
Q

Humira causes what effects?

A

decreases signs and symptoms, and structural damage

43
Q

Side effects of Humira

A

Headache, Nausea, rash, injection site reaction

44
Q

Indication for anakinra (Kineret)

A

Treatment of moderate to severe RA in patients who have failed one or more DMARDS

45
Q

Anakinra (Kineret) causes what effects

A

Slows degradation of cartilage and bone loss

46
Q

Side effects of anakinra (Kineret)

A

headache, injection site reaction, infections

47
Q

Name the Antimalarial drugs

A
  1. chloroquine (Aralen)

2. hydroxychloroquine (Plaquenil)

48
Q

Indications of Antimalarial drugs

A

Treatment of RA that is unresponsive to NSAIDS

- may be used in combination with aspirin and/or corticosteroids

49
Q

Effects of antimalarials

A

Slow progression of erosive bone lesions

50
Q

Side effects of Antimalarial drugs

A

Severe effects/toxicity!

  • severe eye damage
  • blue-black intramural pigmentation
51
Q

Action of Penicillamine

A

chelating agent (also used as antidote for heavy metal poisoning)

52
Q

Effects of Penicillamine

A

Slows the progression of bone destruction and RA

53
Q

Mechanism for Penicillamine

A

Depresses circulating IgM rheumatoid factor, depresses T-cell activity

54
Q

Indication for Penicillamine

A

Used for RA treatment after gold salts have failed, but before use of corticosteroids

55
Q

Side effects of Penicillamine

A

dermatologic, nephritis, aplastic anemia

56
Q

Oral complications with penicillamine

A

Infection
Delayed healing
Prolonged bleeding
Oral ulcerations

Pharmacology II (24 decks)

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