Oncology Flashcards

1
Q

What genetic conditions have a predisposition for leukemia?

A
Trisomy 21
NF 1
Shwachman-Diamond syndrome
Li-Fraumeni syndrome
Chromosomal fragility – Bloom’s, Fanconi’s anemia, Ataxia Telangiectasia
Paroxysmal Nocturnal Hemoglobinuria
Diamond-Blackfan Anemia
Kostmann syndrome
SCID (Severe combined immune deficiency)
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2
Q

What are typical findings on CBC in Leukemia?

A

WBC may be low, normal or high.

Hemoglobin and platelets may be normal or low.

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3
Q

What % of patients with leukemia will not have circulating blasts?

A

20%

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4
Q

How do patients with leukemia typically present?

A

Low Hemoglobin
Pallor, fatigue, irritability

Low White cells
Fever, sepsis

Low Platelets
Bruising/bleeding, petechiae

Leukemic Blasts
Bone pain, limp

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5
Q

How do you distinguish between leukemia and sJIA?

A

Wbc low (<4),
Plt low normal (150-250),
Night time pain

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6
Q

What x-ray findings do you see in leukemia?

A

Transverse radiolucent metaphyseal growth arrest lines
Periosteal elevation with reactive Subperiosteal cortical thickening
Osteolytic lesions
Diffuse osteopenia/ osteoporosis

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7
Q

What are some clinical features of leukemia that indicate extramedullary disease?

A
Lymphadenopathy
HSM
Gingival hyperplasia
Leukemia Cutis
Chloroma (subcutaneous collection of AML cells)
Lymphomatous mass
CNS disease*
Testicular disease*
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8
Q

What are indications for BMA?

A

Unexplained and significant depression ≥ 1 peripheral blood cell elements

Blasts on peripheral smear

Leukoerythroblastic changes on peripheral smear

Association with unexplained lymphadenopathy or hepatosplenomegaly

Association with an anterior mediastinal mass

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9
Q

What is the most common type of ALL?

A

80-85% are precursor B, remainder precursor T

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10
Q

What is the prognosis of ALL?

A

90% cure

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11
Q

How long is treatment for ALL?

A

2.5-3.5 years

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12
Q

How long is treatment for AML?

A

6 months, intensive

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13
Q

What is the prognosis of AML?

A

60% cure

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14
Q

What are poor prognostic signs in ALL?

A

AGE: < 1 and > 10 yrs*

WHITE CELL COUNT: > 50 *

CNS and/or TESTICULAR DISEASE

CYTOGENETICS
Good:t (12;21) = TEL-AML; hyperdiploidy
Poor: MLL gene rearrangement (11q23)
Very Poor: t (9;22) = Ph chromosome, and hypodiploidy

DISEASE RESPONSE
As assessed by minimal residual disease (MRD) testing at the end of induction chemotherapy

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15
Q

What is a differential diagnosis for cervical adenopathy?

A
Viral URI
Bacterial adenitis
EBV
Cat scratch
Atypical mycobacterium
Malignancy
Kawasaki
TB
Rare infections-toxo, tularemia, brucellosis, leptospirosis
Sarcoidosis
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16
Q

Differential diagnosis of generalized adenopathy?

A

Syphilis
HIV
CMV
Toxo

Rare: leukemia, TB, serum sickness, SLE, JRA, sarcoidosis, fungal, histoplasmosis, LCH

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17
Q

What are the predictive factors for malignancy with lymphadenopathy?

A

Age >10
Node >2.5 cm
Supraclavicular (TB in ddx)

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18
Q

What are the indications for excisional biopsy with lymphadenopathy?

A
>2 cm
Increase over 2 weeks
No decrease in size after 4 weeks
Supraclavicular
Hard, matted, rubbery consistency
Abnormal CXR
Fever
Weight loss
HSM
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19
Q

What are the types of lymphoma in children?

A

Hodgkins

  • Classical (chemo + rads)
  • Lymphocyte predominant (only surgery if localized)

Non-hodgkins

  • Mature B cell: burkitt’s and diffuse B cell
  • Precursor B/T cell: Lymphoblastic lymphoma: like leukemia, except <25% BM involvement
  • Mature T cell: Anaplastic

Rough ddx:
<5 years:
Lymphoblastic lymphoma

> 5 years:
Hodgkin lymphoma

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20
Q

How does Hodgkin’s lymphoma typically present?

A

Painless cervical lymphadenopathy
Slow growing
1/3 present with B symptoms

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21
Q

What tests do you need to do pre-chemo for Hodgkins?

A

PFTs (Bleomycin)

Echo (Anthracyclines)

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22
Q

What is the prognosis of Hodgkin’s lymphoma?

A

> 90% cure

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23
Q

What chemotherapy agents are used in Hodgkin’s treatment and what are their late toxicities?

A

Akylator/Etoposide and RT- any
BUT risk of breast cancer 12-20% by 30y!

Anthracycline and RT- CV ds, heart failure

Bleomycin and RT- pulmonary fibrosis

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24
Q

What is more aggressive, NHL or HL?

A

NHL

Diffuse, aggressive, high grade

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25
Q

What is the average at diagnosis for NHL?

A

8-10yo

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26
Q

What are conditions that predispose to NHL?

A

Think immunodeficiency, especially in younger child with NHL:

Ataxia telangiectasia
Wiskott-Aldrich syndrome
Congenital hypogammaglobulinemia
Post-solid organ transplant
HIV
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27
Q

How does burkitt’s lymphoma typically present?

A
  • 80% have abdominal mass (mimics appendicitis, intussuseption)
  • Can be endemic (EBV driven)
  • High risk of TLS
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28
Q

Differential diagnosis for splenomegaly?

A

1) HEMATOLOGIC

HEMOLYTIC:

  • Thalassemia
  • Sickle cell anemia
  • Hereditary spherocytosis
  • Autoimmune hemolysis

LYMPHOPROLIFERATIVE:

  • Leukemia
  • Lymphoma
  • ALPS

MYELOPROLIFERATIVE:

  • CML
  • Polycythemia vera
  • Essential thrombocytosis, Myelofibrosis

HISTIOCYTOSES:

  • HLH
  • LCH

ONCOLOGIC

  • Neuroblastoma
  • Metastases
  • Hemangioma

INFECTIOUS
EBV, CMV, Toxoplasmosis, Viral hepatitis, Typhoid, Tuberculosis, Syphilis, HIV
Malaria, Leishmaniasis, Schistosomiasis

RHEUMATOLOGIC / INFLAMMATORY
Systemic lupus erythematosus
Rheumatoid arthritis
Sarcoidosis

INFILTRATIVE
Gaucher’s disease, Amyloidosis

CONGESTIVE
Sequestration
Hypersplenism
Cirrhosis / Liver failure
Hepatic vein thrombosis
Cardiac failure
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29
Q

Differential diagnosis of anterior mediastinal mass?

A

Lymphoma

  • Hodgkins
  • NHL

Thymus

Teratoma

Thyroid

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30
Q

Name 4 complications of a mediastinal mass

A

Tracheal/Bronchial compression

SVC compression/obstruction (SVC Syndrome)‏

RVOT Obstruction

Pericardial effusion/tamponade

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31
Q

What are the two most common tumour to cause diplopia, headache and ataxia?

A

Posterior fossa-cerebellar astrocytoma, medulloblastoma

Brainstem gliomas are unlikely to cause raised ICP

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32
Q

Name 5 types of pediatric brain tumours

A
Low Grade/Pilocytic Astrocytoma
Medulloblastoma (MOST COMMON PEDIATRIC MALIGNANT BRAIN TUMOUR)
Ependymoma
Glioblastoma Multiforme
Brain Stem Glioma
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33
Q

How do supratentorial tumours typically present?

A

Localizing signs

SEIZURES
Visual changes
Hemiparesis , hemisensory loss, hyperreflexia

Subtle localizing signs/symptoms:

Behavioral problems: frontal lobe

Neuroendocrine deficits: hypothalamus/pituitary
DI, precocious/delayed puberty, hypothyroidism

Diencephalic syndrome in <3yo: FTT, hunger, euphoria

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34
Q

In what age group are supratentorial tumours more common?

A

Infants

Teens/adults

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35
Q

What is the differential for supratentorial tumours?

A

1) Glioma (low or high grade)
- Optic pathway/hypothalamic (eg NF1)
- Cerebral
2) Craniopharyngioma
3) Ependymoma

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36
Q

How do infratentorial tumours typically present?

A

Raised ICP (cerebellar>brainstem)
Ataxia(clumsineness, nystagmus)
Long tract signs (worsening handwriting, appendicular dysmetria)
Cranial Neuropathy (diplopia, difficulty swallowing)

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37
Q

In what age group are infratentorial tumours more common?

A

Children

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38
Q

What is the differential for infratentorial tumours?

A

1) Glioma (low or high grade)
- Cerebellar
- Brainstem
2) Medulloblastoma
3) Ependymoma

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39
Q

How do you distinguish between a brainstem and cerebellar tumour?

A

CN neuropathy, long tract signs, ataxia=Brainstem tumor

↑ ICP, ataxia in absence of other signs= Cerebellar tumor

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40
Q

What are headache red flags?

A

Change in type, increasing severity/frequency

Sudden/severe onset

Associated with trauma

Early AM, awakens from sleep, assoc w/ straining

Abnormal neurologic signs/symptoms

Seizures or loss of consciousness

Linear growth regression

School or behavior change

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41
Q

What type of brain tumour does CT head often miss?

A

Posterior fossa tumours

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42
Q

What are the clinical features of osteoid osteoma?

A

Dull pain worse at night

Better with NSAIDs

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43
Q

What are x-ray findings in osteoid osteoma?

A

Well-defined lucency surrounded by sclerotic bone

Proximal femur and tibia are most common sites

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44
Q

What are clinical features of osteochondroma?

A

Asymptomatic or non-painful bony mass

Lesion enlarges until reach skeletal maturity

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45
Q

What are the x-ray findings in osteochondroma?

A

Usually at metaphysis of long bones

Stalk/broad-based projection

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46
Q

What is an enchondroma?

A

Benign lesion of hyaline cartilage centrally in bone, often in hands

Asymptomatic usually

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47
Q

What is an aneurysmal bone cyst?

A

Reactive lesion of bone seen in persons <20 yr of age

Cavernous spaces filled with blood and solid aggregates of tissue

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48
Q

Where are aneurysmal bone cysts usually found?

A

Metaphysis of any bone

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49
Q

How do malignant bone tumours present?

A

Pain
Limp
Swelling
Nighttime awakening

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50
Q

At what age does osteosarcome typically present?

A

Around puberty (rapid bone growth)

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51
Q

What part of bones is osteosarcoma usually located?

A

Metaphysis of long bones (distal femur, proximal tibia/fibula)

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52
Q

What is the typical x-ray appearance of osteosarcoma?

A
Sunburst appearance***
Hair on end
Osteoblastic activity
Severe periosteal reaction with new bone formation
Periosteal elevation
Mottling***
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53
Q

Where does osteosarcoma metastasize?

A

Lungs

Bone

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54
Q

In what bones is Ewing’s sarcoma typically found?

A

Diaphysis of long bones or flat bones

Axial skeleton more common

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55
Q

What is the appearance of Ewing’s sarcoma on XR?

A

Onion-skinning on XR
Primary lytic lesion (moth-eaten radiolucency) with multilaminar periosteal reaction
Cortical destruction
Soft tissue mass

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56
Q

Where does Ewing’s metastasize?

A

Lungs
Bone
Bone marrow

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57
Q

How can you tell if leg pains are growing pains?

A
Children 4-12y
Poorly localized, often lower limbs
Occur at night but never persists until morning
No disability
Normal physical exam
Normal x-rays
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58
Q

What is the malignant differential for abdominal mass?

A

In younger kids (<5yo), think of embryonal tumors (“blastoma”)
Wilms (nephroblastoma)
Neuroblastoma
Hepatoblastoma (< 3yo)

In older, think of:
Lymphoma - Burkitt’s! (older than 3yo)
Germ Cell Tumour (bimodal)
Sarcoma (EWS, Rhabdo)

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59
Q

What investigations do you order for abdominal mass?

A

Ultrasound
CT

CBC and Diff, lytes, urate, LDH
Liver enzymes/function
AFP, BHCG (GCTs)
Urinanalysis
Urine HVA/VMA (NB)
Consider BMA
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60
Q

What is the clinical presentation of neuroblastoma?

A

Adrenal: Abdo mass, hypertension

Thoracic: Dyspnea or Horner syndrome

Paraspinal: spinal cord compression

Bone and Bone Marrow involvement:
Anemia, bruising, periorbital ecchymosis

Paraneoplastic syndrome:
Opsoclonus-Myoclonus-Ataxia
VIP-induced diarrhea

61
Q

What are good prognostic factors in neuroblastoma?

A

Age, age, age, age - young age is better
Less than 12 – 18 months

Stage
CT/MRI, MIBG, bone scan, BM, Urine HVA/VMA

Biology 
Histology
N-Myc amplification
Ploidy
Others:  1p deletion, 17q gain
62
Q

What is Stage 4S neuroblastoma?

A

Skin involvement ONLY
Nontender, bluish subcutaneous nodules
Massive hepatomegaly
BM involvement <10%

63
Q

What does the presence of opscolonus myoclonus imply for prognosis in neuroblastoma?

A

Good tumor, bad cognition

64
Q

How do you treat opsoclonus myoclonus in neuroblastoma?

A

Steroids, IVIG

65
Q

What age does hepatoblastoma typically present?

A

<3 years

66
Q

What are risk factors for hepatoblastoma?

A

BWS
Hemihypertrophy
Family Hx of FAP
Prematurity

67
Q

What is the biochemical marker in hepatoblastoma?

A

90% have ↑↑↑ alphafetoprotein (AFP)

68
Q

What is the prognosis of hepatoblastoma?

A

Good prognosis for localized

Unresectable may require liver transplant

69
Q

How does Wilm’s tumour present?

A

Painless abdo mass
Hematuria
Abdo pain with rupture
Also detected with screening at-risk patients

70
Q

What is the prognosis of Wilm’s tumour?

A

Excellent prognosis for localized and regional spread

71
Q

What conditions increase your risk of TLS?

A

Leukemia with high WBC count (>50)
Lymphoma (esp lymphoblastic lymphoma, Burkitt)
Advanced solid tumours
Pre-existing renal issues

72
Q

What are the electrolyte abnormalities associated with TLS?

A

High K, PO4, urate

Low Ca

73
Q

How do you treat TLS?

A

HYDRATION, diuresis
Anti-urate therapy (allopurinol, rasburicase)
Monitoring and management of electrolyte abnormalities

74
Q

What is the WBC cut off for hyperleukocytosis?

A

WBC >100,000/mm3

75
Q

What is the clinical presentation of hyperleukocytosis?

A

Pulmonary: exertional dyspnea, severe respiratory distress, hypoxemia

Neurological: confusion, somnolence, stupor, coma, headache, dizziness, gait instability, blurred vision, papilloedema, cranial nerve defects

Renal: decreased urine output, elevated creatinine

76
Q

What is the most common cause of death in hyperleukocytosis?

A

Most early deaths are due to respiratory failure and intracranial hemorrhage

77
Q

How do you treat hyperleukocytosis?

A

Hydration
Rasburicase
Platelet transfusion-to prevent ICH
Antibiotics

Avoid prBC tx (if need to small amounts 2-5 ml’/kg) because increases viscosity!

78
Q

What types of cancers can cause spinal cord compression?

A

Sarcomas
Neuroblastoma
Lymphoma
CNS tumor mets

79
Q

What are the signs of spinal cord compression?

A
Back pain
Local tenderness
Neurologic sx
Urinary retention
Constipation
Hyper-reflexia
Babinski
Parasthesias
80
Q

What treatment should you add for prolonged febrile neutropenia?

A

Anti-fungal

81
Q

What are factors that can influence fertility in cancer patients?

A

Type and cumulative doses of chemotherapy

Radiation fields

82
Q

What options do oncology patients have to deal with infertility?

A

Sperm banking

Counseling about donor sperm, adoption…

83
Q

What side effects are common to all chemotherapy?

A
Fatigue
Nausea/vomiting
Bone marrow suppression
Hair loss
Mucositis
Skin rash
84
Q

Acute toxicity associated with vincristine

A

SIADH
Peripheral Neuropathy
-constipation, hyporeflexia, CNs

85
Q

Late toxicity associated with vincristine

A

None

86
Q

Acute toxicity associated with bleomycin

A

Pulmonary
Hypersensitivity
Rash

87
Q

Late toxicity associated with bleomycin

A

Pulmonary fibrosis

88
Q

Acute toxicity associated with cyclophosphamide/ifosfamide

A

Hemorrhagic cystitis

Encephalopathy (ifosfamide)

89
Q

Late toxicity associated with cyclophosphamide/ifosfamide

A
Infertility
Cardiac dysfunction
SMN
Pulmonary fibrosis
POF
90
Q

Acute toxicity associated with L-asparginase

A

Allergic reaction
Hepatopathy
Coagulopathy/thrombosis
Pancreatitis

91
Q

Late toxicity associated with L-asparginase

A

None

92
Q

Acute toxicity associated with doxorubicin

A

Dilated cardiomyopathy

Mucositis

93
Q

Acute toxicity associated with anthracyclines (doxorubicin)

A

Dilated cardiomyopathy

Mucositis

94
Q

Late toxicity associated with anthracyclines (doxorubicin)

A

Cardiomyopathy

Secondary leukemia

95
Q

Late toxicity associated with etoposide

A

Secondary leukemia

96
Q

Acute toxicity associated with cisplatin

A

Emesis

97
Q

Late toxicity associated with cisplatin

A

Ototoxicity

Nephrotoxicity

98
Q

Acute toxicity associated with methotrexate

A

Renal failure

Mucositis

99
Q

Late toxicity associated with methotrexate

A

Leukoencephalopathy

100
Q

Late toxicity associated with steroids

A

AVN, cataracts

101
Q

List 6 long-term side effects of Hodgkin’s Lymphoma treatment - radiation to neck and chest, chemo including doxorubicin, cyclophosphamide, bleomycin, etoposide, and steroids

A
Hypothyroidism (RT)
Infertility (Cyclopphosphamide, RT)
Cardiomyopathy, CAD (doxorubicin
Pulmonary Fibrosis (Bleomycin, RT)
Second CA – breast, thyroid, skin, …(RT)
MDS/Leukemia (Cyclophosphamide)
Avascular Necrosis (Steroid)
102
Q

What is the pathology in LCH?

A

Clonal proliferation of epidermal dendritic cells

103
Q

Clinical presentation of LCH

A

Exam presentation: Exopthalmos, refractory diaper rash, HSM, bony lucencies of skull of XR

Single bone lesion
Multiple bone lesions 
Multi-organ involvement:
Bone (skull, limb, single or multiple, BM)- 80%
Skin/scalp (scaly, waxy rash) – 50%
CNS, Pituitary (DI) 
Lungs 
GI, liver, spleen
Eyes, ears, mouth
104
Q

What are poor progonistic signs in LCH?

A
Young age (<18 months) at diagnosis 
Hepatomegaly 
Anemia and/or thrombocytopenia 
Bone marrow involvement 
Hemorrhagic skin lesions
105
Q

How do you treat LCH?

A

Observe if localized

Chemotherapy if systemic

106
Q

What are the diagnostic criteria for HLH?

A

Need 5 out of 8:

fever
bicytopenia
splenomegaly	
hemophagocytosis
hyperferritinemia 	
increased sIL2R
hypertriglyceridemia
hypofibrinogemia
low/absent NK cell activity
107
Q

How do you treat HLH?

A

IVIG

Chemo : Steroids, Etoposide (VP-16)

108
Q

What are indications for allogeneic BMT?

A
Hematologic malignancy
Bone marrow failure
Select immunodeficiencies
Regfactory/relapsed lymphoma
Metabolic disorders
Hemoglobinopathies
Osteopetrosis
109
Q

What are indications for autologous BMT?

A

Autologous transplant is basically a ‘rescue’ from ultra high dose chemotherapy
(For example, after chemotherapy for NB, you do autologous BMT to reconstitute the BM)

110
Q

What is GVHD?

A

Only in allogeneic transplants

GVHD occurs when immune cells transplanted from a non-identical donor (the graft) recognize the transplant recipient (the host) as foreign, thereby initiating an immune reaction that causes disease in the transplant recipient

111
Q

What are risk factors for GVHD?

A

Mismatched and unrelated donor
Bone marrow more than cord
Increasing age

112
Q

What systems are involved in acute GVHD?

A

Skin
Liver
Gut

113
Q

What systems are involved in chronic GVHD?

A

Any system can be involved

114
Q

After how many days would you consider GVHD chronic?

A

> 100 days

115
Q

What is osteopetrosis?

A

Inherited bone disease involving dense, sclerotic bones prone to fracture

116
Q

What are clinical features of osteopetrosis?

A
Growth impairment
Fractures
Dental abnormalities
Hepatosplenomegaly
Epilepsy
Intellectual disability
Bone marrow can be affected due to bone density causing cytopenias
117
Q

What is Kasabach Meritt syndrome?

A

Vascular tumor (hemangiomas) leads to sequestration/destruction of platlets, thrombocytopenia and consumptive coagulopathy (DIC)

118
Q

What is the most common type of tumour associated with Kasaback Meritt syndrome?

A

Kaposiform hemangioendotheliomas

119
Q

How do you treat Kasabach Meritt?

A

Steroids

Chemotherapy

120
Q

What is the impact of a cancer diagnosis on siblings?

A

Siblings are at risk both during illness and after death

Parents have extraordinary demands placed on them to meet needs of ill child – healthy children may feel own needs aren’t being met or acknowledged and this may lead to concerns about own health and resentment

Normal response/encouragee to maintain normal routines

Siblings tend to adjust better at the time of and after death

Acknowledge and validate the sibling’s feelings

121
Q

Name 4 principles of treatment with opoids for palliative oncology patients

A

Characterize the pain: neuropathic or mixed?

Decide on route of administration: can she swallow?

Dose with long acting opiods with short acting breakthrough

Ensure timely reassessment of symptoms

Decide if adjuvant medications are required: gabapentin for neuropathic pain

122
Q

Associated malignancies with Down’s Syndrome

A

TMD
ALL
AMKL

123
Q

Associated malignancies with Beckwith-Wiedemann

A

Wilm’s tumour

Hepatoblastoma

124
Q

Associated malignancies with WAGR (Wilms, Aniridia, GU abnormalities, Retardation)

A

Wilm’s tumour

125
Q

Associated malignancies with NF-1

A

Optic pathway glioma
Astrocytoma, brainstem gliomas
Soft tissue sarcoma
Leukemia

126
Q

Associated malignancies with Retinoblastoma (RB1)

A

Retinoblastoma
Osteosarcoma
Melanoma

127
Q

Associated malignancies with Li Fraumeni (p53)

A

Bone, soft tissue sarcomas
Brain tumours
Breast
Others

128
Q

Associated malignancies with Multiple Endocrine Neoplasia

A

MEN1=Parathyroid glands, anterior pituitary, and entero-pancreatic endocrine cells
MEN2=Medullary thyroid CA, pheochrompcytoma

129
Q

Associated malignancies with Familial Adenomatous Polyposis

A

Colorectal carcinoma
Hepatoblastoma
Thyroid cancer

130
Q

What percentage of patients with Down Syndrome have TMP?

A

10%

131
Q

What are the clinical and laboratory features of TMP?

A

↑ WBC
Peripheral blasts
Pancytopenia
Hepatosplenomegaly

132
Q

How do you treat TMP?

A

Most = no treatment, resolves over days-weeks

133
Q

What cancer does TMP put you at risk for?

A

AML

134
Q

What are the clinical features of Beckwith Wiedemann?

A
Hemihypertrophy
Macrosomia
Macroglossia
Visceromegaly
Omphalocele
Umbilical hernia
Neonatal hypoglycemia
135
Q

What is the genetic mutation in Beckwith Wiedemann?

A

11p15 imprinting/uniparental disomy

136
Q

How often and with what do you screen patients with Beckwith Wiedemann for malignancy?

A

Screen every 3 months with:
AFP until age 4
Abdo U/S until age 8

137
Q

What conditions are associated with Wilm’s tumour?

A

Beckwith-Wiedemann
WAGR (Wilms, Aniridia, GU abnorm, Retardation)
Denys Drash (renal dz, pseudohermaphroditism, Wilms)
11p deletions
Hemihypertrophy

138
Q

When do you screen for subependymal astrocytomas in TS?

A

1-3 years of age

139
Q

What are the important emergency department management steps for all children with suspected leukemia?

A
TLS bloodwork
CXR
Hyperhydration 
Allopurinol (or raburicase)
Antibiotics if febrile regardless of WBC count
140
Q

What are benign causes of abdominal mass?

A

Hydronephrosis
Liver/spleen
Fecal mass
Renal vein thrombosis

141
Q

What is the most common risk factor for renal vein thrombosis in neonates?

A

Mother with GDM

142
Q

What is the most common cause of abdominal mass in a neonate?

A

MCDK

143
Q

What are 5 physical exam findings associated with neuroblastoma

A
Hypertension (catecholamine release)
Abdominal mass
Hyperreflexia (SCC compression)
Opsoclonus-myoclonus (paraneoplastic)
Bruising/petechiae (BM involvement)
Periorbital ecchymosis (mets)
144
Q

Until how many months after chemo do you give VZIg if an oncology patient is exposed to chicken pox?

A

3-6 months

145
Q

What are two factors associated with cancer treatment than can effect fertility?

A

Type and cumulative dose of chemotherapy

Radiation fields

146
Q

What are 2 options for dealing with infertility to offer cancer patients?

A

Sperm banking

Counseling about donor sperm and adoption

147
Q

What chemotherapy would cause sinus vinus thrombosis (oncology patient with headache)?

A

L-asparginase

148
Q

How do you diagnose LCH?

A

Skin biopsy

149
Q

Describe xray findings in aneurysmal bone cyst

A

Eccentric lytic destruction and expansion of the metaphysis surrounded by a thin sclerotic rim of bone