Chapter 3 Flashcards

1
Q

What is hematopoiesis?

A

Process of forming blood

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2
Q

What is plasma?

A

Liquid protein

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3
Q

What are leukocytes?

A

White blood cells

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4
Q

What are erythrocytes?

A

red blood cells

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5
Q

What are the 2 components of erythrocytes?

A

hemoglobin and hematocrit

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6
Q

What is the purpose of hemoglobin?

A

the oxygen carrying component

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7
Q

What is the purpose of hematrocrit?

A

amount of blood volume occupied by erythrocytes

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8
Q

What are thrombocytes?

A

platelets

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9
Q

What is hemostasis?

A

stops the blood flow

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10
Q

What is normal hemostasis?

A

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

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11
Q

what is abnormal hemostasis?

A

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

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12
Q

What are the 5 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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13
Q

What is the role of leukocytes?

A

key players in the inflammatory response and in fighting infections

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14
Q

What are the normal ranges of leukocytes?

A

5,000 to 10,000 cells/mL3 blood

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15
Q

What is leukopenia?

A

decreased levels of leukocytes

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16
Q

What is leukocytosis?

A

increased levels of leukocytes

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17
Q

What are neutrophils?

A

a type of leukocyte and the first to arrive at the site of infection

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18
Q

What is the normal range of neutrophils?

A

2,000–7,500 cells/mL

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19
Q

What is neutropenia?

A

When Neutrophils < 1500 cells/mL

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20
Q

What are the causes of neutropenia?

A
Increased usage
Drug suppression
Radiation therapy
Congenital conditions
Bone marrow cancers
Spleen destruction
Vitamin deficiency
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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)
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22
Q

How do you diagnose neutropenia?

A

neutrophil levels and bone marrow biopsy

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23
Q

What is the treatment for Neutropenia?

A

antibiotic therapy and hematopoietic growth factors

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24
Q

What is infectious mononucleosis?

A

“Kissing disease”—oral transmission.

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25
Q

What causes infectious mononucleosis?

A

Caused by Epstein-Barr virus in the herpes family.

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26
Q

Do you have infectious mononucleosis?

A

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.

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27
Q

What are the manifestations of infecticous mononucleosis?

A
  • 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.
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28
Q

What are the treatments for inefectious mononucleosis?

A

symptomatic and supportive

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29
Q

What are lymphomas?

A

Cancers that affect the lymphatic system

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30
Q

What are the 2 main types of lymphoma cancer?

A

Hodgkins and Non-Hodgkins

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31
Q

Is hodgkins or non-hodgkins more common?

A

Non-hogdkins

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32
Q

What is hodgkins lymphoma?

A

Solid tumors with the presence of Reed-Sternberg cells

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33
Q

Where does hodgkins orginate?

A

Typically originate in the lymph nodes of the upper body

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34
Q

Is hodgkins treatable?

A

very with treatment

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35
Q

What are the manifestations of hodgkins and non-hodgkins?

A

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

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36
Q

How is hodgkins diagnosed?

A

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

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37
Q

What is the treatment for hodgkins and non hodgkins?

A

chemotherapy, radiation, and surgery

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38
Q

Is Non-hodgkins treatable?

A

yes, but not a good prognosis

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39
Q

Where does non-hodgkins originate from?

A

Can originate in the T or B cells

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40
Q

Does non-hodkins lymphoma have Reed-Sternberg cells?

A

NO

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41
Q

How commom is Leukemia?

A

second most common blood cancer

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42
Q

What is leukemia?

A

cancer of the leukocytes

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43
Q

What happens with leukemia?

A

Leukemia cells abnormally proliferate, crowding normal blood cells

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44
Q

What are the risk factors of leukemia?

A

exposure to chemical, viral, and radiation mutagens; smoking; use of chemotherapies; certain disease conditions (e.g., Down syndrome); and immunodeficiency disorder

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45
Q

What are the types of Leukemia?

A

Acute lymphoblastic leukemia, Acute myeloid leukemia, Chronic lymphoid leukemia, Chronic myeloid leukemia

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46
Q

Facts about Acute lymphoblastic leukemia

A
  • Affects primarily children
  • Responds well to therapy
  • Good prognosis
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47
Q

Facts about 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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48
Q

Facts about Chronic lymphoid leukemia

A
  • Affects primarily adults

- Responds poorly to therapy, yet most patients live many years after diagnosis

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49
Q

Facts about Chronic myeloid leukemia

A
  • Affects primarily adults

- Responds poorly to chemotherapy, but the prognosis is improved with allogeneic bone marrow transplant

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50
Q

What are the 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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51
Q

How do you diagnose Leukemia?

A

a history, physical examination, complete blood count, and bone marrow biopsy

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52
Q

What is the treatment for Leukemia?

A

chemotherapy and bone marrow transplant

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53
Q

What is Multiple Myeloma?

A
  • 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
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54
Q

Is multiple myeloma caught early?

A

NO, often well advanced upon diagnosis

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55
Q

What are the manifestations of multiple myeloma?

A

Silent onset

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

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56
Q

How is Multiple Myeloma diagnosed?

A

serum and urine protein, calcium, renal function tests, complete blood count, biopsy, X-rays, CT scan and MRI

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57
Q

What is the treatment for multiple myeloma?

A

chemotherapy and complication management

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58
Q

What is erythropoiesis?

A

red blood cell disorder;

  • Production of erythrocytes
  • Regulated by erythropoietin
  • Occurs in bone marrow
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59
Q

What is anemia?

A

Insufficient numbers of RBC’s or an Insufficient amount of hemoglobin in the blood

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60
Q

What are the normal ranges of RBC?

A

Men 4.5-6 x 106/L

Women 4-5.5 x 106/L

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61
Q

What are the normal ranges of Hemoglobin?

A

Men 14-18 g/dl

Women 12.0-16 g/dl

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62
Q

What are the normal ranges of hematocrit?

A

Men 40-50 %

Women 35-45 %

63
Q

What does anemia result from?

A

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

64
Q

What does anemia do?

A

Decreases O2-carrying capacity, leading to tissue hypoxia

65
Q

What are the manifestations of anemia?

A

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

66
Q

What causes iron-deficiency anemia?

A

decreased iron consumption, decreased iron absorption, or increased bleeding

67
Q

What are the manifestations of iron-deficiency anemia?

A

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

68
Q

How is Iron- Deficiency diagnosed?

A

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

69
Q

What is the treatment for Iron-deficiency anemia?

A

identify and treat cause, increase dietary intake, and administer iron supplements

70
Q

What is pernicious anemia?

A

Vitamin B12 deficiency usually caused by a lack of intrinsic factor.

71
Q

What is the cause of pernicious anemia?

A

autoimmune.

72
Q

What is required for DNA synthesis?

A

Vitamin B12 is required for DNA synthesis.

73
Q

What does pernicious anemia lead to?

A

Leads to decreased maturation and cell division.

74
Q

What may we see with pernicious anemia?

A

May see myelin breakdown and neurological complications.

75
Q

What are the manifestations of pernicious anemia?

A

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
Q

How is pernicious anemia diagnosed?

A

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

77
Q

What is the treatment for pernicious anemia?

A

injectable B12

78
Q

What is aplastic anemia?

A

Bone marrow depression of all blood cells (pancytopenia).

79
Q

What are the causes of aplastic anemia?

A

idiopathic, autoimmune, medications, medical treatments, viruses, and genetic abnormalities.

80
Q

What is the onset of aplastic anemia like?

A

Onset may be insidious, sudden, and severe.

81
Q

What are the manifestations of aplastic anemia?

A

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

82
Q

How is aplastic anemia diagnosed?

A

complete blood count and bone marrow biopsy

83
Q

What is the treatment for aplastic anemia?

A

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

84
Q

What is hemolytic anemia?

A

Excessive erythrocyte destruction

85
Q

What are the causes of hemolytic anemia?

A

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

86
Q

What are the types of hemolytic anemia?

A

Several types including sickle cell anemia, thalassemia, and erythroblastosis fetalis

87
Q

Is sickle cell anemia recessive or dominant?

A

neither; its co dominant

88
Q

What is sickle cell anemia?

A

Hemoglobin S causes erythrocytes to be abnormally shaped.

89
Q

What is the problem with abnormal erythroctyes?

A

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

90
Q

Is is more likely to have sickle cell anemia?

A

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
Q

What is the pathogenisis of sickle cell disease?

A

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
Q

What are the 3 forms of sickle cell anemia?

A

Sickle cell trait.
Heterozygous.
Less than half of erythrocytes are sickled

93
Q

What is sickle cell disease?

A

Homozygous.
Most severe.
Almost all erythrocytes are sickled.

94
Q

When does sickle cell anemia appear?

A

around 4 months old

95
Q

What is sickle cell crisis?

A

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
Q

What are the manifestations of sickle cell anemia?

A

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
Q

how is sickle cell anemia diagnosed?

A

complete blood count and bilirubin test

98
Q

What is the treatment for sickle cell anemia?

A
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
Q

What is Thalassemia?

A

Autosomal dominant inheritance

Abnormal hemoglobin from a lack of one of two proteins that make up hemoglobin (alpha and beta globin)

100
Q

How is mostly seen with thalassemia?

A

Most common in people of Mediterranean descent

Also seen in those of Asian, Indian, and African descent

101
Q

What are the manifestations of thalassemia?

A

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

102
Q

What can severe cases of thalassemia lead to?

A

Severe cases can lead to death in childhood.

103
Q

How can the life expectancy of someone with thalassemia increase?

A

Life expectancy can improve with effective management.

104
Q

How is thalassemia diagnosed?

A

complete blood count and iron levels.

105
Q

What is the treatment for thalassemia?

A

blood transfusion and splenectomy.

106
Q

What is polycythemia?

A

Abnormally high erythrocytes

Increased blood volume and viscosity, leading to tissue ischemia and necrosis

107
Q

Is polycythemia rare or common?

A

rare

108
Q

What is polycythemia considered?

A

Considered a neoplastic disease

109
Q

What are the complications of polycythemia?

A

thrombosis, hypertension, heart failure, hemorrhage, splenomegaly, hepatomegaly, and acute myeloblastic leukemia

110
Q

What are the manifestations of polycythemia?

A

cyanotic or ruddy skin, high blood pressure, tachycardia, dyspnea, headaches, visual abnormalities

111
Q

How is polycythemia diagnosed?

A

complete blood counts, bone marrow biopsy, and uric acid levels

112
Q

What is the treatment for polycythemia?

A

chemotherapy, radiation, phlebotomy

113
Q

What is the normal range of platelets?

A

Normal platelet levels range from 150,000 to 400,000 cells/mL3

114
Q

What is thrombocytosis?

A

increased levels of platelets

115
Q

What is thrombocytopenia?

A

decreased levels of platelets

116
Q

What happens when there is a decrease in platelet levels?

A

Decreased platelet function
Decreased platelets in circulation
Platelets used up in clotting

117
Q

What happens when there is impaired coagulation?

A

Impaired platelet function

118
Q

What are the signs of blood loss?

A
Fatigue
Weakness
Fainting
Dizziness
Tachycardia – increased heart rate
Hypotension – low blood pressure
119
Q

What is hemophilia A?

A

X-linked recessive bleeding disorder

Deficiency or abnormality of clotting factor VIII

120
Q

What are the manifestations of Hemophilia A?

A

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

121
Q

How is Hemophilia A diagnosed?

A

clotting studies and serum factor VIII levels

122
Q

What is the treatment for Hemophilia A?

A

clotting factor transfusions, clotting factors, and bleeding precautions

123
Q

How common is it to have a factor 8 deficiency?

A

90%

124
Q

How common is it for factor 8 to be deffective?

A

10%

125
Q

What is the most common hereditary bleeding disorder?

A

Von Willebrands disorder

126
Q

What is Von willedbrands?

A

Decreased platelet adhesion and aggregation

127
Q

What are the manifestations of von willebrands?

A

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

128
Q

How many types of von willebrands are there?

A

3

129
Q

What are the charateristics of type 1 von willebrands?

A

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

130
Q

What are the charateristics of type 2 von willebrands?

A
  • Either autosomal dominant or recessive.
  • Five subtypes.
  • von Willebrand’s factor building blocks are smaller than usual or break down easily.
131
Q

What are the charateristics of type 3 von willebrands?

A
  • Follows autosomal recessive
  • No measurable von Willebrand’s factor or factor VIII
  • Causes severe bleeding problems
132
Q

What is acquired type von willebrand?

A

Occurs with congenital heart disease, systemic lupus erythematosus, and hypothyroidism

133
Q

How is von willebrands diagnosed?

A

bleeding studies and factor VIII levels

134
Q

What is the treatment for von willebrands?

A
  • Mild cases usually do not require treatment
  • Clotting factor infusions
  • Administration of medication to release vW factor
  • Bleeding precautions
  • Measures to control bleeding
135
Q

What is Disseminated Intravascular Coagulation (DIC)?

A
  • Life-threatening complication of many conditions

- Widespread coagulation followed by massive bleeding because of the depletion of clotting factors

136
Q

What does DIC result from?

A

Results from an inappropriate immune response

137
Q

What are the manifestations of DIC?

A

tissue ischemia and abnormal bleeding

138
Q

What are the complications of DIC?

A

shock and multisystem organ failure

139
Q

How is DIC diagnosed?

A

complete blood count and bleeding studies

140
Q

What is the treatment for DIC?

A

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

141
Q

What are the manifestations of thrombocytopenia?

A

Petechiae – pinpoint bleed
Ecchymosis – bruising
Purpura – purple rash
Prolonged bleeding

142
Q

What is Idiopathic Thrombocytopenia Purpura (ITP)?

A

Hypocoagulation resulting from an autoimmune destruction of platelets

143
Q

What is the acute form of ITP like?

A
  • More common in children
  • Sudden onset
  • Self-limiting
144
Q

What is the chronic form of ITP like?

A
  • More common in adults age 20–50

- More common in women

145
Q

What are the causes of ITP?

A

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

146
Q

What are the manifestations of ITP?

A

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

147
Q

How is ITP diagnosed?

A

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

148
Q

What is the treatment for ITP?

A

Acute ITP: steroids, immunoglobulins, plasmapheresis

Chronic ITP: steroids, immunoglobulins, splenectomy, blood transfusions, and immunosuppressant therapy

149
Q

What is Thrombotic Thrombocytopenic Purpura (TTP)?

A

Deficiency of enzyme necessary for cleaving von Willebrand’s factor, leading to hypercoagulation.
Hypercoagulation depletes platelet levels.

150
Q

How is TTP characterized?

A

Characterized by thromboses, thrombocytopenia, and bleeding

151
Q

What are the causes of TTP?

A

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

152
Q

What are the manifestations of TTP?

A

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

153
Q

How is TTP diagnosed?

A

complete blood counts, blood smears, and lactate dehydrogenase levels

154
Q

What is the treatment for TTP?

A

plasmapheresis, splenectomy, and steroids