Medication Summary
The goals of pharmacotherapy are to reduce morbidity and prevent complications.
Corticosteroids
Class Summary
These agents have antiinflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Prednisone (Sterapred)
Used as an immunosuppressant in the treatment of vasculitis and autoimmune disorders. It decreases inflammation by suppression of migration of polymorphonuclear leukocytes and reversal of increased capillary permeability, suppresses the immune system by reducing activity and volume of the lymphatic system, and suppresses adrenal function at high doses.
Immunosuppressant agents
Class Summary
These agents interfere with processes that promote immune reactions resulting from diverse stimuli.
Cyclophosphamide (Cytoxan, Neosar)
Alkylating agent. Activated in the liver to its active metabolite, 4-hydroxycyclophosphamide, which alkylates the target sites in susceptible cells. The mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.
When used in autoimmune diseases, mechanism of action is thought to involve immunosuppression due to destruction of immune cells via DNA cross-linking.
In high doses, affects B cells by inhibiting clonal expansion and suppression of production of immunoglobulins. With long-term, low-dose therapy, affects T cell functions.
Azathioprine (Imuran)
Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. Mechanism whereby azathioprine affects autoimmune diseases unknown. Works primarily on T cells. Suppresses hypersensitivities of cell-mediated type and causes variable alterations in antibody production. Immunosuppressive, delayed hypersensitivity, and cellular cytotoxicity tests are suppressed to a greater degree than antibody responses. Works very slowly; may require 6-12 mo of trial prior to effect. Up to 10% of patients may have idiosyncratic reaction disallowing use. Do not allow WBC count to drop below 3000/mL or lymphocyte count to drop below 1000/mL.
Calcium channel blockers
Class Summary
Inhibits calcium ions from entering slow channels or select voltage-sensitive areas of vascular smooth muscle.
Nifedipine (Adalat, Procardia)
Inhibits calcium ion from entering the slow channels or select voltage-sensitive areas of vascular smooth muscle producing vasodilation.
Nimodipine (Nimotop)
For improvement of neurologic impairments resulting from cerebrovascular spasms.
Nimodipine shares the pharmacology of other calcium channel blockers; animal studies indicate that nimodipine has a greater effect on cerebral arteries than other arteries; this increased specificity may be due to the drug's increased lipophilicity.
Verapamil (Calan, Calan SR, Covera-HS, Verelan)
Inhibits calcium ion from entering the slow channels or select voltage-sensitive areas of vascular smooth muscle during depolarization; produces relaxation of vascular smooth muscle and vasodilation; slows automaticity and conduction of AV node.
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Lateral right internal carotid angiogram shows beading of anterior cerebral arteries (arrowheads) and beading (straight arrows), segmental dilatation (curved arrow), and narrowing of middle cerebral arteries (open arrow).
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Low power view of inflamed vessel in the subarachnoid space shows fibrinoid necrosis (pink areas) superiorly.
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Higher power view of small inflamed vessel in the medulla, with fibrinoid necrosis in the wall and chronic transmural inflammation.
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(a) T1-weighted left parasagittal MRI showing hypointense lesions in the cortical and subcortical white matter of the left superior temporal gyrus and frontal and frontoparietal operculum with sulcal obliteration. (b) The postgadolinium MRI at this level showing nodular parenchymal and linear pial enhancement.
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(a) T2-weighted axial MRI showing hyperintense lesions in the lentiform nuclei, head of the caudate nuclei and frontoparietal subcortical white matter. (b) On T1-weighted (postgadolinium) axial image, the lentiform nuclei and head of caudate nuclei are heterogeneously hypointense, while subcortical white matter lesions are isointense. Linear areas of pial enhancement are seen bilaterally.
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(a) T2-weighted axial MRI showing large, well-defined hyperintense lesions in the left frontal and parietal lobes. (b) Postgadolinium T1-weighted axial MRI showing nodular parenchymal and cortical-pial enhancement of the lesion. A follow up (after 3 mo) T2-weighted axial (c) and postgadolinium (d) T1-weighted axial MRIs showing significant reduction of the lesion size and nodular enhancing areas.
