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Genetics Lecture 5

Total questions: 82

Worksheet time: 44mins

Name
Class
Date
1.

uncontrolled granulocyte production

a)

myeloid leukemia

b)

lymphoid leukemia

2.

uncontrolled lymphocyte production

a)

myeloid leukemia

b)

lymphoid leukemia

3.

phagocytic-bacteria and fungi

a)

neutrophils

b)

eosinophils

c)

basophils

4.

parasites, allergy inflammation response

a)

neutrophils

b)

eosinophils

c)

basophils

5.

release histamine

a)

neutrophils

b)

eosinophils

c)

basophils

6.

granulocytes

a)

neutrophils

b)

eosinophils

c)

basophils

7.

Leukemia

a)

cancer of hemopoietic tissue that usually produces an extraordinary high number of circulating leukocytes and their precursors

b)

acute, self-limiting viral infection of B lymphocytes

c)

Immune-mediated, adverse drug reaction caused by IgG antibodies against the heparin–platelet factor 4 complex leading to platelet activation through platelet FcγIIa receptors

d)

Makes IgG antibodies against an antigen inherited from dad and found on fetal platelets but not on maternal platelets

8.

Chronic Myelogenous Leukemia

a)

Myeloproliferative disorder of granulocytic cells

b)

Abnormal cell line is increased in number, but cells produced are functionally inert

c)

Lack of Factor VIII

d)

Decreases fibrin production

e)

Production of functionally impaired factor IX proteins

9.

In CML: The _______ the tumor burden of these abnormal cells, the ______ marrow space and resources exist for other cells such as healthy white blood cells, red blood cells, and platelets

a)

greater ; less

b)

smaller ; more

c)

greater ; more

d)

smaller ; less

10.

CML can result in infections, anemias, and bleeding from the burden of the abnormal cells

a)

True

b)

False

11.

Chronic Myelogenous Leukemia

a)

Uncontrolled production of mature and maturing granulocytes

b)

Uncontrolled production of immature granulocytes

12.

Chronic Myelogenous Leukemia

a)

Predominantly neutrophils, but also basophils and eosinophils

b)

Predominantly basophils, but also neutrophils and eosinophils

c)

Predominantly eosinophils, but also basophils and neutrophils

13.

Risk Factors for CML include:

a)

prior high dose radiation

b)

exposure to certain organic solvents

c)

older age (median age: 55)

d)

young age (median age: 25)

e)

gender (male > female)

14.

Chronic Myeloid Leukemia Clinical Presentation

a)

asymptomatic

b)

symptomatic

15.

Chronic Myeloid Leukemia Clinical Presentation

a)

Fatigue, night sweats, weight loss, fever

b)

Abdominal fullness, pain and/or early satiety

c)

Easy bruising and purpura

d)

Sternal tenderness

e)

prolonged bleeding after injury, surgery, or tooth extraction

16.

When CML is asymptomatic, elevated white blood count (usually >25,000/L) is discovered incidentally

a)

True

b)

False

17.

Which CML clinical presentation is due to splenomegaly?

a)

Fatigue, night sweats, weight loss, fever

b)

Abdominal fullness, pain and/or early satiety

c)

Easy bruising and purpura

d)

Sternal tenderness

18.

Which CML presentation may be a sign of marrow overexpansion?

a)

Fatigue, night sweats, weight loss, fever

b)

Abdominal fullness, pain and/or early satiety

c)

Easy bruising and purpura

d)

Sternal tenderness

19.

The genetics of CML is the fusion of 2 genes which are...

a)

BCR

b)

ABL1

c)

CML

d)

CBL1

20.

BCR on chromosome

a)

22

b)

9

21.

ABL1 on chromosome

a)

22

b)

9

22.

The genetics of CML is the fusion of 2 genes and results in

a)

BCR-ABL1 fusion gene

b)

CML-ABL1 fusion gene

c)

BCR-ABL2 fusion gene

d)

CML-ABL2 fusion gene

23.

Abnormal chromosome ____ called Philadelphia (Ph) chromosome

a)

22

b)

9

24.

BCR-ABL1 fusion protein, a dysregulated _____________

a)

tyrosine kinase

b)

factor IX proteins

c)

Factor VIII

25.

The phase of disease (CML) is assigned based on two factors

a)

the number of immature cells in the blood and bone marrow biopsy

b)

the severity of the patient’s symptoms

c)

the amount of symptoms the patient presents

d)

the number of mature cells in the blood and bone marrow biopsy

26.

< 10% blast cells in blood and bone marrow samples

a)

Early stage (CML)

b)

Accelerated phase (CML)

c)

Final/blastic phase (CML)

27.

10-20% blasts, platelet counts decline, usually occurs within 6 to 8 months

a)

Early stage (CML)

b)

Accelerated phase (CML)

c)

Final/blastic phase (CML)

28.

20% or more blasts, median survival at this point is often less than 4 months

a)

Early stage (CML)

b)

Accelerated phase (CML)

c)

Final/blastic phase (CML)

29.

Blastic crisis: cellular criteria of blast phase accompanied by

a)

fatigue

b)

fever

c)

splenomegaly

d)

resembles acute leukemia

e)

<10% blast cells

30.

Tyrosine kinase inhibitor

a)

Hydroxyurea

b)

Imatinib mesylate

31.

Chemotherapeutic agents

a)

Hydroxyurea

b)

Imatinib mesylate

32.

Inducing apoptosis in cells with the bcr/abl oncogene

a)

Tyrosine kinase inhibitors

b)

Chemotherapeutic agents

c)

Allogeneic bone marrow transplantation

33.

Often used in high doses for Blast phase CML

a)

Tyrosine kinase inhibitors

b)

Chemotherapeutic agents

c)

Allogeneic bone marrow transplantation

34.

Over 70% of patients on ____ will have a complete cytogenetic response (no Philadelphia chromosome detected)

a)

Tyrosine kinase inhibitors

b)

Chemotherapeutic agents

c)

Allogeneic bone marrow transplantation

35.

Effective for shorter durations and requires higher doses in more advanced disease

a)

Tyrosine kinase inhibitors

b)

Chemotherapeutic agents

c)

Allogeneic bone marrow transplantation

36.

Rarely used for patients in chronic phase.

a)

Tyrosine kinase inhibitors

b)

Chemotherapeutic agents

c)

Allogeneic bone marrow transplantation

37.

A good option for younger, otherwise healthy patients in accelerated or blast phases. Less successful in the Blast phase

a)

Tyrosine kinase inhibitors

b)

Chemotherapeutic agents

c)

Allogeneic bone marrow transplantation

38.

induces rapid disease control often necessary prior to transplant

a)

Tyrosine kinase inhibitors

b)

Chemotherapeutic agents

c)

Allogeneic bone marrow transplantation

39.

The BCR (breakpoint cluster region) gene is located on chromosome 22 and

a)

needs enzyme to activate

b)

is constitutively active

40.

The _______ ABL on chromosome 9 codes for a tyrosine kinase involved in growth regulation and has a well regulated expression pattern

a)

protooncogene

b)

tumor supressor gene

41.

Translocation t(9;22) results in a fusion gene with ____ of expression regulation, leading to increased tyrosine kinase activity and increased cell proliferation

a)

loss

b)

gain

42.

Oligomerization of bcr/abl is crucial for oncogenicity ***

a)

True

b)

False

43.

Demonstrating the presence of the t(9;22) or its gene product is absolutely essential in diagnosing a patient with ____

a)

CML

b)

Hemophilia A

c)

Hemophilia B

44.

______________ is needed in all cases at diagnosis

a)

Cytogenetic analysis (karyotype) of bone marrow

b)

Fluorescence in situ hybridization (FISH)

c)

Quantitative polymerase chain reaction (PCR)

45.

Identifies Philadelphia chromosome and other chromosomal abnormalities

a)

Cytogenetic analysis (karyotype) of bone marrow

b)

Fluorescence in situ hybridization (FISH)

c)

Quantitative polymerase chain reaction (PCR)

46.

Can identify bcr/abl rearrangement even if Philadelphia chromosome cannot be identified by cytogenetic analysis

a)

Cytogenetic analysis (karyotype) of bone marrow

b)

Fluorescence in situ hybridization (FISH)

c)

Quantitative polymerase chain reaction (PCR)

47.

Baseline measure of bcr/abl transcript levels prior to the start of therapy

a)

Cytogenetic analysis (karyotype) of bone marrow

b)

Fluorescence in situ hybridization (FISH)

c)

Quantitative polymerase chain reaction (PCR)

48.

Factor VIII deficiency

a)

Hemophilia A

b)

Hemophilia B

49.

Factor IX deficiency

a)

Hemophilia A

b)

Hemophilia B

50.

__________ is the most frequent of the severe blood coagulation disorders

a)

Hemophilia A

b)

Hemophilia B

51.

Genetics of Hemophilia A: ________ for Factor VIII

a)

X-linked gene

b)

Mitochondrial linked

52.

Genetics of Hemophilia A: Lack of _______, normally part of activation of Factor X at start of Common pathway

a)

Factor VIII

b)

Factor IX

53.

Decreases fibrin production *end result

a)

Hemophilia A

b)

Hemophilia B

54.

Genetics of Hemophilia A: only males are affected, females are carriers

a)

True

b)

False

55.

responsible for making coagulation Factor VIII

a)

F8 gene

b)

F9 gene

c)

chromosome 9

d)

chromosome 22

56.

The F8 gene for factor VIII is located close to the end of the _____ arm of the X chromosome

a)

long

b)

short

57.

Genetics of Hemophilia B: Defect in ______ gene on X-chromosome

a)

Factor VIII

b)

Factor IX

58.

Genetics of Hemophilia B

a)

X-linked

b)

Mitochondrial linked

59.

Known as Christmas disease because first identified in Stephen Christmas

a)

Hemophilia A

b)

Hemophilia B

60.

Hemophilia B

a)

seen in males

b)

seen in females

61.

Results in production of functionally impaired factor IX proteins

a)

Hemophilia A

b)

Hemophilia B

62.

Genetics of Hemophilia B: Clinical manifestations proportional to the amount of normal ______ present

a)

F8 protein

b)

F9 protein

c)

chromosome 9

d)

chromosome 22

63.

The mutation seen in European Royals is in ________, “Royal Disease”

a)

Hemophilia A

b)

Hemophilia B

64.

Screen all bleeding disorders by

a)

APTT measurement

b)

a PT measurement

c)

a bleeding time measurement

d)

a platelet count

e)

specific coagulation Factor assays

65.

Order ____________ based on results from screening.

a)

APTT measurement

b)

a PT measurement

c)

a bleeding time measurement

d)

a platelet count

e)

specific coagulation Factor assays

66.

good measure of the intrinsic pathway

a)

APTT

b)

PT

67.

evaluates the extrinsic pathway

a)

APTT

b)

PT

68.

Management and treatment: __________ can be used to increase the levels of factors VIII and IX.

a)

Estrogens

b)

Oral contraceptives

c)

epinephrine

d)

desmopressin acetate

e)

vigorous exercise

69.

Specific factor deficiencies can be corrected through ________

a)

epinephrine

b)

desmopressin acetate

c)

vigorous exercise

d)

infusion of synthetic Factors

70.

Referral to hemophilia treatment centers provides:

a)

Federally funded hospitals

b)

Team approach to treatment comprehensive care

c)

Lower mortality rates

d)

Higher mortality rates

e)

Vigorous exercise

71.

bleeding disorder associated with low factor VIII activity in which von Willebrand factor (vWF) is missing or does not function properly

a)

Von Willebrand's disease

b)

Factor XI deficiency

c)

Hemophilia B Leyden

d)

Acquired Hemophilia

72.

also known as plasma thromboplastin antecedent (PTA deficiency) or Hemophilia C is a deficiency of Factor XI

a)

Von Willebrand's disease

b)

Factor XI deficiency

c)

Hemophilia B Leyden

d)

Acquired Hemophilia

73.

is second only to von Willebrand’s disease among bleeding disorders affecting females

a)

Factor XI deficiency

b)

Hemophilia B Leyden

c)

Acquired Hemophilia

74.

Factor XI deficiency

a)

autosomal recessive

b)

autosomal dominant

75.

Factor XI deficiency

a)

Mild, most don’t require treatment

b)

Severe, most require treatment

76.

a rare variant of hemophilia B inherited in an X-linked pattern

a)

Von Willebrand's disease

b)

Factor XI deficiency

c)

Hemophilia B Leyden

d)

Acquired Hemophilia

77.

similar to inherited Hemophilia, but due to autoantibodies and usually first appears in adulthood

a)

Von Willebrand's disease

b)

Factor XI deficiency

c)

Hemophilia B Leyden

d)

Acquired Hemophilia

78.

Altered developmental expression of Factor IX

a)

Von Willebrand's disease

b)

Factor XI deficiency

c)

Hemophilia B Leyden

d)

Acquired Hemophilia

79.

Associated with several point mutations in the gene for factor IX

a)

Von Willebrand's disease

b)

Factor XI deficiency

c)

Hemophilia B Leyden

d)

Acquired Hemophilia

80.

Episodes of excessive bleeding in childhood that resolve after puberty.

a)

Von Willebrand's disease

b)

Factor XI deficiency

c)

Hemophilia B Leyden

d)

Acquired Hemophilia

81.

Normal function of vWF: forms a complex with _______

a)

Factor VIII

b)

Factor XI

82.

Normal function of vWF: vWF interacts with platelets and collagen during clotting to form the platelet plug

a)

True

b)

False

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