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SMIT Pathology > Chapter 3 Hemopoietic Functions > Flashcards

Chapter 3 Hemopoietic Functions Flashcards

1
Q

Hematopoiesis

A

Process of forming blood, primarily in the bone marrow

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2
Q

Plasma

A

liquid protein

transport medium that carries the blood cells as well as antibodies, nutrients, electrolytes, hormones, lipids, and waste products

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3
Q

Leukocytes

A
  • white blood cells
  • key players in the inflammatory response and infectious process
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4
Q

Erythrocytes

A
  • red blood cells
  • Hemoglobin – oxygen-carrying component
  • Hematocrit - the amount of blood volume occupied by erythrocytes
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5
Q

Thrombocytes

A

– platelets

– along with clotting factors, control coagulation

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6
Q

Hemostasis

A

process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel

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7
Q

Normal Hemostasis

A

when it seals a blood vessel to prevent blood loss and hemorrhage.

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8
Q

Abnormal Hemostasis

A

when it causes inappropriate clotting or when clotting is insufficient to stop blood flow

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9
Q

Stages of Hemostasis

A
  1. Vessel spasm
  2. Formation of platelet plug
  3. Blood coagulation
  4. Clot retraction
  5. Clot dissolution
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10
Q

Leukopenia

A

Decreased leukocytes level

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11
Q

Leukocytosis

A

Increased leukocytes level

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12
Q

Neutrophils

A
  • One type of leukocytes
  • Usually the first to arrive at the site of infection
  • Normal range is 2,000–7,500 cells/µL
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13
Q

Describe neutropenia

A

Neutrophils < 1500
Less ability to fight infections

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14
Q

Etiology of neutropenia

A

Increased usage eg., infection
Drug suppression eg., immunosuppressant
Radiation therapy
Congenital conditions
Bone marrow cancers
Spleen destruction
Vitamin deficiency

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15
Q

Clinical manifestations of neutropenia

A

Depends on severity and cause

Infections and ulcerations especially of the respiratory tract, skin, vagina, and gastrointestinal tract

Signs and symptoms of infection (e.g., fever, malaise, and chills)

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16
Q

Diagnosis of neutropenia

A

neutrophil levels
bone marrow biopsy

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17
Q

Treatment of neutropenia

A

Antibiotic therapy
hematopoietic growth factors

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18
Q

Describe infectious mononucleosis

A

“Kissing Disease”-oral transmission
Self-limiting
Most prevalent in adolescents and young adults

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19
Q

Etiology of infectious mononucleosis

A

Epstein-Barr virus in the herpes family

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20
Q

Pathophysiology of infectious mononucleosis

A

EBV -> Infects B lymphocytes -> Antibody production -> Infectious mononucleosis

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21
Q

Clinical manifestations of Infectious Mononucleosis

A

Insidious onset
Incubation = 4 to 8 weeks
Initially see anorexia, malaise, and chills
Manifestations intensify to include leukocytosis, fever, chills, sore throat, and lymphopathy
Acute illness usually last 2-3 weeks; may not fully recover for 2-3 months

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22
Q

Lymphomas

A

Group of blood cell tumors that develop from lymphocytes
Most common hematologic cancer in the US
Two main types
1. Hodgkin’s
2. Non-Hodgkin’s

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23
Q

Hodgkin’s Lymphoma

A

Least common of the two
Solid tumors with the presence of Reed-Sternberg cells
Typically originate in the lymph nodes of the upper body
Several subtypes - Very curable with treatment

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24
Q

Clinical manifestations of Hodgkin’s lymphoma

A

painless enlarge nodes, weight loss, fever, night sweats, pruritis, coughing, difficulty breathing, chest pain, recurrent infections, and splenomegaly

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25
Q

Stage 1 of Hodgkin’s lymphoma

A

The lymphoma cells are in one lymph node group or one part of a tissue or an organ.

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26
Q

Stage 2 of Hodgkin’s lymphoma

A

The lymphoma cells are in at least two lymph node groups on the same side of the diaphragm, or the lymphoma cells are in one part of a tissue or an organ and the lymph nodes near that organ.

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27
Q

Stage 3 of Hodgkin’s lymphoma

A

The lymphoma cells are in lymph nodes above and below the diaphragm. Lymphoma cells may be found in one part of a tissue or an organ near these lymph node groups. Cells may also be found in the spleen.

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28
Q

Stage 4 of Hodgkin’s lymphoma

A

Lymphoma cells are found in several parts of one or more organs or tissues, or the lymphoma cells are in an organ and in distant lymph nodes

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29
Q

Recurrent stage of Hodgkin’s lymphoma

A

The disease returns after treatment.

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30
Q

Diagnosis of Hodgkin’s lymphoma

A

physical examination

presence of Reed-Sternberg cells in a lymph node biopsy

complete blood count

chest X-rays

computed tomography scan

magnetic resonance imaging

positron emission tomography scan

bone marrow biopsy

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31
Q

Treatment of Hodgkin’s Lymphoma

A

chemotherapy

radiation

surgery

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32
Q

Non-Hodgkin’s Lymphoma

A

More common

Poor prognosis

Many different types

Similar to Hodgkin’s manifestations, staging, and treatment

Different in the spread and diagnosis

Can originate in the T or B cells

No Reed-Sternberg cells

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33
Q

Leukemia

A

Cancer of the leukocytes
Leukemia cells abnormally proliferate, crowding normal blood cells

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34
Q

Types of Leukemia

A

Acute lymphoblastic leukemia (ALL)
Acute myeloid leukemia (AML)
Chronic lymphoid leukemia (CLL)
Chronic myeloid leukemia (CML)

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35
Q

Acute lymphoblastic leukemia

A

Affects primarily children
Responds well to therapy
Good prognosis

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36
Q

Acute myeloid leukemia

A

Affects primarily adults
Responds fairly well to treatment
Prognosis somewhat worse than that of acute lymphoblastic leukemia

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37
Q

Chronic lymphoid leukemia

A

Affects primarily adults
Responds poorly to therapy, yet most patients live many years after diagnosis

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38
Q

Chronic myeloid leukemia

A

Affects primarily adults
Responds poorly to chemotherapy, but the prognosis is improved with allogenic bone marrow transplant

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39
Q

Clinical manifestations of Leukemia

A

leukopenia, anemia, thrombocytopenia, lymphadenopathy, joint swelling, bone pain, weight loss, anorexia hepatomegaly, splenomegaly, and central nervous system dysfunction

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40
Q

Diagnosis of leukemia

A

a history, physical examination

peripheral blood smears

complete blood count

bone marrow biopsy

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41
Q

Treatment of leukemia

A

chemotherapy and bone marrow transplant

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42
Q

Multiple Myeloma

A

Plasma cell cancer

Excessive numbers of abnormal plasma cells in the bone marrow crowd the blood-forming cells

cause Bence Jones proteins to be excreted in the urine

Bone destruction leads to hypercalcemia and pathologic fractures

Often well advanced upon diagnosis

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43
Q

Bence Jones Proteins

A

antibodies
are produced by neoplastic plasma cells.

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44
Q

Clinical manifestations of Multiple Myeloma

A

Insidious onset
Include: anemia, thrombocytopenia, leukopenia, decreased bone density, bone pain, hypercalcemia, and renal impairment

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45
Q

Diagnosis of Multiple myeloma

A

serum and urine protein, calcium,

renal function tests,

complete blood count,

biopsy,

X-rays, computed tomography, and magnetic resonance imaging

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46
Q

Treatment of Multiple Myeloma

A

chemotherapy
complication management

47
Q

Anemia

A

Results from decreased number of erythrocytes, reduction of hemoglobin, or abnormal hemoglobin

Decreases O2 carrying capacity, leading to tissue hypoxia

Several types with varying etiology

48
Q

General manifestations of Anemia

A

weakness, fatigue, pallor, syncope, dyspnea, and tachycardia

49
Q

In males with anemia, Hemoglobin concentration falls to

A

<13.5 g/dL

50
Q

In females with anemia, Hemoglobin concentration falls to

A

<12 g/dL

51
Q

Causes of Iron-deficiency Anemia

A

decreased iron consumption, decreased iron absorption, and increased bleeding

52
Q

Additional manifestation of Iron-deficiency Anemia

A

cyanosis to sclera, brittle nails, decreased appetite, headache, irritability, stomatitis, pica, and delayed healing

53
Q

Diagnosis of iron-deficiency Anemia

A

complete blood count (low hemoglobin, hematocrit, MCV, and MCHC), serum ferritin, serum iron, and transferrin saturation

54
Q

Treatment of Iron-deficiency Anemia

A

identify and treat the cause,

increase dietary intake (e.g., liver, red meat, fish, beans, raisins, and green leafy vegetables), and iron supplements.

Foods or supplements high in vitamin C should be increased because vitamin C increases the absorption of iron.

55
Q

Pernicious Anemia

A

Vit B12 deficiency usually caused by a lack of intrinsic factor that is required for vit B12 absorption in the stomach.

56
Q

Etiology of Pernicious Anemia

A

Autoimmune

57
Q

Pathophysiology of Pernicious Anemia

A

Vit B12 is required for DNA synthesis  decreased maturation & cell division

May see myelin breakdown & neurological complications

58
Q

Clinical manifestations of of Pernicious Anemia

A

bleeding gums, diarrhea, impaired smell, loss of deep tendon reflexes, anorexia, personality or memory changes, positive Babinski’s sign, stomatitis, paresthesia, and unsteady gait

59
Q

Diagnosis of Pernicious Anemia

A

serum B12 levels, Schilling’s test, complete blood count, gastric analysis, and bone marrow biopsy

60
Q

Treatment of Pernicious Anemia

A

injectable B12

61
Q

Aplastic Anemia

A

Bone marrow depression of all blood cells (pancytopenia)

62
Q

Etiology of Aplastic Anemia

A

insidious, autoimmune, medications, medical treatments, viruses, and genetic

Onset may be insidious sudden & severe

63
Q

Clinical manifestations of Aplastic Anemia

A

Anemia (e.g., weakness, pallor, dyspnea)
Leukocytopenia (e.g., recurrent infections)
Thrombocytopenia (e.g., bleeding)

64
Q

Diagnosis of Aplastic Anemia

A

complete blood count and bone marrow biopsy

65
Q

Treatment of Aplastic Anemia

A

identify and manage underlying cause, oxygen therapy, infection control, infection treatment, bleeding precautions, blood transfusions, and bone marrow transplants

66
Q

Hemolytic Anemia

A

Excessive erythrocyte destruction

67
Q

Etiology of Hemolytic Anemia

A

idiopathic, autoimmune, genetics, infections, blood transfusion reactions, and blood incompatibility in the neonate

68
Q

Sickle Cell Anemia

A

Autosomal recessive

Hemoglobin S causes erythrocytes to be abnormally shaped

Abnormal erythrocytes carry less oxygen and clog vessels, causing hypoxia and tissue ischemia

More common in people of African and Mediterranean descent

69
Q

Sickle cell trait

A

Heterozygous
Less than half of erythrocytes are sickled

70
Q

Sickle cell disease (forms of sickle cell anemia)

A

Homozygous
Most severe
Almost all erythrocytes are sickled

71
Q

Clinical manifestations of Sickle Cell Anemia

A
  • Typically appear around 4 months of age
  • Sickle cell crisis
    Painful episodes that can last for hours to days
    Pain is caused by tissue ischemia and necrosis
    Triggered by dehydration, stress, high altitudes, and fever
72
Q

Diagnosis of Sickle Cell Anemia

A

hemoglobin electrophoresis, complete blood count, and
bilirubin test

Life expectancy improving with better management

73
Q

Treatment of Sickle Cell Anemia

A

No cure, palliative
Stem cell research showing promise
Medications (e.g., Hydrea [hydroxyurea])

74
Q

Thalassemia

A

Autosomal dominant inheritance
Abnormal hemoglobin from a lack of one of two proteins that makes up hemoglobin (alpha and beta globin)
Most common in people of Mediterranean descent

75
Q

Clinical manifestations of Thalassemia

A

abortion, delayed growth, and development, fatigue, dyspnea, heart failure, hepatomegaly, splenomegaly, bone deformities, jaundice

Severe cases can lead to death in childhood

Life expectancy can improve with effective management

76
Q

Diagnosis of Thalassemia

A

complete blood count (low MCV, MCHC) and iron levels

77
Q

Treatment of Thalassemia

A

blood transfusion, chelation therapy, and splenectomy

78
Q

Polycythemia Vera

A

chronic myeloproliferative neoplasms  increased red blood cells, white blood cells, and platelets

79
Q

Complications associated with Polycythemia Vera

A

Thrombosis
Bleeding

80
Q

Clinical manifestations of Polycythemia Vera

A

itself is often asymptomatic

eventually the increased red cell volume and viscosity cause weakness, headache, light-headedness, visual disturbances, fatigue, and dyspnea.

81
Q

Diagnosis of Polycythemia Vera

A

complete blood counts

bone marrow biopsy

uric acid levels

82
Q

Treatment of Polycythemia Vera

A

phlebotomy and managing clotting disorders

83
Q

Thrombocytosis

A

increased levels of platelet – causes thrombus (blood clots)

84
Q

Thrombocytopenia

A

Decreased levels of platelet - causes bleeding

85
Q

Hemophilia A

A

X-linked recessive bleeding disorder

Deficiency or abnormality of clotting factor VIII

Varies in severity - depending on the amount of factor VIII present in the blood.

86
Q

Diagnosis of Hemophilia A

A

clotting studies and serum factor VIII levels

87
Q

Treatment of Hemophilia A

A

clotting factor transfusions, recombinant clotting factors, desmopressin, and bleed precautions

88
Q

Clinical manifestations of Hemophilia A

A

prolonged bleeding

indications of bleeding (e.g. bruising, petechia, etc)

prolonged clotting time

89
Q

Von Willebrand’s Disease

A

Most common hereditary bleeding disorder

Deficit of the von Willebrand factor - decreased platelet adhesion and aggregation

90
Q

Clinical manifestations of Von Willebrand’s Disease

A

bleeding or indications of bleeding (e.g. bruising, petechia, etc)

91
Q

Type 1 of Von Willebrand’s Disease

A

Most common and mildest form
Autosomal dominant
Reduced von Willebrand’s factor levels
Can cause significant bleeding with trauma or surgery

92
Q

Diagnosis of Type 1 of Von Willebrand’s Disease

A

bleeding studies and factor VIII levels

93
Q

Treatment of Type 1 of Von Willebrand’s Disease

A

Mild cases usually do not require treatment
Cryoprecipitate infusions
Desmopressin (DDAVP)
Bleeding precautions
Measures to control bleeding

94
Q

Disseminated Intravascular Coagulation (DIC)

A

Life-threatening complications of many conditions - Blood transfusion reaction, cancer, sepsis, pregnancy complications

95
Q

In persons with DIC, clotting factors become

A

abnormally active.

96
Q

Pathophysiology of DIC

A

Results from an inappropriate immune response
Widespread coagulation -> massive bleeding because of the depletion of clotting factors

97
Q

Clinical manifestations of DIC

A

tissue ischemia and bleeding

98
Q

Complications associated with DIC

A

shock and multisystem organ failure

99
Q

Diagnosis of DIC

A

complete blood count and bleeding studies

100
Q

Treatment of DIC

A

identify and treat underlying cause, replace clotting components, and preventing activation of clotting mechanisms

101
Q

Idiopathic Thrombocytopenic Purpura (ITP)

A

Hypocoagulation resulting from an autoimmune destruction of platelets

102
Q

Acute form of ITP

A

More common in children
Sudden onset
Self-limiting

103
Q

Chronic form of ITP

A

More common in adults age 20-50
More common in women

104
Q

Etiology of ITP

A

idiopathic, autoimmune diseases, immunizations with a live vaccine, immunodeficiency disorders, and viral infections

105
Q

Clinical manifestations of ITP

A

bleeding or indications of bleeding (e.g. bruising, petechia, etc)

106
Q

Diagnosis of ITP

A

complete blood count (platelet levels < 20,000) and bleeding studies

107
Q

Treatment of acute ITP

A

glucocorticoid steroids, immunoglobulins, plasmapheresis, and platelet pheresis

108
Q

Treatment of chronic ITP

A

glucocorticoid steroids, immunoglobulins, splenectomy, blood transfusions, and immunosuppressant therapy

109
Q

Thrombotic Thrombocytopenic Purpura

A

Deficiency of enzyme necessary for cleaving von Willebrand’s factor, leading to hypercoagulation

Hypercoagulation depletes platelet levels -> bleeding

Characterized by thromboses, thrombocytopenia, and bleeding

110
Q

Etiology of Thrombotic Thrombocytopenic Purpura

A

idiopathic causes, heredity, bone marrow transplants, cancer, medications, pregnancy, and HIV

111
Q

Clinical manifestations of Thrombotic Thrombocytopenic Purpura

A

purpura, changes in consciousness, confusion, fatigue, fever, headache, tachycardia, pallor, dyspnea on exertion, speech changes, weakness, and jaundice

112
Q

Diagnosis of Thrombotic Thrombocytopenic Purpura

A

complete blood counts, blood smears

113
Q

Treatment of Thrombotic Thrombocytopenic Purpura

A

plasmapheresis, splenectomy, and glucocorticoid steroids

SMIT Pathology (4 decks)

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