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12 Cards in this Set
- Front
- Back
10. List the three treatments used for Vitiligo, and know their mechanism of action(s). Be clear which repigment versus which depigment.
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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 |
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12. Recognize the role of antibody AGGREGATES in SLE. How do these aggregate particularly hurt the circulatory system?
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a. Aggregates in SLE cause inflammation and tissue damage
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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 |
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14. Be able to give the names in a short-answer question of the 3 drugs most likely to induce DILE.
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b. Tope 3 inducers of DILE: procainamide, hydralazine, quinidine
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know the two major tissue pathologies characteristic of RA
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1. Bone loss, synovial membrane overgrowth and inflammation
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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 |
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17. Recognize that MS patients have both increased ____ activity and ____ levels
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T-cell, antibody
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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
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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. |
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list the effects on the CNS/PNS of MS
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i. CNS effects: balance, depression, cognitive deficit
ii. PNS effects: numbness, pain, motor deficit, vision problems |
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19. List the first-line therapies used for treatment of MS.
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a. Avonex/Rebif/ Betaseron: Inhibits TH-cell proliferation
b. Copaxone: antibodies attack drug (myelin-like) |
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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!
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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. |
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21. Recognize the 2 general toxicities believed to be common to all immunosuppressant drugs.
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i. Increased susceptibility to INFECTION
ii. Increased CANCER risk: body won’t be able to attacks and kill cancerous cells if immunosuppressed. |