Exam 3: Autoimmune diseases Flashcards Preview

Pharmacology II > Exam 3: Autoimmune diseases > Flashcards

Flashcards in Exam 3: Autoimmune diseases Deck (56):
1

What occurs during immune system dysfunction

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

2

What genes predispose to autoimmune disease

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

3

List diseases classified as familial autoimmunity:

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

4

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

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

5

How do autoantibodies initiate disease and give example of each

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

6

Organ specific autoimmune disease is mediated by what cells?

Mediated by T lymphocytes

7

Treatment for oran specific autoimmune disease

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

8

Why are steroids considered for Organ Specific autoimmune diseases?

1. suppress the growth of lymph tissues
2. decrease T lymphocytes and antibodies produced from B lymphocytes

9

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

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

10

Main ideas for autoimmune disease treatment

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

11

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

False, therapy goals are palliative
- Reduce joint inflammation and swelling
- relieve pain and stiffness
- encourage normal function

12

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

Aspirin and NSAIDS are cornerstones
- reduce inflammation (swelling), pain and fever

13

List the adverse effects of aspirin on autoimmune disease

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

14

What is the sign of toxicity to aspirin

Tinnitus

15

Name some oral complications of aspirin and NSAIDS

Prolonged bleeding
Oral aphthous ulceration/Aphthous stomatitis

16

Action of sulfasalazine (Azulfidine)

Interferes with prostaglandin synthesis

17

Indication of sulfasalazine (Azulfidine)

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

18

Side effects of sulfasalazine (Azulfidine)

headache, photosensitivity, GI distress, anorexia

19

Is it ok to use celebrex with aspirin?

Yes, OK to use with low dose aspirin

20

List the adverse cardiovascular risks of celebrex

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

21

Celebrex is contraindicated in what patients

1. Aspirin/NSAID allergic patients
2. Allergic to sulfonamides

22

Define DMARDS

Disease-modifying anti-rheumatic drugs

23

In what patients are DMARDS used

Used for treatment of RA and OA
Patients who do not respond to COX-2 inhibitors

24

How quickly do DMARDS act?

Slow onset of action
- May take 3-4 months to see effects

25

Name the 4 preparations of DMARDS

1. Immune modulator
2. Antimalarials
3. Penicillamine
4. Gold compounds

26

List the immune modulator drug names

1. methotrexate
2. leflunomide (Arava)

27

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

Response within 3-6 weeks
- faster than other DMARDS

28

What are the two indications for methotrexate?

1. High dose = chemotherapy
2. Low dose = immune modulator for autoimmune diseases

29

List the adverse effects of methotrexate

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

30

Mechanism of leflunomide (Arava)

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

31

Effects of leflunomide (Arava)

- reduces pain and inflammation
- Slows progression of structural damage

32

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

methotrexate

33

Most common side effects of leflunomide (Arava)

headache
diarrhea
nausea

34

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

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

Name the anticytokine therapy drugs

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

Indication of etanercept (Enbrel)

Moderate to severe RA

37

Side effects and risks of Enbrel

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

38

Mechanism of action for infliximab (Remicade)

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

39

What occurs with long-term use of infliximab?

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

40

Side effects of infliximab

infections leading to pneumonia, cellulitis; blood dyscrasias

41

Indication for Humira

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

42

Humira causes what effects?

decreases signs and symptoms, and structural damage

43

Side effects of Humira

Headache, Nausea, rash, injection site reaction

44

Indication for anakinra (Kineret)

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

45

Anakinra (Kineret) causes what effects

Slows degradation of cartilage and bone loss

46

Side effects of anakinra (Kineret)

headache, injection site reaction, infections

47

Name the Antimalarial drugs

1. chloroquine (Aralen)
2. hydroxychloroquine (Plaquenil)

48

Indications of Antimalarial drugs

Treatment of RA that is unresponsive to NSAIDS
- may be used in combination with aspirin and/or corticosteroids

49

Effects of antimalarials

Slow progression of erosive bone lesions

50

Side effects of Antimalarial drugs

Severe effects/toxicity!
- severe eye damage
- blue-black intramural pigmentation

51

Action of Penicillamine

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

52

Effects of Penicillamine

Slows the progression of bone destruction and RA

53

Mechanism for Penicillamine

Depresses circulating IgM rheumatoid factor, depresses T-cell activity

54

Indication for Penicillamine

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

55

Side effects of Penicillamine

dermatologic, nephritis, aplastic anemia

56

Oral complications with penicillamine

Infection
Delayed healing
Prolonged bleeding
Oral ulcerations