Chapter 3 Flashcards
1
Q
What is hematopoiesis?
A
Process of forming blood
2
Q
What is plasma?
A
Liquid protein
3
Q
What are leukocytes?
A
White blood cells
4
Q
What are erythrocytes?
A
red blood cells
5
Q
What are the 2 components of erythrocytes?
A
hemoglobin and hematocrit
6
Q
What is the purpose of hemoglobin?
A
the oxygen carrying component
7
Q
What is the purpose of hematrocrit?
A
amount of blood volume occupied by erythrocytes
8
Q
What are thrombocytes?
A
platelets
9
Q
What is hemostasis?
A
stops the blood flow
10
Q
What is normal hemostasis?
A
Normal when it seals a blood vessel to prevent blood loss and hemorrhage
11
Q
what is abnormal hemostasis?
A
Abnormal when it causes inappropriate clotting or when clotting is insufficient to stop blood flow
12
Q
What are the 5 stages of hemostasis?
A
- Vessel spasm
- Formation of platelet plug
- Blood coagulation
- Clot retraction
- Clot dissolution
13
Q
What is the role of leukocytes?
A
key players in the inflammatory response and in fighting infections
14
Q
What are the normal ranges of leukocytes?
A
5,000 to 10,000 cells/mL3 blood
15
Q
What is leukopenia?
A
decreased levels of leukocytes
16
Q
What is leukocytosis?
A
increased levels of leukocytes
17
Q
What are neutrophils?
A
a type of leukocyte and the first to arrive at the site of infection
18
Q
What is the normal range of neutrophils?
A
2,000–7,500 cells/mL
19
Q
What is neutropenia?
A
When Neutrophils < 1500 cells/mL
20
Q
What are the causes of neutropenia?
A
Increased usage Drug suppression Radiation therapy Congenital conditions Bone marrow cancers Spleen destruction Vitamin deficiency
21
Q
What are the 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)
22
Q
How do you diagnose neutropenia?
A
neutrophil levels and bone marrow biopsy
23
Q
What is the treatment for Neutropenia?
A
antibiotic therapy and hematopoietic growth factors
24
Q
What is infectious mononucleosis?
A
“Kissing disease”—oral transmission.
25
What causes infectious mononucleosis?
Caused by Epstein-Barr virus in the herpes family.
26
Do you have infectious mononucleosis?
yes; Once the disease is eliminated, a few B cells remain altered, giving the individual an asymptomatic infection for life and the potential to occasionally spread the EBV to others.
27
What are the manifestations of infecticous mononucleosis?
- Insidious onset.
- Incubation = 4–8 weeks.
- Initially see anorexia, malaise, and chills.
- Manifestations intensify to include leukocytosis, fever, chills, sore throat, and lymphopathy.
- Acute illness usually lasts 2–3 weeks; may not fully recover for 2–3 months.
28
What are the treatments for inefectious mononucleosis?
symptomatic and supportive
29
What are lymphomas?
Cancers that affect the lymphatic system
30
What are the 2 main types of lymphoma cancer?
Hodgkins and Non-Hodgkins
31
Is hodgkins or non-hodgkins more common?
Non-hogdkins
32
What is hodgkins lymphoma?
Solid tumors with the presence of Reed-Sternberg cells
33
Where does hodgkins orginate?
Typically originate in the lymph nodes of the upper body
34
Is hodgkins treatable?
very with treatment
35
What are the manifestations of hodgkins and non-hodgkins?
painless enlarged nodes, weight loss, fever, night sweats, pruritus, coughing, difficulty breathing, chest pain, recurrent infections, and splenomegaly
36
How is hodgkins diagnosed?
physical examination, presence of Reed-Sternberg cells in a lymph node biopsy, complete blood count, chest X-rays, diagnostic imaging (CT scan and MRI), and bone marrow biopsy
37
What is the treatment for hodgkins and non hodgkins?
chemotherapy, radiation, and surgery
38
Is Non-hodgkins treatable?
yes, but not a good prognosis
39
Where does non-hodgkins originate from?
Can originate in the T or B cells
40
Does non-hodkins lymphoma have Reed-Sternberg cells?
NO
41
How commom is Leukemia?
second most common blood cancer
42
What is leukemia?
cancer of the leukocytes
43
What happens with leukemia?
Leukemia cells abnormally proliferate, crowding normal blood cells
44
What are the risk factors of leukemia?
exposure to chemical, viral, and radiation mutagens; smoking; use of chemotherapies; certain disease conditions (e.g., Down syndrome); and immunodeficiency disorder
45
What are the types of Leukemia?
Acute lymphoblastic leukemia, Acute myeloid leukemia, Chronic lymphoid leukemia, Chronic myeloid leukemia
46
Facts about Acute lymphoblastic leukemia
- Affects primarily children
- Responds well to therapy
- Good prognosis
47
Facts about Acute myeloid leukemia
- Affects primarily adults
- Responds fairly well to treatment
- Prognosis somewhat worse than that of acute lymphoblastic leukemia
48
Facts about Chronic lymphoid leukemia
- Affects primarily adults
| - Responds poorly to therapy, yet most patients live many years after diagnosis
49
Facts about Chronic myeloid leukemia
- Affects primarily adults
| - Responds poorly to chemotherapy, but the prognosis is improved with allogeneic bone marrow transplant
50
What are the manifestations of leukemia?
leukopenia, anemia, thrombocytopenia, lymphadenopathy, joint swelling, bone pain, weight loss, anorexia, hepatomegaly, splenomegaly, and central nervous system dysfunction
51
How do you diagnose Leukemia?
a history, physical examination, complete blood count, and bone marrow biopsy
52
What is the treatment for Leukemia?
chemotherapy and bone marrow transplant
53
What is Multiple Myeloma?
- Plasma cell cancer (third most common)
- Excessive numbers of abnormal plasma cells in the bone marrow, crowding the blood-forming cells and causing Bence Jones proteins to be excreted in the urine
- Bone destruction leads to hypercalcemia and pathologic fractures
54
Is multiple myeloma caught early?
NO, often well advanced upon diagnosis
55
What are the manifestations of multiple myeloma?
Silent onset
| Include: anemia, thrombocytopenia, leukopenia, decreased bone density, bone pain, hypercalcemia, and renal impairment
56
How is Multiple Myeloma diagnosed?
serum and urine protein, calcium, renal function tests, complete blood count, biopsy, X-rays, CT scan and MRI
57
What is the treatment for multiple myeloma?
chemotherapy and complication management
58
What is erythropoiesis?
red blood cell disorder;
- Production of erythrocytes
- Regulated by erythropoietin
- Occurs in bone marrow
59
What is anemia?
Insufficient numbers of RBC’s or an Insufficient amount of hemoglobin in the blood
60
What are the normal ranges of RBC?
Men 4.5-6 x 106/L
| Women 4-5.5 x 106/L
61
What are the normal ranges of Hemoglobin?
Men 14-18 g/dl
| Women 12.0-16 g/dl
62
What are the normal ranges of hematocrit?
Men 40-50 %
| Women 35-45 %
63
What does anemia result from?
Results from a decreased number of erythrocytes, reduction of hemoglobin, or presence of abnormal hemoglobin
64
What does anemia do?
Decreases O2-carrying capacity, leading to tissue hypoxia
65
What are the manifestations of anemia?
weakness, fatigue, pallor, syncope, dyspnea, and tachycardia
66
What causes iron-deficiency anemia?
decreased iron consumption, decreased iron absorption, or increased bleeding
67
What are the manifestations of iron-deficiency anemia?
cyanosis to sclera, brittle nails, decreased appetite, headache, irritability, stomatitis, pica, and delayed healing
68
How is Iron- Deficiency diagnosed?
complete blood count (low hemoglobin, hematocrit, MCV, and MCHC), serum ferritin, serum iron, and transferrin saturation
69
What is the treatment for Iron-deficiency anemia?
identify and treat cause, increase dietary intake, and administer iron supplements
70
What is pernicious anemia?
Vitamin B12 deficiency usually caused by a lack of intrinsic factor.
71
What is the cause of pernicious anemia?
autoimmune.
72
What is required for DNA synthesis?
Vitamin B12 is required for DNA synthesis.
73
What does pernicious anemia lead to?
Leads to decreased maturation and cell division.
74
What may we see with pernicious anemia?
May see myelin breakdown and neurological complications.
75
What are the manifestations of pernicious anemia?
bleeding gums, diarrhea, impaired sense of smell, loss of deep tendon reflexes, anorexia, personality or memory changes, positive Babinski’s sign, stomatitis, paresthesia, and unsteady gait
76
How is pernicious anemia diagnosed?
serum B12 levels, Schilling’s test, complete blood count, gastric analysis, and bone marrow biopsy
77
What is the treatment for pernicious anemia?
injectable B12
78
What is aplastic anemia?
Bone marrow depression of all blood cells (pancytopenia).
79
What are the causes of aplastic anemia?
idiopathic, autoimmune, medications, medical treatments, viruses, and genetic abnormalities.
80
What is the onset of aplastic anemia like?
Onset may be insidious, sudden, and severe.
81
What are the manifestations of aplastic anemia?
Anemia (e.g., weakness, pallor, dyspnea)
Leukocytopenia (e.g., recurrent infections)
Thrombocytopenia (e.g., bleeding)
82
How is aplastic anemia diagnosed?
complete blood count and bone marrow biopsy
83
What is the treatment for aplastic anemia?
identify and manage underlying cause, oxygen therapy, infection control, infection treatment, bleeding precautions, blood transfusions, and bone marrow transplants
84
What is hemolytic anemia?
Excessive erythrocyte destruction
85
What are the causes of hemolytic anemia?
idiopathic, autoimmune, genetics, infections, blood transfusion reactions, and blood incompatibility in the neonate
86
What are the types of hemolytic anemia?
Several types including sickle cell anemia, thalassemia, and erythroblastosis fetalis
87
Is sickle cell anemia recessive or dominant?
neither; its co dominant
88
What is sickle cell anemia?
Hemoglobin S causes erythrocytes to be abnormally shaped.
89
What is the problem with abnormal erythroctyes?
Abnormal erythrocytes carry less oxygen and clog vessels, causing hypoxia and tissue ischemia.
90
Is is more likely to have sickle cell anemia?
More common in people of African and Mediterranean descent.
| Also seen in people from South and Central America, the Caribbean, and the Middle East
91
What is the pathogenisis of sickle cell disease?
HgbS and low oxygen conditions
Aggregation of HgbS into larger molecules
Change in shape and rigidity of RBC’s
Hemolysis of sickled cells
Vascular occlusion
92
What are the 3 forms of sickle cell anemia?
Sickle cell trait.
Heterozygous.
Less than half of erythrocytes are sickled
93
What is sickle cell disease?
Homozygous.
Most severe.
Almost all erythrocytes are sickled.
94
When does sickle cell anemia appear?
around 4 months old
95
What is sickle cell crisis?
Painful episodes that can last for hours to days
Pain caused by tissue ischemia and necrosis
Triggered by dehydration, stress, high altitudes, and fever
96
What are the manifestations of sickle cell anemia?
include abdominal pain, bone pain, dyspnea, delayed growth and development, fatigue, fever, jaundice, pallor, tachycardia, skin ulcers, angina, excessive thirst, frequent urination, and vision impairment
97
how is sickle cell anemia diagnosed?
complete blood count and bilirubin test
98
What is the treatment for sickle cell anemia?
```
No cure, palliative
Stem cell research showing promise
Medications
Avoid sickling triggers
Other strategies: oxygen therapy, hydration, pain management, infection control, vaccinations, blood transfusions, bone marrow transplants, genetic counseling
```
99
What is Thalassemia?
Autosomal dominant inheritance
| Abnormal hemoglobin from a lack of one of two proteins that make up hemoglobin (alpha and beta globin)
100
How is mostly seen with thalassemia?
Most common in people of Mediterranean descent
| Also seen in those of Asian, Indian, and African descent
101
What are the manifestations of thalassemia?
abortion, delayed growth and development, fatigue, dyspnea, heart failure, hepatomegaly, splenomegaly, bone deformities, jaundice
102
What can severe cases of thalassemia lead to?
Severe cases can lead to death in childhood.
103
How can the life expectancy of someone with thalassemia increase?
Life expectancy can improve with effective management.
104
How is thalassemia diagnosed?
complete blood count and iron levels.
105
What is the treatment for thalassemia?
blood transfusion and splenectomy.
106
What is polycythemia?
Abnormally high erythrocytes
| Increased blood volume and viscosity, leading to tissue ischemia and necrosis
107
Is polycythemia rare or common?
rare
108
What is polycythemia considered?
Considered a neoplastic disease
109
What are the complications of polycythemia?
thrombosis, hypertension, heart failure, hemorrhage, splenomegaly, hepatomegaly, and acute myeloblastic leukemia
110
What are the manifestations of polycythemia?
cyanotic or ruddy skin, high blood pressure, tachycardia, dyspnea, headaches, visual abnormalities
111
How is polycythemia diagnosed?
complete blood counts, bone marrow biopsy, and uric acid levels
112
What is the treatment for polycythemia?
chemotherapy, radiation, phlebotomy
113
What is the normal range of platelets?
Normal platelet levels range from 150,000 to 400,000 cells/mL3
114
What is thrombocytosis?
increased levels of platelets
115
What is thrombocytopenia?
decreased levels of platelets
116
What happens when there is a decrease in platelet levels?
Decreased platelet function
Decreased platelets in circulation
Platelets used up in clotting
117
What happens when there is impaired coagulation?
Impaired platelet function
118
What are the signs of blood loss?
```
Fatigue
Weakness
Fainting
Dizziness
Tachycardia – increased heart rate
Hypotension – low blood pressure
```
119
What is hemophilia A?
X-linked recessive bleeding disorder
| Deficiency or abnormality of clotting factor VIII
120
What are the manifestations of Hemophilia A?
Manifestations: bleeding or indications of bleeding (e.g., bruising, petechia, etc.)
121
How is Hemophilia A diagnosed?
clotting studies and serum factor VIII levels
122
What is the treatment for Hemophilia A?
clotting factor transfusions, clotting factors, and bleeding precautions
123
How common is it to have a factor 8 deficiency?
90%
124
How common is it for factor 8 to be deffective?
10%
125
What is the most common hereditary bleeding disorder?
Von Willebrands disorder
126
What is Von willedbrands?
Decreased platelet adhesion and aggregation
127
What are the manifestations of von willebrands?
bleeding or indications of bleeding (e.g., bruising, petechia, etc.)
128
How many types of von willebrands are there?
3
129
What are the charateristics of type 1 von willebrands?
-Most common and mildest form
-Follows autosomal dominant
Reduced von Willebrand’s factor levels
-Can cause significant bleeding with trauma or surgery
130
What are the charateristics of type 2 von willebrands?
- Either autosomal dominant or recessive.
- Five subtypes.
- von Willebrand’s factor building blocks are smaller than usual or break down easily.
131
What are the charateristics of type 3 von willebrands?
- Follows autosomal recessive
- No measurable von Willebrand’s factor or factor VIII
- Causes severe bleeding problems
132
What is acquired type von willebrand?
Occurs with congenital heart disease, systemic lupus erythematosus, and hypothyroidism
133
How is von willebrands diagnosed?
bleeding studies and factor VIII levels
134
What is the treatment for von willebrands?
- Mild cases usually do not require treatment
- Clotting factor infusions
- Administration of medication to release vW factor
- Bleeding precautions
- Measures to control bleeding
135
What is Disseminated Intravascular Coagulation (DIC)?
- Life-threatening complication of many conditions
| - Widespread coagulation followed by massive bleeding because of the depletion of clotting factors
136
What does DIC result from?
Results from an inappropriate immune response
137
What are the manifestations of DIC?
tissue ischemia and abnormal bleeding
138
What are the complications of DIC?
shock and multisystem organ failure
139
How is DIC diagnosed?
complete blood count and bleeding studies
140
What is the treatment for DIC?
identify and treat underlying cause, replace clotting components, and prevent activation of clotting mechanisms
141
What are the manifestations of thrombocytopenia?
Petechiae – pinpoint bleed
Ecchymosis – bruising
Purpura – purple rash
Prolonged bleeding
142
What is Idiopathic Thrombocytopenia Purpura (ITP)?
Hypocoagulation resulting from an autoimmune destruction of platelets
143
What is the acute form of ITP like?
- More common in children
- Sudden onset
- Self-limiting
144
What is the chronic form of ITP like?
- More common in adults age 20–50
| - More common in women
145
What are the causes of ITP?
idiopathic, autoimmune diseases, immunizations with a live vaccine, immunodeficiency disorders, and viral infections
146
What are the manifestations of ITP?
bleeding or indications of bleeding (e.g., bruising, petechia, etc.)
147
How is ITP diagnosed?
complete blood count (platelet levels < 20,000/mL) and bleeding studies
148
What is the treatment for ITP?
Acute ITP: steroids, immunoglobulins, plasmapheresis
| Chronic ITP: steroids, immunoglobulins, splenectomy, blood transfusions, and immunosuppressant therapy
149
What is Thrombotic Thrombocytopenic Purpura (TTP)?
Deficiency of enzyme necessary for cleaving von Willebrand’s factor, leading to hypercoagulation.
Hypercoagulation depletes platelet levels.
150
How is TTP characterized?
Characterized by thromboses, thrombocytopenia, and bleeding
151
What are the causes of TTP?
idiopathic causes, heredity, bone marrow transplants, cancer, medications, pregnancy, and HIV.
152
What are the manifestations of TTP?
purpura, changes in consciousness, confusion, fatigue, fever, headache, tachycardia, pallor, dyspnea on exertion, speech changes, weakness, and jaundice
153
How is TTP diagnosed?
complete blood counts, blood smears, and lactate dehydrogenase levels
154
What is the treatment for TTP?
plasmapheresis, splenectomy, and steroids
