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Clin Med II > HemeOnc > Flashcards

HemeOnc Flashcards

1
Q

HCT criteria for diagnosing anemia in a male

A

< 41%

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2
Q

Hgb criteria for diagnosing anemia in a male

A

< 13.5 g/dL

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3
Q

HCT criteria for diagnosing anemia in a female

A

< 37%

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4
Q

Hgb criteria for diagnosing anemia in a female

A

< 12 g/dL

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5
Q

Patient with liver disease presents for his bimonthly LFTs. In addition to the LFT report, you see that the lab tech has noted inc. ferritin, dec. iron, and dec. RBC MCV. diagnosis?

A

Anemia of chronic disease

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6
Q

While treating a chronic renal failure patient for her anemia with Erythropoietin, what should you be cautious of?

A

Watch her iron stores, since she’s likely on dialysis. We don’t want to overload the kidneys with iron.

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7
Q

Condition of bone marrow failure that arises from injury to or suppression of the hematopoietic stem cell

A

Aplastic anemia

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8
Q

Anemia involving pancytopenia, no abnormal cells on PBS, and hypocellular bone marrow

A

Aplastic anemia

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9
Q

Most common cause of aplastic anemia

A

T-cell mediated autoimmune bone marrow failure - shuts down blood cell production

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10
Q

Patient presents with weakness, fatigue, increased bleeding time, pallor, purpura, petechia, and seems to have had a series of infections in the last 6 months. Diagnosis?

A

Aplastic anemia

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11
Q

Refractory aplastic anemia tx

A

IV Cyclophosphamide

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12
Q

Treatment for severe aplastic anemia

A

-If 40, anti-thymocyte globulin + Cyclosporine or Tacrolimus

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13
Q

How does antithymocyte globuline (ATG) work?

A

Works at the thymus to reduce T-cell production

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14
Q

Why do we give steroid with anti-thymocyte globulin (ATG) treatment?

A
  • to avoid serum sickness
  • the globulin we’re giving is a foreign protein and we don’t want someone to have a massive reaction to it
  • steroids reduce this chance
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15
Q

Why is Vit. B12 important?

A

It’s a cofactor for steps in DNA synthesis, particularly in erythroid progenitor cells

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16
Q

Macrocytic (Megaloblastic) anemia with macro-ovalocytes and hypersegmented neutrophils

A
  • B12 or folate deficiency!

- Have to check levels of both

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17
Q

Why can a decrease in intrinsic factor lead to a B12 deficiency?

A

Intrinsic factor is needed to absorb B12

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18
Q

Vit. B12 deficiency might be associated with what other kind of anemia?

A

Pernicious anemia

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19
Q

Severe B12 deficiency anemia can mimic what other type of anemia, and how can you tell them apart?

A
  • Aplastic anemia

- MCV is large in B12 deficiency and normal in aplastic anemia

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20
Q

Patient presents with red and swollen tongue, diarrhea, and anorexia. On exam, you note a loss of proprioception, balance, and vibratory sensation. Diagnosis?

A

-Vit. B12 deficiency anemia

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21
Q

Peripheral blood smear with the following findings:

  • elevated MCV
  • Anisocytes and Poikilocytes
  • Macro-ovalocytes
  • hypersegmented neutrophils
A

Vitamin B12 or Folate deficiency anemia

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22
Q

Patient presents with a red and swollen tongue, anorexia, and diarrhea. You suspect an anemia. What kind?

A

Folate deficiency

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23
Q

Iron deficiency anemia is caused by _______ until proven otherwise

A

Bleeding

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24
Q

Most common cause of anemia worldwide

A

Iron deficiency anemia

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25
Q

Where is 70-95% of our iron contained?

A

In Hgb

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26
Q

How much of our dietary iron is usually absorbed, and what can we increase it to?

A
  • 10%

- Can be increased to 20% if our body needs it

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27
Q

Patient presents with easy fatigability, heart palpitations, and tachypnea. She says she’s had a weird craving to eat things that aren’t food. You note tachycardia. Suspected diagnosis?

A

Iron deficiency anemia

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28
Q

Peripheral blood smear with:

  • hypochromic RBCs
  • target cells
  • Elliptocytes
A

Iron deficiency anemia

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29
Q

What would you add with PO ferrous sulfate to decrease GI effects and increase iron absorption?

A

Vitamin C

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30
Q

Hereditary enzyme defect that causes episodic hemolytic anemia because of the decreased ability of RBCs to deal with oxidative stress

A

G6PD deficiency anemia

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31
Q
  • X-linked recessive disorder in American black men or Mediterranean patients
  • Episodic hemolysis
  • Minimally abnormal peripheral blood smear
A

G6PD deficiency anemia

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32
Q

What types of cells might you see during an “episode” in a G6PD deficiency anemia patient?

A
  • Increased retics
  • blister/bite cells
  • Heinz bodies
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33
Q

Why do we see Blister and Bite cells in G6PD deficiency anemia?

A

-Because the Hgb is crystallizing

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34
Q

Patient presents RUQ pain and the feeling of being slightly out of breath. While performing an ultrasound for suspected gallstones, you note pallor and jaundice. Underlying cause of symptoms?

A

Hemolytic anemia

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35
Q

PBS shows elevated retics and nRBCs. Increased plasma Hgb and indirect bilirubin also noted. Diagnosis?

A

Hemolytic anemia

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36
Q

Genetic mutation that causes Sickle Cell Anemia?

A

-A point mutation, changing a Valine for a Glutamine on the 6th spot of the beta hemoglobin chain

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37
Q

What can the hemolytic anemia that’s associated with sickle cell anemia cause?

A
  • Jaundice
  • Gallstones
  • Hepatosplenomegaly
  • Poorly healing ulcers over the lower tibia
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38
Q

Patient presents with ulcerations over the lower tibia that won’t seem to heal. On exam, you note jaundice and hepatosplenomegaly. You draw blood. What do you expect to find on the PBS?

A
  • Sickle cells
  • Reticulocytes
  • Howell-Jolly bodies
  • Target cells
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39
Q

Hgb F characteristics

A
  • Very high affinity for oxygen

- Can cause hypoxia in tissues

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40
Q

Hereditary disorder characterized by reduction in the synthesis of globin chains

A

Thalassemias

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41
Q

-Microcytosis disproportionate to the degree of anemia with elevated RBC count

A

Thalassemia

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42
Q

Classification of a thalassemia that has no clinical impact

A

Trait

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43
Q

Classification of a thalassemia that sometimes requires RBC transfusions, but otherwise has only a moderate clinical impact

A

Intermedia

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44
Q

Classification of a thalassemia that involves transfusion-dependence

A

Major

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45
Q

Type of genetic mutation that results in alpha-thalassemias

A

Gene deletions

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46
Q

Thalassemia that produces no change in the percentage distibution of Hgb A, A2, or F

A

Alpha

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47
Q

Type of genetic mutation that causes beta-thalassemias

A

Point mutations, which result in premature chain termination or in problems with RNA transcription

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48
Q

Beta null thalassemia

A

Absent globin chain production

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49
Q

Beta plus thalassemia

A

Reduced globin chain synthesis

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50
Q

What do the RBCs look like in a patient with a thalassemia?

A

Small (microcytic) and hypochromic

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51
Q

Which chromosome contains the genes with information for alpha globin chains?

A

Chromosome 16

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52
Q

Which chromosome contains the genes with information for beta globin chains?

A

Chromosome 11

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53
Q

Consequence of an alpha-thalassemia in which three genes are deleted

A

Hgb H

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54
Q

Consequence of an alpha-thalassemia in which 4 genes are deleted?

A

Hydrops fetalis (fluid overload causes fetal heart failure)

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55
Q

Consequence of an alpha-thalassemia in which 2 genes are deleted

A

“Trait”

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56
Q

Ethnicity of many patients with beta-thalassemias

A

Mediterranean

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57
Q

Anemia involving:

  • MCV 60-75
  • HCT: 28-40%
  • PBS: microcytes, hypochromia, target cells, acanthocytes
  • Electrophoresis: no increase in Hgb A2, F, and Hgb H is absent
A

Alpha-thalassemia trait (2 gene deletion)

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58
Q

Anemia involving:

  • MCV: 60-70
  • HCT 22-32%
  • PBS: microcytes, hypochromia, target cells, poikilocytosis
  • Electrophoresis: Hgb H
A

Alpha-thalassemia Hgb H disease (3 genes deleted)

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59
Q

Anemia involving:

  • MCV: 55-75
  • HCT: 28-40%
  • PBS: hypochromia, microcytes, target cells, basophilic stippling
  • Electrophoresis: Hgb A2 and Hgb F
A

Beta-thalassemia minor

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60
Q

Anemia involving:

  • HCT: < 10%
  • PBS: poikilocytosis, hypochromia, microcytes, target cells, basophilic stippling, nRBCs
  • Electrophoresis: Hgb F is major Hgb present
A

Beta-thalassemia Major

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61
Q

Hgb H disease tx

A
  • Folate supplementation

- Avoid iron and oxidative drugs

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62
Q

Severe thalassemia tx

A
  • Transfusions
  • Folate supplementation
  • Bone marrow transplant for beta major
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63
Q

Acquired myeloproliferative bone marrow disorder that causes overproduction of all three cell lines

A

Polycythemia vera

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64
Q

What causes polycythemia vera?

A

Mutation of the JAK2 gene

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65
Q

Patient presents after an episode of extreme itching after getting out of the shower. He says it’s happened many times and that he’s lately developed tinnitus, blurred vision, a HA, and fatigue. Suspicion?

A

Polycythemia vera

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66
Q

What might you find on physical exam of someone with polycythemia vera?

A
  • Plethora (excess blood)
  • Engorged retinal veins
  • Palpable spleen
67
Q

Major complication of polycythemia vera

A
  • Thrombosis

- Due to increased blood viscosity and abnormal platelet function

68
Q

Is bleeding time of polycythemia vera increased or decreased?

A

Increased (paradoxical)

69
Q

Hallmark lab finding of HCT > 54% in males and 51% in females

A

Polycythemia vera

70
Q

What’s associated with:

  • Inc. RBC mass
  • Inc. WBC and RBC count
  • Basophilia and Eosinophilia
  • Low erythropoietin
  • Decreased iron stores
A

Polycythemia vera

71
Q

Treatment of choice for polycythemia vera

A

Intentional phlebotomy

72
Q

Malignancy of the hematopoietic progenitor cell; cells proliferate in an uncontrolled fashion and replace normal bone marrow elements

A

Acute Leukemia

73
Q
  • Short duration of fatigue, fever, bleeding
  • Cytopenia or pancytopenia
  • > 20% blasts in bone marrow (increased)
  • Blast cells in peripheral blood
A

Acute Leukemia

74
Q

Leukemia that occurs primarily in adults > 60yo and is associated with auer rod cells

A

AML

75
Q

Leukemia that occurs primarily in children

A

ALL

76
Q

13-yo WF presents with HA, dyspnea, and repetitive nosebleeds. PMH significant for menorrhagia and diffuse bone pain. Suspicion?

A

ALL

77
Q

65yo WM presents with mucosal bleeding and diffuse pain in his bones and joints. He thinks it’s arthritis, but you note no inflammation in joints and hypertrophy of his gums. What’s your suspicion?

A

AML

78
Q

6yo patient presents with small “bruises” on her body and bone pain. On physical exam, you note hepatosplenomegaly and enlarged lymph nodes. You draw blood and find a decrease in all three cell lines. Suspicion?

A

ALL

79
Q

What medical treatment do you provide for adult patients after ALL remission has been achieved via combination chemo?

A

CNS prophylaxis, because some leukemic cells can sequester in the brain

80
Q

Why do acute leukemia patients experience HA, confusion, and dyspnea?

A

They have an increase in circulating blasts, which can impair circulation

81
Q

AML treatment

A

Anthracyclines + Cytarabine

82
Q

Chromosomal abnormality associated with chronic myeloid leukemia?

A

Philadelphia chromosome

83
Q

Myeloproliferative disorder characterized by overproduction of myeloid cells

A

Chronic myeloid leukemia

84
Q

56 yo WM presents with complaint of fatigue and night sweats. Patient is slightly febrile (100.0’F) and has splenomegaly. You note very elevated WBCs on CBC with a left shift. Suspicion?

A

CML

85
Q

PBS showing left shift, basophilia, eosinophilia and VERY elevated WBCs

A

AML

86
Q

CML Treatment

A
  • Imatinib mesylate

- Dastinib and Nilotinib attack the Philadelpia chromosome directly

87
Q

Clonal malignancy of B lymphocytes

A

CLL

88
Q

Isolated lymphocytosis, fatigue or lymphadenopathy, hepatosplenomegaly, and immunosuppression

A

CLL

89
Q

CLL staging: lymphocytosis only

A

0

90
Q

CLL staging: anemia

A

III

91
Q

CLL staging: organomegaly

A

II

92
Q

CLL staging: lymphocytosis + lymphadenopathy

A

I

93
Q

CLL staging: thrombocytopenia

A

IV

94
Q

What lymphocyte lineage markers are associated with CLL?

A

CD19 and CD5

95
Q

CLL Treatment

A

Fludarabine + Rituximab + Cyclophosphamide

96
Q

Heterogenous group of cancers of lymphocytes that usually present as enlarged lymph nodes

A

Non-Hodgkin Lymphoma

97
Q

Painless lymphadenopathy that spreads in a non-contiguous fashion whose diagnosis is made by a tissue exam

A

Non-Hodgkin Lymphoma

98
Q

Patient presents with a high fever, weight loss, drenching night sweats, and large masses in her neck and inguinal area. You suspect infection, but upon palpation, the lymph nodes are non-tender. Suspicion?

A

Non-Hodgkin lymphoma

99
Q

What might you see on a CXR of a Non-Hodgkin lymphoma patient?

A

Mediastinal mass

100
Q

Prognostic marker associated with NHL

A

LDH

101
Q

How do you make a diagnosis of Non-Hodgkin Lymphoma or Hodgkin lymphoma?

A

Tissue biopsy

102
Q

NHL treatment

A
  • Radiation

- Combination chemo for aggressive lymphomas

103
Q

Lymphocytic cancer associated with Reed-Sternberg cells

A

Hodgkin Lymphoma

104
Q

Painless lymphadenopathy that spreads in a contiguous fashion

A

Hodgkin lymphoma

105
Q

Typical age of Hodgkin lymphoma patients

A
  • Bimodal age distribution

- 20’s, then again in the 50’s

106
Q

Patient presents with a high fever, weight loss, drenching night sweats, and large masses behind her ear, in her neck and under her arm (axilla). You suspect infection, but upon palpation, the lymph nodes are non-tender. Suspicion?

A

Hodgkin lymphoma

107
Q

Non-tender lymphadenopathy, but sometimes associated with pain after ETOH consumption

A

Hodgkin lymphoma

108
Q

Ann Arbor Hodgkin Lymphoma Stage I

A

One lymph node region is involved

109
Q

Ann Arbor Hodgkin Lymphoma Stage II

A

Involvement of 2 lymph node ares on the same side of the diaphragm

110
Q

Ann Arbor Hodgkin Lymphoma Stage III

A

Lymph node regions on either side of the diaphragm are involved

111
Q

Ann Arbor Hodgkin Lymphoma Stage IV

A

disseminated disease with bone marrow or liver involvement

112
Q

Hodgkin Lymphoma stage A

A

Lack of constitutional symptoms

113
Q

Hodgkin Lymphoma Stage B

A
  • > 10% weight loss over 6 months

- Fever or night sweats

114
Q

Hodgkin Lymphoma Stage IA tx

A

Radiation

115
Q

Hodgkin Lymphoma Stages I and II tx

A

Short course of ABVD

116
Q

Hodgkin Lymphoma Stages III or IV tx

A

Full course of ABVD

117
Q

Malignancy of hematopoietic stems cells terminally differentiated as plasma cells

A

Multiple myeloma

118
Q

Bone pain, monoclonal paraproteins in serum, clonal plasma cells in bone marrow, organ damage due to plasma cells

A

Multiple myeloma

119
Q

67 yo WM presents with mucosal bleeding, nausea, visual disterbances, and hard deposits of tissue in his tongue. Suspicion?

A

Multiple myeloma

120
Q

What kind of symptoms would you expect to find in a patient with multiple myeloma?

A
  • pallor
  • bone tenderness
  • soft tissue masses
  • amyloid symptoms (enlarged tongue, neuropathy, CHF, hepatomegaly)
  • neurologic sings
121
Q

Why might you find neurologic signs and symptoms in a patient with multiple myeloma?

A

-because amyloid deposits may compress the spinal cord

122
Q

What might you expect to find on a PBS of a patient with multiple myeloma?

A

Rouleaux formations

123
Q

Paraprotein on Serum Protein Electrophoresis (SPEP)

A

Multiple myeloma

124
Q

If a patient had severe symptoms with multiple myeloma, what might you do if they were < 76 yo?

A

Autologous stem cell transplantation

125
Q

Recurrent episodes of hemarthroses and arthorpathy

A

Hemophilia A or B

126
Q

What should you look for in an older patient with a hemophilia?

A

HIV or Hep C from contaminated blood products

127
Q

Congenital deficiency of coagulation factor VIII

A

Hemophilia A

128
Q

Chance of developing an inhibitor antibody in hemophilia A

A

25%

129
Q

Would PTT, PT, or BT be prolonged in hemophilia A?

A

PTT

130
Q

Tx for hemophilia A

A
  • Cryoprecipitate
  • DDAVP (Desmopressin acetate)
  • COX 2 inhibitor for arthritis
131
Q

Congenital deficiency of F. IX

A

Hemophilia B

132
Q

Chance of developing an inhibitory antibody in hemophilia B

A

< 5%

133
Q

PTT, PT, or BT prolonged in hemophilia B?

A

PTT

134
Q

Hemophilia B treatment

A
  • FFP
  • DDAVP not useful
  • COX-2 inhibitor for arthritis
135
Q

Hemophilia C deficiency in what clotting factor?

A

XI

136
Q

Hemophilia A deficient in what clotting factor?

A

VIII

137
Q

Hemophilia B deficient in what clotting factor?

A

F. IX

138
Q

Autoimmune condition in which pathogenic antibodies bind platelets, resulting in an accelerated platelet clearance

A

Immune Thrombocytopenia (TTP)

139
Q

Isolated thrombocytopenia

A

Immune thrombocytopenia

140
Q

Treat immune thrombocytopenia if PLT count gets below what?

A

< 20,000 or 30,000

141
Q

Initial treatment of immune thrombocytopenia

A
  • Prednisone +/- IVIG

- Anti-D

142
Q

Treatment for severe immune thrombocytopenia

A

Splenectomy

143
Q

Thrombocytopenia and microangiopathic hemolytic anemia

A

Thrombotic Thrombocytopenic Purpura

144
Q

Cause of thrombotic thrombocytopenic purpura

A
  • Autoantibody against vWFCP
  • Congenital (vWFCP decreased)
  • Pregnancy-associated antibody against vWFCP
145
Q

Another thrombotic microangiopathy that’s sometimes confused with thrombotic thrombocytopenic purpura

A

Hemolytic uremic syndrome

146
Q

Signs and symptoms associated with thrombotic thrombocytopenic purpura

A
  • anemia (pallor)
  • bleeding
  • neurologic problems
147
Q

Thrombotic thrombocytopenic purpura treatment

A
  • plasma exchange
  • FFP
  • blood transfusions
148
Q

The most common inherited bleeding disorder

A

-Von Willebrand’s Disease

149
Q

Function of vWF

A
  • bridges platelets together and tethers them to the subendothelial matrix at the site of vascular injury
  • prolongs half-life of F. VIII
150
Q

Type I vWF disease

A

-quantitative abnormality of vWF

151
Q

Type 2 A or 2B vWF disease

A

-qualitative defect of vWF

152
Q

Type 2M vWF disease

A

Defect in vWF that decreases binding to platelets

153
Q

Type 2N vWF disease

A

Defect in vWF that decreases binding to V. FIII

154
Q

Type 3 vWF disease

A
  • undetectable levels of vWF

- Rare

155
Q

Signs and symptoms of vWF type 1

A

Mild-moderate platelet-type bleeding (skin and mucosal)

156
Q

Type 2 vWF disease signs and symptoms

A

Moderate-severe bleeding

157
Q

Mild-moderate bleeding; vWF activity and antigen are mildly depressed

A

Type I vWF disease

158
Q

Moderate to severe bleeding; vWF antigen to activity is 2:1

A

Type 2A or 2B vWF disease

159
Q

vWF disease platelet count

A

normal - decreased

160
Q

vWF disease PT

A

normal

161
Q

vWF disease PTT

A

Normal - prlonged

162
Q

vWF disease bleeding time

A

prolonged

163
Q

vWF disease fibrinogen time

A

normal

164
Q

vWF disease tx

A
  • DDAVP
  • Antifibrinolytic therapy
  • Cryoprecipitate if severe

Clin Med II (9 decks)

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