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HLSC 222 Pathophysiology 🧫 > Chapter 21- Alteration in Haematological function > Flashcards

Chapter 21- Alteration in Haematological function Flashcards

1
Q

What are some alterations in eythrocytes?

A

Anemias
Polycythemias

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2
Q

What are Anemias?

A

Condition of too few erythrocytes or an insufficient volume of them in blood

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3
Q

What are Polycythemias?

A

Erythrocyte (RBC) numbers or volume is excessive

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4
Q

What are some alterations in Leukocytes?

A

Leukocytosis
proliferative disorders

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5
Q

What is Leukocytosis?

A

Increased numbers of leukocytes (response to infections, etc.)

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6
Q

What is an example of a proliferative disorder altering leukocytes?

A

Leukemia

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7
Q

What is the purpose of clotting?

A

To stop bleeding

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8
Q

What is clotting?

A

interaction between endothelium, platelets and clotting componenets

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9
Q

What do clotting disorders result from?

A

Alterations in any of the three components
-Endothelium, platelets and clotting

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10
Q

Anemia

A

reduction in the total number of RBCs in blood or decrease in quality or quantity of hemoglobin

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11
Q

How is anemia classified?

A

Based on changes that affect cells’ size and hemoglobin content

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12
Q

What do terms that end in ‘cytic’ refer to?

A

Cell size

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13
Q

What do terms that end in ‘chromic’ refer to?

A

Hemoglobin content

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14
Q

Anisocytosis

A

RBCs varying in size

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15
Q

Poikilocytosis

A

RBCs assuming various shapes

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16
Q

What is the main alteration caused by anemia?

A

Reduced oxygen-carrying capacity of blood

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17
Q

What is the effect of reduced RBC concentration in blood?

A

Reduction in consistency and volume of blood

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18
Q

What is the end result of reduced RBC concentration?

A

Decreased blood viscosity
Blood flows faster

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19
Q

What is the effect of blood flowing faster as a result of anemia?

A

Increased heart rate
Increased stroke volume

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20
Q

Hypoxemia

A

Reduced oxygen levels in the blood

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21
Q

How does the body compensate for hypoxemia?

A

Dilation of vessels
—> Decreased systemic resistance
Increased blood flow through vessels
Increased blood flow to the heart
Increased heart rate and stroke volume

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22
Q

Compensation of Hypoxemia can result in ____ ______?

A

Heart failure

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23
Q

What are 3 kinds of Anemias?

A
  1. Macrocytic-Normochromic Anemias
  2. Microcytic-Hypochromic Anemia
  3. Normocytic-Normochromic Anemia
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24
Q

What is Macrocytic-Normochromic Anemia?

A

Large stem cells (megaloblasts) in bone marrow that form unusually large RBC

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25
Q

Macrocytic-Normochromic Anemia: Hemoglobin?

A

Normal content of hemoglobin

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26
Q

What causes Macrocytic-Normochromic Anemia?

A

Ineffective RBC DNA synthesis

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27
Q

What leads to ineffective RBC DNA synthesis?

A

Vit B and Folic acid deficiencies

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28
Q

What is the result of ineffective RBC DNA synthesis?

A

Affected RBC die in circulation ultimately decreasing RBC concentration and leading to anemia

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29
Q

What is Eryptosis?

A

Premature death of damaged erythrocytes

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30
Q

What are some Macrocytic-Normochromic Anemias?

A

Pernicious Anemia
Folate Deficiency Anemia

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31
Q

What is the most common Macrocytic type of anemia?

A

Pernicious Anemia (PA)

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32
Q

What causes Pernicious Anemia?

A

Vit B deficiency

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33
Q

Pernicious

A

Highly injurious or destructive

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34
Q

What is Pernicious anemia?

A

An autoimmune condition that prevents your body from absorbing vitamin B12

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35
Q

How does pernicious anemia prevent the absorption of Vit B12?

A

PA individuals produce antibodies against parietal cells
—> Parietal cells produce intrinsic factor
—> Intrinsic factor required for Vit B12 absorption

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36
Q

What is Vitamin B12 needed for?

A

DNA synthesis in RBC

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37
Q

What past bacterial infection can cause Pernicious anemia?

A

H. pylori

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38
Q

How does Pernicious Anemia develop?

A

Slowly over 20-30 years
-Situation is severe when the patient gets treatment

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39
Q

Describe pernicious anemia early symptoms.

A

Non-specific and often ignored

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40
Q

What are Normal Hb lvels?

A

> 120 g/L

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41
Q

What is the Hb level of someone with PA when they start to experience classic symptoms?

A

70-80g/L

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42
Q

What are the classic symptoms of Pernicious Anemia?

A

Fatigue
Paresthesia of feet and fingers
Abdominal pain
Nerve demyelination

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43
Q

Paresthesia

A

Tingling, prickling feeling

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44
Q

Are symptoms of PA reversible?

A

No
They are irreversible

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45
Q

What is Folate deficiency anemia?

A

Folic acid (folate) deficiency affecting RBC production

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46
Q

What is Folate’s purpose?

A

Essential vitamin for RBC, RNA and DNA synthesis

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47
Q

What are folates?

A

Coenzymes that are required for synthesis of thymine and purines which affects RBC undergoing rapid cell reproduction

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48
Q

How do humans meet daily folate requirements?

A

Entirely depends on diet

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49
Q

What is the daily folate requirement?

A

50-200mg/day

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50
Q

What is folate deficiency anemia similar to appearance wise?

A

Malnourished appearance

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51
Q

What is a specific manifestation of folate deficiency anemia?

A

Scales on mouth and burning mouth syndrome
(red beefy tongue)

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52
Q

How is folate deficiency anemia treated?

A

Oral folate administration

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53
Q

if treatment/administration is effective what happens to folate deficiency anemia?

A

Anemia disappears in 1-2 weeks

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54
Q

What are Microcytic Hypochromic Anemias?

A

Abnormally small RBC

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55
Q

Microcytic Hypochromic Anemias: Hemoglobin?

A

Reduced amounts of Hb

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56
Q

What causes Microcytic Hypochromic Anemias?

A

iron metabolism disorders
-heme synthesis disorders
-globin synthesis disorders

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57
Q

What is the result of iron metabolism disorders?

A

iron deficeny anemia
Thalassemia

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58
Q

Thalassemia

A

An inherited disorder causing reduced hemoglobin concentration

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59
Q

What causes Iron deficiency anemia?

A

Chronic blood loss
Inadequate iron intake
Metabolic iron deficiency

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60
Q

Is chronic blood loss/inadequate iron intake related to iron metabolism dysfunction?

A

No
-They have no intrinsic dysfunction of iron metabolism

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61
Q

What is metabolic iron deficiency?

A

Dysfunction in iron metabolism
-insufficient iron delivery to bone marrow or impaired iron absorption into bone marrow

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62
Q

How much blood needs to be lost to cause iron deficiency anemia?

A

2-4mL/day

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63
Q

How does blood loss lead to iron deficiency anemia?

A

Normally iron can be recycled by blood loss disrupts this balance

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64
Q

What can cause iron deficiencies?

A

Medications causing GI bleeding
Surgical procedures
Insufficient iron intake
Pica

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65
Q

What kind of surgical procedures lead to iron deficiency?

A

Procedures that decrease transit time and absorption

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66
Q

What kind of mediactions cause GI bleeding and lead to iron deficiency?

A

Aspirin
NSAIDS

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67
Q

What is Pica?

A

disorder causing the eating of non-nutritional substances (dirt, chalk, paper)

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68
Q

Iron deficiency anemia is developped in how many stages?

A

3

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69
Q

Iron deficiency anemia development: Stage 1?

A

irons stores depleted
RBC production remains normal

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70
Q

Iron deficiency anemia development: Stage 2?

A

Insufficient iron transported to bone marrow
iron-deficient RBC production begins

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71
Q

Iron deficiency anemia development: Stage 3?

A

Hemoglobin-deficient RBC begin to replace normal RBCs that are being destroyed
-Anemia

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72
Q

What stage of IDA development does anemia occur?

A

Stage 3

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73
Q

At what level of Hb is Iron deficiency Anemia noticed?

A

70-80 g/L
-This is when the patient experiences classic symptoms

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74
Q

What are some symptoms of progressive reductions in Hb level?

A

Structural changes in epithelial tissue
Koilonychia
Glossitis
Dysphagia

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75
Q

Koilonychia

A

Finger nails become brittle and “spoon-shaped”

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76
Q

Glossitis

A

Tongue papillae atrophy

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77
Q

What is the dysphagia associated with reductions in Hb level caused by?

A

Web of mucus and inflammatory cells at esophageal opening

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78
Q

How is Iron deficiency anemia directly diagnosed?

A

iron stores measure by bone marrow biopsy

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79
Q

How is iron deficiency anemia indirectly diagnosed?

A

Measurement of serum levels of…
-Ferritin
-Transferrin saturation
-or Total iron-binding capacity

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80
Q

What is the first step in iron deficiency anemia treatment?

A

Eliminate the source of blood loss

81
Q

What is the second step in iron deficiency anemia treatment?

A

iron replacement therapy until serum ferritin level reaches 50 ug/L
(50 millionth of a gram/Liter)

82
Q

What is Normocytic Normochromic anemias?

A

Normal size and normal hemoglobin content but insufficient in numbers

83
Q

What are the four distinct normocytic normochromic anemias?

A

Aplastic
Posthemorrhagic
Hemolytic
Chronic inflammation

84
Q

What is aplastic anmeia?

A

Infliltrative disorders of bone marrow
-Body stops producing enough new blood cells

85
Q

What is posthemorrhagic anemia?

A

Sudden blood loss with normal iron states

86
Q

What are the 3 subdivisions of hemolytic anemia?

A

Acquired
Hereditary
Hemolysis

87
Q

What is acquired hemolytic anemia?

A

Destruction of RBC developed after birth
-Not congenital/hereditary

88
Q

What is hemolytic hereditary anemia?

A

Destruction of RBC inherited
e.g Sickle cell anemia

89
Q

What is hemolysis?

A

Destruction of RBC by erytosis

90
Q

Erytosis

A

Premature death of damaged erythrocytes

91
Q

What is chronic inflammation anemia?

A

Inflammatory disease

92
Q

Leukocytosis

A

WBC count is higher than normal
-Causes
-Symptoms

93
Q

Why does leukocytosis occur?

A

Normal protective response to physiological stressors

94
Q

When does leukocytosis rarely happen?

A

Rarely in acute bacterial infection

95
Q

When does leukocytosis commonly happen?

A

Acute viral infections
Especially Epstein-Barr virus

96
Q

When do alterations in leukocytes affect people?

A

If there are too many or too few WBCs present in the blood
If WBCs in blood are structurally/functionally defective

97
Q

What is Leukopenia?

A

WBC count is lower than normal
Absolute WBC count <4.0 x 10^9

98
Q

Is the presence of Leukopenia normal?

A

NO its presence is never normal

99
Q

What is the normal WBC count?

A

4.5 to 11.0 x 10^9/L

100
Q

Increased risk of infection is associated with what?

A

Reduction in neutophils

101
Q

When does infection increase rapidly?

A

Neutrophil count below 1.0 x 10^9/L

102
Q

When does the possibility of life-threatening infection occur?

A

Neutrophil count below 0.5 X 10^9/L

103
Q

What is Infectious mononucleosis? (IM)

A

Benign, acute, self-limiting characterised by infection of B-lymphocytes

104
Q

What is a common cause of Infectious mononucleosis?

A

Epstein-Barr virus (EBV)
-85% of IM

105
Q

What are other less common causes of IM?

A

HIV
Hepatitis A
Rubella

106
Q

What percentage of people who get EBV, are infected during early childhood?

A

95%

107
Q

Do most EBv cases develop into IM and why?

A

No, EBV rarely develops into IM because early infections asymptomatic and supply immunity to EBV

108
Q

How is EBV transmitted in teenagers and young adults?

A

Through saliva
-aka Kissing disease

109
Q

How does EBV infection begin?

A

Invasion of B cells which have receptors for EBV

110
Q

Where does EBV infection first appear?

A

In throat area epithelial cells and spreads to lymphoid tissues

111
Q

life-cycle of EBV

A
112
Q

What is leukemia?

A

Malignant, very infec tious disorder of bone marrow and usually blood

113
Q

What is the main feature of leukemia?

A

The main feature is the uncontrolled proliferation of malignant leukocytes causing decreased production of hematopoietic cells

114
Q

What is common in leukemia?

A

Chromosomal abnormalities and translocations

115
Q

How do WHO guidelines divide lymphoid neoplasms?

A

Five categories defined by cell of origin

116
Q

What are the 5 categories of lymphoid neoplasms?

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

What are hematopoietic cells?

A

Immature cells that can develop into all types of blood cells

118
Q

What are the 2 kinds of leukemia?

A

Acute
Chronic

119
Q

What is acute leukemia?

A

undifferentiated and immature cells (blast cells)
the onset of disease is rapid
short survival time

120
Q

What is chronic leukemia?

A

more differentiated cells but not functionally normal
-slow progression

121
Q

What do most lymphoid neoplasms arise from?

A

B-cells and T-cell differentiation pathways

122
Q

What kind of disorders are leukemias?

A

Clonal disorders are driven by genetically abnormal stem-like cancer cells (SLCCs)

123
Q

During leukemia, what are the abnormal WBCs called?

A

Leukemic blasts

124
Q

What do leukemic blasts do?

A

Fill bone marrow and spill into the blood

125
Q

What happens when normal bone marrow cells stop functioning during leukemia infection?

A

Pancytopenia

126
Q

What is Pancytopenia?

A

Reduction in production of all blood cellular components

127
Q

After pancytopenia, what occurs during leukemia infection?

A

Translocations occur

128
Q

What kind of translocation can occur during leukemia infection?

A

Philadelphia chromosome translocations

129
Q

What chromosomes are involved in Philadelphia chromosome translocations?

A

Chromosome 9 and 22

130
Q

What kind of leukemia has a 95% chance of Philadelphia chromosome translocations?

A

Chronic myeloid leukemia

131
Q

What kind of leukemia has a 30% chance of Philadelphia chromosome translocations?

A

Acute Lymphocytic Leukemia

132
Q

What is the result of leukemia chromosome mutations?

A

Unique protein (BCR-ABL) results in reduced apoptosis and release of immature cells into circulation

133
Q

What are the two types of acute leukemia?

A

ALL: Acute Lymphocytic Leukemia
AML: Acute Myeloid Leukemia

134
Q

What cells are affected by Acute Lymphocytic Leukemia?

A

B-cells
T-cells
NK cells

135
Q

What cells are affected by Acute Myeloid Leukemia?

A

RBC
Platelets
Eosinophils
Neutrophils
Basophils

136
Q

Who are most cases of ALL?

A

Children
1-10 years old

137
Q

Who are most cases of AML?

A

Older adults

138
Q

AML has a decreased rate of what?

A

Apoptosis and differentiation in affected cells

139
Q

Because of decreased apoptosis/differentiation AML people blood becomes?

A

Populated with dysfunctional blood cells

140
Q

Signs/symptoms of Acute leukemia?

A

Fatigue
Bleeding
Fever

141
Q

What causes acute leukemia fatigue?

A

Anemia

142
Q

What causes acute leukemia bleeding?

A

Low platelet count

143
Q

What causes acute leukemia fever?

A

Infections caused by dysfunctional immune response

144
Q

What are the 2 kinds of chronic leukemia?

A

CLL: Chronic Lymphocytic leukemia
CML: Chronic Myeloid leukemia

145
Q

What is Chronic Lymphocytic leukemia

A

Slow-growing cancer with too many immature lymphocytes found cells in bone and blood

146
Q

What is the most common leukemia in the Western world IN ADULTS?

A

Chronic Lymphocytic leukemia

147
Q

What is Chronic Myeloid Leukemia?

A

Slow developing cancer
Too many myeloid cells (RBC and Platelets) being made in bone marrow

148
Q

What is the main deficit in CLL?

A

B cells fail to mature into Plasma cells

149
Q

What affects 60% of patients with CLL?

A

Inability to synthesize antibodies.

150
Q

What is the main effect of CML?

A

Philadelphia chromosome and presence of BCR-ABL protein (present in 95% of CML patients)

151
Q

What is the only known cause of CML?

A

exposure to ionizing radiation

152
Q

What are the 3 CML phases?

A
  1. Chronic Phase
  2. Accelerated Phase
  3. Terminal Blast Phase
153
Q

What is the chronic phase (CML)?

A

Lasts 2-5 years
May be asymptomatic

154
Q

What is the accelerated phase of CML?

A

Lasts 6-18months
Proliferation of malignant cells
Splenomegaly
Infections

155
Q

Splenomegaly

A

Enlarged spleen

156
Q

What is the terminal phase of CML?

A

Survival 3-6 months
Rapid and progressive leukocytosis (increased WBC count)

157
Q

What does the spleen control?

A

Blood level of white blood cells, red blood cells and platelets

158
Q

How is CLL diagnosed?

A

Tests for accumulation of monoclonal B cells in blood

159
Q

What are monoclonal B cells?

A

condition in which a higher-than-normal number of identical B cells are found in blood.

160
Q

Is there a survival advantage for immediate versus delayed treatment of CLL?

A

No

161
Q

How is Progressive CLL treated?

A

Chemotherapy
-Its not curative

162
Q

What has achieved prolonged disease-free treatment of CLL?

A

Stem cell transplants

163
Q

How is CML treated?

A

Not very treatable
-Current modalities do not cure the disease

164
Q

What is Lymphadenopathy? (LO)

A

Enlarged lymph nodes due to an increase in lymphocytes and monocytes

165
Q

Lymphadenopathy enlarged lymph nodes are?

A

Palpable and painful to touch

166
Q

What does localized LO indicate?

A

Drainage from an infected area

167
Q

When does Generalized LO occur?

A

Occurs less often
With the occurrence of infection or malignant disease in adults

168
Q

What are the causes of Lymphadenopathy (LO)?

A
  1. Neoplastic disease
  2. Immune or inflammatory conditions
  3. Endocrine disorders
  4. Lipid storage diseases
169
Q

Malignant

A

very virulent or infectious

170
Q

What are the 2 classifications of malignant lymphomas?

A

Hodgkin’s
Non-Hodkin’s

171
Q

What are the basic groups of Hodgkin’s and Non-Hodkin’s?

A

B-cell neoplasms
T-cell neoplasms
NK-cell neoplasms

172
Q

What are maliganant lymphomas?

A

Proliferation of malignant lymphocytes in lymph system

173
Q

Lymphomas are the result of what?

A

Genetic mutation of infection which causes cell with uncontrolled and excessive growth to accumulate in lymph nodes

174
Q

What is the most common blood cancer in Canada?

A

Lymphoma

175
Q

How much has the Canadian incidence of Lymphoma increased since 1970?

A

Double since 1970

176
Q

What has the Canadian incidence of lymphoma increased?

A

Immune disorders
Diet
metabolic syndrome
Environmental factors

177
Q

What are Hodgkin’s lymphoma?

A

Malignant lymphoma that progresses from one group of lymph nodes to another

178
Q

Presence of what cells are used to diagnose HL but don’t always appear with cancer?

A

Unique B cells called Reed-Sternberg cells

179
Q

Which gender is the incidence of Hodgkin’s lymphoma higher?

A

Male

180
Q

What is the median age for HL?

A

Median = 64
Peaks: 20-40 and 60-70 yoa

181
Q

What are Reed-Sternberg cells?

A

Large binuclear B cells

182
Q

What type of cell is accepted as the malignant transformed lymphocyte in Hodgkin’s Lymphoma (HL)?

A

Reed-Sternberg cells

183
Q

What is the triggering mechanism for the transformation of Reed-Sternberg (RS) cells in Hodgkin’s Lymphoma (HL)?

A

The triggering mechanism for cell transformation is unknown

184
Q

What is Hodgkin’s Lymphoma derived from?

A

B cells that have not undergone Successful Immunoglobulin Rearrangement (SIR)

185
Q

What is SIR?

A

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

186
Q

What does proper SIR induce?

A

Apoptosis

187
Q

What is the survival of SIR linked to?

A

EBV providing factors that expand tissue growth

188
Q

What is the first sign of HL?

A

Enlarged painless lymph node on neck

189
Q

What are the common systemic symptoms of HL?

A

Fever without infection
Drenching night sweats
Itchy skin (Pruritus)
Weight loss

-Combined appearance of these symptoms = poor prognosis

190
Q

How is HL diagnosed with blood work?

A

Complete blood count (CBC), sedimentation rate and lymph node biopsy

191
Q

What are Non-Hodgkin’s Lymphoma?

A

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

192
Q

What are WHO classifications of NHL?

A

cell neoplasms: originate from B cells at various levels of differentiation
T cell neoplasms: originate from T cells at various levels of differentiation
NK-cell neoplasms: originate NK cells at various levels of differentiation

193
Q

How are NHL and HL differentiated from one another?

A

NHL lack Reed-sternberg cells

194
Q

What is the best way to describe NHLs?

A

A progressive clonal expansion of B, T and NK cells

195
Q

What percentage of NHLs are from B-cells?

A

90%

196
Q

What activates oncogenes during NHLs?

A

Translocations

197
Q

How does NHL spread?

A

Unpredictable manner and spreads early (unlike HL)

198
Q

What is the most common NHL?

A

Diffuse B cell NHL

199
Q

What are risk factors of NHL?

A

Old, male and white
Autoimmune disease
Infection of cancer-related virus (HIV, EBV, Hep C)
Immune suppressants bc of Organ transplant
Gastric infection with H. pylori

HLSC 222 Pathophysiology 🧫 (16 decks)

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