Chapter 3 Hemopoietic Functions Flashcards
1
Q
Hematopoiesis
A
Process of forming blood, primarily in the bone marrow
2
Q
Plasma
A
liquid protein
transport medium that carries the blood cells as well as antibodies, nutrients, electrolytes, hormones, lipids, and waste products
3
Q
Leukocytes
A
- white blood cells
- key players in the inflammatory response and infectious process
4
Q
Erythrocytes
A
- red blood cells
- Hemoglobin – oxygen-carrying component
- Hematocrit - the amount of blood volume occupied by erythrocytes
5
Q
Thrombocytes
A
– platelets
– along with clotting factors, control coagulation
6
Q
Hemostasis
A
process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel
7
Q
Normal Hemostasis
A
when it seals a blood vessel to prevent blood loss and hemorrhage.
8
Q
Abnormal Hemostasis
A
when it causes inappropriate clotting or when clotting is insufficient to stop blood flow
9
Q
Stages of Hemostasis
A
- Vessel spasm
- Formation of platelet plug
- Blood coagulation
- Clot retraction
- Clot dissolution
10
Q
Leukopenia
A
Decreased leukocytes level
11
Q
Leukocytosis
A
Increased leukocytes level
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
13
Q
Describe neutropenia
A
Neutrophils < 1500
Less ability to fight infections
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
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)
16
Q
Diagnosis of neutropenia
A
neutrophil levels
bone marrow biopsy
17
Q
Treatment of neutropenia
A
Antibiotic therapy
hematopoietic growth factors
18
Q
Describe infectious mononucleosis
A
“Kissing Disease”-oral transmission
Self-limiting
Most prevalent in adolescents and young adults
19
Q
Etiology of infectious mononucleosis
A
Epstein-Barr virus in the herpes family
20
Q
Pathophysiology of infectious mononucleosis
A
EBV -> Infects B lymphocytes -> Antibody production -> Infectious mononucleosis
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
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
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
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
25
Stage 1 of Hodgkin's lymphoma
The lymphoma cells are in one lymph node group or one part of a tissue or an organ.
26
Stage 2 of Hodgkin's lymphoma
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.
27
Stage 3 of Hodgkin's lymphoma
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.
28
Stage 4 of Hodgkin's lymphoma
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
29
Recurrent stage of Hodgkin's lymphoma
The disease returns after treatment.
30
Diagnosis of Hodgkin's lymphoma
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
31
Treatment of Hodgkin's Lymphoma
chemotherapy
radiation
surgery
32
Non-Hodgkin's Lymphoma
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
33
Leukemia
Cancer of the leukocytes
Leukemia cells abnormally proliferate, crowding normal blood cells
34
Types of Leukemia
Acute lymphoblastic leukemia (ALL)
Acute myeloid leukemia (AML)
Chronic lymphoid leukemia (CLL)
Chronic myeloid leukemia (CML)
35
Acute lymphoblastic leukemia
Affects primarily children
Responds well to therapy
Good prognosis
36
Acute myeloid leukemia
Affects primarily adults
Responds fairly well to treatment
Prognosis somewhat worse than that of acute lymphoblastic leukemia
37
Chronic lymphoid leukemia
Affects primarily adults
Responds poorly to therapy, yet most patients live many years after diagnosis
38
Chronic myeloid leukemia
Affects primarily adults
Responds poorly to chemotherapy, but the prognosis is improved with allogenic bone marrow transplant
39
Clinical manifestations of Leukemia
leukopenia, anemia, thrombocytopenia, lymphadenopathy, joint swelling, bone pain, weight loss, anorexia hepatomegaly, splenomegaly, and central nervous system dysfunction
40
Diagnosis of leukemia
a history, physical examination
peripheral blood smears
complete blood count
bone marrow biopsy
41
Treatment of leukemia
chemotherapy and bone marrow transplant
42
Multiple Myeloma
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
43
Bence Jones Proteins
antibodies
are produced by neoplastic plasma cells.
44
Clinical manifestations of Multiple Myeloma
Insidious onset
Include: anemia, thrombocytopenia, leukopenia, decreased bone density, bone pain, hypercalcemia, and renal impairment
45
Diagnosis of Multiple myeloma
serum and urine protein, calcium,
renal function tests,
complete blood count,
biopsy,
X-rays, computed tomography, and magnetic resonance imaging
46
Treatment of Multiple Myeloma
chemotherapy
complication management
47
Anemia
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
General manifestations of Anemia
weakness, fatigue, pallor, syncope, dyspnea, and tachycardia
49
In males with anemia, Hemoglobin concentration falls to
<13.5 g/dL
50
In females with anemia, Hemoglobin concentration falls to
<12 g/dL
51
Causes of Iron-deficiency Anemia
decreased iron consumption, decreased iron absorption, and increased bleeding
52
Additional manifestation of Iron-deficiency Anemia
cyanosis to sclera, brittle nails, decreased appetite, headache, irritability, stomatitis, pica, and delayed healing
53
Diagnosis of iron-deficiency Anemia
complete blood count (low hemoglobin, hematocrit, MCV, and MCHC), serum ferritin, serum iron, and transferrin saturation
54
Treatment of Iron-deficiency Anemia
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
Pernicious Anemia
Vit B12 deficiency usually caused by a lack of intrinsic factor that is required for vit B12 absorption in the stomach.
56
Etiology of Pernicious Anemia
Autoimmune
57
Pathophysiology of Pernicious Anemia
Vit B12 is required for DNA synthesis decreased maturation & cell division
May see myelin breakdown & neurological complications
58
Clinical manifestations of of Pernicious Anemia
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
Diagnosis of Pernicious Anemia
serum B12 levels, Schilling’s test, complete blood count, gastric analysis, and bone marrow biopsy
60
Treatment of Pernicious Anemia
injectable B12
61
Aplastic Anemia
Bone marrow depression of all blood cells (pancytopenia)
62
Etiology of Aplastic Anemia
insidious, autoimmune, medications, medical treatments, viruses, and genetic
Onset may be insidious sudden & severe
63
Clinical manifestations of Aplastic Anemia
Anemia (e.g., weakness, pallor, dyspnea)
Leukocytopenia (e.g., recurrent infections)
Thrombocytopenia (e.g., bleeding)
64
Diagnosis of Aplastic Anemia
complete blood count and bone marrow biopsy
65
Treatment of Aplastic Anemia
identify and manage underlying cause, oxygen therapy, infection control, infection treatment, bleeding precautions, blood transfusions, and bone marrow transplants
66
Hemolytic Anemia
Excessive erythrocyte destruction
67
Etiology of Hemolytic Anemia
idiopathic, autoimmune, genetics, infections, blood transfusion reactions, and blood incompatibility in the neonate
68
Sickle Cell Anemia
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
Sickle cell trait
Heterozygous
Less than half of erythrocytes are sickled
70
Sickle cell disease (forms of sickle cell anemia)
Homozygous
Most severe
Almost all erythrocytes are sickled
71
Clinical manifestations of Sickle Cell Anemia
- 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
Diagnosis of Sickle Cell Anemia
hemoglobin electrophoresis, complete blood count, and
bilirubin test
Life expectancy improving with better management
73
Treatment of Sickle Cell Anemia
No cure, palliative
Stem cell research showing promise
Medications (e.g., Hydrea [hydroxyurea])
74
Thalassemia
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
Clinical manifestations of Thalassemia
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
Diagnosis of Thalassemia
complete blood count (low MCV, MCHC) and iron levels
77
Treatment of Thalassemia
blood transfusion, chelation therapy, and splenectomy
78
Polycythemia Vera
chronic myeloproliferative neoplasms increased red blood cells, white blood cells, and platelets
79
Complications associated with Polycythemia Vera
Thrombosis
Bleeding
80
Clinical manifestations of Polycythemia Vera
itself is often asymptomatic
eventually the increased red cell volume and viscosity cause weakness, headache, light-headedness, visual disturbances, fatigue, and dyspnea.
81
Diagnosis of Polycythemia Vera
complete blood counts
bone marrow biopsy
uric acid levels
82
Treatment of Polycythemia Vera
phlebotomy and managing clotting disorders
83
Thrombocytosis
increased levels of platelet – causes thrombus (blood clots)
84
Thrombocytopenia
Decreased levels of platelet - causes bleeding
85
Hemophilia 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
Diagnosis of Hemophilia A
clotting studies and serum factor VIII levels
87
Treatment of Hemophilia A
clotting factor transfusions, recombinant clotting factors, desmopressin, and bleed precautions
88
Clinical manifestations of Hemophilia A
prolonged bleeding
indications of bleeding (e.g. bruising, petechia, etc)
prolonged clotting time
89
Von Willebrand's Disease
Most common hereditary bleeding disorder
Deficit of the von Willebrand factor - decreased platelet adhesion and aggregation
90
Clinical manifestations of Von Willebrand's Disease
bleeding or indications of bleeding (e.g. bruising, petechia, etc)
91
Type 1 of Von Willebrand's Disease
Most common and mildest form
Autosomal dominant
Reduced von Willebrand’s factor levels
Can cause significant bleeding with trauma or surgery
92
Diagnosis of Type 1 of Von Willebrand's Disease
bleeding studies and factor VIII levels
93
Treatment of Type 1 of Von Willebrand's Disease
Mild cases usually do not require treatment
Cryoprecipitate infusions
Desmopressin (DDAVP)
Bleeding precautions
Measures to control bleeding
94
Disseminated Intravascular Coagulation (DIC)
Life-threatening complications of many conditions - Blood transfusion reaction, cancer, sepsis, pregnancy complications
95
In persons with DIC, clotting factors become
abnormally active.
96
Pathophysiology of DIC
Results from an inappropriate immune response
Widespread coagulation -> massive bleeding because of the depletion of clotting factors
97
Clinical manifestations of DIC
tissue ischemia and bleeding
98
Complications associated with DIC
shock and multisystem organ failure
99
Diagnosis of DIC
complete blood count and bleeding studies
100
Treatment of DIC
identify and treat underlying cause, replace clotting components, and preventing activation of clotting mechanisms
101
Idiopathic Thrombocytopenic Purpura (ITP)
Hypocoagulation resulting from an autoimmune destruction of platelets
102
Acute form of ITP
More common in children
Sudden onset
Self-limiting
103
Chronic form of ITP
More common in adults age 20-50
More common in women
104
Etiology of ITP
idiopathic, autoimmune diseases, immunizations with a live vaccine, immunodeficiency disorders, and viral infections
105
Clinical manifestations of ITP
bleeding or indications of bleeding (e.g. bruising, petechia, etc)
106
Diagnosis of ITP
complete blood count (platelet levels < 20,000) and bleeding studies
107
Treatment of acute ITP
glucocorticoid steroids, immunoglobulins, plasmapheresis, and platelet pheresis
108
Treatment of chronic ITP
glucocorticoid steroids, immunoglobulins, splenectomy, blood transfusions, and immunosuppressant therapy
109
Thrombotic Thrombocytopenic Purpura
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
Etiology of Thrombotic Thrombocytopenic Purpura
idiopathic causes, heredity, bone marrow transplants, cancer, medications, pregnancy, and HIV
111
Clinical manifestations of Thrombotic Thrombocytopenic Purpura
purpura, changes in consciousness, confusion, fatigue, fever, headache, tachycardia, pallor, dyspnea on exertion, speech changes, weakness, and jaundice
112
Diagnosis of Thrombotic Thrombocytopenic Purpura
complete blood counts, blood smears
113
Treatment of Thrombotic Thrombocytopenic Purpura
plasmapheresis, splenectomy, and glucocorticoid steroids
