Hematology Flashcards
1
Q
what is blood?
A
blood is a specialized body fluid
2
Q
what are the four main components of blood?
A
- plasma
- RBCs
- WBCs
- platelets
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
4
Q
what are the two types of stem cells?
A
myeloid and lymphoid
5
Q
what are the 3 types of myeloid stem cells?
A
- erythrocytes
- leukocytes
- platelets
6
Q
what are the two types of lymphoid cells?
A
- T lymphocytes
2. B Lymphocytes
7
Q
what are erythrocytes also known as?
A
red blood cells
8
Q
what do erythrocytes do?
A
carrying oxygen to tissues and removing carbon dioxide from tissues.
9
Q
what are leukocytes also known as?
A
White blood cells
10
Q
what do leukocytes do?
A
fight infection
11
Q
how many types of WBCs are there?
A
5
12
Q
what do platelets do?
A
stop bleeding. they form blood clots
13
Q
what are platelets also known as?
A
thrombocytes
14
Q
T/F
platelets have no nucleus.
A
true
15
Q
what are platelets derived from?
A
fragments of cytoplasm which are derived from megakaryocytic of the bone marrow, then enter the circulation
16
Q
What are B lymphocytes used for?
A
Creating antibodies
17
Q
where are B lymphocytes produced?
A
bone marrow
this is also where they mature
18
Q
What are T lymphocytes used for?
A
controlling immune response
19
Q
where are the precursors of T cells produced?
A
bone marrow
20
Q
where do T cells mature?
A
T cells leave the bone marrow and mature in the thymus
21
Q
what do T lymphocytes do?
A
direct immune response, and evaluate immune function
22
Q
what are the 5 types of WBC’s?
A
- neutrophils
- eosinophils
- basophils
- monocytes
- lymphocytes
23
Q
what do neutrophils do?
A
primary pathogen fighting cells
24
Q
what do eosinophils do?
A
help control allergic response, and fight parasites
25
what do basophils do?
release heparin, histamine, and other inflammatory mediators
26
what do monocytes do?
fight bacteria, fungi, and viruses
27
where are monocytes formed?
bone marrow
28
what is the largest WBC?
monocytes
29
what do lymphocytes do?
determine the specificity of immune response to infectious microorganisms
30
what percent of WBCs do lymphocytes make up?
20-40%
31
what is leukemia?
neoplastic proliferation of one cell
32
what is a common indicator of leukemia?
unregulated proliferation of leukocytes in bone marrow
33
what does unregulated proliferation of leukocytes cause?
little room for normal cell production
34
how is leukemia classified?
according to stem cell line, either lymphoid or myeloid
35
how is leukemia classified?
acute or chronic`
36
how is acute leukemia characterized?
abrupt onset, development of healthy cells halted at blast phase
37
how is chronic leukemia characterized?
symptoms evolve over months to years, majority of leukocytes mature
38
how is leukemia often noticed?
by elevate WBCs
39
what does ineffective and quick WBC replication cause?
no normal cell production
40
what is the blast phase associated with?
acute leukemia
41
what happens in the blast phase?
in this phase patients have more blast cells in the blood and bone marrow samples, blast cells frequently invade other tissues and organs
42
what happens during the blast phase?
the disease transforms into an aggressive and acute leukemia
43
what percent of leukemia is AML?
70%
44
what percent of leukemia in ALL?
30%
45
what is a blast cell?
primitive undifferentiated blood cell, often found in the blood of those with acute leukemia
46
what type of cells does AML effect ?
monocytes, erythrocytes and platelets
47
what age Is AML most common in?
all ages, but over age 55 most common
48
what previous cancer is AML related to?
Hodgkins lymphoma
49
what is the manifestation of AML?
sudden onset with signs and symptoms over period of weeks, with flu like symptoms
50
what is pancytopenia?
every type of cell is low
51
signs of AML??
proliferation of leukemic cells in organs
pain from hepatomegaly or splenomegaly
hyperplasia of gums
bone pain
52
what causes spleen and liver enlargement in AML?
with the proliferation of cells, they start to go into organs and become enlarged and painful
53
what diagnostics will show evidence of AML?
CBC, bone marrow biopsy, bruising, bleeding,
54
what will a CBC look like in someone who has AML?
low RBC, and platelets
excess blast cells (>20%)
low neutrophils
55
where do we see evidence of the blast phase?
in the bone marrow
56
why may ecchymosis and petechiae occur with AML?
risk for major bleeding if platelet count is <10,000
| vessels are infiltrated with cells
57
what type of precautions will an AML patient be in?
neutropenic precautions
58
treatment of AML?
induction therapy
consolidation therapy
bone marrow transplant
palliative care
59
what is induction therapy ?
aggressive chemotherapy for several weeks
60
how does induction chemo work?
chemo destroys leukemic and normal cells
| this is the initial blast of chemo in a high dose to wipe out the blast cells
61
how does consolidation chemo work?
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
when is consolidation therapy used?
- once patient is recovered from induction therapy
| - this is maintenence therapy, post remission tx to get rid of any remaining leukemic cells
63
what is a bone marrow transplant?
destruction hematopoietic function bone marrow, replaced with donor stem cells
64
what is a possible complication of AML treatment?
tumor lysis syndrome
65
what is tumor lysis syndrome?
release of intracellular electrolytes and fluids into systemic circulation
66
what does tumor lysis syndrome cause r/t uric acid?
increased uric acid and phosphorus risk gout, renal stones and colic, leading to ARF
67
what does tumor lysis syndrome cause r/t electrolytes?
hyperlkalemia and hypocalcemia
68
what can electrolyte imbalances from tumor lysis syndrome cause ?
cardiac dysrhythmias, hypotension, neuromuscular effects, confusion, seizures
69
how to treat gout?
allopurinol prophylaxis
70
how to treat electrolyte imbalances r/t TLS?
high fluid intake, kayexalate to bind and flush out potassium, hemodialysis
71
what is chronic myeloid leukemia?
mutation in myeloid stem cells
72
what type of cell is present 90-95% of the time in CML?
philadelphia chromosome; which is a section of DNA missing from chromosome 22, which is translocated onto chromosome 9
73
why does this gene mutation cause CML?
breakpoint cluster region gene chromosome 22 and ABL viral gene of chromosome 9. when fused, produce abnormal protein causing rapid dividing of leukocytes
74
what age group is CML most common in?
uncommon in younger than 20, incidence increases with age (mean of 67)
75
what are the phases of CML?
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
how does CML present?
mild signs and symptoms until the patients suddenly get very sick and they have a blast crisis in acute form
77
treatment options for CML?
treatment with tyrosine kinase inhibitor; Gleevec which blocks signal within leukemia cells preventing chemical reactions causing cell growth and division
78
what should the nurse do to protect herself when giving Gleevec?
wear gloves
79
when is Gleevec most effective?
chronic phase, can induce complete remission at cellular and molecular level
80
what cannot be given when a patient is on Gleevec?
antacids and grapefruit juice
81
what can we do for the patient if the initial round of chemo drugs does not worK?
when remission not obtained or maintained, may increase the dose, add another inhibitor, or have a BMT
82
what is the treatment of a crises in CML?
acute form tx resembles induction therapy; blasting cells and killing off blasts
83
how long must a patient be in remission to be declared cured?
5 years
84
what is induction therapy?
aggressive chemotherapy for several weeks ; high does chemo destroying leukemic and normal cells causing severe pancytopenia, requiring supportive care and neutropenic precautions
85
What is acute lymphocytic leukemia?
proliferation of immature lymphoid stem cells (lymphoblasts)
| production of immature lymphocytes impedes production of normal myeloid cells- results in pancytopenia
86
what age is ALL most common in?
children (0-15) and older adults (>50)
87
what age group has the highest survival rate of ALL?
children (80%)
88
what type of cells are more common in ALL?
infiltration leukemic cells to other organs more common with ALL. this can cause liver and spleen enlargement, bone pain, CNS involvement
89
what is the goal of all cancer treatment?
remmission
90
treatment of ALL?
-preventative cranial irradiation or intrathecal chemo to decrease CNS involvement
91
induction tx in ALL?
lymphoid blast cells sensitive to corticosteroids and vinca alkaloids- goal is to wipe everything out
92
consolidation tx in ALL?
3 years, goal is to improve outcomes in those with high risk of relapse.
93
when do we count from for remission?
the end of consolidation treatment
94
what is chronic lymphocytic leukemia?
malignant clone of B lymphocytes in bone marrow, most cells mature, T lymphocyte CLL is rare
95
what is the thought of CLL?
may be that cells some how escape apoptosis
96
pathophysiology of CLL?
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
what may happen in the later stages of CLL?
anemia
| thrombocytopenia related to immune response
98
what lymph nodes are most indicative of CLL?
the enlargement of clavicular chain lymph nodes are indicative of CLL
99
what are the s/s of CLL?
leukocytosis, lymph node enlargement flu like symptoms, risk of infections
100
tx of CLL?
treatment can result in 70% 5 year remission rate, tx results in longterm prolonged bone marrow suppression.
101
What is lymphoma?
neoplasms of cells of lymphoid origin, typically originating in lymph nodes but can involve lymphoid tissue in spleen, GI tract, liver, bone marrow
102
what are the two categories of lymphoma?
Hodgkin and Non-Hodgkin
103
what is Hodgkin lymphoma?
malignant cells, spreading contiguously along lymphatic system, originating in a single node.
104
who is Hodgkin lymphoma most common in?
pts receiving immunosupresssive treatment, and veterans exposed to agent orange
105
when in peak occurrence of Hodgkin Lymphoma?
early 20s and after age 50
106
what type of cell is a marker for Hodgkin lymphoma?
Reed Sternberg cells
107
what are reed Sternberg cells?
pathologic marker for disease
108
how to identify reed Sternberg cells?
through biopsy, may take multiple biopsies to identify the cells
109
what is the preceding factor to reed Sternberg cells?
thought to be a viral component. Epstein Barr Virus!
110
how does Hodgkin Lymphoma present?
presents with painless enlarged nodes on one side of the neck, most common cervical supraclavicular, mediastinal.
111
when are B symptoms in Hodgkin Lymphoma?
in 40% of cases, most often with advanced disease
112
how is Hodgkin Lymphoma diagnosed?
eliminating infectious cause of symptoms
| lymph node biopsy and reed Sternberg cells
113
what diagnostic testing is used for HL?
CXR, CT chest, CT abd, CT pelvis for extent of lymphadenopathy, bone marrow if suspect marrow involvement, and CBC
114
are Hogkin or Non Hodgkin patients sicker?
Hodgkin patients are sicker.
115
what is the treatment of HL in early stages?
tx dependent on stage of disease
| early stage: short course chemo: 2-4 months (chemo followed by radiation)
116
what is the tx of HL in late stage dx?
combo chemo tx: ABVD - doxorubicin, bleomycin, vinblastine, dacarbazine
117
what is the risk after treatment of HL?
long term risk of secondary malignancy, breast and lung cancer and AML
118
what is non Hodgkin Lymphoma?
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
how does NHL spread?
spread occurs unpredictably, localization is rare. may infiltrate lymph nodes as well as non lymph tissue
120
what increases risk of NHL?
age, immunodeficiency, autoimmune disorder, cancer tx, organ transplant, virus, agent orange exposure
121
symptoms of NHL?
lymphadenopathy most common, flu-like symptoms, CNS involvement
122
how is NHL dx?
CT, PET scans, bone marrow biopsy, CSF analysis
123
how is NHL tx?
dependent on classification and disease, prior tx, pts ability to tolerate therapy, radiation, monoclonal antibodies, intrathecal chemo, cranial radiation
124
what is DIC?
disseminated intravascular coagulation: abnormal function of clotting and bleeding. sign of underlying condition such as sepsis, trauma, cancer, shock, toxins, allergy.
125
what will the platelet count look like in DIC?
it will be decreased
126
what is a normal platelet count?
150-450K/mm3
127
what is a normal PT?
11-12.5 sec
128
what will PT look like in DIC?
it will be increased
129
what will PTT look like in DIC?
It will be increased
130
what is a normal PTT?
23-35 sec
131
what is a normal TT?
8-11 sec
132
what will TT look like in DIC?
it will be increased
133
what is a normal fibrinogen?
170-340mg/dL
134
what will fibrinogen look like in DIC?
it will be decreased
135
what will the D-dimer look like in DIC?
it will be increased
136
what is a normal D-dimer?
0-250mg/mL
137
what will fibrin degrad prod look like in DIC?
Increased
138
what is a normal fibrin degrad prod?
0-5mcg/mL
139
what will euglobulin clot lysis look like in DIC?
<1 hr
140
what is a normal euglobulin clot lysis?
>2hr
141
clinical manifestation of DIC?
```
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
tx of DIC?
tx of underlying cause
supportive care
oxygen, fluids, pressors, fibrinogen, Factor 5 and factor 7, FFP
