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12 Cards in this Set

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10. List the three treatments used for Vitiligo, and know their mechanism of action(s). Be clear which repigment versus which depigment.
i. Repigmentation
1. Topical immunosuppressants-reduce autoimmune attack
2. Psoralen PhotoChemotherapy (PUVA)
a. MOA: psoralens react with UV to produce growth factors that stimulate melanocyte proliferation.
ii. Depigmentation-complete
1. Hydroquinone
a. MOA: inhibit tyrosinase enzyme, blocks melanin synthesis
12. Recognize the role of antibody AGGREGATES in SLE. How do these aggregate particularly hurt the circulatory system?
a. Aggregates in SLE cause inflammation and tissue damage
13. List the 7 major tissues affected, and the corresponding pathophysiologies seen with SLE.

(draw your simplified body picture (bleeding) here with the organs affected drawn in)
a. Systemic Lupis Erythematosus - immune aggregates in 7 tissues.

1. Skin Rash
2. Joints/Muscles Arthritis
3. Lung Blood clots. Inflammation
4. Brain Neurological disorder. Seizures
5. Blood Circulatory problems to digits. Hemolytic anemia
6. Kidney Glomerulonephritis
7. Heart Pericardial Inflammation
14. Be able to give the names in a short-answer question of the 3 drugs most likely to induce DILE.
b. Tope 3 inducers of DILE: procainamide, hydralazine, quinidine
know the two major tissue pathologies characteristic of RA
1. Bone loss, synovial membrane overgrowth and inflammation
16. Recognize that RA patients have both increased ____ activity and ____ levels.

Recognize the two major inflammatory mediators released in the synovial space during RA.
T-cell, antibody
IL-1, TNFa
17. Recognize that MS patients have both increased ____ activity and ____ levels
T-cell, antibody
18. ID the main protein target of AI attack in Multiple Sclerosis. Recognize the effect of the loss of this protein on nerve conduction, and the ensuing effects on the CNS/PNS. Explain exactly how and why glatiramer acetate blocks this attack
a. Multiple Sclerosis: auto-immune attack of myelin basic protein - axons no longer effectively conduct signals  nerve cells in the brain and spinal cord fail to communicate with each other.
i. CNS effects: balance, depression, cognitive deficit
ii. PNS effects: numbness, pain, motor deficit, vision problems
b. Glatiramer Acetate (Copaxone) – mimics myelin: antibodies that attack myelin in CNS will attack the drug instead.
list the effects on the CNS/PNS of MS
i. CNS effects: balance, depression, cognitive deficit
ii. PNS effects: numbness, pain, motor deficit, vision problems
19. List the first-line therapies used for treatment of MS.
a. Avonex/Rebif/ Betaseron: Inhibits TH-cell proliferation
b. Copaxone: antibodies attack drug (myelin-like)
20. Explain why glatiramer acetate and natalizumab (Tysabri) are only used for treatment of MS, and not other AI disorders. The answer has to do with their MOAs!
Natalizumab –MS involves demyelination of white matter in CNS. Drug prevent immune cells from leaving the bloodstream to CNS-stopping them from reaching MS lesions in the brain and spinal cord.

Glatiramer Acetate (Copaxone) – mimics myelin.

a. Other AI disorders are not involved with myelin destruction and are not involved with ANS/PNS.
21. Recognize the 2 general toxicities believed to be common to all immunosuppressant drugs.
i. Increased susceptibility to INFECTION
ii. Increased CANCER risk: body won’t be able to attacks and kill cancerous cells if immunosuppressed.