Blood Flashcards

1
Q

What is the most common cause of microcytic anemia

A

Iron deficiency

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2
Q

What is the most common cause of macrocytic /megaloblastic anemia

A

Vitamin B 12 deficiency and or folate deficiency

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3
Q

Primary causes of macrocytic (megaloblastic) anemia?

A

Vitamin B12 deficiency (pernicious) MCC , folic acid deficiency, drug induced, idiopathic

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4
Q

Clinical manifestations of vitamin B 12/pernicious anemia

A

Beefy, red, sore tongue, anorexia, malabsorption, neurological manifestations

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5
Q

Are there neurological manifestations in folate deficiency?

A

No

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6
Q

Mechanism for vitamin B 12 anemia or pernicious anemia

A

Lack of intrinsic factor from gastric parietal cells

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7
Q

What are the gastric parietal cells required for

A

Vitamin B 12 absorption

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8
Q

What is the most common cause of vitamin B 12 malabsorption

A

Lack of intrinsic factor made by the parietal cells of the stomach

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9
Q

Is vitamin B 12 deficiency anemia/pernicious anemia auto immune?

A

Yes

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10
Q

What is the underlying pathology associated with pernicious anemia

A

Lack of IF

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11
Q

What are B12 and folic acid important for

A

Nucleic acid and Myelin metabolism

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12
Q

What does lack of B12 or folic acid limit

A

DNA synthesis

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13
Q

What does lack of B12 lead to

A

Loss of folic acid and abnormal Mylelin synthesis

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14
Q

Clinical manifestations of iron deficiency anemia

A

Thin, brittle, coarsely ridged, spoon shaped nails, red and sore painful tongue

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15
Q

What is the most common red blood cell anemia

A

Iron deficiency anemia

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16
Q

Causes of Iron deficiency anemia?

A

Blood loss, in adequate dietary iron, inability to absorb enough iron

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17
Q

Is iron deficiency anemia microcytic or macrocytic? Hypochromic or normochromic?

A

Microcytic hypochromic

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18
Q

What does the blood results of iron deficiency anemia look like

A

Low serum iron, ferritin, and transferrin with high TIBC

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19
Q

Mechanism of sideroblastic anemia

A

Altered mitochondrial metabolism causing ineffective iron uptake resulting in dysfunctional hemoglobin synthesis

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20
Q

What is diagnostic of sideroblastic anemia

A

Ring decider of Blas within the bone marrow

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21
Q

What are sideroblasts

A

Erythrocytes that contain iron granules that have not been synthesized into hemoglobin

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22
Q

What are the two types of normalchromic normocytic anemias

A

Aplastic anemia and post hemorrhagic anemia

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23
Q

What are the three types of aplastic anemia’s

A

Pancytopenia, pure red cell aplasia, Fanconi anemia

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24
Q

Pancytopenia?

A

Deficiency of all three cellular components (RBCs WBCs, and platelets)

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25
Q

Pure red cell aplasia?

A

Isolated decline of red blood cells

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26
Q

Fanconi anemia?

A

Autosomal recessive syndrome

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27
Q

Post hemorrhagic anemia?

A

Acute blood loss from the vascular space

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28
Q

Aplastic anemia?

A

Blood disorder where the bodies bone marrow does not make enough new blood cells

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29
Q

What is the mechanism of a plastic anemia?

A

Immune mediated; set a toxic T lymphocytes target hematopoietic stem cells

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30
Q

Signs and symptoms of a plastic anemia?

A

Thrombocytopenia, neutropenia, no splenomegaly or lymphadenopathy

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31
Q

What can aplastic anemia progressed to

A

Acute leukemia

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32
Q

What is hemolytic anemia?

A

Red blood cells are destroyed and removed from the blood stream before the lifespan is over

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33
Q

Is hemolytic anemia hereditary or acquired

A

Can be either

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34
Q

Is sickle cellanemia microcytic or normocytic or macrocytic? Hypochromic or normochromic?

A

Normalchromic normocytic

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35
Q

Is sickle cell anemia genetic?

A

Yes it’s autosomal recessive

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36
Q

What is the most common complication of sickle cell disease

A

Pain

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37
Q

What is the primary mechanism of anemia of chronic disease

A

White blood cell production of cytokines. Decreased iron release, shortened RBC survival, impaired EPO levels

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38
Q

Polycythemia

A

Increase in RBC due to persistent overproduction

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39
Q

Leukemia ‘s?

A

Wbc cancer characterized by extensive bone marrow replacement with neoplastic WBCs

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40
Q

Multiple myeloma

A

Cancer of plasma cells arising from bone marrow

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41
Q

Lymphomas

A

Cancer of white blood cells characterized by involvement of sites other than the bone marrow or blood. Usually lymphocytic origin

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42
Q

Relative polycythemia

A

Fluid loss results in relative increase of RBC account and hemoglobin and hematocrit values. Resolves with fluid intake

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43
Q

Polycythemia Vera

A

Chronic neoplastic non-malignant condition. Over production of RBC and platelets. Splenomegaly and aquagenic pruritis

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44
Q

What gene is mutated in polycythemia Vera

A

Janus kinase 2 (JAK2)

45
Q

What can polycythemia Vera convert into

A

Acute myeloid leukemia

46
Q

What is aquagenic pruritis a symptom of

A

polycythemia Vera

47
Q

What is aquagenic pruritis

A

Intense painful itching intensified by heat or exposure to water

48
Q

Risk factors of leukemia’s?

A

Smoking, benzene, radiation, hiv, hep c, HTLV1, drugs causing bone marrow depression

49
Q

Leukemia ‘s?

A

Malignant disorders of the blood and blood forming organs. Uncontrolled proliferation of malignant leukocytes

50
Q

Acute leukemia?

A

Undifferentiated or immature cells, rapid onset with short survival

51
Q

Chronic leukemia?

A

Mature cell that does not function normally, slow progression

52
Q

Clinical manifestations of leukemia

A

Fatigue, bleeding, fever, anorexia, difficulty swallowing, CNS involvement

53
Q

What kind of test do you do to see if someone has leukemia

A

Blood smear or bone marrow test

54
Q

Complications of leukemia’s?

A

Anemia, neutropenia, low WBC count

55
Q

What type are the majority of childhood leukemia’s?

A

ALL

56
Q

Where do malignancies arise in ALL?

A

T or B cell lymphocytes but usually B cell lymphocytes

57
Q

Most common genetic translocation in ALL?

A

Philadelphia chromosome

58
Q

Most common adult leukemia?

A

AML

59
Q

Is AML more common in men or women

A

Men

60
Q

Where is the mutation in AML?

A

Receptor tyrosine kinase FLT3

61
Q

Is a ML immune mediated or genetic

A

Genetic

62
Q

Is CLL hereditary or immune mediated

A

Hereditary

63
Q

What type of cells does CLL affect?

A

Monoclonal B lymphocytes

64
Q

Who is CLL common in?

A

Adults older than 50

65
Q

What type of translocation is usually present in CML?

A

Philadelphia chromosome

66
Q

Who is CML usually diagnosed in?

A

Adults

67
Q

What type of leukemia is asymptomatic at the time of diagnosis

A

CLL

68
Q

What is the most common finding in CLL?

A

Lymphadenopathy

69
Q

What are the three phases of CML?

A

Chronic, accelerated, terminal blast

70
Q

Clinical manifestations of CML?

A

Infections, fever, and weight loss

71
Q

When does splenomegaly develop in CML

A

Accelerated phase

72
Q

Where are smudgecells found?

A

CLL

73
Q

Where are auer rods found?

A

AML

74
Q

What is lymphadenopathy?

A

Enlarged lymph nodes that become palpable and tender

75
Q

Local lymphadenopathy?

A

Drainage of an inflammatory lesion located near the enlarged node

76
Q

When does General lymphadenopathy occur

A

Presence of malignant or non-malignant disease

77
Q

Malignant lymphoma?

A

Group of neoplasms that develop from population of malignant lymphocytes

78
Q

What is included in primary lymphoid tissue

A

Thomas, bone marrow

79
Q

What is included in secondary lymphoid tissue?

A

Lymph nodes, spleen, tonsils, intestinal lymphoid tissue

80
Q

Two categories of malignant lymphoma’s?

A

Hodgkin lymphoma and non-Hodgkin’s lymphoma

81
Q

Are malignant lymphoma’s genetic or autoimmune

A

They are either genetic or from a viral infection

82
Q

What is necessary for the diagnosis of Hodgkin lymphoma

A

Read Sternberg cells. These are not specific to Hodgekin lymphoma though

83
Q

What are reed Sternberg cells derived from

A

Malignant B cells

84
Q

What do reed Sternberg cells release

A

Cytokines

85
Q

Two types of Hodgkin lymphoma?

A

Classic non-Hodgkin lymphoma and nodular lymphocyte predominant Hodgkin

86
Q

Clinical manifestations of Hodgkin lymphoma?

A

Enlarged painless neck lymph nodes, lymphadenopathy, mediastinal mass, fever, weight loss, night sweats, pruritus, and fatigue

87
Q

What is non-Hodgkin’s lymphoma now called

A

B cell neoplasm’s

88
Q

What kind of neoplasms does non-Hodgkin lymphoma include

A

T cell and NK cell neoplasm’s

89
Q

Clinical manifestations of Non-Hodgkin lymphoma

A

Painless lymphadenopathy, nodal enlargement, retroperitoneal and abdominal masses with symptoms of abdominal fullness, ascites and leg swelling

90
Q

What is Burkett lymphoma

A

Aggressive B cell non-Hodgkin lymphoma

91
Q

Are Burkitt lymphoma tumors fast or slow growing? Where are they located

A

Fast growing tumor of the jaw and facial bones

92
Q

What do you usually find in the United States for people who have Burkitt lymphoma

A

Abdominal swelling

93
Q

Is lymphoblastic lymphoma categorized under Hodgkin or non-Hodgkin lymphoma

A

Non-Hodgkin

94
Q

Are tumors of lymphoblastic lymphoma usually from T or B cell origin

A

T cell origin

95
Q

Mechanism of lymphoblastic lymphoma?

A

Clones of relatively immature T cells become malignant in the thymus

96
Q

First sign of lymphoblastic lymphoma?

A

Painless lymphadenopathy neck

97
Q

What are some conditions that mimic lymphomas

A

TB, syphilis, SLE, lung cancer, bone cancer

98
Q

What type of lymphadenopathy do lymphoma’s usually involve

A

Localized lymphadenopathy

99
Q

2 types of plasma cell malignancies

A

Multiple myeloma and Waldenström’s macroglobulinemia

100
Q

What occurs in multiple myeloma

A

Plasma cells proliferate in bone marrow

101
Q

What translocation occurs in multiple myeloma

A

Immunoglobulin heavy chain on chromosome 14

102
Q

What is malignant plasma cells produce and in multiple myeloma

A

Large amounts of IgM and Bence Jones proteins

103
Q

What do Bence Jones proteins do and what are they

A

They are unattached light chains of immunoglobulins that pass through the glomerulus and damage renal tubular cells

104
Q

What disorder are punched out lytic lesions common in

A

Multiple myeloma

105
Q

What is monoclonal gammopathy of undetermined significance

A

When M proteins are in the blood or urine that occurs before multiple myeloma

106
Q

What is Waldenström macroglobulinemia/Lymphoplasmacytic lymphoma

A

Slow growing plasma tumor cell that secretes a monoclonal IgM

107
Q

What does Waldenström macroglobulinemia/Lymphoplasmacytic lymphoma arise from

A

Plasma cells with genetic defects

108
Q

Clinical manifestations of Waldenström macroglobulinemia/Lymphoplasmacytic lymphoma

A

Weakness, fatigue, bruising, weight loss, bruising