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HEMATOLOGY & ONCOLOGY > HemeOnc > Flashcards

HemeOnc Flashcards

Exam review

1
Q

What is the leukocyte count difference between a leukomoid reaction and Chronic Myeloid Leukemia?

A

> 50,000 leukocytes in a leukomoid reaction. >100,000 leokocytes.

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2
Q

What do the neutrophil precursors look like in leukomoid reaction vs CML

A

They are more mature in the case of leukomoid reaction. They have more metamyelocytes than myelocytes. In CML, they are less mature, we have more myelocytes than metameylocytes. Absolute basophilia is present in CML.

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3
Q

Besides consulting with RADONC and Neurosurgery, how should I manage spinal cord compression - usually a result of MVC, malignancy or infection?

A

Emergency MRI, IV glucocorticoids

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4
Q

compare and contrast Early vs Late signs of spinal cord compression.

A

Early signs vs Late Signs
- Symetric LE Weakness Paraparesis/paraplegia
- Hypoactive/absent DTR Bilat Babinski
- Decreased rectal tone
Increased DTR
Sensory Loss

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5
Q

Besides alcohol abuse, liver disease, folate and B12 defficiency, what are the other 4 causes of macrocytic anemia?

A
  • Myelodysplastoc syndromes
  • Acute Myeloid Leukemia (AML)
  • Drug-induced (hydorcyurea, Zidovudine, chemo agents)
  • Hypothyroidism
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6
Q

What do all these symptoms tell me about this patient’s underlying probem?

  1. Oral Candidiasis
  2. Hairy Leukoplakia
  3. Aggressive Seborrheic dermatitis
  4. Peripheral neuropathy
  5. unexplained weight loss
  6. Generalized Lymphadenopathy
  7. Fever of unknown rigin
  8. Disseminated herpes Zoster
  9. opportunistic infections
  10. Kaposi’s sarcoma
  11. B cell lymphoma
  12. Unexplained Cytopenias
A

Clinical Findings in chronic HIV infection

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7
Q

In polycythemia there are 2 possibilities: primary polycythemia or secondary polycythemia. What is the difference between these?

A

Primary polycythemia vs Secondary Polycythemia

  • Low Erythropoetin -Normal or high EPO
  • Polycythemia Vera (JAK2 mut) -hypoxemia
  • primary familial (EPO recptor mutation)
  • congenital (EPO R mut) -congenital (high affinity Hb)
    - Hepatic or renal tumors
    - post-renal tx
    - Androgen supplementaion
    e. g testosterone
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8
Q

two types of Heparin-Induced thrombocytopenia

A

Type 1 ( Non-immune mediated) and Type 2 (immune-mediated)

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9
Q

What is the timing of both type 1 and type 2 Heparin-Induced thrombocytopenia

A

1-4 days after Heparin for type 1 (non-immune-mediated)

5-10 days after Heparin for type 2 (immune-mediated)

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10
Q

platelet count numbers in HIT type 1 and Type 2 HIT

A

type 1 non-immune-mediated (>100,000/ul of platelets), Type 2 immune-mediated (>20,000/ul of platelets)

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11
Q

How do I manage type 1 and type 2 HIT?

A

Continue Heparin and observe in the case of type 1 HIT (non-immune-mediated), for type 2 (immune-mediated, , 5, occurs 5-10 days after heparin. STOP HEPARIN, SWITCH ANTICOAGULANTS.

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12
Q

What are the clinical outcomes of the two types of HIT?

A

Type-1 : No clinical manifestations

Type 2: Necrotic skin lesions at heparin injection sites, Acute systemic reactions.

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13
Q

What type of transfusion reaction occurs within an hour to 6 hours of a transfusion.

A

Febrile nonhemolytic

TRALI

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14
Q 
Patients with these conditions have what type of hemolysis?
1. Micorangiopathic hemolytic anemia
2. Transfusion reactions
3. Infections 
4. Paroxysmal Nocturnal Hemoglobinuria
Rho D infusion
A

Intravascular Hemolysis

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15
Q

These patient’s have what condition?

  1. Intrinsic RBC enzyme deficiencies like G6PD
  2. Hemoglobinopathies like sickle cell and thalassemia
  3. Membrane defects like hereditary spherocytosis
  4. Hypersplenism, IV immunoglobulin infusion
  5. Warm or cold-agglutinin autoimmune hemolytic anemia (most cases)
  6. Infections like malaria or bartonella
A

Extravascular hemolysis

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16
Q

These anticoagulants prevent the conversion of fibrinogen to fibrin by inhibiting 2a (thrombin)

A

Direct Thrombin inhibitors like Argatroban, Bivalirudin and Dabigatran

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17
Q

These antocoagulants prevent the formation of thrombin by inhibting factor Xa which conducts the conversion fron factor 2 to 2a (thrombin)

A

Direct factor xa inhibitors: Rivaroxaban, Apixaban

Indirect factor xa inhibitors: Fondaparinux

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18
Q

Both warm and cold agglutinin autoimmune hemolytic anemia are coombs positive, but what are the differences in their immunoglobulins?

A

anti-IgG and anti-C3 or both for warm agglutinin autoimmune hemolytic anemia. Anti C3 or anti-IgM for the cold agglutinin autoimune hemolytic anemia.

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19
Q

Treatment differs in the case of warm agglutinin and cold agglutinin hemolytic anemia. How do their treatments differ?

A

Cold agglutinin HA: Avoid cold temperatures, Rituximab and Fludarabine
Warm agglutinin HA: Corticosteroids and splenectomy for refractory disease.

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20
Q

What are the only two causes of cold agglutinin Autoimmune hemolytic anemia?

A

Infections like mycoplasma pneumonia infection and infectious mononucleosis. then lymphoproliferative diseases like CLL.

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21
Q

What is the only abnormal lab in a hemophilia patient?

A

Prolonged APTT (Activated Partial Thromboplastin Time)

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22
Q

Labs that remain normal in hemophilia?

A

platelet count, bleeding time and prothrombin time

only factors 8 and 9 will be low or absent.

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23
Q

In the case of hemphilia A, What else besides replacing the missing factor will you do as part of treatment for the condition?

A

Desmopressin for mild hemophilia A

24
Q

Possible disorders in the case of low hemoglobin, normal MCV and a decreased reticulocyte count?

A

it could be:

  • leukemia
  • Aplastic Anemia
  • Infection
  • Medication side effect
25
Q

Likely condition in the case of a low hemoglobin, normal mcv and increased reticulocyte count?

A

Pt likely has hemorrhage or hemolysis going on.

26
Q

Besides anemia and an elevated lead level, what other serum findings or peripheral smear findings will I see in a patient with lead poisoning.

A

Elevated serum zinc protoporphyrin level

Basophiic Stippling on peripheral smear

27
Q

Severe lymphocytosis and the presence of smudge cells tells me my patient has what?

A

CLL (Chronic Lymphocytic Leukemia)

28
Q

complications of CLL?

A

Infection
Autoimmune hemolytic anemia
Secondary Malignancies

29
Q

A couplepresent to my office with the following complains:
Husband: gynecomastia, low sperm count
Wife: Acne, hirsutism, deepening of her voice, menstrual irregularities
What are they doing?

A

Androgen abuse - both are in the WWE

30
Q

Cardiovascular effects of androgen abuse?

A

Left Ventricular Hypertrophy, decreased HDL and ELEVATED LDL.

31
Q

Hematologic effects of of androgen abuse?

A

Polycythemia , possible hypercoagulability

32
Q

What should I do for a solitary pulmonary nodule which is low to intermediate risk and happens to be >8mm.

A

I will order an 18-fluorodeoxyglucose PET scan or biopsy. If results are suspicious for malignancy, I will excise. If not suspicious for malignancy, I will do SERIAL CT SCANS.

33
Q

A patient of Northern European descent presents with hemolytic anemia, jaundice and splenomegaly. What is my diagnosis?

A

Hereditary Spherocytosis

34
Q

Besides spherocytes on peripheral smear and an increased osmotic fragility on acidified glycerol lysis test, what are the other lab findings in hereditary spherocytosis?

A
  1. Increased MCV
  2. Negative Coombs Test
  3. Abnormal eosin-5-maleimide binding test
35
Q

treatment for hereditary spherocytosis?

A
  1. Folic acid supplementation
  2. Blood Transfusions
  3. Splenectomy
36
Q

complications of hereditary spherocytosis?

A

1.Pigment gallstones

2, Aplastic Crises from PArvovirus B-19 infection

37
Q

If within seconds to minutes of a blood transfusion, shock, angioedema/urticaria and respiratory distress occurs, what is my diagnosis and what is the molecular cause of it?

A

Anaphylaxis - caused by recipient anti-IgA antibodies

38
Q

If after 6 hours of a blood tranfusion, ,y patient develops respiratory distress and signs of noncardiogenic pulmonary edema, what is my dx? what os the molecular cause of it?

A

TRALI (transfusion-related acute lung injury)

caused by donor anti-leukocyte antibodies.

39
Q

A patient on an ace inhibitor develops hypotension within minutes of a blood tranfusion, what is my diagnosis and what is the cause?

A

Primary hypotension reaction

caused by bradykinin in blood products. It is normally degraded by ACE

40
Q

If within minutes to hours of a blood transfusion, my patient develops fever, chills, septic shock and DIC, WHAT is my dx?

A

Bacterial Sepsis

41
Q

yes or no? Alcohol use and b12 and folate defficiency can cause decreased platelet destruction and cause thrombocytopenia

A

yes

42
Q

what do these disorders have in common ?

SLE, Heparin use, ITP, DIC, TTP, HUS and antiphospholipid syndrome?

A

All cause increased platelet destruction and resulting thrombocytopenia.

43
Q

within 1hr after a blood transfusion, my patient develops fever, flank pain, hemoglobinuria, renal failure and DIC. What is the cause of this acute hemolytic immunologic reaction?

A

ABO Incompatibility

44
Q

1-6 hours after a blood transfusion, my patient develops fever and chills. What is the cause of this transfusion immunologic reaction?

A

cytokine accumulation during blood storage

This is the most common blood transfusion reaction - called Febrile nonhemolytic reaction

45
Q

My patient develops mild fever and hemolytic anemia within 2-10 days after transfusion, they also have a positive direct coombs test and a positive new antibody screen. What is the dx?

A

Delayed hemolytic transfusion reaction

caused by anamnestic antibody response

46
Q

What is the criteria for diagnosing antiphospholipid antibody syndrome in my patients?

A

1 clinical and 1 lab criteria must be met.

47
Q

What are the clinical criteria for antiphospholipid antibody syndrome?

A

Arterial/Venous thrombosis

pregnancy morbidity

48
Q

What are the laboratory criteria for antiphospholipid antibody syndrome?

A

Lupus anticoagulant
Anticardiolipin antibody
Anti b2GP1 antibody

49
Q

In the case of immune thrombocytopenia, what must precede the clinical presentation?

A

Antecedent Viral Infection

50
Q

What is the only abnormality seen in the lab results of a patient with immune thrombocytopenia?

A

Megakaryocytes on peripheral smear

51
Q

How do I treat my patient with Immune thrombocytopenia who is actually bleeding.

A

IVIG or Glucocorticoids

52
Q

Finding in peripheral blood smear in a patient with thalessemia?

A

Target cells

53
Q

I have 3 patients who received iron transfusions to treat their anemia. Who will have a response to iron supplementation?

  1. Patient with iron deficiency anemia
  2. patient with B-thal
  3. Patient with a-thal
A

Pt with iron deficiency anemia will have an elevated hemoglobin after iron supplementation.

54
Q
  1. Patient with iron deficiency anemia
  2. patient with B-thal
  3. Patient with a-thal

Which of these patients will have an abnormal hemoglobin electrophoresis

A

B-thalassemia minor patient will have an elevated hemoglobin A2

55
Q

Gold standard confirmatory test for type 2 heparin induced thrombocytopenia?

A

Serotonin release assay

Start treatment in suspected cases prior to confirmatory test.

56
Q

Treatment for type 2 heparin induced thrombocytopenia?

A
  1. stop all heparin products

2. start a diret thrombin inhibitor ike argatroban or fundaparinux (synthetic pentasaccharide)

HEMATOLOGY & ONCOLOGY (1 decks)

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