Consider the following medical report that includes the patient's historical health records. Use it to predict the disease that the patient is high likely exposed to. 

 Medical Report: allergies: phenobarbital attending: chief complaint: intraparenchymal hemorrhage major surgical or invasive procedure: endotracheal intubation radial arterial line placement history of present illness: 82 yo woman wtih history of htn, hl, tia, persistent afib on coumadin was transferred from osh for right parenchymal hemorrhage. 2am, she was noticed to be confused by husband. over the day, she remained confused, and she was brought into osh ed. there she developed gtc seizure (duration not documented) and intubated for airway protection. she received ativan (unknown amount) which resolved seizure. head ct showed 2 x2 cm r occipital parenchymal hemorrhage. she was transferred to ed for further care. ros: unable to obtain from patient. past medical history: hypertension hypercholesterolemia sdh tia paf on coumadin social history: no etoh,smoking, drugs. family history: non-contributory physical exam: t98.7 hr105 bp180/66 rr17 sao2 100% intubated. general: intubated, no distress. heent: conjunctiva not anemic, sclera not icteric. neck: supple, no carotid bruit cv: rrr, nl s1 and s2, no murmurs/gallops/rubs lung: clear to auscultation bilaterally abd: soft, flat, no tenderness ext: no arthralgia, no deformities, no edema neurological exam: mental status: opens eyes with voice. opens and closes right hand, but inconsistently. able to follow command to move eyes with full eom. cranial nerves: r surgical pupil. l eye reactive, 4 to 3mm. does not blink to the threat from the right. eye closure is weaker at the left side. motor: keeps flexed arms. hypotonic at the left arm. bilateral legs have spasticity. poor spontaneous movement at the left. sensation: withdrawal at all extrimeties, more so at the right. reflexes: b t br pa ankle right 3 3 3 3 3 left 3 3 3 3 3 toes up at the left, mute at the right. meningeal sign: negative brudzinski sign. no nucal rigidity. pertinent results: labs: 128 91 7 - - - - - - gluc 125 3.4 23 0.6 ck: 80 mb: pnd wbc 8.3 hct 38.1 plt 333 n:83.3 l:13.0 m:2.9 e:0.5 bas:0.1 pt: 31.8 ptt: 37.9 inr: 3.4 head ct (@osh): 2 cm x 2 cm r parieto-occipital hemorrhage with small surrounding edema, no mass effect. head ct (@ ed): stable size (21x23mm) intraparenchymal hemorrhage. small edema, no mass effect. ct head w/o contrast 10:45 am again seen is a right parieto-occipital hematoma measuring approximately 2.7 cm in size with surrounding vasogenic edema which is not significantly changed allowing for technical differences. no new intracranial hemorrhages are identified. the ventricles and sulci are prominent as before. there are extensive white matter hypodensities which likely represent chronic microangiopathic changes. vascular calcifications are noted bilaterally. the visualized orbits show cataract surgical changes. right-sided nasogastric tube is in place. the visualized paranasal sinuses, mastoid air cells, middle ear cavities are clear. no suspicious bony abnormalities are seen. impression: no significant change in the right parieto-occipital hematoma with surrounding vasogenic edema compared to . ekg : technically difficult study sinus rhythm with atrial premature complexes cannot rule out atrial fibrillation with pvcs intraventricular conduction delay incomplete lbbb inferior/lateral st-t changes may be due to myocardial ischemia since previous tracing of , rhythm more irregular, qrs interval wider mri/a brain: findings: the right medial parietal lobe hemorrhage is re-demonstrated, with a moderate amount of surrounding edema. within the hemorrhage is a small fluid level. there iss extensive high t2 signal within the periventricular white matter of both cerebral hemispheres, as well as a probable punctate focus within the right cerebellar hemisphere. these abnormalities are consistent with chronic small vessel infarction, and appear to have been present on a prior mr study obtained at this institution on . additionally, as was noted on the prior study, there are numerous tiny foci of susceptibility scattered throughout the brain. as many of them have a somewhat peripheral location, as was suggested before, amyloid angiopathy may be present, and if so, would certainly account for the new right medial parietal lobe hemorrhage. there were no areas of pathological enhancement seen intracranially, including the area of hemorrhage within the right parietal lobe. the principal vascular flow patterns are observed, aside from the proximal basilar artery. this latter finding, in retrospect was probably present on the prior mr scan and raises the question of a proximal occlusion or high-grade stenosis of this vessel. conclusion: 1. right parietal lobe hemorrhage, probably related to underlying amyloid angiopathy. 2. findings raise the question of a proximal basilar artery occlusion or high-grade stenosis, likely seen on the prior study as well. mr angiography of the circle of and its tributaries technique: three-dimensional time-of-flight imaging with multiplanar reconstructions. findings: unfortunately the image quality of the mr p images is degraded by extensive overlying t1 hyperintensity from fat within the skull base. nevertheless, when reviewing the source images, there is the impression that the proximal basilar artery is occluded, aside from a small segment in its distal portion. as was stated above, this finding was probably present at the time of the study. conclusion: findings suggest the presence of a proximal basilar artery occlusion, likely chronic in age. the remaining vascular tributaries of the circle of are patent. 2 chest xrays confirm placement of ngt, show no infiltrate, show some mild left-sided atelectasis brief hospital course: 82 yo woman wtih history of htn, hl, tia, persistent afib on coumadin was transferred from osh for right parenchymal hemorrhage. initial neurological examination showed left hemiplegia and also possible right side upper motor neuron signs as well, suggesting a possible old stroke on the left in addition to new pathology in the right hemisphere. she had been reversed with ffp and vitamin k at an outside hospital prior to transfer to the er at , and she received more of each while at . she was loaded with dilantin and transferred to the icu for further monitoring on the stroke/icu service. head ct showed a right parieto-occipital hemorrhage. mri/a confirmed the location of the hemorrhage, and as several "microbleeds" were apparent, the etiology of the hemorrhage was felt to be related to an underlying diagnosis of amyloid angiopathy, with elevated risk of hemorrhage on coumadin (with supratherapeutic inr reported as "11"). her inr normalized after further reversal and she had no more seizures. she was extubated without complications. in the icu, she was noted to have waxing and mental status, thought in part due to the location of the hemorrhage (right hemisphere) and compounded by worsening of her baseline hyponatremia. her blood pressure was elevated and she was thus maintained on an esmolol drip in the icu for several days before being transferred to the floor. she was maintained on standing dilantin for seizure control. her hyponatremia (na 126 range) gradually corrected with fluid restriction, and over time it normalized to her "baseline" of 134 range. her mental status improved with this change, and by the time of discharge she was alert and conversant, despite occasionally falling asleep during conversation. though she could not name the hospital itself, she knew she was in the hospital in , and she knew the season was fall (guessed , rather than ). her naming was somewhat poor due to some inattention and perseveration as well, connoting perhaps a pre-stroke diagnosis of frontal lobe dysfunction, exacerbated by the hemorrhage itself. these mental status findings were felt by the stroke team to likely improve with time. fluid restriction was discontinued and salt tabs were continued. she should have her sodium level rechecked at rehab in days to ensure stability. her swallowing ability was initially impaired following the cerebral hemorrhage and exacerbated by her decreased level of alertness. a nasogastric tube was placed for nutrition for several days before she was felt by swallow specialists to be safe to take in a modified diet. calorie counts were recommended, to ensure adequate caloric intake. a swallow evaluation should be repeated in several days after discharge in order to advance her diet further. her family was counseled on the increased risks of bleeding associated with amyloid angiopathy and anticoagulation, and despite the history of atrial fibrillation, avoidance of coumadin in the future was recommended. she was started on aspirin on , nine days after the hemorrhage. at discharge, keppra was started (she was given one dose), with plans to discontinue dilantin after discharge following one day of overlap. she should follow up with neurology after discharge from rehab, or in weeks. medications on admission: coumadin (dose unknown), simvastatin, levoxyl, xalatan, lisinopril, norvasc, isosorbide, vicodin. discharge medications: 1. acetaminophen 325 mg tablet sig: 1-2 tablets po q6h (every 6 hours) as needed for fever/pain. 2. bisacodyl 5 mg tablet, delayed release (e.c.) sig: two (2) tablet, delayed release (e.c.) po daily (daily) as needed. 3. docusate sodium 50 mg/5 ml liquid sig: one (1) po bid (2 times a day). 4. famotidine 20 mg tablet sig: one (1) tablet po bid (2 times a day). 5. ipratropium bromide 0.02 % solution sig: one (1) inhalation q6h (every 6 hours) as needed for wheezing. 6. heparin (porcine) 5,000 unit/ml solution sig: one (1) injection tid (3 times a day). 7. levothyroxine 25 mcg tablet sig: one (1) tablet po daily (daily). 8. sodium chloride 1 gram tablet sig: two (2) tablet po tid (3 times a day). 9. phenytoin 50 mg tablet, chewable sig: two (2) tablet, chewable po three times a day for 1 days: for three more doses after initiation of keppra, then discontinue. 10. artificial tear with lanolin 0.1-0.1 % ointment sig: one (1) appl ophthalmic prn (as needed). 11. miconazole nitrate 2 % powder sig: one (1) appl topical qid (4 times a day) as needed. 12. metoprolol tartrate 25 mg tablet sig: three (3) tablet po bid (2 times a day). 13. aspirin 325 mg tablet sig: one (1) tablet po daily (daily). 14. levetiracetam 500 mg tablet sig: one (1) tablet po bid (2 times a day). 15. norvasc 2.5 mg tablet sig: one (1) tablet po once a day: hold for sbp<100; increase to home dose in one week. 16. lisinopril 5 mg tablet sig: one (1) tablet po once a day: increase to home dose in one week as blood pressure tolerates. 17. simvastatin 10 mg tablet sig: one (1) tablet po once a day: resume home dose in one week. discharge disposition: extended care facility: rehabilitation center discharge diagnosis: right parieto-occipital cerebral hemorrhage amyloid angiopathy hyponatremia (acute on chronic) discharge condition: improved: mental status improving but still inattentive with some anomia and oriented to 'hospital,' 'fall ' and name. residual left-sided weakness (mild, at best umn pattern). discharge instructions: please md if patient experiences another seizure, or if she has new signs of stroke or hemorrhage, including acute visual change, trouble speaking or swallowing, or worsening weakness or numbness. please check chem-7 in days after discharge to ensure stability of sodium, considering hyponatremia. avoid all coumadin/warfarin. continue calorie counts at rehab, and supplement diet as needed. please have swallow ability re-evaluated in days, in order to consider advancing diet. followup instructions: 1) please follow up with your primary care physician, . () after discharge from rehab. 2) please follow up with dr. (neurology) after discharge from rehab (or in weeks); please call ( for an appointment. (.) md procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours insertion of endotracheal tube arterial catheterization transfusion of other serum diagnoses: abnormal coagulation profile unspecified essential hypertension hyposmolality and/or hyponatremia atrial fibrillation other convulsions intracerebral hemorrhage other and unspecified hyperlipidemia long-term (current) use of anticoagulants anticoagulants causing adverse effects in therapeutic use amyloidosis, unspecified 

Answer: The patient is high likely exposed to