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Critical Care Nursing Exam 4 > Hematology > Flashcards

Hematology Flashcards

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1
Q

what is blood?

A

blood is a specialized body fluid

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2
Q

what are the four main components of blood?

A
  • plasma
  • RBCs
  • WBCs
  • platelets
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3
Q

what is blood responsible for?

A
  • transporting oxygen and nutrients to lungs and tissues
  • forming blood clots to prevent excess blood loss
  • carrying cells and antibodies to fight infection
  • bring waste products to the kidneys and liver, filtering and cleaning the blood
  • regulate body temp
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4
Q

what are the two types of stem cells?

A

myeloid and lymphoid

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5
Q

what are the 3 types of myeloid stem cells?

A
  1. erythrocytes
  2. leukocytes
  3. platelets
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6
Q

what are the two types of lymphoid cells?

A
  1. T lymphocytes

2. B Lymphocytes

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7
Q

what are erythrocytes also known as?

A

red blood cells

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8
Q

what do erythrocytes do?

A

carrying oxygen to tissues and removing carbon dioxide from tissues.

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9
Q

what are leukocytes also known as?

A

White blood cells

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10
Q

what do leukocytes do?

A

fight infection

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11
Q

how many types of WBCs are there?

A

5

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12
Q

what do platelets do?

A

stop bleeding. they form blood clots

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13
Q

what are platelets also known as?

A

thrombocytes

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14
Q

T/F

platelets have no nucleus.

A

true

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15
Q

what are platelets derived from?

A

fragments of cytoplasm which are derived from megakaryocytic of the bone marrow, then enter the circulation

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16
Q

What are B lymphocytes used for?

A

Creating antibodies

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17
Q

where are B lymphocytes produced?

A

bone marrow

this is also where they mature

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18
Q

What are T lymphocytes used for?

A

controlling immune response

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19
Q

where are the precursors of T cells produced?

A

bone marrow

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20
Q

where do T cells mature?

A

T cells leave the bone marrow and mature in the thymus

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21
Q

what do T lymphocytes do?

A

direct immune response, and evaluate immune function

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22
Q

what are the 5 types of WBC’s?

A
  • neutrophils
  • eosinophils
  • basophils
  • monocytes
  • lymphocytes
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23
Q

what do neutrophils do?

A

primary pathogen fighting cells

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24
Q

what do eosinophils do?

A

help control allergic response, and fight parasites

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25
Q

what do basophils do?

A

release heparin, histamine, and other inflammatory mediators

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26
Q

what do monocytes do?

A

fight bacteria, fungi, and viruses

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27
Q

where are monocytes formed?

A

bone marrow

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28
Q

what is the largest WBC?

A

monocytes

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29
Q

what do lymphocytes do?

A

determine the specificity of immune response to infectious microorganisms

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30
Q

what percent of WBCs do lymphocytes make up?

A

20-40%

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31
Q

what is leukemia?

A

neoplastic proliferation of one cell

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32
Q

what is a common indicator of leukemia?

A

unregulated proliferation of leukocytes in bone marrow

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33
Q

what does unregulated proliferation of leukocytes cause?

A

little room for normal cell production

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34
Q

how is leukemia classified?

A

according to stem cell line, either lymphoid or myeloid

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35
Q

how is leukemia classified?

A

acute or chronic`

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36
Q

how is acute leukemia characterized?

A

abrupt onset, development of healthy cells halted at blast phase

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37
Q

how is chronic leukemia characterized?

A

symptoms evolve over months to years, majority of leukocytes mature

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38
Q

how is leukemia often noticed?

A

by elevate WBCs

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39
Q

what does ineffective and quick WBC replication cause?

A

no normal cell production

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40
Q

what is the blast phase associated with?

A

acute leukemia

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41
Q

what happens in the blast phase?

A

in this phase patients have more blast cells in the blood and bone marrow samples, blast cells frequently invade other tissues and organs

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42
Q

what happens during the blast phase?

A

the disease transforms into an aggressive and acute leukemia

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43
Q

what percent of leukemia is AML?

A

70%

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44
Q

what percent of leukemia in ALL?

A

30%

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45
Q

what is a blast cell?

A

primitive undifferentiated blood cell, often found in the blood of those with acute leukemia

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46
Q

what type of cells does AML effect ?

A

monocytes, erythrocytes and platelets

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47
Q

what age Is AML most common in?

A

all ages, but over age 55 most common

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48
Q

what previous cancer is AML related to?

A

Hodgkins lymphoma

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49
Q

what is the manifestation of AML?

A

sudden onset with signs and symptoms over period of weeks, with flu like symptoms

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50
Q

what is pancytopenia?

A

every type of cell is low

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51
Q

signs of AML??

A

proliferation of leukemic cells in organs
pain from hepatomegaly or splenomegaly
hyperplasia of gums
bone pain

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52
Q

what causes spleen and liver enlargement in AML?

A

with the proliferation of cells, they start to go into organs and become enlarged and painful

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53
Q

what diagnostics will show evidence of AML?

A

CBC, bone marrow biopsy, bruising, bleeding,

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54
Q

what will a CBC look like in someone who has AML?

A

low RBC, and platelets
excess blast cells (>20%)
low neutrophils

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55
Q

where do we see evidence of the blast phase?

A

in the bone marrow

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56
Q

why may ecchymosis and petechiae occur with AML?

A

risk for major bleeding if platelet count is <10,000

vessels are infiltrated with cells

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57
Q

what type of precautions will an AML patient be in?

A

neutropenic precautions

58
Q

treatment of AML?

A

induction therapy
consolidation therapy
bone marrow transplant
palliative care

59
Q

what is induction therapy ?

A

aggressive chemotherapy for several weeks

60
Q

how does induction chemo work?

A

chemo destroys leukemic and normal cells

this is the initial blast of chemo in a high dose to wipe out the blast cells

61
Q

how does consolidation chemo work?

A

multiple cycles of chemo agents, usually some form of cytarabine
in lower doses than induction, so is less toxic and has less side effects.
a small dose over a longer period of time

62
Q

when is consolidation therapy used?

A
  • once patient is recovered from induction therapy

- this is maintenence therapy, post remission tx to get rid of any remaining leukemic cells

63
Q

what is a bone marrow transplant?

A

destruction hematopoietic function bone marrow, replaced with donor stem cells

64
Q

what is a possible complication of AML treatment?

A

tumor lysis syndrome

65
Q

what is tumor lysis syndrome?

A

release of intracellular electrolytes and fluids into systemic circulation

66
Q

what does tumor lysis syndrome cause r/t uric acid?

A

increased uric acid and phosphorus risk gout, renal stones and colic, leading to ARF

67
Q

what does tumor lysis syndrome cause r/t electrolytes?

A

hyperlkalemia and hypocalcemia

68
Q

what can electrolyte imbalances from tumor lysis syndrome cause ?

A

cardiac dysrhythmias, hypotension, neuromuscular effects, confusion, seizures

69
Q

how to treat gout?

A

allopurinol prophylaxis

70
Q

how to treat electrolyte imbalances r/t TLS?

A

high fluid intake, kayexalate to bind and flush out potassium, hemodialysis

71
Q

what is chronic myeloid leukemia?

A

mutation in myeloid stem cells

72
Q

what type of cell is present 90-95% of the time in CML?

A

philadelphia chromosome; which is a section of DNA missing from chromosome 22, which is translocated onto chromosome 9

73
Q

why does this gene mutation cause CML?

A

breakpoint cluster region gene chromosome 22 and ABL viral gene of chromosome 9. when fused, produce abnormal protein causing rapid dividing of leukocytes

74
Q

what age group is CML most common in?

A

uncommon in younger than 20, incidence increases with age (mean of 67)

75
Q

what are the phases of CML?

A
  1. chronic: few symptoms, and are very subtle
  2. transformation: process of change to acute form. may have bone pain, fever, weight loss
  3. Acute form: Blast crises. Life threatening infection and bleeding risk
76
Q

how does CML present?

A

mild signs and symptoms until the patients suddenly get very sick and they have a blast crisis in acute form

77
Q

treatment options for CML?

A

treatment with tyrosine kinase inhibitor; Gleevec which blocks signal within leukemia cells preventing chemical reactions causing cell growth and division

78
Q

what should the nurse do to protect herself when giving Gleevec?

A

wear gloves

79
Q

when is Gleevec most effective?

A

chronic phase, can induce complete remission at cellular and molecular level

80
Q

what cannot be given when a patient is on Gleevec?

A

antacids and grapefruit juice

81
Q

what can we do for the patient if the initial round of chemo drugs does not worK?

A

when remission not obtained or maintained, may increase the dose, add another inhibitor, or have a BMT

82
Q

what is the treatment of a crises in CML?

A

acute form tx resembles induction therapy; blasting cells and killing off blasts

83
Q

how long must a patient be in remission to be declared cured?

A

5 years

84
Q

what is induction therapy?

A

aggressive chemotherapy for several weeks ; high does chemo destroying leukemic and normal cells causing severe pancytopenia, requiring supportive care and neutropenic precautions

85
Q

What is acute lymphocytic leukemia?

A

proliferation of immature lymphoid stem cells (lymphoblasts)

production of immature lymphocytes impedes production of normal myeloid cells- results in pancytopenia

86
Q

what age is ALL most common in?

A

children (0-15) and older adults (>50)

87
Q

what age group has the highest survival rate of ALL?

A

children (80%)

88
Q

what type of cells are more common in ALL?

A

infiltration leukemic cells to other organs more common with ALL. this can cause liver and spleen enlargement, bone pain, CNS involvement

89
Q

what is the goal of all cancer treatment?

A

remmission

90
Q

treatment of ALL?

A

-preventative cranial irradiation or intrathecal chemo to decrease CNS involvement

91
Q

induction tx in ALL?

A

lymphoid blast cells sensitive to corticosteroids and vinca alkaloids- goal is to wipe everything out

92
Q

consolidation tx in ALL?

A

3 years, goal is to improve outcomes in those with high risk of relapse.

93
Q

when do we count from for remission?

A

the end of consolidation treatment

94
Q

what is chronic lymphocytic leukemia?

A

malignant clone of B lymphocytes in bone marrow, most cells mature, T lymphocyte CLL is rare

95
Q

what is the thought of CLL?

A

may be that cells some how escape apoptosis

96
Q

pathophysiology of CLL?

A

leukocytes small so do not interfere with flow through microvasculature, but do get trapped din lymph nodes- the nodes enlarge sometimes painful. development of liver and spleen enlargement and cause enlarged lymph nodes.

97
Q

what may happen in the later stages of CLL?

A

anemia

thrombocytopenia related to immune response

98
Q

what lymph nodes are most indicative of CLL?

A

the enlargement of clavicular chain lymph nodes are indicative of CLL

99
Q

what are the s/s of CLL?

A

leukocytosis, lymph node enlargement flu like symptoms, risk of infections

100
Q

tx of CLL?

A

treatment can result in 70% 5 year remission rate, tx results in longterm prolonged bone marrow suppression.

101
Q

What is lymphoma?

A

neoplasms of cells of lymphoid origin, typically originating in lymph nodes but can involve lymphoid tissue in spleen, GI tract, liver, bone marrow

102
Q

what are the two categories of lymphoma?

A

Hodgkin and Non-Hodgkin

103
Q

what is Hodgkin lymphoma?

A

malignant cells, spreading contiguously along lymphatic system, originating in a single node.

104
Q

who is Hodgkin lymphoma most common in?

A

pts receiving immunosupresssive treatment, and veterans exposed to agent orange

105
Q

when in peak occurrence of Hodgkin Lymphoma?

A

early 20s and after age 50

106
Q

what type of cell is a marker for Hodgkin lymphoma?

A

Reed Sternberg cells

107
Q

what are reed Sternberg cells?

A

pathologic marker for disease

108
Q

how to identify reed Sternberg cells?

A

through biopsy, may take multiple biopsies to identify the cells

109
Q

what is the preceding factor to reed Sternberg cells?

A

thought to be a viral component. Epstein Barr Virus!

110
Q

how does Hodgkin Lymphoma present?

A

presents with painless enlarged nodes on one side of the neck, most common cervical supraclavicular, mediastinal.

111
Q

when are B symptoms in Hodgkin Lymphoma?

A

in 40% of cases, most often with advanced disease

112
Q

how is Hodgkin Lymphoma diagnosed?

A

eliminating infectious cause of symptoms

lymph node biopsy and reed Sternberg cells

113
Q

what diagnostic testing is used for HL?

A

CXR, CT chest, CT abd, CT pelvis for extent of lymphadenopathy, bone marrow if suspect marrow involvement, and CBC

114
Q

are Hogkin or Non Hodgkin patients sicker?

A

Hodgkin patients are sicker.

115
Q

what is the treatment of HL in early stages?

A

tx dependent on stage of disease

early stage: short course chemo: 2-4 months (chemo followed by radiation)

116
Q

what is the tx of HL in late stage dx?

A

combo chemo tx: ABVD - doxorubicin, bleomycin, vinblastine, dacarbazine

117
Q

what is the risk after treatment of HL?

A

long term risk of secondary malignancy, breast and lung cancer and AML

118
Q

what is non Hodgkin Lymphoma?

A

hetergenous group cancers originate from neoplastic growth lymphoid tissue
thought to arise from single clone of lymphocyte, most malignant B lymphocytes
lymphoid tissue infiltrated with malignant cells

119
Q

how does NHL spread?

A

spread occurs unpredictably, localization is rare. may infiltrate lymph nodes as well as non lymph tissue

120
Q

what increases risk of NHL?

A

age, immunodeficiency, autoimmune disorder, cancer tx, organ transplant, virus, agent orange exposure

121
Q

symptoms of NHL?

A

lymphadenopathy most common, flu-like symptoms, CNS involvement

122
Q

how is NHL dx?

A

CT, PET scans, bone marrow biopsy, CSF analysis

123
Q

how is NHL tx?

A

dependent on classification and disease, prior tx, pts ability to tolerate therapy, radiation, monoclonal antibodies, intrathecal chemo, cranial radiation

124
Q

what is DIC?

A

disseminated intravascular coagulation: abnormal function of clotting and bleeding. sign of underlying condition such as sepsis, trauma, cancer, shock, toxins, allergy.

125
Q

what will the platelet count look like in DIC?

A

it will be decreased

126
Q

what is a normal platelet count?

A

150-450K/mm3

127
Q

what is a normal PT?

A

11-12.5 sec

128
Q

what will PT look like in DIC?

A

it will be increased

129
Q

what will PTT look like in DIC?

A

It will be increased

130
Q

what is a normal PTT?

A

23-35 sec

131
Q

what is a normal TT?

A

8-11 sec

132
Q

what will TT look like in DIC?

A

it will be increased

133
Q

what is a normal fibrinogen?

A

170-340mg/dL

134
Q

what will fibrinogen look like in DIC?

A

it will be decreased

135
Q

what will the D-dimer look like in DIC?

A

it will be increased

136
Q

what is a normal D-dimer?

A

0-250mg/mL

137
Q

what will fibrin degrad prod look like in DIC?

A

Increased

138
Q

what is a normal fibrin degrad prod?

A

0-5mcg/mL

139
Q

what will euglobulin clot lysis look like in DIC?

A

<1 hr

140
Q

what is a normal euglobulin clot lysis?

A

> 2hr

141
Q

clinical manifestation of DIC?

A 
thrombocytopenia
petechia of skin 
spontaneous bleeding of skin, mucous membranes, or into foley
prolonged bleeding time
hemorrhage into subcut tissue
ecchymosis
purpura
oozing from multiple sites, including incisions, needle sites
142
Q

tx of DIC?

A

tx of underlying cause
supportive care
oxygen, fluids, pressors, fibrinogen, Factor 5 and factor 7, FFP

Critical Care Nursing Exam 4 (4 decks)

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