By B. Berek. Oklahoma State University. 2017.
On physical examination cheap 20mg levitra jelly visa, the circumference of her right leg is increased trusted 20mg levitra jelly. Which of the following tests would be helpful in the acute setting to determine the cause of her sus- pected hypercoagulable state? AT-III level Key Concept/Objective: To understand the implications of timing on the workup of a hypercoag- ulable state In this young woman with a history of DVTs, a hypercoagulable state should be suspect- ed. In acute thrombosis, many clotting factor inhibitors are consumed, and therefore, an assessment of the levels of these inhibitors would not be useful. If plasma levels are high, it would be possible to argue that the patient does not have a hereditary deficiency; levels could be low secondary to the acute event or to an inherited cause. Some of the coagula- tion cascade inhibitors that are consumed immediately after a clotting event are protein C, protein S, and AT-III. Factor V Leiden mutations can be tested at any time. A 44-year-old white woman presents with pain and swelling in her left lower extremity. In the past, she experienced one other episode of DVT, for which she underwent treatment with warfarin for 6 months. She takes no medications except oral contracep- tive pills. Her family history is significant in that, last year, a younger sister was diagnosed as having DVT. Which of the following statements is true regarding the treatment of this patient? She should again be treated with warfarin for 6 months B.
The optic nerve leaves the orbit through the optic canal (lesser wing of the sphenoid bone) order levitra jelly 20mg amex, in close proximity to the ophthalmic artery and the cavernous sinus levitra jelly 20 mg line. The optic nerve enters the middle cranial fossa and joins the optic nerve from the other eye to form the optic chiasm. Signs While direct pupillary reaction to light is absent, the pupillary reaction can be evoked indirectly. Toxic optic neuropathy: Alcohol Anilin dye Amoproxan Ara C (high dose) Arsenic Aspidium (antihelmintic drug) Cafergot Carbon disulfide Carbon tetrarchloride Chinin Chinolin derivates Chlorambucil (edema of the retina) Chloramphenicol Digitalis Disulfiram Docetaxel: may cause visual sensations (“visual field flash”) Ethambutol Isoniazid Lead Mercury (Hg) Nitrosurea and radiation Nitrous oxide (N2O) Thallium Vincristine Vascular: Ischemic optic neuropathy due to: Amyloidosis Arteritis cranialis Herpes zoster Retrobulbar optic neuropathy Systemic lupus erythematosis (SLE) 37 Infectious: Meningitis Sarcoid Syphilis Tuberculosis Focal infection: Granulomatous disease Sinusitis Inflammatory: Optic neuritis due to demyelinating diseases (MS, neuromyelitis optica) Nutritive: Alcohol ingestion B12 anemia Cuban neuropathy Methylol toxicity Strachan’s syndrome Tobacco alcohol amblyopia Compression: Apoplexy of the pituitary Carotid aneurysm Endocrine orbitopathy Orbital tumors Inflammatory causes of compression: syphilis, tuberculosis, arachnitis opto- chiasmatica Tumors: Metastases Melanocytoma Meningeal carcinomatosis (see Fig. Compression occurs in 50% of pituitary adenomas; other potential causes include craniopharyngeoma (in childhood), meningeoma of the tuberculum sellae, aneurysm, tumors of the chiasm itself (spongioblastoma, meningioma, neuronoma, or retinoblastoma). Paraneoplastic: Rarely involved in paraneoplastic dysfunction: CAR (carcinomatous retino- pathy) Hereditary: Charcot-Marie-Tooth (CMT) Leber’s disease Lysosomal disease Storage disease (Tay Sachs) Spinocerebellar disease 38 Ataxias: Friedreich’s ataxia Mitochondrial – NARP Syndrome: (Neuropathy; Ataxia; Retinitis Pigmentosa) Posterior column ataxia + Retinitis pigmentosa Iatrogenic: Pressure on the eye bulb caused by anesthesia (ischemic optic nerve neuro- pathy), blepharoplasty, fractures of the orbit, or surgery of the nasal sinus. Radiation: Radiation therapy of brain tumors, pituitary tumors, metastases, or ENT tumors can cause uni- or bilateral loss of vision with long latencies. Progressive optic nerve atrophy is seen within 6 weeks of exposure to 70 Gy (units of gray). Trauma: “Blow out” fractures Gunshot wounds Penetrating trauma Trauma of the orbit Traumatic optic neuropathy Diagnosis Diagnosis is based on X-ray, CT, or MRI imaging, visual function and color discrimination tests, ophthalmoscopic exam, visual evoked potentials (VEP), and electroretinogram (ERG). Differential diagnosis Other causes of papilledema should be considered, including increased intra- cranial pressure (ICP) and pseudotumor cerebri. Therapy Treatment depends upon the cause of the lesion. References Acheson J (2000) Optic nerve and chiasmal disease. J Neurol 247: 587–596 Lee AG, Brazis PW (2000) Neuro-ophthalmology. In: Evans RW, Baskin DS, Yatsu FM (eds) Prognosis of neurological disorders.
