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: penicillins / heparin agents attending: chief complaint: headache in the setting of dehydration (significant nausea and vomiting) major surgical or invasive procedure: decompressive right hemicraniectomy with partial right temporal lobectomy history of present illness: per admitting resident: the pt is a 47 y/o rhw with a history of uc (no current flare) presented with ha x days. she states that on monday night she suffered from diarrhea and vomiting x 24 hours, on wed morning she awoke with a headache worse on the right side associated with right eye pain. the pain was getting gradually worse, aggravated by activity. because of the pain she showed up in the ed. here her only complaints are headache and right eye pain. she notes no other problems, no weakness, no fever, chills, no current nasuea or vomiting, chest pain, sob, palpitations, pain in her extremities, diplopia, or numbness. no neck pain past medical history: ulcerative colitis (well controlled, not currently medicated) social history: no drugs, etoh, smoking family history: father had dm and died of complications from such. physical exam: on admission: vitals: 98.8 62 116/72 16 100% general: awake, cooperative, nad. heent: nc/at, mmm. neck: supple, no carotid bruits appreciated. no nuchal rigidity pulmonary: lungs cta bilaterally cardiac: rrr, nl. s1s2 abdomen: soft, nt/nd. extremities: no edema or deformities. skin: no rashes or lesions noted. neurologic: -mental status: alert, oriented x 3. able to relate history without difficulty. language is fluent with intact repetition and comprehension. there were no paraphasic errors. speech was not dysarthric. able to follow both midline and appendicular commands. there was no evidence of apraxia or neglect or graphesthesia. -cranial nerves: i: olfaction not tested. ii: perrl 3 to 2mm and brisk. vff to confrontation. iii, iv, vi: eomi without nystagmus. normal saccades. v: facial sensation intact to light touch. vii: left nl fold flat at rest. viii: hearing intact to finger-rub bilaterally. ix, x: palate elevates symmetrically. : 5/5 strength in trapezii and scm bilaterally. xii: tongue protrudes in midline. -motor: normal bulk, tone throughout. no pronator drift bilaterally. no tremor, asterixis noted. delt bic tri wre ffl fe io ip quad ham ta l 5 5 5 5 5 5 5 5 5 5 5 5 5 r 5 5 5 5 5 5 5 5 5 5 5 5 5 -sensory: no deficits to light touch, cold sensation, proprioception throughout. no extinction to dss (touch). -dtrs: tri pat ach l 1 0 0 0 0 r 1 0 0 0 0 plantar response was flexor bilaterally. -coordination: no dysmetria on fnf bilaterally. .... on discharge: ? pertinent results: admission labs: 09:15pm blood wbc-12.1* rbc-4.49 hgb-9.6* hct-32.2* mcv-72* mch-21.4* mchc-29.9* rdw-18.5* plt ct-392 09:15pm blood pt-12.2 ptt-23.3* inr(pt)-1.1 03:15am blood esr-29* 03:26pm blood sickle-neg 03:15am blood fibrino-450* 09:30am blood aca igg-2.5 aca igm-6.0 03:26pm blood lupus-neg 03:26pm blood at-93 protcfn-100 protsfn-58 03:26pm blood aca igg-2.7 aca igm-6.0 09:15pm blood glucose-85 urean-7 creat-0.7 na-139 k-3.7 cl-102 hco3-23 angap-18 05:00am blood alt-52* ast-26 ld(ldh)-198 alkphos-35 totbili-0.2 12:58am blood ck-mb-1 ctropnt-<0.01 05:20am blood ck-mb-1 ctropnt-<0.01 03:53pm blood ck-mb-1 ctropnt-<0.01 03:15am blood calcium-8.4 phos-4.2 mg-2.0 cholest-165 03:47am blood caltibc-335 ferritn-13 trf-258 03:26pm blood d-dimer-1100* 03:15am blood %hba1c-5.6 eag-114 03:15am blood triglyc-85 hdl-50 chol/hd-3.3 ldlcalc-98 09:30am blood homocys-6.0 03:15am blood crp-78.6* 03:15am blood hcg-<5 05:45am blood asa-neg acetmnp-13 bnzodzp-neg barbitr-neg tricycl-neg 09:15pm urine blood-neg nitrite-neg protein-neg glucose-neg ketone-10 bilirub-neg urobiln-neg ph-6.0 leuks-neg 09:15pm urine color-yellow appear-clear sp -1.032 microbiology reports: 7:00 pm swab right cranial bone flap. gram stain (final ): no polymorphonuclear leukocytes seen. no microorganisms seen. wound culture (final ): no growth. anaerobic culture (preliminary): no growth. reports nchct : large right temporal and occipital hypodense region which is slightly expansile with effacement of -white matter differentiation worrisome for infarction with areas of subarachnoid and probable intraparenchymal hemorrhage, overall worrisome for infarction which could be seen with venous thrombosis. less likely considerations include a primary neoplasm with hemorrhagic features. evaluation with mri/mrv can is recommended to aid in understanding the etiology. cta head/neck : although the major arteries are patent, there appears to be a linear high-density area in the right occipital lobe which could be due to a thrombosed vein or a thrombosed branch of the posterior cerebral artery. in addition, some prominent vascular structures in the right sylvian fissure could be due to prominent cortical veins. the findings in correlation with the mri examination obtained subsequently are suggestive of either a cortical venous thrombosis or in situ arterial thrombosis secondary to vasospasm. findings were discussed with dr. at the time of interpretation of this study. mri : although no major vascular occlusion is seen around the circle of , it appears that the linear hyperintensity intensity area seen in the right occipital lobe on t1 images could be connecting to the calcarine branch of the right posterior cerebral artery. alternatively this could also be a venous structure as described. mid basilar artery is not well seen on the maximum intensity projections but is visualized on t2-weighted images as flow void and on the cta and is likely artifactual. echo : the left atrium is elongated. left ventricular wall thicknesses are normal. the left ventricular cavity size is normal. overall left ventricular systolic function is normal (lvef>55%). tissue doppler imaging suggests a normal left ventricular filling pressure (pcwp<12mmhg). right ventricular chamber size and free wall motion are normal. the aortic valve leaflets (3) are mildly thickened. there is no aortic valve stenosis. trace aortic regurgitation is seen. the mitral valve appears structurally normal with trivial mitral regurgitation. the estimated pulmonary artery systolic pressure is normal. there is no pericardial effusion. agitated saline contrast study revealed trace borderline evidence of an intracardiac shunt (one bubble seen within 3 beats of right atrial opacification with valsalva release). lenis : no evidence of dvt in bilateral lower extremity veins. cta head/neck: : 1. interval increase in the large region of, primarily, vasogenic edema, with worsening mass effect. decrease in size of hemorrhagic foci within this process, as well as the subarachnoid blood. the prominent peripherally-enhancing vessel in the right occipital lobe is still present, which likely represents a thrombosed cortical vein. of note, the appearance and evolution of this infarct, and this finding, suggest a venous rather than an arterial etiology. technical difficulties limit the assessment of vessel narrowing or vasospasm. however, allowing for these limitation, the major arteries of the anterior and posterior circulation enhance symmetrically and the venous sinuses are unremarkable. ekg : sinus bradycardia. normal tracing. no previous tracing available for comparison. intervals axes rate pr qrs qt/qtc p qrs t 55 142 76 39 nchct : 1. interval worsening of mass effect caused by large infarct of the right mca and pca territories. right uncal herniation is again noted, although it is unclear whether it has worsened compared to prior exam. nchct : decrease in the degree of leftward shift of the normally midline structures compared to previous examination. mrv : no pelvic venous clot. fibroid uterus. bilateral simple ovarian cysts, likely follicular in a patient of this age. cholelithiasis. diagnostic 4 vessel angiogram : underwent cerebral angiography which showed a paucity of venous structures in the right temporal area consistent with a right vein of occlusion. nchct : no significant interval change compared to . severe right hemispheric mass effect and uncal herniation. nchct am: minimal increase in leftward shift in normally midline structures from 10 mm to 12 mm, likely due to minimal increase in surrounding vasogenic edema. severe right hemispheric mass effect and uncal herniation persist. nchct pm: minimal increase in leftward shift in normally midline structures from 10 mm to 12 mm, likely due to minimal increase in surrounding vasogenic edema. severe right hemispheric mass effect and uncal herniation persist. nchct pm: stable appearance of right parietal, temporal and occipital lobe infarction. significant mass effect on the right lateral ventricle, leftward shift of approximately 11 mm, and right uncal herniation is stable since the earlier study of 9:06 a.m. nchct am: stable large right hemispheric venous infarction with surrounding vasogenic edema involving the midbrain and basal ganglia. increase in leftward midline shift and the degree of cerebral herniation through the craniectomy defect. unchanged right uncal herniation. nchct : impression: persistent but decreased mass effect in the right cerebral hemisphere. nchct : prelim read: decreased mass effect. . conventional cerebral angiography (): impression: underwent cerebral angiography which showed a paucity of venous structures in the right temporal area consistent with a right vein of occlusion. brief hospital course: ms. is a 47 year-old woman with a history of ulcerative colitis (untreated) who presented to the emergency department a few days following 'violent' nausea and vomiting with severe right-sided headache. a non-contrast ct showed hypodensities in the right hemisphere (middle cerebral artery and posterior cerebral artery territories) with a hemorrhagic component and midline shift. the etiology of the syndrome was not immediately clear. she was admitted to the stroke service from until for further evaluation and care. . further investigation included vessel imaging, which showed the presence of a fetal posterior cerebral artery on the right (in this anatomical variant the blood supply to the middle cerebral artery and posterior cerebral artery comes from the same source - the internal carotid artery). accordingly, ischemic right mca and pca strokes in the setting of cardioembolic disease (eg from valsalva during recent vomiting) was considered a possible explanation. given the severity of headache and evidence of hemorrhage in the hypodensities, cerebral vasoconstriction (with secondary arterial occlusion) was also thought to be a viable cause. as ulcerative colitis, dehydration, and the use of an estrogen patch (for birth control) can predispose to hypercoaguability, there was also concern for venous thrombosis. however, there was no clear evidence of venous sinus thrombosis on initial imaging. although there was a suggestion of a thrombosed vein, the distribution of venous drainage at the area of this clot was not thought to be sufficient to explain the degree of her cerebral edema. . to evaluate for arterial embolic sources, a transthoracic echocardiogram was done. the study identified a patent foramen ovale. lower extremity dopplers were negative for dvt and an mrv of her pelvis did not show any evidence of proximal thrombi or thrombogenic sources. telemetry monitoring showed no contributory arrhythmias. aspirin was started as empiric treatment. a heparin drip was deferred in the context of hemorrhage; however, subcutaneous heparin heparin was started. . to address the potential role of reversible cerebral vasoconstriction, verapamil was started. unfortunately, the medication did not translate into clear relief. angiography and transcranial doppler studies showed no obvious evidence of arterial vasospasm. . in the setting of persistent headache and cerebral edema (with midline shift), arterial and venous vessel imaging was repeated with the thought that progressive venous processes might be more evident. the tests were unrevealing. she ultimately underwent conventional cerebral angiography which revealed thrombus in the right vein of . accordingly, a heparin drip was started with a goal of transitioning to coumadin (inr goal ). . the patient's examination worsened slightly, with the development of a right ptosis, partial right third nerve palsy, and subtle left pronator drift. as the headache was also unremitting, she was given a mannitol challenge. the mannitol provided relief. in the setting of radiological shift, examination change, and symptomatic relief, scheduled mannitol was started. hypertonic saline was subsequently added. decadron was implemented. . despite aggressive osmotic management, the patient's examination ultimately worsened. a very mild and subtle left hemiparesis progressed gradually to include a complete left hemiplegia, slight right hemiparesis and a pupil sparing right third nerve palsy. she became more lethargic. neurosurgery was consulted and she ultimately underwent an emergent right hemicraniectomy and partial temporal lobectomy. keppra was started for seizure prophylaxis. she received two units of prbcs in the or. . two days following her surgery, her exam was such that she was awake, alert and oriented without speech or language deficits. she had no visual or sensory extiction to stimuli on the left, but did have a dense left homonymous hemianopia. her pupils were equal and briskly reactive to light with full extraocular movements. she displayed full strength on the right and full sensation throughout her body. she did have quite a dense hemiparesis on the left arm and leg without face involvement. there were perhaps a trace of movements in her left fingers and toes. at this time, she was able to tolerate pos and she passed her bedside swallow evaluation. . given her stable clinical picture, she was transferred to the neuro-step down unit. she was restarted on a heparin drip as a bridge to coumadin, and per neurosurgery recs, she was quickly tapered off of her decadron and remained on keppra seizure prophylaxis. the dose was decreased to 500 mg po bid prior to discharge. prior to discharge, the inr became therapeutic. the heparin was stopped. a non-contrast head ct was repeated; there was no evidence of new hemorrhage and the edema had markedly decreased. the initially visualized hypodensities are thought to represent edema rather than infarct. accordingly, she is expected to regain function in the left limbs. . ** patient will need to have prothrombin gene mutation and factor 5 leiden drawn as an outpatient to complete hypercoagulability work up. medications on admission: - none discharge medications: 1. senna 8.6 mg tablet sig: one (1) tablet po daily (daily). 2. sodium phosphates 19-7 gram/118 ml enema sig: one (1) rectal daily (daily) as needed for constipation. 3. bisacodyl 5 mg tablet, delayed release (e.c.) sig: two (2) tablet, delayed release (e.c.) po daily (daily). 4. levetiracetam 500 mg tablet sig: one (1) tablet po bid (2 times a day). 5. simvastatin 10 mg tablet sig: two (2) tablet po daily (daily). 6. docusate sodium 100 mg capsule sig: one (1) capsule po bid (2 times a day). 7. pantoprazole 40 mg tablet, delayed release (e.c.) sig: one (1) tablet, delayed release (e.c.) po q24h (every 24 hours). 8. warfarin 5 mg tablet sig: one (1) tablet po once daily at 4 pm. 9. oxycodone 5 mg tablet sig: one (1) tablet po q4h (every 4 hours) as needed for pain. 10. hydromorphone 2 mg tablet sig: one (1) tablet po q6h (every 6 hours) as needed for pain. 11. ondansetron 4 mg iv q8h:prn nausea discharge disposition: extended care facility: - discharge diagnosis: venous sinus thrombosis cerebral edema s/p craniectomy ulcerative colitis iron deficiency anemia discharge condition: mental status: clear and coherent. level of consciousness: alert and interactive. activity status: out of bed with assistance to chair or wheelchair. neurological examination is notable for inattention (able to do doy backwards but not ), right ptosis, left visual field deficit, and left hemiparesis. more specifically, on the left there is 0/5 strength in the deltoid, biceps, ecr, and finger extensors. 4/5 strength at the triceps and finger flexors. strength in the ip, quad; at the ham and adductors. 0/5 in the ta and ; and in the and abductors. there is occasional extinction of left-sided stimuli to double simultaneous stimulation. discharge instructions: dear ms. , you were admitted to the neurology wards and the neuro-intensive care unit of the for an evaluation of symptoms of headaches that you were experiencing at home. through a series of physical examinations, laboratory studies, neuroimaging modalities and other medical tests, we were able to determine that the cause for your symptoms was an occlusion (or blockage) of one of the veins in the right part of your brain. this blockage unfortunately lead to a large amount of swelling (probably from increased backflow and obstruction) which ultimately caused worsening weakness of your left side of the body, problems with moving your right eye, as well as difficulties staying awake. you received a number of treatments including aspirin therapy, heparin therapy and a "decompressive hemicraniectomy", which is a procedure designed to remove the skull over a part of the brain so that the underlying brain can be allowed to swell. - we were able to organize a rehabilitation facility for you, where skilled therapists will continue to help you regain the strength on your left side. you will be discharged to - . - we have arranged a helmet for you to wear so that your brain can be protected in the absence of the overlying skull (on the right). please keep this helmet on at all times. - we have started you on a medication to thin your blood called warfarin while on this medication, there is a higher risk of bleeding problems such as lower intestinal bleeding or traumatic bleeding in your head. please be sure to seek medical attention following a fall or after hurting yourself. - as part of your work-up, we sent bloodwork to look for any additional disorders that may make you more likely to develop blood clots. two tests, the prothrombin gene mutation and factor 5 leiden will need to be drawn in our outpatient bloodwork lab on the . an order for this has been placed in our computer system. please have this done when you return for follow up with the neurology or neurosurgery clinics. . medication changes: - coumadin (warfarin) was started. followup instructions: please follow up with your primary care physician . @ 1020am , , phone: fax: please also follow up with dr. of the department of neurology, vascular division. the clinic is located on the , bldg, . we have made an appointment for you on at 3:30pm. provider: , md phone: date/time: 3:30 please follow up with dr. in the clinic in regard to replacing the bone flap in your skull. you will have a cat scan done prior to your appointment as scheduled below. provider: scan phone: date/time: 10:00 provider: , md phone: date/time: 10:45 md procedure: venous catheterization, not elsewhere classified other operations on extraocular muscles and tendons other excision or destruction of lesion or tissue of brain arteriography of cerebral arteries arterial catheterization central venous catheter placement with guidance diagnoses: abnormal coagulation profile subarachnoid hemorrhage ostium secundum type atrial septal defect cerebral edema iron deficiency anemia, unspecified diarrhea ulcerative colitis, unspecified hemiplegia, unspecified, affecting unspecified side third or oculomotor nerve palsy, partial phlebitis and thrombophlebitis of intracranial venous sinuses muscle weakness (generalized) other facial nerve disorders 

Answer: The patient is high likely exposed to