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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
Pure red cell aplasia?
Isolated decline of red blood cells
26
Fanconi anemia?
Autosomal recessive syndrome
27
Post hemorrhagic anemia?
Acute blood loss from the vascular space
28
Aplastic anemia?
Blood disorder where the bodies bone marrow does not make enough new blood cells
29
What is the mechanism of a plastic anemia?
Immune mediated; set a toxic T lymphocytes target hematopoietic stem cells
30
Signs and symptoms of a plastic anemia?
Thrombocytopenia, neutropenia, no splenomegaly or lymphadenopathy
31
What can aplastic anemia progressed to
Acute leukemia
32
What is hemolytic anemia?
Red blood cells are destroyed and removed from the blood stream before the lifespan is over
33
Is hemolytic anemia hereditary or acquired
Can be either
34
Is sickle cellanemia microcytic or normocytic or macrocytic? Hypochromic or normochromic?
Normalchromic normocytic
35
Is sickle cell anemia genetic?
Yes it’s autosomal recessive
36
What is the most common complication of sickle cell disease
Pain
37
What is the primary mechanism of anemia of chronic disease
White blood cell production of cytokines. Decreased iron release, shortened RBC survival, impaired EPO levels
38
Polycythemia
Increase in RBC due to persistent overproduction
39
Leukemia ‘s?
Wbc cancer characterized by extensive bone marrow replacement with neoplastic WBCs
40
Multiple myeloma
Cancer of plasma cells arising from bone marrow
41
Lymphomas
Cancer of white blood cells characterized by involvement of sites other than the bone marrow or blood. Usually lymphocytic origin
42
Relative polycythemia
Fluid loss results in relative increase of RBC account and hemoglobin and hematocrit values. Resolves with fluid intake
43
Polycythemia Vera
Chronic neoplastic non-malignant condition. Over production of RBC and platelets. Splenomegaly and aquagenic pruritis
44
What gene is mutated in polycythemia Vera
Janus kinase 2 (JAK2)
45
What can polycythemia Vera convert into
Acute myeloid leukemia
46
What is aquagenic pruritis a symptom of
polycythemia Vera
47
What is aquagenic pruritis
Intense painful itching intensified by heat or exposure to water
48
Risk factors of leukemia’s?
Smoking, benzene, radiation, hiv, hep c, HTLV1, drugs causing bone marrow depression
49
Leukemia ‘s?
Malignant disorders of the blood and blood forming organs. Uncontrolled proliferation of malignant leukocytes
50
Acute leukemia?
Undifferentiated or immature cells, rapid onset with short survival
51
Chronic leukemia?
Mature cell that does not function normally, slow progression
52
Clinical manifestations of leukemia
Fatigue, bleeding, fever, anorexia, difficulty swallowing, CNS involvement
53
What kind of test do you do to see if someone has leukemia
Blood smear or bone marrow test
54
Complications of leukemia’s?
Anemia, neutropenia, low WBC count
55
What type are the majority of childhood leukemia’s?
ALL
56
Where do malignancies arise in ALL?
T or B cell lymphocytes but usually B cell lymphocytes
57
Most common genetic translocation in ALL?
Philadelphia chromosome
58
Most common adult leukemia?
AML
59
Is AML more common in men or women
Men
60
Where is the mutation in AML?
Receptor tyrosine kinase FLT3
61
Is a ML immune mediated or genetic
Genetic
62
Is CLL hereditary or immune mediated
Hereditary
63
What type of cells does CLL affect?
Monoclonal B lymphocytes
64
Who is CLL common in?
Adults older than 50
65
What type of translocation is usually present in CML?
Philadelphia chromosome
66
Who is CML usually diagnosed in?
Adults
67
What type of leukemia is asymptomatic at the time of diagnosis
CLL
68
What is the most common finding in CLL?
Lymphadenopathy
69
What are the three phases of CML?
Chronic, accelerated, terminal blast
70
Clinical manifestations of CML?
Infections, fever, and weight loss
71
When does splenomegaly develop in CML
Accelerated phase
72
Where are smudgecells found?
CLL
73
Where are auer rods found?
AML
74
What is lymphadenopathy?
Enlarged lymph nodes that become palpable and tender
75
Local lymphadenopathy?
Drainage of an inflammatory lesion located near the enlarged node
76
When does General lymphadenopathy occur
Presence of malignant or non-malignant disease
77
Malignant lymphoma?
Group of neoplasms that develop from population of malignant lymphocytes
78
What is included in primary lymphoid tissue
Thomas, bone marrow
79
What is included in secondary lymphoid tissue?
Lymph nodes, spleen, tonsils, intestinal lymphoid tissue
80
Two categories of malignant lymphoma’s?
Hodgkin lymphoma and non-Hodgkin’s lymphoma
81
Are malignant lymphoma’s genetic or autoimmune
They are either genetic or from a viral infection
82
What is necessary for the diagnosis of Hodgkin lymphoma
Read Sternberg cells. These are not specific to Hodgekin lymphoma though
83
What are reed Sternberg cells derived from
Malignant B cells
84
What do reed Sternberg cells release
Cytokines
85
Two types of Hodgkin lymphoma?
Classic non-Hodgkin lymphoma and nodular lymphocyte predominant Hodgkin
86
Clinical manifestations of Hodgkin lymphoma?
Enlarged painless neck lymph nodes, lymphadenopathy, mediastinal mass, fever, weight loss, night sweats, pruritus, and fatigue
87
What is non-Hodgkin’s lymphoma now called
B cell neoplasm’s
88
What kind of neoplasms does non-Hodgkin lymphoma include
T cell and NK cell neoplasm’s
89
Clinical manifestations of Non-Hodgkin lymphoma
Painless lymphadenopathy, nodal enlargement, retroperitoneal and abdominal masses with symptoms of abdominal fullness, ascites and leg swelling
90
What is Burkett lymphoma
Aggressive B cell non-Hodgkin lymphoma
91
Are Burkitt lymphoma tumors fast or slow growing? Where are they located
Fast growing tumor of the jaw and facial bones
92
What do you usually find in the United States for people who have Burkitt lymphoma
Abdominal swelling
93
Is lymphoblastic lymphoma categorized under Hodgkin or non-Hodgkin lymphoma
Non-Hodgkin
94
Are tumors of lymphoblastic lymphoma usually from T or B cell origin
T cell origin
95
Mechanism of lymphoblastic lymphoma?
Clones of relatively immature T cells become malignant in the thymus
96
First sign of lymphoblastic lymphoma?
Painless lymphadenopathy neck
97
What are some conditions that mimic lymphomas
TB, syphilis, SLE, lung cancer, bone cancer
98
What type of lymphadenopathy do lymphoma’s usually involve
Localized lymphadenopathy
99
2 types of plasma cell malignancies
Multiple myeloma and Waldenström’s macroglobulinemia
100
What occurs in multiple myeloma
Plasma cells proliferate in bone marrow
101
What translocation occurs in multiple myeloma
Immunoglobulin heavy chain on chromosome 14
102
What is malignant plasma cells produce and in multiple myeloma
Large amounts of IgM and Bence Jones proteins
103
What do Bence Jones proteins do and what are they
They are unattached light chains of immunoglobulins that pass through the glomerulus and damage renal tubular cells
104
What disorder are punched out lytic lesions common in
Multiple myeloma
105
What is monoclonal gammopathy of undetermined significance
When M proteins are in the blood or urine that occurs before multiple myeloma
106
What is Waldenström macroglobulinemia/Lymphoplasmacytic lymphoma
Slow growing plasma tumor cell that secretes a monoclonal IgM
107
What does Waldenström macroglobulinemia/Lymphoplasmacytic lymphoma arise from
Plasma cells with genetic defects
108
Clinical manifestations of Waldenström macroglobulinemia/Lymphoplasmacytic lymphoma
Weakness, fatigue, bruising, weight loss, bruising

Pathophysiology (17 decks)

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