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ABIM > Oncology > Flashcards

Oncology Flashcards

1
Q

Surveillance for Asian man above age 40 with HCC

A

6 monthly ultrasound

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2
Q

Sickle-cell-anemia: why do they not have splenomegaly?

Meta: rationale

A

Even mild disease: splenic infarcts from childhood

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3
Q

Sickle-cell disease: sickle trait:

Clinical phenotype

A

Asymptomatic

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4
Q

Sickle-cell: Stroke prophylaxis

A

Exchange transfusion

Hydroxyurea takes several weeks to reduce sickle hemoglobin concentrations. Mechanism of stroke in sickle: sickled cells.

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5
Q

90 to 95% of urothelial cancers

A

Transitional cell

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6
Q

A group of patients with NSCLC have tumors with inversion in chromosome 2 that juxtaposes the 5’ end of the echinoderm microtubule-associated protein-like 4 (EML4) gene with the 3’ end of the anaplastic lymphoma kinase (ALK) gene, resulting in the fusion oncogene EML4-ALK.

This fusion oncogene rearrangement is transforming both in vitro and in vivo.

Rx?

A

Crizotinib

ALK inhibitor

“ALK-positive” tumors are highly sensitive to tALK-targeted inhibitors.

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7
Q

alpha fetoprotein

A
  1. nonseminomatous GCTs
  2. HCC

AFP is not elevated in patients with pure seminomas.

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8
Q

Bladder cancer biopsy: Quality Criterion

A

should include bladder wall muscle

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9
Q

Bladder cancer: DxStagingEval

A
  1. Excretory urography/intravenous pyelogram followed by cystoscopy
  2. Retrograde pyelography ( upper tract lesions)
  3. Urine cytology; brush biopsies may increase the diagnostic yield
  4. Biopsies of any lesion must be of adequate size to include bladder wall muscle
  5. CT abdomen: Evaluate for local extension and nodal involvement
  6. bone scan if bony symptoms
  7. CXR staging evaluation
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10
Q

Bladder cancer: DxMethod

A

Excretory urography/intravenous pyelogram followed by cystoscopy

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11
Q

When cancer of the upper urinary tract is diagnosed, there is a _% to _% chance of cancer of the bladder.

When bladder cancer is diagnosed, there is a _% to _% chance of developing cancer of upper urinary tract.

A

When cancer of the upper urinary tract is diagnosed, there is a 30% to 50% chance of cancer of the bladder.

When bladder cancer is diagnosed, there is a 2% to 3% chance of developing cancer of upper urinary tract.

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12
Q

Exposure to aryl amines increases risk for _ cell cancer, while Schistosoma haematobium infection is associated with _ cell cancer of the bladder

A

Exposure to aryl amines increases risk for transitional bladder cancer, while Schistosoma haematobium infection usually associated with squamous cell carcinoma of the bladder

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13
Q

Bladder cancer: symptoms

A
  1. Hematuria: painless
  2. frequency, urgency, or dysuria
  3. Vesical irritation without hematuria: Common in carcinoma in situ of bladder
  4. Symptoms of advanced disease: Pain from metastatic sites, edema of lower extremities, cough or dyspnea from lung metastases
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14
Q

CA 125

A

Epithelial ovarian cancer

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15
Q

CA 19-9

A

Pancreatic cancer

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16
Q

Cancer associated with: membranous nephropathy, MAHA, PAN

A

Gastric cancer

OpenQuestion -what drives autoimmunity?

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17
Q

CEA

A
  1. GI tumors
  2. Some lung
  3. Some breast
  4. Some MCT
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18
Q

Chronic diarrhea after pancreatectomy

Rx

A

Oral pancreatic enzyme

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19
Q

When should first degree relatives of patients who have colon cancer before age 60 be screened?

A

40 or 10 years prior to dx whichever is first

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20
Q

Cryptorchidism: risk of testicular cancer is bilateral

A

True

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21
Q

Majority of testicular cancer in cryptorchid testicles

A

Pure seminoma

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22
Q

Diarrhea associated with carcinoid and VIP

A

octreotide

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23
Q

A familial nephropathy of unknown cause that results in progressive inflammation of the renal parenchyma, leading to renal failure and multifocal, superficial, low-grade cancers of the renal pelvis and ureters

A

Balkan nephropathy

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24
Q

Extracolonic cancer in Lynch syndrome

A

Endometrial

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25
Q

Febrile neutropenia: low risk vs high risk

Low risk neutropenia: MxL

A
  1. Expected duration of neutropenia of 7 days or less
  2. No evidence of sepsis
  3. No co-existing conditions (what does that mean?)
  4. No hepatic or renal dysfunction

Low risk neutropenia:

  1. No need to admit
  2. home on ciprofloxacin + Augmentin
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26
Q

ß-HCG: marker for

A

Germ cell tumor

gestational trophoblastic disease (GTD), testicular tumors, ovarian germ cell tumors, teratomas, and, rarely, other human chorionic gonadotropin (hCG)-secreting tumors

27
Q

Irregular vaginal bleeding after sex

A

Cervical cancer

28
Q

LCIS: ER status

A

Nearly always ER+

29
Q

LCIS: Mx

A
  1. Surgical excision
  2. Annual mammogram
  3. Risk reduction counseling
  4. Tamoxifen
30
Q

55 to 74 year old patient with 30 pack year history, currently smoke or have quit in 15 years

A

Yearly low dose CT

31
Q

Lynch syndrome

A
  1. Autosomal dominant
  2. Error in DNA mismatch repair system
  3. AKA HNPCC
  4. Adenocarcinoma of the proximal colon, splenic flexure
  5. Amsterdam criteria: all have to be met
32
Q

Lynch syndrome: lifetime risk of cancer

A

70%

33
Q

Malignant tumor: most common men 25-35

A

Testicular

34
Q

Morphine dosing rule in palliation

A

10% of daily total dose every hour (PO) or every 30 minutes IV

35
Q

Morphine: time to peak effect

A

30 to 60 minutes

36
Q

Nonsmoker with metastatic adenocarcinoma: OnDx

A

Test for EGFR, ALK

If EGFR +ve, erlotinib or geftinib

If ALK+ve: crizotinib

37
Q

Palliation: morphine failure at high doses

Severe, continued pain in spite of high dose long acting, frequent high dose short acting

A

Switch to methadone

38
Q

Post menopausal bleeding + Hx tamoxifen use: Mx

A

In-office endometrial biopsy

39
Q

Postmenopausal bleeding: imaging

A

Pelvic USG, saline sonography

Endometrial thickness < 4 mm has NPV 99% for endometrial cancer

40
Q

Prostate cancer: castration resistant, metastatic

A

docetaxel

41
Q

Prostate cancer: life expectancy < 10 years

A
  1. No symptoms: Active surveillance
    • Symptoms: Radiation (same efficacy as surgery)
42
Q

Risk of lung cancer in smokers

(Model derived from CARET study)

A
  1. duration of smoking,
  2. number of cigarettes smoked per day,
  3. duration of abstinence
  4. age

http://nomograms.mskcc.org/Lung/Screening.aspx

10 year risk:

  1. 51-year-old woman who smoked one pack per day for 29 years but stopped smoking 9 years : 0.8%
  2. 68-year-old man who smoked two packs a day for the past 50 years and continued to smoke: 15%
43
Q

Suspected ovarian cancer: first investigation?

A

Transvaginal ultrasound

44
Q

Tamoxifen: can cause which cancer?

A

Uterine carcinoma and sarcoma

(Because it has both antiestrogenic and pro-estrogenic effects; can cause endometrial proliferation)

45
Q

HIT: when does it occur?

A

Typically 5-14 days after exposure

46
Q

HIT: Pre-test probability assessment

A

The score assesses the degree of Thrombocytopenia, the Timing relative to heparin exposure, the presence of Thrombosis, and oTher causes for thrombocytopenia. Points are assigned as follows:

47
Q

Microcytosis: mild anemia

MCV 60s

A

Beta-Thal trait

48
Q

Budd-Chiari: Commonest risk factor

A

MPN

Myeloproliferative neoplasm

49
Q

Acute porphyria: FirstTest

Meta: FirstTest

A

Rapid urine screen for porphobilinogen

50
Q

Sickle-cell: Acute chest syndrome: Severe:

Rx other than supportive

A

Exchange transfusion

51
Q

β-thalassemia intermeda: why are they prone to venous thrombosis?

A

Abnormal erythrocytes which express prothrombotic phospholipids; activated clotting factors and activated platelets.

Meta: never seen a case

Several reports have described an increased risk of thromboembolic complications in thalassemia [68-70]. In a retrospective series of 584 individuals with beta thalassemia intermedia, thrombosis was observed in 82 (14 percent) [71]. (See “Clinical manifestations and diagnosis of the thalassemias”.)

The mechanisms are incompletely understood. It has been suggested that increased phosphatidylserine (PS) on the outer leaflet of the RBC membrane may promote thrombosis, similar to the role of PS in promoting coagulation on the surface of activated platelets [72]. (See “Overview of hemostasis”, section on ‘Multicomponent complexes’.)

Other hemostatic changes may include alterations in the levels of procoagulant or anticoagulant factors, and/or chronic activation of platelets, endothelial cells, or white blood cells [68]. Splenectomy may also increase the risk of thrombosis [73,74]. Similarity to the increased risk of thromboembolism in sickle cell disease has also been suggested. However, as high quality evidence for the increased risk of thrombophilia is lacking, we manage patients with thalassemia similar to the general population. Further study of this issue is warranted

52
Q

β-thalassemia: classification-basis

A

Degree of beta-globin reduction

Beta thalassemia is further classified as:

  1. beta thalassemia major,
  2. beta thalassemia intermedia, or
  3. beta thalassemia minor (also called beta thalassemia trait) according to the degree of reduction in beta globin
53
Q

β-thalassemia: causes of anemia

A
  1. Intramedullary hemolysis
  2. Reduced RBC survival

Beta thalassemia is caused by one or more mutations in the beta globin gene (figure 1) that result in an imbalanced ratio of alpha to beta globin. This imbalance in turn leads to impaired red blood cell (RBC) maturation and destruction of developing RBC precursors in the bone marrow, called ineffective erythropoiesis or intramedullary hemolysis; as well as hemolysis, with reduced RBC survival in the peripheral blood. The severity of beta thalassemia may also be affected by other mutations that affect the ratio of alpha globin to beta globin, including concomitant alpha thalassemia, hereditary persistence of fetal hemoglobin, concomitant sickle hemoglobin mutation, or concomitant hemoglobin E. (See ‘Imbalanced ratio of alpha to beta globin’ above.)

54
Q

β-thalassemia: causes of organ damage

Meta: PathophysiologicMechanism

A

Organ damage in beta thalassemia (renal disease, cardiomyopathy, diabetes) is due to the combined effects of anemia, chronic hypoxia, iron overload, and possibly other disease features such as a chronic inflammatory state. (See ‘Organ damage’ above.)

55
Q

CGD

A

recurrent, life-threatening bacterial and fungal infections and granuloma formation. Most diagnosed before age of five years.

Caused by defects in phagocyte enzyme complex which is responsible for the phagocyte respiratory burst.

lifelong antifungal plus antibacterial prophylaxis +/- immunomodulatory therapy

56
Q

ITP: DxMethod

Meta: DxOfExclusion

A

Ruling out other causes of thrombocytopenia

The pathogenesis of immune thrombocytopenia (ITP) is related to a combination of increased platelet destruction and impaired platelet production caused by anti-platelet autoantibodies.

57
Q

ITP: Rx

Meta: FirstLine, SecondLine

A
  1. FirstLine: prednisone/IVIG
  2. SecondLine: splenectomy, rituximab, thrombopoietin receptor agonists or immunosuppressive therapy
58
Q

GM-CSF: evidence for use during sepsis + neutropenia

A

Not that great

Granulocyte colony stimulating factors (G-CSFs) have been widely evaluated to minimize the extent and duration of neutropenia associated with myelosuppressive cytotoxic chemotherapy or radiation therapy (RT) for conditions other than acute leukemia, myelodysplastic syndrome, and in the setting of hematopoietic cell transplantation (HCT). Despite their effects on neutropenia, prophylactic use of G-CSFs has not been shown to have an impact on survival in most clinical situations.

59
Q

Aplastic anemia vs MDS: difference

A

In Myelodysplastic Syndrome (MDS), there is impaired production of myeloid class of blood cells by the bone marrow whereas aplastic anemia is a condition in which the bone marrow is damaged leading to decreased new blood cell production.

In MDS, the bone marrow produces new blood cells but they are abnormal and deformed whereas in aplastic anemia, the bone marrow stops producing new blood cells.

Read more: Difference Between Aplastic Anemia and Myelodysplastic Syndrome | Difference Between http://www.differencebetween.net/science/health/disease-health/difference-between-aplastic-anemia-and-myelodysplastic-syndrome/#ixzz4eqINRJn6

60
Q

MDS vs myelofibrosis

A
  1. Myelofibrosis: leukoerythroblastic picture
  2. Myelofibrosis: splenomegaly
61
Q

MPN: Common MPNs

A
  1. CML
  2. PV
  3. PMF
  4. ET

CML = chronic myeloid leukemia; PV = polycythemia vera; PMF = primary myelofibrosis; ET = essential thrombocythemia; IG = immature granulocytes; Megas = megakaryocytes; EPO = erythropoietin

See: http://surgpathcriteria.stanford.edu/mdsmps/primary-myelofibrosis/differential-diagnosis.html

62
Q

Leukoerythroblastic

A

Neutrophilia and nucleated red blood cells may also be associated with teardrop shaped RBCs and early granulocytes in the blood, the so-called leukoerythroblastic blood picture (picture 7A-B). This combination suggests the presence of infiltrative marrow disease (eg, myelofibrosis, malignancy, granulomatous disease, inflammation or infection in the marrow itself).

63
Q

5q minus syndrome

A

MDS subtype: severe anemia, normal platelet counts, and del(5q)

Approximately 5 percent of patients with MDS present with “5q minus syndrome” characterized by severe anemia, preserved platelet counts, and del(5q) as the sole cytogenetic abnormality. Patients with 5q minus syndrome with or without other cytogenetic abnormalities have demonstrated high response rates to treatment with low-dose lenalidomide.

64
Q

MDS: Rx

A
  1. No standard Rx
  2. symptomatic anemia and an erythropoietin level >500 mU/mL who are not good candidates for immunosuppressive Rx, azacitidine, decitabine, or lenalidomide
  3. serum erythropoietin level >500 mU/mL, and a good probability of responding to immunosuppressive therapy, we suggest a trial of antithymocyte globulin (ATG) plus cyclosporin

ABIM (36 decks)

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