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Hematology week 2

by: Hanyao Foong

Hematology week 2 1002

Hanyao Foong
Leonard M. Miller School of Medicine

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Chase notes for 2nd week of hematology .
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This 15 page Class Notes was uploaded by Hanyao Foong on Saturday February 7, 2015. The Class Notes belongs to 1002 at Leonard M. Miller School of Medicine taught by in Winter2015. Since its upload, it has received 37 views.

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Date Created: 02/07/15
Oncology Lecture WI Dr Fein 23 January 2012 The Topic of This Lecture ls Paraneopastic Syndromes gt A paraneoplastic syndrome is de ned by symptoms attributable to a tumor but not due to metastasis 0 As generic groups there are immunemediated and hormonemediated syndromes 0 Interestingly treating the cancer causing paraneoplastic syndrome can shorten life spans Symptoms of paraneoplastic syndrome can precede svmptoms of the primary cancen gt LambertEaton syndrome is a classic neurologic syndrome associated with small cell lung cancer 0 Antibodies target QZ channels at NMls causing proximal weakness especially the legs and trunk LES resembles myasthenia gravis antiAChR but the patients do not get weaker over time It develops because there are shared antigens of the tumor and the Ca2v channels 0 It39s proposed that neural antigens are more primitive so tumors make them as they degenerate There39s more in ammation in patients with neurologic syndromes better prognosis 0 As this is immunemediated steroids and IVIG are used as treatments Plasma exchange works too gt Cachexia is a wholebody syndrome of weight loss and muscle wasting seen in states of chronic disease 0 It s a hvpermetabolic state induced by chronic systemic in ammation It s not like starvation In a way the cancer is consuming calories Eating more can39t counteract the weight loss The weight loss gt5 of body weight is coupled with anorexia and early satiety o Anorexia is associated with chemotherapy radiation depression and uncontrolled pain 0 In cachexia there s excessive lipolvsis as TNFu suppresses lipoprotein lipase lipid mobilizing factor Skeletal muscle is depleted by proteolysisinducing factor PIF and acute phrase reactants Certain cytokines TNFcx lL1 and lL6 attenuate cachexia and induce weight loss 0 Treatments include anabolic steroids corticosteroids and weed no seriously dronabinol works gt Muscle weakness and a rash raccoon eyes shawl sign and Gottren39s papules signify dermatomyositis o Biopsies show Tcells within skeletal muscle along with elevated blood CK and aldolase 0 Like LES this is an immunemediated response and it can be treated accordingly gt Hypercalcemia has a huge differential but almost all cases are primary hyperparathyroidism or malignancy 0 Unfortunately hypercalcemia signi es a poor prognosis and advanced disease 0 There39s production of PTHrP and calcitriol as well as osteolysis and higher prostaglandin formation PTHrP blocks osteoblasts and stimulates osteoclasts This clearly promotes bone resorption Additionally it diminishes one39s ability to excrete Ca2 in the urine o Hypercalcemia is de ned as Ca2 084Alb gt 105 Clinically it39s associated with many symptoms There39s fatigue weakness confusion constipation polyuria kidney stones and a short QT o The rst treatment is volume repletion with normal saline to dilute the Ca2 and a bisphosphonate Calcitonin is able to inhibit osteoclasts and steroids inhibit intestinal absorption of Ca2 gt Cushing syndrome is an endocrinemediated phenomenon due to excessive levels of cortisol 0 There39s weight gain with redistribution of fat moon facies central obesity and a buffalo hump Plus there s glucose intolerance hypertension easy bruising edema proximal myopathy 0 Causes of Cushing syndrome pituitary adenoma adrenal tumor or ectopic ACTH neuroendocrine As an iatrogenic cause chronic use of corticosteroids leads to a Cushingoid syndrome 0 To diagnose use a dexamethasone suppression test Cortisol levels drop unless there s ectopic ACTH gt Hyponatremia is usually hypoosmotic lt39s then interpreted with regard to how much volume there is o Hypovolemia can be from excessive natriuresis Na gt H20 In this case ADH levels are appropriate o If it39s euvolemia it39s probably SIADH ln hypervolemia it39s cirrhosis nephrotic syndrome or CHF SIADH is associated with small cell lung cancer There39s too much ductal H20 resorption The urine osmolarity will be gt 100 mOsm while serum Na can drop below 115 Tx Restrict H2O intake give hypertonic saline if needed ADH receptor blockers tolvaptan gt Thrombophilia of cancer Trousseau syndrome is associated with excessive clotting and thus DVTs 0 Patients tend to have Virchow39s triad venous stasis vascular injury and a hypercoagulable state The latter is due to tumorassociated cytokines distal and local impaired epithelial defense mechanisms and direct injury to the vascular endothelium by tumor cells 0 It s recommended that cancer patients should be chronically treated with LMWH or warfarin Suspect a clot if there39s edema The only caution is renal failure not even brain cancer Oncology Lecture WI Dr Fein 23 January 2012 The Topic of This Lecture ls Oncologica Emergencies gt Cancer can lead to mechanical complications Most importantly is pain Treat it as aggressively as possible gt Spinal cord compression from vertebral column metastasis is debilitating and life threatening 0 Associated tumors are breast lung prostate kidney lymphoma and multiple myeloma Everv cancer patient that comes in with back pain must be evaluated for compression 0 The pain is exacerbated by coughing straining and lying at There may also be proximal weakness Hyperre exia may be noted on PE Anv autonomic dvsfunction is an emergency Patients should get an MRICT quickly with dexamethasone treatment begun immediately 0 Treat rst ask questions later Period Start steroid treatment before m gt Lung breast and melanomas like to metastasize to the brain The rst sign is often a persistent headache 0 There may be focal weakness neurologic de cit or cognitive changes Evaluate with a contrast CT 0 For a solitary lesion see if a neurosurgeon can cut it out with minimal brain damage If it s multiple the only hope is irradiation and a pulse of IV dexamethasone 0 Anyone with a brain tumor should avoid activities that39d be risky due to the potential for seizures gt Pleural effusions can be from increased hydrostatic pressure CHF or capillary permeability malignancy 0 Lymphatic obstruction can lead to extravasation of lymph uid chylous This is fairly rare 0 Malignant effusions tend to be exudative or bloody though cancer cells aren39t always present Everv pleural effusion should be tapped both for therapeutic and diagnostic purposes 0 Similarly pericardial effusions can be caused by cancer It s an emergency if it gets to tamponade The uid should be drained ASAP A surgeon can cut a window into the pericardium too gt SVC syndrome is caused by a compressing tumor It s almost alwavs lung cancer Others are from lymphoma 0 There39s dyspnea coughing facialarm swelling JVD prominent chest wall veins amp Horner svndrome The tumor is typically in the apex of the lung which is why it presses on nearby structures 0 It s not really an emergency lust get a diagnosis Get a CT scan and then do biobsies to con rm A tissue diagnosis is absolutelv essential to guide therapv Don39t irradiate all willynilly o Elevating the head of the bed or reducing hypervolemia can manage symptoms of dyspnea gt Bone lesions that require immediate intervention are those that are in longbones like the femur gt Renal failure can occur in cancer due to obstructive urobathv and hvdronephrosis of BOTH kidneys o This is diagnosed by an ultrasound or CT and it s treated simply by stenting gt Chemotherapy has its own problems It induces vomiting mucositis 9 anorexia and febrile neutropenia o Mucositis is due to destruction of cells in the mouth and gut It is painful and greatly reduces 00L 0 Febrile neutropenia is due to suppression of bone marrow cells with neutrophils dropping to lt 500 These patients get ooportunistic infections Pseudomonas and bacteremia from gut ora Symptoms start 710 days after chemo Prophylactic antibioticsantifungals must be given 0 Tumor lysis syndrome is a massive release of intracellular electrolytes subsequent to cell death Without excretion high levels of K phosphate and uric acid will kill the patient 0 Think about it If phosphate is high it binds Ca2 leading to hypocalcemia Tx diuresis and allopurinol xanthine oxidase inhibitor or rasburicase urate oxidase Cancers most associated with this leukemia Burkitt s lymphoma and small cell lung cancer gt Patients with unresectable tumors or metastases get palliative care Half of patients have no hope of cure 0 Surgery is done to avoid bowel obstruction Also mild chemo or radiation can be given 0 Poor prognostic signs are hypercalcemia CNS metastases spinal cord compression cachexia etc 0 Once the patient is dying take care of the family and ensure that there is comfort care OxyContin DO NOT CODE A DYING CANCER PATIENT Oncology Lecture WI Dr GanjejAzar 24 January 2012 The Topic of This Lecture ls Gynecologic Cancers gt Cervical carcinomas are essentially STDs as they result from HPV infections HPV DNA in patients gt 30 0 They39re the most readilv screened dvnecolodic cancer The peak age is 3045 0 O O They are usually asvmptomatic except for postcoital vaginal bleeding or spotting Currently they are screened for by a Pap smear and diagnosed by cytology Precancerous lesions are in the transformation zone endo 9 ectocervix evidenced by dysplasia In development exposed columnar epithelium undergoes metaplasia 9 squamous Cervical intraepithelial neoplasias CIN are asymptomatic which is why we do Pap smears CIN is graded from I mild to lll carc in situ l is lowgrade ll amp III are high grade Grading is by atypia r NC ratio loss of polarity hyperchromasia and loss of maturation HPVinduced lesions lie at the surface They39re cancer once they invade the basement membrane Koilocytes are cellular evidence of HPV infection The cells look like they have halos They don39t signifv what tvpe of HPV The highrisk ones are 16 amp 18 lowrisk are 6 amp 11 Highrisk ones induce cancer by producing oncoproteins that mess with p53 and Rb As HPV tests improve testing is become the standard of care in conjunction with cytology Only signi cantly invasive cervical squamous cell carcinomas are visible Cancer is seen in a group 10 vears older than those who have precancerous lesions About 15 of cervical cancers are adenocarcinomas They tend to not be visible Advanced cervical carcinomas can cause ureteric obstruction and lethal renal complications gt Endometrial cancers are the most common uterine malignancies with a peak age of 55 65 0 There is atypical endometrial hyperplasia and they cause bleeding in post menobausal women Unfortunately there is no screening test Diagnoses are made by endometrial sampling Those that are due to excess estroden stimulation are easier to treat than the clear cthype They are commonly associated with obesity diabetes HTN and infertility Endometrial hyperplasia turns into cancer if the PTEN tumor suppressor is inactivated That39s what is seen in endometrioid cancers Clearcell ones involve Q53 Clearcell carcinomas are seen in older women They are not estrogen dependent so they are not associated with premalignant hyperplasia They are much more invasive Simple hyperplasia lacks atypia and is benign Precancerous lesions are complex with atypia EIN Younger women can attempt a trial of prodestin Those past menopause get hysterectomies The behavior of the cancer is based on depth of invasion and myometrial thickness O Grading of the cancer is based on the solidity of the mass lt 5 1 while gt 50 3 Patients with Lynch syndrome HNPCC are at risk for colorectal and endometrial cancers There are inactivated DNA mismatch repair genes leading to microsatellite instability These patients should be identi ed MLH or MSH genes and screened regularly for cancer gt Ovarian cancer is the most deadly gynecological cancer It s often asvmptomatic and there s no screen 0 O 0 It occurs especially in women gt 40 who have not had children Diagnosis is by CT or laparotomy Most neoplasms are from the surface epithelium In those lt 20 suspect a germ cell tumor Surface epithelial tumors are often bilateral They39re either cystic or solid and either papillary or solid Tumors are classi ed as benign adenoma borderline or malignant carcinoma The only way we have to identify ovarian cancers without nuclear medicine is a vaginal ultrasound There are no known precancerous lesions Most patients present in stage III or IV If a mucinous tumor ruptures cysts are seeded within the abdomen pseudomyxoma peritoneii Oncology Lecture WI Dr Baracco 24 January 2012 The Topic of This Lecture ls Infections in Patients with Cancer Oh God More Microbiology Febrile neutropenia occurs 710 days after induction chemotherapy once the absolute count is lt 500 o The duration of the neutropenia is based on how much the bone marrow is involved 0 As we already learned oral mucositis occurs due to the rapid turnover of those cells This is an important loss of passive immunitv as skin and mucosa are barriers to infection 0 It is often dif cult to nd the source of the infection as there are many possible sources of fever Mucositis in the upper GI leads to susceptibility to Gram cocci like 5 viridans Translocation 9 bacteremia o In the lower GI the worries are enteric Gram rods Pseudomonas and Candida o The line used as a chemotherapv port is a nidus for Gram cocci S aureus Bacillus Coryneba cterium o In the urine it39s probably E coli If there39s meningitis it39s S pneumoniae or Cryptococcus o In the lungs it s S pneumoniae S aureus or Pseudomonas or other Gram rods With longer periods of neutropenia we might worry about fungi Aspergillus or Nocardia It s important to comprehensivelv repeat the phvsical exam as symptoms may be more subUe o The signs we associate with infections are the immune response which is lacking in neutropenia o For imaging get a CXR or CT Also get serial blood cultures 3 a UA a urine culture maybe an LP When a patient is severely neutropenic err on the side of caution and use potent empirical therapy 0 Therapy is guided based on the most likely organisms and susceptibility what was the prophylaxis o Ideally go with something broad that covers Gram Gram Pseudomonasl and anaerobes Broad spectrum things are cefepime piperacillintazobactam imipenemcilastatin etc If there39s a lack of improvement do not discontinue the antibiotics Think about why they wouldn39t work 0 It could be an abscess or a fastidious bug some odd fungus or a noninfectious cause Infections are a byproduct of immunosuppression coupled with disruption of protective barriers 0 There are potentially opportunistic pathogens many of which carry drug resistance 0 Empiric therapy is absolutely required since we cannot wait for cultures to get back Don39t stop until the patient is afebrile and the absolute neutr0phi count has recovered Oncology Lecture WI Dr Wolfson 24 January 2012 The Topic of This Lecture ls Principles of Radiation Oncology RadOnc uses precisely measured doses of ionizing radiation to a de ned tumor sparing normal tissue 0 The goal is to increase survival without destrovind function orjust providing palliation The clinical evaluation involves the history chart review physical and most importantly Imaging 0 Patients are intimately involved in the therapeutic decision as there must be informed consent 0 There is treatment planning including simulations and ensuring radiation is targeted appropriately Target volume localization is accomplished by CT Critical organs must be avoided The nal plan is developed by a dosimetrist with quality assurance by a medical physicist Intensitymodulated radiation therapy IMRT allows for selective dose distributions dose painting 0 Plans are then evaluated based on the doses going to each structure heart esophagus lungs etc Dose limitations have been quanti ed for pretty much every structure Imageguided radiation therapy IGRT uses previous imaging and aliens it with the radiation plan 0 The patient must be in the same place for every treatment dose IGRT ensures that happens 0 Cells that divide less rapidly require higher doses of radiation and more treatments Fractionation ensures selectivity toward mitotic cells leaving normal cells intact The therapeutic ratio tumor susceptibility vs normal tissue varies on location and type ofcancen o The minimal tolerance dose is TD55 radiation dose with lt 5 severe complications within 5 vears For more severe complications like optic chiasm blindness a TDos is used Ionizing radiation IR mediates aDODtosis via p53 but later in the treatment course it unregulates both VEGF and Bcl2 while decreasing levels of Bax Tumor cells adapt and try to survive 0 IR induces GZ arrest and cells are particularly sensitive in 62 and M They39re resistant in S A new treatment is brachytherapy BT in which radioactive pellets are inserted into the prostate Benign diseases can be treated with IR but there s a fear of secondarv malignancv Oncology Lecture WI Dr Beiarano 25 January 2012 The Topic of This Lecture ls Lung Cancer gt Smoking induces metaplasia of the respiratory epithelium It becomes squamous and then dysplastic o It should be columnar pseudostrati ed and ciliated All of that is lost with continued smoking gt The vast majority 80 of lung carcinomas are nonsmall cell either adenocarcinoma or squamous cell 0 NSCCs are best treated with surgery Only squamous cell carcinomas are associated with smoking 0 Adenocarcinomas are usually peripherally located They arise from bronchial glands or pneumocytes Tumors that have a consolidated pattern in lung architecture are bronchioloalveolar These tumors can be eliminated by drugs with speci c targets such as EGFR Other variants are tubularacinar in the stroma or papillary more brovascular Some tumors lack good morphology so they39re labeled as solid Mucin stains identify them Adenocarcinomas are positive for TTF1 speci c for lung and for CEA nonspeci c o Squamous cell carcinomas arise from the airway near the hilum They are often wellcircumscribed They produce keratin pearls They tend to cavitate over time with central necrosis 0 Adenosquamous tumors are exactly what they sound like They share morphology with both types 0 Large cell tumors are bulky with lots of hemorrhaging and necrosis They39re often quite aggressive The cells in these carcinomas are able to phaqocvtize PMNs They are huge gt The other carcinomas are small cell These carry a much higher mortality and are treated only by chemo 0 SCC cells aren39t cohesive They look like Ivmphocvtes with little cytoplasm and no membrane They may be confused with lymphoma so pathologists used a keratin stain 0 They like to cluster near blood vessels They induce extravasation of chromatin Azzopardi effect gt SCCs are an aggressive type of neuroendocrine tumor NET Others are typical or atypical carcinoids 0 Typical carcinoid tumors are lowgrade atypical ones are intermediate grade 0 Carcinoid tumors are malignant They arise from large bronchi and have abundant vasculature They affect mostly patients under 45 and are the most common lund tumor of kids 0 Typical ones do not have mitotic activity or pleomorphism just a monotonous population of cells The term that we need to know for NETs is quotrosettesquot cells around a small lumen gt A small number of tumors in the lung are from metastasis as in lymphatic spread of colon cancer 0 The characteristic appearance is multiple lesions The source is identi ed by antibody panels IHC o IHC shows 39lTFl if it39s a primary lung cancer estrogen receptors ER for breastovary or CK7 for GI gt Pleural tumors are much more likely to be metastatic from the lung breast ovary GI etc o Mesothelioma is a primary malignancy almost always from asbestos exposure Cells are keratin calretinin and CEA Tumors are epithelial or sarcomatous mesothelial o Clusters of cohesive cells with globules coupled with in ammatory cells signify malignancy EMA staining is membranous for mesothelioma and cytoplasmic for adenocarcinoma Oncology Lecture WI Dr Jorda 25 January 2012 The Topic of This Lecture ls Renal and Urologic Cancer gt Any papillary tumor in the kidney that s lt 5 mm is a benign adenoma If it39s more it39s a papillary carcinoma o If there is hemorrhage and necrosis one can undoubtedly say that the tumor is malignant o Angiomyolipomas are a type of hamartoma They are benign but associated with tuberous sclerosis o Oncocytomas are always benign They are grossly mahogany but eosinophilic on microscopy These tumors arise from the intercalated cells of collecting ducts They have a central scar The color granular qualities and eosinophilia are due to abundance of mitochondria The malignant version of this tumor is a chromophobe carcinoma gt Renal clear cell carcinomas RCCCs are located in the periphery with the epicenter in the cortex 0 Most of the tumors have a vellowish dualitv due to glycogen These are conventional 70 of RCCCs Conventional RCCCs have mutations in their von HippelLindau gene VHL on Chr 3p Familial cases are rare but have the whole VHL syndrome Most cases are spontaneous In VHL syndrome there are multifocal bilateral cysts not single tumors 0 For sampling the familial one is in the blood It39s a germline mutation not somatic VHL protein mutations lead to accumulation of HlFcx and thus PDGF VEGF and EGF For conventional RCCCs antiVEGF and antiEGF antibodies are effective treatments 0 RCCCs HCCs and prostatic carcinomas all metastasize through veins not through lymph gt Papillary renal carcinomas have a brovascular core that allows for growth The tips are poorly vascularized o All papillary tumors have psammona bodies which are deposits of Ca2 also seen in meningiomas These bodies are seen at the tips of the papillae due to necrosis of hypoxic cells 0 Familial cases HPRC are AD and they are from mutations in c met a proto oncogene on Chr 7 As in VHL syndrome there are multiple bilateral carcinomas o c metis also implicated in some sporadic cases There39s proliferation of hepatocyte growth factor A tyrosine kinase inhibitor may be able to shut down this process gt Chromophobe carcinomas are also from intercalated cells The FH gene furamate hydratate is implicated 0 As such these malignant tumors do not respond to antiVEGF or antiEGF therapies gt A sarcomatoid carcinoma has spindle cell morphology but it39s not actually mesenchvmal 0 These tumors are the result of dedifferentiation of another tumor type They39re highly aggressive gt Tumors that originate from the renal pelvis are urothelial carcinomas They can also be seen in ureters 0 When in the ureter they can induce obstruction which generates hydronephrosis Bladder tumors are papillary or at and they can be invasive or noninvasive o The normal urothelium has a at shinv surface umbrella cells with few layers 0 Grossly carcinoma in situ appears diffuser and multifocally as at reddishwhite m Huge malignant cells can be seen in the urine if there is carcinoma in situ o Lowgrade papillary tumors can be removed curatively but they often recur o A cystectomy may be required for highgrade urothelial cancers that invade smooth muscle A subset of bladder tumors have keratin pearls signifying that they are squamous cell carcinomas 0 These are associated with schistosomiasis They are most often seen near the urachal remnants Most urachal cancers are still adenocarcinomas Renal adenocarcinomas are due to infections and intestinal metaplasia Prostatic carcinomas are the most frequent cancers of men The cancer cells are polyclonal 0 Those forming normal glands rather than fused ones in a cribriform pattern have good prognoses o A Gleason score of lt 7 is considered good 710 are bad tumors that metastasize Metastatic prostate tumors are osteoblastic PSA scores will also be high Perineural invasion coupled with a lack of glands signi es a Gleason 55 score Testicular cancer is treated with bleomycin cisplatin and vinblastine Oncology Lecture WI Dr Gomez 26 January 2012 The Topic of This Lecture ls Breast Cancer gt The majority of breast biopsies just show brocystic changes They39re scar tissue lled with clear uid 0 Most are not proliferative but intraductal hvperplasia esp after menopause is a cancer risk If dysplasia or pleomorphism is noted the hyperplasia is labeled as atypical higher risk 0 Fibroadenomas are wellcircumscribed benidn ne0pasms that do not invade at all o If there39s more stromal cellularitv and a leaflike pattern it39s a phyllodes tumor Due to the increased mesenchymal tissue this is a type of sarcoma Its severity varies While these tumors must be completely resected they do not invade lymph nodes gt lntraductal papillomas can induce bloodv nipple discharge from lactiferous ducts gt Breast carcinomas are either ductal or Iobular Those that are noninvasive are Iow or highgrade in situ 0 Even in highgrade ductal carcinoma in situ with necrosis comedocarcinoma there39s no invasion Based on the malignant potential of these cells they must be surgically removed 0 Mammary Paget39s is seen in nipple tissue They39re glandular cells within squamous epithelium o Lobular carcinomas in situ are not precursors but they are a marker of risk of breast cancen Invasive Iobular carcinomas are harder to detect and thus more likely to metastasize gt Every pathology report discusses invasive carcinomas based on size nodal status histologic grade Nottingham score histologic typesubtype and steroid receptor status 0 For lymph nodes sentinel nodes are identi ed to avoid removing unnecessary ones 0 For grading formation of tubules separation of cells and a lack of mitosis yield a low score 0 For subtypes tubular colloid and papillary carcinomas are ER and favorable for treatment 0 6070 of tumor cells have estrogen receptors ER so they will respond to tamoxifen The presence of ER is also a sign of good prognosis even without treatment gt When overexpressed HERZ is a poor prognosticator However it is another target for therapy 0 Herceptin is an antiHER2 antibodv that works alone and as a potentiator for other chemo drugs The actual name of Herceptin is trastuzumab o Basallike tumors suck because they are both ER and HER2 They39re hard to treat Oncology Lecture WI Dr Petito 26 January 2012 The Topic of This Lecture ls CNS Tumors Meningiomas develop along the calvaria They39re often discrete benign masses located parasagittally 0 Women have a greater risk as these tumors express estrogen and progesterone receptors 0 These tumors are treated surgically perhaps with prophylactic antiepileptics Astrocytomas are glial tumors that diffuser in ltrate brain tissue There39s no focal mass lesion 0 Pleomorphic xanthoastrocytomas and subependymal giant cell astrocytomas are excep ons Glioblastoma multiforme GBM grade lV glioma yields jagged regions of necrosis which expand Medulloblastomas tend to be midline tumors They are not cystic They grow fairly rapidly 0 Growth of these tumors can yield hvdrocephalus with symptoms of nausea and vomiting 0 They are malignant tumors that frequently spread through the CSF Metastatic carcinomas appear as multiple ringenhancing lesions They39re usually from lung or breast Treating brain tumors is tricky due to the bloodbrain barrier so drugs can be given intrathecally o The rididitv of the skull makes benign tumors problematic And the CSF allows for rapid spread 0 While CNS tumors pass in the CSF and in ltrate diffusely thev39re rarelv metastatic to other organs Pilocytic astrocytomas are grade I gliomas that appear in children They39re focal and treated surdicallv Diffuse astrocytomas grade II are usually treated surdicallv with subsequent observation 0 Demyelination is an important risk of radiation therapy so watchful waiting is preferred Anaplastic astrocytoma Ill and GBM IV are treated with radiation and temozolomide alkylating agent 0 Temozolomide sensitizes GBM tumors to radiation Avastin can be used in conjunction Oligodendrogliomas may have a LoH at lp19d If so there s sensitivity to chemo so radiation isn39t needed Pleomorphic xanthoastrocytomas are slowgrowing discrete grade II tumors with mural nodules in a cvst 0 These are treated surgically as they39re usually super cial They prefer the temporal lobe o PXAs are welldemarcated and benign though they may appear microsc0picav to be malignant These must be kept on the differential to avoid giving a wrong diagnosis of malignancy Subependymal giant cell astrocytomas are slowgrowing intraventricular tumors that affect people lt 20 0 They are associated with tuberous sclerosis a mutation in TSCl 9p hamartin or TSC2 19p tuberin 0 Still these tumors are benign grade I and treated with excision for they are encapsulated They have IHC components of astrocytes GFAP and neurons synaptophysin gt Tumors associated with VHL disease include hemangiobloastomas in the CNS and retinal angiomas gt Inexplicably this lecture is not on the exam so why the fuck did I take extensive notes


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