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U World Step 2 > Hematology/Oncology > Flashcards

Hematology/Oncology Flashcards

1
Q

Chronic Lymphocytic Leukemia

  1. Clinical
  2. Diagnostic
  3. Prognostic
  4. Complicatons
  5. Treatment
A
  1. Treatment: Rituximab (anti-CD20)
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2
Q

Indications for treatment of CLL

A

Patients with CLL have a median survival of 10 years, and treatment is not beneficial if a patient is asymptomatic

  1. Progressive bone marrow failure (causing cytopenias)
  2. Massive lymphadenopathy/splenomegaly
  3. Presence of severe B symptoms (night sweats, weight loss)
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3
Q

Etiology of infections in sickle cell

  1. Pneumonia
  2. Osteomyelitis/septic arthritis
  3. Bacteremia/sepsis
  4. Meningitis
A
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4
Q

Laboratory abnormalities during vaso-occlusive pain crisis due to sickle cell

A

Anemia

Leukocytosis

SIgns of hemolysis (elevated LDH and indirect bilirubin)

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5
Q

Multiple myeloma

  1. Pathophysiology
  2. Manifestations
  3. Laboratory
  4. Radiology
A
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6
Q

Etiology of renal failure in multiple myeloma (MM)

A
  1. Myeloma cast nephropathy: Monoclonal light chains clog renal tubules, causing intratubular cast formation and toxicity - renal tubular injury
  2. Amyloidosis (glomerular injury - nephrotic syndrome)
  3. Monoclonal immunoglobulin deposition disease (glomerular injury - nephrotic syndrome)
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7
Q

Disseminated intravascular coagulation

A

Most common coagulopathy in malignancy (gastric, breast, lung cancer)

Thrombocytopenia

Decreased fibrinogen

Increased INR

-Anemia due to hemolysis from microangiopathic hemolytic anemia (MAHA)

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8
Q
A

Hyposegmented/hypogranulated neutrophils

Characteristic of myelodysplastic syndrome

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9
Q

Myelodysplastic syndrome

  1. Epidemiology
  2. Manifestations
  3. Diagnosis
  4. Treatment
A
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10
Q

Pernicious anemia

A

Anti-intrinsic factor antibodies

B12 deficiency

Increased methylmalonic acid

Macrocytic anemia

Hypersegmented neutrophils

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11
Q
A

Rouleaux formation

Characteristic of multiple myeloma

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12
Q
A

Smudge cells (fragile but mature lymphocytes)

Characteristic of chronic lymphocytic leukemia

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13
Q
A

Hypersegmented neutrophils

Characteristic of B12 deficiency

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14
Q
A

Lymphoblasts

Seen in acute lymphoblastic leukemia

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15
Q
A

Auer rods

Seen in acute promyelocytic leukemia (APML)

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16
Q
A

Teardrop shaped red blood cells

Seen in myelofibrosis or beta thalessemia (especially after splenectomy)

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17
Q

Febrile nonhemolytic transfusion reactions (time course)

A

1-6 hours

Benign

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18
Q
A

Hereditary spherocytosis

Increased risk of bilirubin gallstones

Treat with blood transfusions and folic acid supplementation, consider splenectomy

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19
Q

Secondary thrombocytosis

A

Caused by cytokines promoting platelet production

Usually driven by an inflammatory state (infection, recent surgery, malignancy)

Often occurs after splenectomy: Typically platelet counts normalize after weeks, but patients may have thrombocytosis for months or years.

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20
Q

Initial screening test for a non-African female with a family history of anemia, concerned for hemogloninopathy

A

Complete blood count

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21
Q

Hemophilia A & B

  1. Inheritance
  2. Clinical features
  3. Laboratory findings
  4. Treatment
A
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22
Q
A

Severe hemophilic arthropathy

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23
Q
A

Hemophilic arthropathy

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24
Q

Iron study findings in microcytic/hypochromic anemias

  1. Iron deficiency anemia
  2. Thalassemia
  3. Anemia of chronic disease
  4. Sideroblastic anemia
A
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25
Q

Coagulation cascade pathway

A
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26
Q

Vitamin K deficiency

  1. Risk factors
  2. Clinical features
  3. Laboratory findings
A
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27
Q

Obstructive sleep apnea

  1. Pathophysiology
  2. Symptoms
  3. Sequelae
A
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28
Q

Drugs that cause folic acid deficiency

A

Anti-epileptics: Phenytoin, primidone, phenobarbital

Impair absorption of folic acid in the small intestine

Trimpethoprim: Inhibits dihydrofolate reductase and in high doses can cause megaloblastic pancytopenia

Methotrexate: Inhibits dihydrofolate reductase (treat with leucovorin – folinic acid)

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29
Q

Drug that causes B6 deficiency

A

Isoniazid

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30
Q

Treatment of deep venous thrombosis

A
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31
Q

Immune deficiency in asplenia

A

Defects in antibody response, antibody-mediated phagocytosis/complement activation

At risk for fulminant infection with encapsulated bacteria (Strep pneumo, H. influenzae)

32
Q

Diseases characterized by complement deficiency

A

Systemic lupus erythematosus

Antiphospholipid antibody syndrome

(Increased risk of infection with encapsulated bacteria)

33
Q

Impaired B cell isotype switching

A

Seen in patients with common variable immunodeficiency

Normal B cell numbers but significantly reduced Ig subtypes

Risk for recurrent infection (e.g., sinopulmonary, GI) and antoimmune disease

34
Q

Leukocyte adhesion deficiency

A

Impaired chemotaxis

Recurrent bacterial infections of skin and mucosa

35
Q

Chronic granulomatous disease

A

Impaired oxidative burst

Recurrent bacterial or fungal infections due to catalase-producing organisms (e.g. Asperigillus nidulans, Staphylococcus aureus)

36
Q

Thrombotic thrombocytopenic purpura

  1. Pathophysiology
  2. Clinical features
  3. Management
A
37
Q

Treatment for cancer-related anorexia/cachexia syndrome (CACS)

A
  1. Progresterone analogues (megestrol acetate and medroxyprogesterone acetate)
  2. Corticosteroids

Progesterone analoges prefereed due to decreased incidence of side effects

38
Q
A

RBC agglutination

Seen in Waldenstrom’s macroglobulinemia

Plasma cell neoplasm characterized by excessive monoclonal IgM, end-organ damage, and >10% clonal lymphocytes by bone marrow biopsy. Hyperviscosity syndrome, neuropathy, and cryoglobulinemia are common consequences of elevated serum IgM.

39
Q

Waldenstrom Macroglobulinemia versus Multiple Myeloma

  1. Major manifestations
  2. Monoclonal antibody
  3. Peripheral smear
  4. Bone marrow biopsy
A
40
Q

Clinical features of type 2 heparin-induced thrombocytopenia

  1. Clinical signs
  2. Diagnostic evaluation
  3. Therapy
A

HIT is a life-threatening ocmplication of heparin therapy. HIT is antibody-mediated and causes a mild to moderate thrombocytopenia with minimal bleeding risk. Venous and arterial thrombotic risk is significant, as high as 50% in untreated HIT.

All heparin products should be discontinued immediately.

Warfarin is used for anticoagulation maintenance in HIT but only after the patient has received another anticoagulant and the platelet count is >150,000. Initial treatment with warfarin is contraindicated in HIT as it rapidly lowers protein C levels, which may further increase the risk of thrombus.

41
Q

Anemia of prematurity

  1. Etiology
  2. Clinical manifestations
  3. Laboratory findings
  4. Treatment
A

After birth, circulating EPO decreases due to increased oxygen concnetration in tissue. Decreased EPO causes decreased reticulocyte production in bone marrow.

42
Q
A

Target cells (and hypochromic microcytic RBCs)

Alpha or beta thalassemia

43
Q
A

Bite cells (and Heinz bodies)

Characteristic of glucose-6-phosphate dehydrogenase deficiency

44
Q
A

Sickle cell anemia

(Infants are protected by fetal hemoglobin in first 4-6 months of life)

45
Q

Immune thrombocytopenia

  1. Clinical presentation
  2. Laboratory findings
  3. Treatment: Children, adults
A

Children usually recover spontaneously within 6 months and require only observation, regardless of platelet count. Children with bleeding should receive IvIG or glucocorticoids.

46
Q

Positive Coomb’s test

A

Warm, antibody-type, autoimmune hemolytic anemia

Most commonly seen in women with some underlying disease affective the immune system (e.g., lymphoid neoplasm, collagen vascular disease, congenital immunodeficiency diseases).

47
Q

JAK2 mutation

A

Associated with myeloproliferative diseases, particularly polycythemia vera (PV)

48
Q

Serum protein electrophoresis

A

Can detect elevated levels of monoclonal proteins

Used to diagnose multiple myeloma

49
Q
A

Craniopharyngeoma

Calcified, intracranial tumors that occur in the supresellar region.

Presenting symptoms include bitemporal hemianopsia and pituitary hormonal deficiencies (e.g., diabetes insipidus, growth hormone deficiency)

50
Q
A

Empty sella syndrome

Sella turcica is often enlarged and contains no discernible pituitary gland.

Patient may be asymptomatic or present with hypopituitarism.

51
Q

Key features of craniopharyngioma

A
52
Q

Iron studies in microcytic anemia

  1. Cause
  2. MCV
  3. Iron
  4. TIBC
  5. Ferritin
  6. Transferrin saturation (Iron/TIBC)
A
53
Q

Leukemoid reaction versus Chronic myeloid leukemia

  1. Leukocyte count
  2. Cause
  3. LAP score
  4. Neutrophil precursors
  5. Absolute basophilia
A

LAP: Leukocyte alkaline phosphatase

CML is characterized by a low LAP score due to cytochemically abnormal neutrophils

54
Q

Anticoagulants and their mechanism of action

A
55
Q

Treatment of acute deep venous thrombosis/pulmonary embolism

  1. Mechanism of action
  2. Therapeutic onset
  3. Overlap needed?
  4. Laboratory monitoring?
A
56
Q
A

Skin necrosis at injection site

Classic for heparin induced thrombocytopenia (HIT)

57
Q

Clinical Manifestations of Fanconi Anemia

  1. Bone Marrow
  2. Appearance
  3. Skin
  4. Eyes/ears
A

Fanconi’s anemia caused by defective DNA repaire genes

Diagnosis made by chromosomal breaks on genetic analysis

58
Q

Acquired causes of Aplastic Anemia

A
59
Q

Cancers associated with pernicious anemia

A

Gastric cancer

Gastric carcinoid tumors

60
Q

Thalassemias (alpha, beta)

  1. Disorder (genotype)
  2. Hb electrophoresis
  3. Anemia severity
A
61
Q

Iron deficiency anemia, alpha thalassemia minor, beta thalassemia minor

  1. MCV
  2. RDW
  3. RBCs
  4. Peripheral smear
  5. Serum iron studies

6. Response to iron supplementation

  1. Hemoglobin electrophoresis
A
62
Q

Differential diagnosis of a mediastinal mass

A

4 Ts

Thymoma

Teratoma (and other germ cell tumors)

Thyroid neoplasm

Terrible lymphoma

63
Q

Nonseminomatous germ cell tumors

A

Elevated AFP

May have an elevated beta-hCG

64
Q
A

Hairy cell leukemia

65
Q

Hairy cell leukemia

  1. Features
  2. Manifestations
  3. Diagnosis
  4. Treatment
A
66
Q
A

Lymphoblasts

Lymphoblasts on peripheral blood smear is a sign of acute lymphoblastic leukemia

Primarily seen in children

67
Q
A

Reed Sternberg cells

Characteristic of Hodgkin lymphoma (B cell neoplasm)

Manifests with a mediastinal mass and a painless, enlarged lymph node

68
Q

Diamond-Blackfan anemia (DBA)

A

Congenital macrocytic pure red cell aplasia

Presents in the first 3 months of life with pallor and poor feeding.

CBC reveals a normocytic or macrocytic anemia with reticulocytopenia.

Normal WBC and platelet counts.

Short stature, webbed neck, cleft lip, shielded crest, and triphalangeal thumbs

69
Q
A

Schistocytes

Seen in microangiopathic hemolytic anemia (e.g., HUS)

70
Q
A

Dactylitis (hand-foot syndrome)

Can be the earliest manifestation of vaso-occlusion in sickle cell disease

Presents at 6 months to 4 years with an acute onset of pain and symmetric swelling of the hands and feet.

71
Q

Differential diagnosis of bone pain in sickle cell disease

  1. Cause
  2. Clinical features
A
72
Q

Recommendations for lung cancer screening

  1. Recommended test
  2. Recommended interval
  3. Age for screening
  4. Eligibility for screening based on smoking history
  5. Termination of screening
A
73
Q

Nontender, solitary node in the head and neck

A

Concerning for squamous cell carcinoma

74
Q

Indications for specialized RBC treatments

A

During blood storage, small amounts of leukocyte debris remains in red cell concentrate. These leukocytes release cytokines, which can cause transient fevers, chillds, and malaise, without hemolysis.

Leukoreduction involves reducing the number of leukocytes, which can prevent febrile nonhemolytic reaction and reduce risk of HLA alloimmunization and CMV transmission.

75
Q
A

Chronic myeloid leukemia

BCR-ABL fusion gene

Treat with tyrosine kinase inhibitors

U World Step 2 (22 decks)

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