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HLSC 222 - Pathophysiology Across the Lifespan > Chapter 21 - Alterations in Hematological Function > Flashcards

Chapter 21 - Alterations in Hematological Function Flashcards

1
Q

Alterations in erythrocyte function can be related to either a) or b):

A

a) insufficient or excess number
b) normal number but with abnormal components

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2
Q

Anemia is a condition of too ____ erythrocytes in the blood

A

few

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3
Q

Polycythemia is a condition of too _____ erythrocytes in the blood

A

many

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4
Q

Leukocytosis is an __________ number of leukocytes in response to infection

A

increased

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5
Q

What is blood clotting used for?

A

to stop bleedin

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6
Q

Clotting disorders result from alterations in the interactions between endothelium, platelets, and _________ components

A

clotting

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7
Q

Anemia can be a reduction in the number of RBCs or a decrease in the quality or quantity of ____________

A

hemoglobin

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8
Q

Anemia is classified based on cell _____ and ____ content

A

size; Hb

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9
Q

Terms that end in ‘cytic’ refer to…

A

cell size

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10
Q

Terms that end in ‘chrome’ refer to…

A

Hb content

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11
Q

Anisocytosis is a type of anemia where cells vary in ______

A

size

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12
Q

Poikilocytosis is a type of anemia where cells assume various ______

A

shapes

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13
Q

Anemia reduces the ______ ______ capacity of blood

A

oxygen carrying capacity

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14
Q

Anemia results in a decrease in blood ________, increased ______ rate, and an ________ heart rate and stroke volume

A

viscosity; flow; increased

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15
Q

What is hypoxemia?

A

state of reduced oxygen levels in the blood

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16
Q

How does the body compensate hypoxemia?

A

vasodilation

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17
Q

Vasodilation due to hypoxemia results in…

A

-decreased resistance
-increased flow rate
-increased heart rate and stroke volume

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18
Q

Compensating for hypoxemia due to anemia can result in…

A

heart failure

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19
Q

Anemias are named based on their effects. Match:
a) macro
b) normo
c) micro
d) cytic
e) chromic

i) cell size (RBC)
ii) small
iii) Hb content
iv) large
v) normal

A

a) iv
b) v
c) ii
d) i
e) iii

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20
Q

Macrocytic-Nomochromic Anemia means…

A

-Large RBCs
-normal Hb content

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21
Q

What is the source of large RBCs with Macrocytic-Normochromic Anemia?

A

large stem cells (megaloblasts) in bone marrow

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22
Q

What is the cause of Macrocytic-Normochromic Anemia? (hint: nutrients)

A

inefficient DNA synthesis in RBCs due to vitamin B and Folic acid deficiency

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23
Q

Macrocytic-Normochromic Anemia results in RBCs _______ in circulation due to…

A

dying; DNA synthesis error resulting in eryptosis

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24
Q

Eryptosis`

A

premature death of damaged erythrocytes

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25
Q

What is vit B12 and folic acid used for in erythroblasts (undifferentiated RBCs in bone marrow)?

A

proliferation during differentiation

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26
Q

What is the most common macrocytic type of anemia?

A

Pernicious Anemia

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27
Q

Pernicious anemia is caused by a _______ deficiency

A

vit B

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28
Q

What does pernicious mean?

A

highly injurious or destructive

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29
Q

Pernicious anemia is an __________ condition

A

autoimmune

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30
Q

Pernicious anemia causes the person to produce antibodies against _________ cells

A

parietal

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31
Q

What do parietal cells produce?

A

intrinsic factor (IF) and HCl

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32
Q

What is intrinsic factor used for?

A

absorption of vit B12

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33
Q

What is HCl from parietal cells used for?

A

iron absorption

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34
Q

Pernicious anemia may also result from a past ________ infection

A

H. pylori

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35
Q

Pernicious anemia develops slowly over __-__ years

A

20-30

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36
Q

Pernicious anemia is severe when…

A

the patient seeks treatment

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37
Q

What are the early symptoms of pernicious anemia?

A

unspecific and usually ignored

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38
Q

What is a normal Hb level?

A

> 120 g/L

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39
Q

What is the Hb level of a pernicious anemic person experiencing symptoms?

A

70-80 g/L

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40
Q

What are the symptoms of pernicious anemia?

A

-fatigue
-paresthesia of feet and fingers
-abdominal pain
-nerve demyelination

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41
Q

Paresthesia

A

tingling, prickling feeling

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42
Q

The symptoms of pernicious anemia are ________

A

irreversible

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43
Q

Folate Deficiency anemia is a type of ______-cytic _____-chromic anemia

A

macro; normo

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44
Q

Folate (folic acid) is essential for the _____ and ____ synthesis in RBCs

A

DNA and RNA

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45
Q

Folates are ______________ necessary for t______ and p______ synthesis

A

coenzymes; thymine; purine

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46
Q

How do humans get folate?

A

diet (eating)

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47
Q

What is the daily folate requirement?

A

50-200 mg/day

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48
Q

People with folate deficiency anemia have a ___________ appearance.

A

malnourished

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49
Q

Burning Mouth Syndrome is a symptom of _______ ______ anemia and presents as…

A

folate deficiency; red beefy tongue and scales on the mouth

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50
Q

What is the treatment for folate deficiency anemia?

A

oral folate

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51
Q

Effective Tx for FD anemia will have it disappearing in how long?

A

1-2 weeks

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52
Q

What is Microcytic-Hypochromic Anemia?

A

-small RBC
-reduced Hb amounts

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53
Q

Microcytic-Hypochromic anemia is caused by _____ metabolism disorders

A

iron

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54
Q

Iron metabolism disorders lead to problems with _______ and _______ synthesis

A

heme and globin

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55
Q

Iron deficiency anemia and __________ result from iron metabolism disorders

A

Thalassemia

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56
Q

Thalassemia

A

an inherited disorder causing reduced hemoglobin

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57
Q

Iron deficiency anemia is caused by a) chronic ______ _____ or b) inadequate ________ intake

A

blood loss; iron

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58
Q

There is no intrinsic dysfunction of iron metabolism with ______ _________ anemia

A

iron deficiency

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59
Q

A metabolic iron deficiency results from issues with a) iron delivery to _____ ______ or b) impaired iron __________ into bone marrow

A

bone marrow; absorption

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60
Q

A blood loss of __-__ mL/day can cause iron deficiency anemia

A

2-4 mL/day

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61
Q

Iron can be ___________

A

recycled

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62
Q

Blood loss disrupts iron recycling because…

A

there is no iron to recycle

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63
Q

Iron deficiency is caused by i) m____________ ii) s__________ iii) Pica iv) ______

A

medication; surgery; [iron] intake

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64
Q

Which medications can cause GI bleeding and lead to iron deficiency

A

Aspirin and NSAIDs

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65
Q

How do surgical procedures contribute to iron deficiency?

A

decrease transit time and thus absorption

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66
Q

Pica

A

disorder causing the eating of non-nutritional substances

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67
Q

Stage 1 IDA occurs when iron stores are ________ but RBC production remains normal

A

depleted

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68
Q

Which stage of IDA is characterized by insufficient iron transport to bone marrow and the creation of iron-deficient RBCs?

A

Stage 2

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69
Q

During stage 3 IDA, Hb deficient RBCs ________ normal RBCs and anemia occurs

A

replace

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70
Q

Iron deficiency anemia is not noticed until the Hb level reaches ___-___ g/L

A

70-80

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71
Q

What are the noticeable symptoms of IDA?

A

-changes in epithelial tissue structure
-Koilonychia
-Glossitis
-Dysphagia

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72
Q

Koilonychia

A

brittle and spoon shaped fingernails

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73
Q

Glossitis

A

atrophy of tongue papillae

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74
Q

IDA Dysphagia occurs due to a ____________ and inflammatory cells

A

web of mucus

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75
Q

How is IDA directly diagnosed?

A

bone marrow biopsy to measure iron stores

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76
Q

How is IDA indirectly diagnosed?

A

measure of:
-Ferritin levels
-Transferrin saturation
-Iron-binding capacity

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77
Q

What is the first step of IDA treatment?

A

eliminate sources of blood loss

78
Q

What is the second step of IDA treatment?

A

iron replacement therapy

79
Q

Iron replacement therapy is done until serum Ferritin level reaches __µg/L

A

50

80
Q

What is Normocytic Normochromic Anemia?

A

normal size cells with normal Hb content but insufficient in numbers

81
Q

What are the four normocytic normochromic anemias?

A

aplastic, posthemorrhagic, hemolytic, chronic inflammation

82
Q

Aplastic anemia is an infiltrative disorder of _______ _______

A

bone marrow

83
Q

Posthemorrhagic anemia occurs with sudden ______ _____ and normal _____ stores

A

blood loss; iron

84
Q

Hemolytic anemia involves…

A

the destruction of RBCs

85
Q

Hemolytic anemia can be a_________, h________, or due to hemolysis

A

acquired; hereditary

86
Q

Acquired anemia is developed…

A

after birth

87
Q

What is an example of hereditary anemia?

A

Sickle Cell Anemia

88
Q

Hemolysis

A

destruction of RBCs

89
Q

Hemolytic anemia occurs from the _________ (premature death of damaged erythrocytes)

A

eryptosis

90
Q

Leukocyte alterations may be due to: a) or b)

A

a) too many or too few leukocytes
b) structurally or functionally defective cells

91
Q

Leukocytosis occurs with a WBC count that is…

A

higher than normal

92
Q

When does leukocytosis occur?

A

as a normal protective response to physiological stress

93
Q

Is leukocytosis more common in acute viral or bacterial infections?

A

viral (especially EBV)

94
Q

Leukopenia occurs with a WBC count that is…

A

lower than normal

95
Q

When is the presence of leukopenia normal?

A

never

96
Q

Leukopenia is defined as an absolute WBC count less than ____ x 10⁹/L

A

4.0

97
Q

What is a normal absolute WBC count?

A

4.5 to 11.0 x 10⁹/L

98
Q

Leukopenia is associated with a reduction in __________

A

neutrophils

99
Q

Reduced neutrophils = increased _________________

A

risk of infection

100
Q

A neutrophil count below ____ x 10⁹/L poses risk for a rapidly increasing infection

A

1.0

101
Q

A neutrophil count below ____ x 10⁹/L poses risk for a life-threatening infection

A

0.5

102
Q

Infectious mononucleosis (IM) is an infection of ___ lymphocytes

A

B

103
Q

Mono is b_____, acute, and self-____________

A

benign; limiting

104
Q

Which virus is responsible for 85% of mono cases?

A

Epstein-Barr virus

105
Q

Mono may also be cause by HIV, hep ____, and r_________

A

A; Rubella

106
Q

____% of all people have been infected with EBV, most in early childhood

A

95%

107
Q

Why do early EBV infections rarely develop into mono?

A

the early infection is asymptomatic and supplies the body immunity to EBV

108
Q

Why is mono called the kissing disease?

A

it is transmitted through saliva

109
Q

Why does the mono infection begin with B cells?

A

they have receptors for EBV

110
Q

Mono infection begins in the ___________ cells of the throat area and spreads to __________ tissue

A

epithelial; lymphoid

111
Q

Leukemia is a malignant disease of the _______ _______ and blood

A

bone marrow

112
Q

Leukemia is characterized by uncontrolled proliferation of ________ _________

A

malignant leukocytes

113
Q

The presence of malignant leukocytes decreases production of __________ cells

A

hematopoietic

114
Q

Chromosomal abnormalities and ___________ are common in leukemia

A

translocations

115
Q

Hematopoietic Cells

A

immature cell that can develop into all types of blood cells

116
Q

What are the 5 categories of lymphoid neoplasms defined by WHO?

A
  1. Precursor (immature) B cells
  2. Peripheral (mature) B cells
  3. Precursor (immature) T cells
  4. Peripheral (mature) T cell and NK cells
  5. Hodgkin’s Lymphoma (Reed-Sternberg cells)
117
Q

Acute leukemia involves ______________ and immature cells called ______ cells

A

undifferentiated; blast

118
Q

The onset of acute leukemia is _____ and has a _______ survival time

A

rapid; short

119
Q

Chronic leukemia involves ______________ cells that are not functionally normal

A

differentiated

120
Q

Chronic leukemia has a _______ progression

A

slow

121
Q

Most lymphoid neoplasms arise from ______________ pathways

A

differentiation

122
Q

What genetically abnormal cells drive leukemia?

A

stem-like cancer cells (SLCCs)

123
Q

Leukemias are ________ disorders

A

clonal

124
Q

Which abnormal WBCs fill bone marrow and spill into blood?

A

Leukemic blasts

125
Q

What is bone marrow pancytopenia?

A

a reduction in the production of all blood cellular components

126
Q

The Philadelphia chromosome translocation involved chromosomes ___ and ___

A

9 and 22

127
Q

The Philadelphia chromosome translocation is seen in ___% of Chronic Myeloid Leukemia and ___% of Acute Lymphocytic Leukemia

A

95%; 30%

128
Q

What is the result of the Philadelphia chromosome translocation?

A

a unique protein called BCR-ABL

129
Q

What does the BCR-ABL protein do?

A

reduces apoptosis and the release of immature cells into circulation

130
Q

Acute leukemia can be ______ or _____

A

ALL or AML

131
Q

What does acute lymphocytic leukemia (ALL) affect?

A

B cells, T cells, NK cells

132
Q

What does acute myeloid leukemia (AML) affect?

A

RBCs, platelets, eosinophils, neutrophils, and basophils

133
Q

Most cases of ALL affect…

A

children age 1-10

134
Q

Most cases of AML affect…

A

older adults

135
Q

AML results in a decreased rate of ___________ and differentiation which leaves the blood populated with dysfunctional blood cells

A

apoptosis

136
Q

What are the signs and symptoms of acute leukemia?

A

-fatigue (due to anemia)
-bleeding (due to low platelet count)
-fever (due to infections)

137
Q

Chronic lymphocytic leukemia (CLL) is a _______ growing cancer with many ________ lymphocytes in bone and blood

A

slow; immature

138
Q

What is the most common leukemia in adults in the Western world?

A

Chronic Lymphocytic Leukemia (CLL)

139
Q

Chronic myeloid leukemia is a slow developing cancer with too many _______ cells being made in bone marrow

A

myeloid

140
Q

RBCs and platelets originate from ___________ stem cells

A

myeloid

141
Q

What is the main deficit of CLL?

A

B cells fail to mature into plasma cells and thus they can’t synthesize antibodies

142
Q

What % of CLL patients can’t synthesize antibodies?

A

60%

143
Q

The main effect of CML is…

A

Philadelphia chromosome (BCR-ABL protein)

144
Q

The Philadelphia chromosome is present in ____% of CML patients

A

95%

145
Q

What is the only known cause of CML?

A

exposure to ionizing radiation

146
Q

CML has ____ phases

A

3; chronic, accelerated, terminal blast

147
Q

Stage 1 CML - Chronic Phase: lasts ___ to ___ years and may be asymptomatic

A

2 to 5

148
Q

Stage 2 CML - Accelerated Phase: lats ___ to ___ months and involves…

A

-6-18 months
-proliferation of malignant cells
-splenomegaly
-infections

149
Q

Splenomegaly

A

enlarge spleen

150
Q

Stage 3 CML - Terminal Blast phase: lasts ___-___ months before death and involves rapid __________

A

3-6; leukocytosis

151
Q

What does the spleen do?

A

control levels of WBCs, RBCs, platelets

152
Q

CLL is characterized by the accumulation on monoclonal B cells in blood which means…

A

a higher number of IDENTICAL B cells are found

153
Q

Is there a survival advantage of immediate (vs. delayed) treatment for CLL?

A

no

154
Q

Progressive CLL is treated with ____________ but it is not curative

A

chemotherapy

155
Q

______ _____ transplant achieves prolonged disease-free survival for CLL patients

A

stem cell

156
Q

Is there a cure for CML?

A

no

157
Q

With lymphadenopathy (LO), why are lymph nodes enlarged?

A

due to an increase in lymphocytes and monocytes

158
Q

Enlarged lymph nodes are palpable and ________ to touch

A

painful

159
Q

Localized LO indicates…

A

drainage from an infected area

160
Q

Generalized LO occurs less often with…

A

infection of malignant disease in adults

161
Q

Lymphadenopathy can be caused by… (4)

A
  1. neoplastic disease
  2. immune or inflammatory conditions
  3. endocrine disorders
  4. lipid storage diseases
162
Q

What does malignant mean?

A

very virulent or infectious

163
Q

Hodgkin’s and Non-Hodgkin’s lymphoma can be ____, _____, or ______ cell neoplasms

A

B, T, or NK cell

164
Q

Malignant lymphomas results from the proliferation of malignant lymphocytes into the _________ system

A

lymph

165
Q

Lymphomas result from ________ _________ or infection

A

genetic mutation

166
Q

What is the most common blood cancer in Canada?

A

lymphoma

167
Q

What factors contribute to the lymphoma incidence doubling in Canada since 1970?

A

-immune disorders
-diet
-metabolic syndrome
-environmental factors

168
Q

What is Hodgkin’s lymphoma (HL)?

A

a malignant lymphoma that progresses from one group of lymph nodes to another

169
Q

What cells are used to diagnose HL, but don’t always appear with cancer?

A

Reed-Sternberg cells (unique B cells)

170
Q

HL incidence is high in ________ with an average age of _______

A

males; 64

171
Q

HL incidence peaks at ___-___ years and ___-___

A

20-40; 60-70

172
Q

Reed-Sternberg cells are THE malignant transformed ______________

A

lymphocyte

173
Q

RS cells are _________

A

binuclear

174
Q

What triggers the mechanism for RS cell transformation?

A

unknown

175
Q

HL is caused by B cells that have not undergone SIR which is…

A

successful immunoglobulin rearrangement

176
Q

Proper SIR involves…

A

the alignment of the two light chains and two heavy chains of the antibody

177
Q

Proper SIR = proper _________ induction

A

apoptosis

178
Q

The survival of SIR is linked to ______ providing factors that expand tissue growth

A

EBV

179
Q

What is the first sign of HL?

A

enlarged painless lymph node on the neck

180
Q

Systemic HL Symptoms:

A

-fever but without infection
-night sweats
-pruritus (itchy skin)
-weight loss

181
Q

A combined appearance of HL symptoms means…

A

poor prognosis

182
Q

How is HL diagnosed?

A

complete blood count (CBC), sedimentation rate, lymph node biopsy

183
Q

What is Non-Hodgkin’s lymphoma (NHL)?

A

heterogeneous group of lymphoid tissue neoplasms with differing patterns of activity and responses to treatment

184
Q

With NHL, B, T, and NK cell neoplasms arise when?

A

at various levels of differentiation

185
Q

How does NHL differentiate from HL?

A

lack of RS cells

186
Q

What is the best description of NHL?

A

clonal expansion of B, T, and NK cells

187
Q

___ cells make up 90% of NHLs

A

B

188
Q

What are oncogenes?

A

genes that transform a cell into tumour cells

189
Q

What activates oncogenes?

A

translocations

190
Q

NHL spreads in an _____________ manner and _______

A

unpredictable; early

191
Q

What is the most common NHL?

A

B cell NHL

192
Q

What are the risk factors of NHL?

A

-old, male, white
-autoimmune disease
-cancer related virus infection (HIV, EBV, hep C)
-immune suppressants related to organ transplant
-H. pylori infection

HLSC 222 - Pathophysiology Across the Lifespan (17 decks)

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