Oncology Flashcards

Question

AFP is elevated in

Answer 1

Hepatoblastoma HCC Germ cell tumors Ataxia telangiectasia

Answer 2

cisplatin carboplatin

Answer 3

antidote for cyanide poisoning protects against cisplatin induced hearing loss

Answer 4

begins in cells that give risk to sperm or eggs can occur anywhere in body benign or malignant GCT: 1/3 gonadal, 2/3 extragonadal from aberrant migration Most are curable but some are highly malignant Risk increased with gonadal dysgenesis - eg Kleinfelters- mediastinal GCC Turners - increased risk gonadoblastoma Immature germ cell tumors (malignant) are positive for AFP or bHCG Mature teratomas (benign) are negative for AFP and bHCG **as AFP normal values change with age quickly in first year of life, may need to do serial measurements Rx: platinum chemotherapy (cisplatin or carboplatin) or surgery alone (eg ovarian teratoma doesnt need chemo)

Answer 5

Wilms tumor/Denys Drash/WAGR syndrome AML somatic mutations mean the cancer is there in that tissue germline mutations are inherited and give predisposition to cancer eg WAGR, Denys Drash, Frasier syndrome

Answer 6

urgent MRI spine Alterations in perianal sensation/saddle parasthesia often preceed complete loss of sensation, bladder/bowel incontience and weakness Cauda equine and cord compression may progress or complete in under 24 hours, and defects at that stage are typically irreversible Therefore dont wait for full blown clauda equina, look for subtle signs as the longer the nerve is damaged, the lower the chance of recovery would need high dose steroids and surgery to decompress

Answer 7

yes Autologous transplant to allow more/higher dose chemo to be given **allogenic STC used in leukemias "graft versus disease"

Answer 8

Tumour suppressor genes (inactivation) Regulators of cellular growth and apoptosis Inactivation of BOTH alleles required for a tumour suppressor gene Inheritance of one germline mutation can be AD A second mutation at somatic level still required In inherited mutations, one inactivated allele may be inherited and the other undergoes spontaneous inactivation Examples: P53 (usually initiates apoptosis) , APC, Rb, BRCA Proto-oncogenes (activation) Activating mutation in ONE gene results in an oncogene , via: 1. Amplification 2. Point mutations 3. Translocation These gees interfere with apoptosis, continue to proliferate Examples Chromosome translocation T(1;19) – pre- B ALL T(14:18) – C Myc in Burkitt’s T(9:22) – Philadelphia chromosome in ALL, CML Gene amplification = N myc in neuroblastoma (poor prognosis) Point mutation 1p in AML – NRAS signal transducer, point mutation ***translocations are usually proto onco genes****

Answer 9

C Myc Burkitts lymphoma

Answer 10

Philadelphia chromosome ALL, CML BAD PROGNOSTIC FACTOR

Answer 11

Fanconi anaemia (AR leukaemia) Bloom’s syndrome (AR leukemia and lymphomas) Ataxia-telangiectasia (AR lymphoreticular cancers) Dysplastic nevus syndrome (AD melanoma)

Answer 12

Mutations in telemere maintenance pathways Short telemeres

Answer 13

EBV: Burkitt lymphoma Diffuse large cell B cell lymphoma Hodgkin lymphoma Post-transplant lymphoproliferative disorder Nasopharyngeal carcinoma Leiomyosarcoma Gastric adenocarcinoma Hepatitis B: Hepatocellular carcinoma Hepatitis C: Hepatocellular carcinoma HPV :Cervical carcinomas Anus, penis, vulva/vagina, oropharyngeal carcinomas HHV8: Kaposi’s sarcoma Primary effusion B-cell lymphoma Plasma cell variant of Castleman disease

Answer 14

mutation in p53- inactivation of tumor suppression gene Sarcomas (soft tissue and osteosarcoma), leukeminas,astrocytoma, medulloblastoma, breast cancer, bone, lung, brain If adrenocorticocarcinoma or choroid plexus carcinoma, LFS unless proven otherwise If medulloblastoma + Li-Fraumeni, almost certainly Sonic Hedgehog subtype

Answer 15

optic glioma neurofibroma phaeochromocytma meningioma astrocytoma soft tissue sarcoma breast cancer >age 50

Answer 16

bilateral acoustic neuromas, meningiomas, epyndymomas

Answer 17

Autosomal dominant, mutation of tumour suppressor gene VHL Cysts, benign and malignant tumours hemangioblastoma renal cell carcinoma pheochromocytoma

Answer 18

Short stature, photosensitive telangiectatic erythema (red rash in sun exposed areas, esp face/cheeks) Immune deficiency Excessive number of broken chromosomes due to DNA repair defects Increased risk leukaemia, lymphoma, solid tumours (AML most common

Answer 19

AR Mutation in ATM tumour suppressor gene (11q22-23) Neurodegenerative; ataxia, telangiectasia, immunodeficiency with sinopulmonary infections, impaired organ maturation, X-ray hypersensitivity Lymphoma, leukaemia

Answer 20

Leukaemia+ lymphoma 1. Wiskott-Aldrich 2. SCID, CVID 3. X linked lymphoproliferative syndrome 4. Kostmann syndrome 1. Congenital neutropaenia Risk of myelodysplastic syndrome/ leukaemia

Answer 21

500 fold increase in AML. 25% of kids with TAM develop AML 20 fold increase in ALL

Answer 22

medulloblastoma + BCC

Answer 23

Medullary carcinomas of thyroid PTH adenoma Phaeochromocytoma

Answer 24

Add alkyl groups --> cell cycle arrest --> death Work in all phases of cell cycle Cyclophophamide Ifosfamide - both alkylate guanine and thus inhibit DNA synthesis

Answer 25

N/V Myelosuppresion Alopecia HAEMORRHAGIC CYSTITIS PULMUNARY FIBROSIS SIADH INFERTILITY Secondary neonplasm **use hyperhydration + mesna to prevent haemorrhagic cystitis

Answer 26

N/V Myelosuppression Haemorrhagic cystits (less common than cyclophosphamide) SIADH Iphosphamide encephalopathy (rx thiamine, methylene blue) Renal tubular acidosis (proximal RTA/Fanconi) Infertility

Answer 27

Disrupt DNA synthesis Cause cell death during S phase of cell cycle Eg Methotrexate = folate atagonist, inhibits DNA synthesis 6- mercaptopurine = inhibits purine syntheiss Cytarabine (Ara-C)= pyrimidine analog, inhibits DNA polymerase 5-flurouracil = pyrimidine analog

Answer 28

N/V Hepatitis (LFT derangement) Photosensitive dermatitis Myelosuppression High dose- renal and CNS toxicity (lowers IQ) **can accumilate and cause toxicity in 3rd space fluid eg pleural/ascites** Need hyperhydration, urinary alkalinisation and folinic acid to avoid toxicity

Answer 29

Inhibit microtubule assembly during MITOSIS, causing cell arrest eg Vincristine Vinblastine

Answer 30

constipation abdo pain neuropathy- peripheral, autonomic, cranial nerve jaw pain mucositis phlebitis Alopecia VESICANT IV only Minimal myelosuppression Not ematogenic

Answer 31

Disrupts topoisomerase I and II --> inhibits DNA replication Works in S + G 2 phase of cell cycle eg Etoposide

Answer 32

N/V Myelosuppression Secondary leukemia Type 1 hypersensitivity reactions

Answer 33

increase oxygen free radicals--> cell apoptosis Intercalates DNA Not specific to any phase in cell cycle eg Doxorubicin Danorubicin

Answer 34

N/V Cardiomyopathy Radiation dermatitis Myelosuppression Arrythmia *dexrazoxane reduces risk of cardiotoxicity**

Answer 35

Inhibit DNA synthesis by cross linking DNA Not phase specific eg carboplatin cispatin

Answer 36

HIGHLY EMATOGENIC including delayed N/V Ototoxicity - very common Nephrotoxicity Hypomagnesemia Myelosuppression, seizures, neuropathy- uncommon THROMBOSIS **sodium thiosulfate and amifostine otoprotective

Answer 37

Anaphylaxis Pancreatitis Coagulopathy Hyperglycemia Cerebral sinus thrombosis ***give PEG asparaginase if become allergic to L-asparaginase**

Answer 38

N/V Pneumoatosis Mucocutaneous reactions and dermatitis Alopecia Pulmunary fibrosis- less common NO MYELOSUPPRESSION

Answer 39

N/V Pneumoatosis Pulmunary fibrosis Mucocutaneous reactions and dermatitis NO MYELOSUPPRESSION

Answer 40

Calcineurin inhibitor Reduce IL-2 and IL-2 receptor production

Answer 41

Hirsuitism Gingival hyperplasia Nephrotoicity Tremor Headache Hyperglycemia Elevated LFTs HTN

Answer 42

Vincristine Asparaginase Bleomycin

Answer 43

Vincristine Cyclophosphamide

Answer 44

antimetabolities doxyrubicin bleomycin etoposide

Answer 45

cisplatin carboplatin Cyclophophamide High dose methotrexate Cytarabine

Answer 46

Vincristine Asparaginase Bleomycin Mercaptopurine Low dose methotrexate low- flurouracil, busulfan, low dose cytarabine, doxorubicin, etoposide,

Answer 47

etoposide (AML) Cyclophosphamide (AML) Carboplatin/cisplatin

Answer 48

cyclophosphamide ifosfamide cisplatin

Answer 49

methotrexate cytarabine

Answer 50

S and G2/M

Answer 51

M phase eg vincristine (microtubule formation)

Answer 52

Platinum analgues - cisplatin, carboplatin Anthracyclines- doxorubicin Alkylating agents - cyclophosphamide, ifosfamide busulfan

Answer 53

bleomycin etoposide

Answer 54

fever and flu like symptoms mucositis phlebitis diarrhoea GI ulceration deranged LFT neuro and pulmunary toxicity

Answer 55

acute lung injury or intersitial lung fibrosis N/V Diarrhoea

Answer 56

bleomycn dactinomycin doxorubicin hydroxyurea methotrexate radiation recall only - arsenic, cyclophosphamide, cytarabine, etoposide,

Answer 57

hyperkalemia hyperphosphatemia hyperuricemia hypocalcemia (binds to phosphate)

Answer 58

acute leukemias WCC> 100 Burkitts lymphoma Large tumors eg abdominal patients with preexisitng renal disease/hyperuricemia

Answer 59

usually within 24-48 hours of starting treatment, up to 7 days after starting

Answer 60

hyperuricemia- precipitation uric acid in tubules -- inflammation -- AKI hyperphosphatemia -- precipitates calcium phosphate and uric acid deposition in kidneys --> uric acid nephropathy (in acidic urine), or calcium phosphate nephropathy (at alkaline pH) Hyperkalemia-- arrythmias Hypocalcemia- seizures, muscle cramps, tetany

Answer 61

Hyperhydration Alkalinization is usually necessary to maintain a urine pH of approximately 7.0. The urinary excretion of uric acid is reduced at an acidic pH, whereas the excretion of phosphorus is impaired by over-alkalinization (and they precipitate more at these pHs) Allopurinol - if low risk BLOCKS XANTHINE OXIDASE - blocks catabolism of hypoxanthine and xanthine (more soluable than uric acid)- but xanthine can still precipitate at high levels -*** contraindicated in combination with azathioprine or 6MP as causes severe bone marrow suppression** Rasburicase - if high risk - urate oxidase. Catalyses uric acid into water soluable allantoin

Answer 62

Treatment of hyperkalaemia: 1. Cardiac membrane stabilisation -> IV calcium gluconate immediately 2. Shift of K+ intracellularly -> insulin/glucose infusion, sodium bicarbonate, beta-agonists (salbutamol) 3. Reduction of K+ load -> resonium, loop diuretics, dialysis (last resort) Treatment of hyperphosphatemia: 1. Dietary restriction of phosphate 2. Phosphate binders 3. Dialysis Treatment of hypocalcemia: 1. IV calcium gluconate with caution as can increase precipitation of calcium phosphate (Don’t give if hyperphosphatemia. Don’t treat if asymptomatic)

Answer 63

1. Immature cells = CD34, CD117, HLA-DR 2. T cells = CD2, CD3, CD4, CD8 3. B cells = CD10, CD19, CD20, CD22 4. Myeloid = CD15, CD33

Answer 64

T21 NF1 Bloom syndrome Ataxia telangectasia

Answer 65

i. Lymphadenopathy + hepatosplenomegaly ii. Bone pain +++ – particularly lower extremities, can be severe and wake patient at night iii. T cell disease: mediastinal adenopathy causing major airway compression with stridor and/or superior vena cava obstruction iv. Signs of CNS involvement are INFREQUENT at diagnosis: 1. Headache, nausea and vomiting 2. Irritability, nuchal rigidity and papilledema 3. Cranial nerve involvement – most frequently involving CNVII, CNIII, CNIV, CNVI v. Testicular involvement at diagnosis is rare – appears as painless testicular enlargement and is usually unilateral vi. Fever- inflammatory cascade from tumor cells

Answer 66

i. Age (1-10 years favourable, <1 yr, >10 yrs unfavourable) ii. WCC at presentation (<50 favourable) iii. Cytogenetic/molecular eg Ph+ = risk factor iv. Response to induction (= MRD) – biggest prognostic factor v. Testicular disease, CNS disease poorer prognosis b. Low risk i. High risk features not present ii. Favourable cytogenetics 1. Hyperdiploidy (>50) 2. Trisomies 4, 10 3. ETV-RUNX protein (t12;21) c. Standard risk i. High risk features not present ii. No favourable genetics d. High risk/ very high risk i. Age = <1 or >10 years ii. Presentation 1. WCC > 50 at diagnosis 2. CSF involvement 3. Testicular involvement iii. Additional cytogenetic + molecular features 1. Hypodiploidy (<44) 2. KMT2A/MLL genetic rearrangements - translocations of 11q23 (eg. t4;11) 3. iAMP21 amplification 4. Philadelphia chromosome t(9;22) BCR-ABL fusion protein --> very poor prognosis

Answer 67

CD15 or CD33 positive Negative for CD3 or CD 19 (as not B or T cells) Myeloblasts will stain positive with myeloperoxidase

Answer 68

t (8,21), t (8,17), inv (16) NPM1

Answer 69

t (8,21), t (8,17), inv (16) NPM1

Answer 70

t(15;17)= PML- RARA Chemo= all trans retnoic acid + anthrayclines + cytarabine risk differentiation syndrome and DIC

Answer 71

500 x more likely to develop AML (but better survival than other kids) 30 x more likely to develop ALL GATA1 mutations

Answer 72

Most due to Philadephia chromosome t(9,22) BCR-ABL fusion protein encodes oncogenic protein Philadelphia chromsome on FISH Rx: tyrosine kinase inhibitors (imatinib, dasatinib) - inhibits BSR-ABL tyrosine kinase Hydroxyurea Allogenic SCT

Answer 73

rare cancer of infancy Associated with mutations in RAS/MAP kinase pathway Only curative rx is stem cell transplant Risk factors: - NF1 -Noonan syndrome (mutations in PTPN11, NRAS, KRAS) Ix: monocytosis, thrombocytopenia, anemia, BM= hypercellular myeloid cells, <20% myeloblasts, molecular analysis

Answer 74

Murphy I: Tumor at one site (nodal or extranodal -- “E”) II: Two or more sites; same side of body (or resectable GI primary) III: Both sides of body IV: CNS or marrow involvement

Answer 75

Ann Arbor I: Tumor at one site (nodal or extranodal -- “E”) II: Two or more sites; same side of body (or resectable GI primary) III: Both sides of body IV: Lung, liver, or bone mets A- asymptomatic B- B symptoms present

Answer 76

a. A malignancy of the germinal centre B-Cells that affects the reticuloendothelial and lymphatic systems b. Characterised by the presence of Reed-Sternberg cells (histopathologically) c. Spread: slow, predictable, with extension to contiguous lymph nodes Haematogenous spread also occurs (LESS COMMON)  liver, spleen, bone, bone marrow or brain d. Associated with B symptoms (which are a poor prognostic factor) e. usually presents with painless, firm rubbery cervical /supraclavicular lymphadenopathy. Mediastinal mass of HSM. Most commonly affects teens, rare <5 years Less common than non Hodgkins lymphoma

Answer 77

a. Accounts for 60% of lymphomas in children b. 2nd most commonly malignancy in those 15-35 years old c. Burkitt lymphoma most common in children 0-14 years d. DLBCL most common in adolescents/young adults 2. Key points a. Malignant solid tumour characterised by undifferentiated lymphoid cells b. Spread: aggressive, diffuse, unpredictable c. Involves lymphoid tissue and can infiltrate the BM and CNS d. Characterised by a high growth fraction and doubling time e. Early diagnosis and treatment is critical Rapid chemotherapy response can occur, therefore there is a higher risk for tumour lysis3. Risk factors a. Inherited or acquired immunodeficiency (eg. SCID, Wiskott-Aldrich, HIV) b. Viruses (eg. HIV, EBV) c. Part of genetic syndrome (eg. ataxia-telangiectasia, Bloom syndrome) d. Radiation therapy/ exposure e. Post T cell depleted HSCT Post solid organ transplan

Answer 78

a. Stage I: Involvement of single tumour or single anatomic area excluding the mediastinum or abdomen b. Stage II: Two or more lymph node regions on the same side of the diaphragm or resectable primary abdominal c. Stage III: Involvement of lymph node regions on both sides of the diaphragm; all primary mediastinal, paraspinal or extensive intra-abdominal disease Stage IV: Any of the above and initial involvement of the CNS, BM or both

Answer 79

aka cerebella present as truncal and gait ataxia, CN palsy Usually CN 6 first (abducens)- LR affected, unable to move gaze laterally CN4 (trochlear, SO affected)- double vision CN3- oculomotor- down and out position, dilated pupil, ptosis Nystagmus

Answer 80

CN palsies Nystagmus Gait and coordination difficulties UMN signs- hemiparesis, hyperreflexia, clonus

Answer 81

Lateralized deficits (focal motor weakness, focal sensory changes, language disorders, focal seizures, reflex asymmetry

Answer 82

most common= craniopharyngioma, astrocytoma Visual field defects neuroendocrine defects = obesity, abnormal linear growth velocity, diabetes insipidus, galactorrhoea, precious puberty, delayed puberty and hypothyroidism 1. Di-encephalic syndrome = failure to thrive + emaciation despite normal caloric intake + inappropriately normal or happy affect (tumor in diencephalon (hypothalamus, optic chiasm), most commonly pilocytic astrocytoma)

Answer 83

structures that are on either side of the third ventricle, including the thalamus, the hypothalamus, the epithalamus and the subthalamus Arises from the prosencephalon

Answer 84

Pineal gland tumor/midbrain infarction or haemorrhage/obstructive hydrocephalus Paralysis of upward gaze Pupils not reactive to light (pseudo Argyll RObertson pupil) Nystagmus to convergence eyelid retraction

Answer 85

Gliomas- further divided into: astrocytomas ependmoma oligodendrocytomas mixed glial/neuronal

Answer 86

medulloblastoma neuroblastoma pNET Atypical teratoid/ rhabdoid tumors (ATRT)

Answer 87

arise from lining of ventricles/spinal cord (most in posterior fossa) bimodal- in kids <5 years NF2 have increased risk MRI: calcifications common, arise at ventricles, can look very nasty and heterogenous Histology: pseudorosettes/ependymal rosettes Rx: surgery + radiation, not usualy chemosensitive Worse prognosis if cant do GTR, posterior fossa disease, diseemniated disease

Answer 88

Subset of glioma Can be low grade (eg pilocytic) or high grade (DIPG/GBM) **optic pathway gliomas are low grade astrocytomas** Pilocytic astrocytoma typically in cerebellum NF1= better prognosis MRI: contrast enhanging nodule within wall of cystic mass Histology: Rosenthal fibres (corkscrew pink bundles)

Answer 89

Most common type of low grade astrocytoma Typically in cerebellum, optic pathway, or tectal Commonly in NF1 Locally aggressive but rarely invasive May stabilise or even regress without intervention MRI: contrast enhanging nodule within wall of cystic mass, in posterior fossa or optic tract, often associated with hydrocephalus Histology: Rosenthal fibres (corkscrew pink bundles) Molecular: change in BRAF (RAS/MAPK) pathway (can use BRAF/MEK/mTORinhibitors) Rx: slow growing so dont respond well to chemo. Can do nothing, just watch if normal visual acuity Surgery is first line If progression- small amount of chemo (carboplatin, vincristine, vinblastine) Survival 90%

Answer 90

Anaplastic astrocytoma Glioblastoma multiforme DIPG (midline GBM)- very agressive, 90% mortality within years

Answer 91

Embryonal tumors Include medulloblastoma and ATRT

Answer 92

most common childhod malignant brain tumor Arise from cerebellum- usually vermis 1/3 have mets at presentation - usually to CNS M>F Peak age 3-9 years Prognostic factors: Good= WNT1, age >3 years, localised disease Bad= MYC amplification (Group 3) , p53 Intermediate = Sonic hedgehog (better prognosis in infants; but SHH +p53 are very bad), group 4, >1.5 cm2 residual tumor, large cell anaplastic Babies <3 years automatically high risk - cant do radiation Rx: surgery, chemotherapy, radiation Craniospinal irradiation with a boost to the posterior fossa followed by intensive adjuvant chemotherapy MRI of spine + lumbar CSF obtained at least 10 days after surgery

Answer 93

highly malignnat, fast growing can appear anywhere in brain or spine usually in kids <3 years short clinical hx mets in 20% at presentation small round blue cells + rhabdoid tumor cells deletion/inactivation of INI1/SMARCB1 Poor prognosis, median survival 12 months Increased risk for renal and soft tissue tumors as well

Answer 94

A craniopharyngioma develops from remnant of Rathke’s pouch in sella turcica. Clinically often presents with headache/vomiting, visual disturbances due to the compression of the optic nerves or the optic chiasm (bitemporal hemianopia, optic atrophy, visual loss) About 50% of childhood craniopharyngiomas extend upward into the third ventricle and result in hydrocephalus. Bimodal, age 10-14 yo Endocrine: growth hormone deficiency (75%); thyroid-stimulating hormone deficiency (25-64%); adrenocorticotropic hormone deficiency (25-56%); luteinising hormone or follicle-stimulating hormone deficiency (40-44%); diabetes insipidus (9-17%, but almost 100% post-op). MRI: cystic. most calcified. suprasellar location

Answer 95

fever malaise myalgia/arthralgia after cytarabine

Answer 96

tuberus sclerosis bengin, slow growing, arise in wall of lateral ventricles Treated with mTOR inhibitors (eg everolimus) if unresectable

Answer 97

Extragonadal germ cell tumors (esp mediastinal) Breast cancer

Answer 98

Gonadoblastoma

Answer 99

Neurofibromas (cutaneous, plexiform) Optic pathway gliomas low-grade Other brain tumors- astrocytomas, brainstem gliomas, and high-grade gliomas Malignant peripheral nerve sheath tumors Rhabdomyosarcoma

Answer 100

Vestibular schwannomas Meningiomas Spinal ependymomas

Answer 101

neurological changes 1-5 days after PF tumor resection difficulty verbalising irritability nystagmus mutism emotional lability mutism usually resolves but can take a year

Answer 102

most common high grade glioma in kids usually pons/brainstem Presentation: multiple CN palsies, raised ICP, cerebellar signs, long tract signs (hyperreflexia, increased tone, clonus, Babinski +, motor deficit) Often have basilar artery encasement Clinical + radiological disgnosis as cant biopsy a brainstem Most have histone H3.3 mutation Rx: palliative radiation Prognosis: most survive <1 year. bad

Answer 103

Arise in suprasellar (pituitary, infundibulum) or pineal region More common in Japanse Presentation: pituitary:hormone deficiencies, DI Pineal: usually malignant, short hx, raised ICP, diplopia, parinaud syndrome, hydrocephalus Ix: AFP/bHCG (serum + CSF), MRI brain + spine High AFP= non germinomatous germ cell tumor Rx: chemo + radiation. germinomas are very radiosensitive. NGGCT- chemo + CS radiation. Germinomas + teratomas: AFP + HCG neg Yolk sac- AFP + Choriocarcinoma: HCG +

Answer 104

- Rhabromyosarcoma - Other bladder cancers very rare - Associated with haematuria, obstruction, urinary symptoms - Usually embryonal subtype which is a small round blue cell tumor

Answer 105

radiation/Xrays due to high risk of other cancers

Answer 106

most common benign bone cyst metaphysis of long bone/tendon insertion site Bony, non painful mass XRay- stalk or projection of bone

Answer 107

most commonly on legs unremitting pain often worse at night and relieved by aspirin/NSAIDS exam: limp, atrophy, weakness xray: lucency surrounded by sclerotic bone

Answer 108

benign, aggressive osteogenic bone lesions commonly found in the posterior elements of the spine. Patients typically present between ages 10 and 30 with regional pain with only partial response from NSAIDs. Diagnosis is made radiographically by a characteristic lesion that is > 2 cm in diameter with a sclerotic margin and radiolucent nidus.

Answer 109

Can occur any time when severely immunosuppressed Mostly LUNGS - halo sign and air crescent sign on CT Can also occur in sinuses, brain Rx: voriconazole, caspofungin second line Inherently resistant to fluconazole

Answer 110

Mostly in neutropenic phase, or with prolonged antibiotics in leukemia/lymphoma Mostly LIVER

Answer 111

T15,17 RaRa gene Complications- differentiation syndrome from all trans retinoic acid DIC

Answer 112

Abdominal mass Hematuria HTN fever

Answer 113

Denys Drasha WAGR Fanconi anemia BWS

Answer 114

Lungs IVC tumor thrombus via renal vein

Answer 115

used for high risk neuroblastoma Kills neuroblasts Antibodies bind to antigens on neuroblastoma cells --> active killing of antibody bound tumor cells by NK cells and macrophages GD2 also found on peripheral + central nerves and skin Severe pain when giving this drug- need concurrent morphine infusionAcute toxicity can present with neuropathic pain, hypotension, hypoxia, fever, capillary leak syndrome and hypersensitivity reactions.

Answer 116

GH deficiency

Answer 117

Present within 100 days post HSCT and with classic features of skin involvement (maculopapular rash), gastrointestinal involvement (diarrhoea and abdominal pain) and/or liver involvement (rising serum transaminases and bilirubin). can do a skin biopsy if diagnosis unclear

Answer 118

Topoisomerase inhibitor inhibits the enzyme topoisomerase II, which unwinds DNA, and by doing so causes DNA strands to break. Work in S and G2 phase

Answer 119

Wilms tumor

Answer 120

hemotherapeutic agents and hypertension are both risk factors for PRES. Vision loss suggests the occipital lobes are involved. The lack of diffusion restriction indicates vasogenic oedema rather than cytotoxic oedema that is seen in watershed infarcts.

Answer 121

cryptococcus neoformans india ink stain - cells w surrounding halo

Answer 122

anti-CD19+ and CD-3+ monoclonal antibody with bi-specific T-Cell engagers (BITE) that is used to treat B-cell acute lymphoblastic leukaemia

Answer 123

anti-CD30+ monoclonal antibody indicated for treatment of CD30+ lymphomas.

Answer 124

MYCN amplification

Answer 125

systemic response caused by the release of cytokines as a response to some form of immunotherapy. The exact pathophysiology is unknown, but symptoms can range from mild (fever, arthralgia, nausea) to severe (acute renal failure, seizures and disseminated intravascular coagulopathy). There is a risk of Cytokine Release Syndrome in any form of immunotherapy, but it occurs most commonly in CAR-T cell therapy (for B-ALL). The current theory is that CAR-T cells produce interleukin-1 and interleukin-6 perpetuating a pro-inflammatory response. Monoclonal antibodies and immune checkpoint inhibitors are all forms of immunotherapy and therefore have the same risks. Tocilizumab (interleukin-6 antagonist) is used to treat cytokine release syndrome.

Answer 126

AML Immunohistochemistry is negative for CD3 and CD19 in AML. Myeloblasts will most commonly stain positive with myeloperoxidase

Answer 127

B-lineage lymphoblasts are positive for cell marker CD19 and cytoplasmic markers CD79a and CD22. Although these markers on their own is not specific for B-ALL, high intensity positivity strongly supports the diagnosis. B-ALL must be negative for CD3 and negative on myeloperoxidase staining.

Answer 128

Diagnosis of Differentiation Syndrome is by the presence of three of more of the following features in the absence of another explanation: Fever ≥38° C Weight gain >5 kg Hypotension Dyspnoea Radiographic opacities Pleural or pericardial effusion Acute renal failure

Answer 129

○ vinca alkaloids ○ enzymes (asparaginase) ○ bleomycin steroids

Answer 130

MTX cytarabine

Oncology Flashcards

(158 cards)