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Pathophysiology > Alteration In Hematological Function > Flashcards

Alteration In Hematological Function Flashcards

1
Q

Alterations of erythrocyte (2)

A

-insufficient or excessive
-normal number of cells, with abnormal components

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2
Q

Anemias

A

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

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3
Q

Polycythemias

A

Erythrocyte numbers or volume is excessive

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4
Q

Leukocytosis

A

Increased numbers of leukocytes
-in response to infections

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5
Q

Example of leukocytosis

A

Proliferation disorder such as leukaemia

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6
Q

Function of clotting

A

To stop bleeding

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7
Q

Clotting

A

Interaction between endothelium, platelets, and clotting components

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8
Q

Terms ending in -cytic

A

Refer to cell size

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9
Q

Terms ending in chromic

A

Refer to hemoglobin content

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10
Q

Anisocytosis

A

Varying in size

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11
Q

Poikilocytosis

A

Assuming various shapes

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12
Q

Manifestations of anemia

A

-reduced O2 carrying capacity of blood
-reduction in consistency and volume
-blood flow faster
-increases heart rate and stroke volume

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13
Q

Result of blood viscosity decreasing

A

Increased heart rate and stroke volume

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14
Q

Hypoxemia

A

Reduced oxygen levels in the blood

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15
Q

What does the body to do compensate for hypoxemia

A

Dilation of vessels
-Dec systemic resistance
-inc blood flow, heart rate and stroke volume

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16
Q

Hypoxemia compensation can result in

A

Heart failure

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17
Q

Maccrocytic-normochromic

A

Large stem cells (megaloblasts) in bone marrow that form unusually large RBC
-normal content of hemoglobin

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18
Q

Macrocytic-normochromic is caused by

A

Ineffective RBC DNA synthesis
-defective vitamin B and folic acid

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19
Q

Result of macrocytic-normochromic

A

Affected RBC die in circulation, decreasing RBC in blood and causing anemia

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20
Q

Eryptosis

A

Premature death of damaged erythrocytes

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21
Q

Erythroblasts require ___ and ____ for proliferation during their differentiation

A

Folate, vitamins B12

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22
Q

What is the most common macrocyclic type caused by vitamin B deficiency

A

Pernicious anemia

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23
Q

Pernicious

A

Highly injurious or destructive

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24
Q

Look at diagram on slide nine

A

Draw it out

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25
Q

Pernicious anemia

A

Autoimmunity condition
-produce antibodies against parietal cells

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26
Q

What do parietal cells produce

A

Intrinsic factor

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27
Q

What is the purpose for intrinsic factor

A

It is required for absorption of vitamin B12, which is required for DNA synthesis in RBC

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28
Q

Pernicious anemia may also be result of

A

Past infection of H.pylori

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29
Q

Manifestations of Pernicious anemia

A

slow developing, usually severe once noticed

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30
Q

Early symptoms of Pernicious anemia

A

Often ignored as they are non specific

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31
Q

Normal Hb levels

A

> 120 g/L

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32
Q

When Hb levels reach _____ patient experiences classic Pernicious anemia symptoms

A

70-80 g/L

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33
Q

Classic Pernicious anemia symptoms

A

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

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34
Q

Paresthesia

A

Tingling, prickling feeling

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35
Q

Symptoms of Pernicious anemia are

A

Irreversible

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36
Q

Folate or folic acid

A

Essential vitamin for RBC RNA and DNA synthesis
-coenzyme

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37
Q

Folates are coenzymes required for synthesis of

A

Thymine and purines
-which affect RBC undergoing rapid cell reproduction

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38
Q

What are humans daily folate requirement (found in diet)

A

50-200 mg/day

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39
Q

Manifestations of folate deficiency anemia

A

-Similar to malnourished appearance
-scales on mouth and burning mouth syndrome

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40
Q

Burning mouth syndrome presents as

A

Red beefy tongue

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41
Q

TX for folate deficiency anemia

A

Oral folate administration
-effective administration anaemia will disappear in 1-2 weeks

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42
Q

Microcytic hypochromic anemias

A

Abnormally small RBC with reduced amounts of Hb

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43
Q

What does Microcytic hypochromic anemias cause

A

-Iron metabolism disorders
-heme synthesis disorders
-globin synthesis disorders

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44
Q

Result of Microcytic hypochromic anemias

A

Iron deficiency anemia
-thalassemia

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45
Q

Thalassemia

A

Inherited disorder causing reduced hemoglobin

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46
Q

Iron deficiency anemia is caused by

A

Chronic blood loss, or inadequate iron intake
-not related to intrinsic dysfunction of iron metabolism

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47
Q

Metabolic iron deficiency

A

Insufficient iron delivery to bone marrow or impaired iron absorption into bone marrow
-dysfunction in iron metabolism

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48
Q

What amount of blood loss can cause IDA

A

2-4 mL/day

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49
Q

Can Iron be recycled? what potentially disrupts this balance?

A

Yes
-blood loss disrupts this balance

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50
Q

Iron deficiency anemia: reasons for iron deficiency (four things)

A

-medications causing GI bleeding (aspirin, NSAIDS)
-surgery decreasing transit time and absorption
-insufficient iron intake
-pica

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51
Q

Pica

A

Disorder causing the eating of non nutritional substances
-dirt, chalk, paper

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52
Q

IDA stage one

A

Iron stores depleted, RBC production remains normal

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53
Q

IDA stage 2

A

Insufficient iron transported to marrow, iron deficient RBC production begins

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54
Q

Stage 3 IDA

A

Hemoglobin deficient RBC begin to replace normal RBC that are being destroyed
-anemia occurs

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55
Q

Iron deficiency anemia is not noticed until (what levels of Hb)

A

70-80 g/L of Hb

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56
Q

IDA classic symptoms

A

-structural changes in epithelial tissue
-koilonychia (finger nails brittle and shaped like spoon)
-glossitis (tongue papillae atrophy)
-dysphasia due to web of mucus

57
Q

How do you diagnose IDA (indirect, direct)

A

Indirect : measurement of serum levels of ferritin, trasnferrin saturation or total iron binding capacity

DIrect: iron stores measure by bone marrow biopsy

58
Q

TX for iron deficiency anemia

A

Eliminate sources of blood loss
-iron replacement therapy until ferritin level reaches 50 ug/L

59
Q

Ug/L

A

millionth of a gram/litre

60
Q

Normocytic-normochromic anemias

A

Characterized by normal size and normal Hb levels, but insufficient in numbers

61
Q

Aplastic anemia

A

Infiltrative disorders of bone marrow

62
Q

Posthemorrhagic

A

Sudden blood loss with normal iron stores

63
Q

Acquired hemolytic

A

Destruction of RBC
-developed after birth

64
Q

Hereditary hemolytic

A

Destruction of RBC
-sickle cell anemia

65
Q

Hemolysis

A

Destruction by eryptossi
-premature death of damaged erythrocytes

66
Q

Four normocytic normochromic anemias

A
  1. Aplastic
  2. Posthemorrhage
  3. Hemolytic
  4. Chronic inflammation
67
Q

Draw out diagram on slide 21

A

Now

68
Q

When are we affected by alterations in quantity of leukocytes

A

Too many or too few or structurally defective

69
Q

Leukocytosis

A

WBC count is higher than normal
-due to normal protective response to physiological stressors

70
Q

When is leukocytosis rare vs more common?

A

Rare: acute bacterial infection

More common: in acute viral infections (especially EBV)

71
Q

Lekopenia

A

WBC count is lower than normal
-this is never a normal response

72
Q

Leukopenia vs normal wbc

A

L: <4.0 x 10^9/L

Normal: 4.5 to 11 x 10^9/L

73
Q

Leukopenia is associated with reduction in

A

Neutrophils

74
Q

Neutrophil count below 1.0 x 10^9/L

A

Infection increases rapidly

75
Q

Neutrophil count below 0.5 x 10^9/L

A

Life threatening infection

76
Q

Infectious mononucleosis

A

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

77
Q

Common causes of Infectious mononucleosis

A

EBV (most likely), HIV, HEP A, Rubella

78
Q

____ percent of all humans infected with EBV occurs during childhood

A

95%

79
Q

Early infections are ____ and supply _____ to EBV

A

-asymptomatic
-immunity

Rarely develops into Infectious mononucleosis

80
Q

What is Infectious mononucleosis called in teenagers and YA

A

Kissing disease since it travels through saliva

81
Q

Infectious mononucleosis infection begins with invasion of

A

B cells which have receptors for EBV
-firstly appears in throat area and then spreads to lymphoid tissues

82
Q

Life cycle of EBV (five steps)

A
  1. Infection
  2. Transformation and establishment of viral latency
  3. Proliferation
  4. Lyric cycle and virion release
  5. Travel into B cell (repeat)
83
Q

Leukaemia

A

Malignant disorder of bone marrow and usually also blood

84
Q

Main features of leukaemia

A

Uncontrolled proliferation of malignant leukocytes
-decreasing production of hematopoietic cells

85
Q

WHO guidlines five categories of leukaemia

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 neoplasms (both mature)
  5. HOdgkins lymphoma (reed-sternberg cells)
86
Q

Hematopoietic cells

A

Immature cell that can develop into all types of blood cells

87
Q

Acute leukaemia

A

undifferentiated and immature cells (blast cells)
-onset of disease is RAPID
-short survival time

88
Q

Chronic leukaemia

A

More differentiated cells but not functionally normal
-slow progression

89
Q

Most lymphoid neoplasms arise from

A

Arise from B cells and T cells

90
Q

Leukaemia are clonal disorders driven by

A

Genetically abnormal stem like cancer cells

91
Q

Leukemic blasts

A

Abnormal WBC that fills bone marrow and spills into blood

92
Q

Normal bone marrow cells cease to function resulting in

A

Pancytopenia
-reduction in production of all blood cellular components

93
Q

Leukaemia mutation occurs in

A

Philadelphia chromosome translocation
-chromosome 9 and 22

94
Q

Pdiledelphia cheomsome translocation percentage

A

95% in chronic myeloid leukaemia, 30% acute lymphocytic leukaemia

95
Q

Result of leukaemia mutations

A

Production of a unique protein (BCR-ABL) reduces apoptosis and releases immature cells into circulation

96
Q

ALL

A

Acute lymphocytic leukaemia
-affects B cells, T cells, NK cells

97
Q

AML

A

Acute myeloid leukaemia
-affects RBC, platelets, eosinophils, neutrophils, basophils

98
Q

Most cases of ALL are in

A

Children
1-10 yoa

99
Q

Most cases of AML are in

A

Older adults

100
Q

AML has a decreased rate of

A

Apoptosis
-differentiation in affected cells cause blood to be populated with dysfunctioned blood cells

101
Q

Signs and symptoms of acute leukaemia

A

Fatigue (anemia)
-bleeding due to lower platelet count
-fever due to infections bc of dysfunctional immune response

102
Q

CLL or chronic lymphocytic leukaemia

A

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

103
Q

What is the most common leukaemia in adults

A

Chronic leukaemia
-western world

104
Q

CML or chronic myeloid leukaemia

A

Slow developing cancer
-too many myeloid cells (RBC and platelets) being made in bone marrow

105
Q

CLL main deficit

A

B cells fail to mature into plasma cells
-inability to synthesize antibodies

106
Q

CML main effect

A

Philadelphia chromosome and presence of BCR-ABL protein (95%)

107
Q

Only known cause of CML

A

Exposure to ionizing radiation

108
Q

Chronic phase of CML

A

2-5 years
May be asymptomatic

109
Q

CML Accelerated phase

A

6-18 months
-proliferation of malignant cells
-splenomegaly (enlarged spleen) develops
-infections

110
Q

CML terminal blast phase

A

Survival 3-6 months
-rapid and progressive leukocytosis (inc in number of WBC)

111
Q

Spleen controls

A

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

112
Q

Diagnosis of CLL

A

CLL is characterized by accumulation of of monoclonal B cells in blood

113
Q

Monoclonal B cells

A

Condition in which a higher than normal number of identical B cells are found in blood

114
Q

Progressive CLL TX

A

Chemotherapy
-not curative

115
Q

TX for CLL

A

Stem cell transplant has achieved prolonged disease free survival

116
Q

CML TX

A

Current modalities do not cure the disease

117
Q

Lymphadenopathy is characterized by

A

Enlarged lymph nodes, due to an inc in lymphocytes and monocytes
-palpable and painful

118
Q

Localized LO

A

Indicates drainage from an infected area

119
Q

Generalized LO

A

Occurs less often
-generally with occurrence of infection/malignant disease in adults

120
Q

Causes of LO

A
  1. Neoplastic disease
  2. Immune or inflammatory conditions
  3. Endocrine disorders
  4. Lipids storage diseases
121
Q

Basic groups of Hodgkin and Non Hodgkin

A

B cell, T cell, NK cell neoplasms

122
Q

Malignant lymphomas

A

Proliferation of malignant lymphocytes in lymph system

123
Q

Lymphomas are a result of

A

Genetic mutation of infection

124
Q

Result of malignant lymphomas

A

Cell with uncontrolled and excsssive growth accumulates in lymph nodes

125
Q

Most common blood cancer in Canada

A

Lymphoma

126
Q

Two classifications of lymphoma

A

Hodgkin lymphoma, non Hodgkin lymphoma

127
Q

Hodgkin lymphoma

A

Progresses from one group of lymph node to another
-unique B cells (reed sternberg) used to diagnosis but not always there

128
Q

Hodgkin lymphoma incidence is higher in

A

Males
Media age: 64 (20-40) (60-70)

129
Q

RS cells

A

Are the alignment transformed lymphocyte
-binuclaer cells used diagnosis

130
Q

HL appears to be derived from

A

B cells that have no undergone successful immunoglobulin rearrangement

131
Q

SIR

A

Proper alignment of the two light chains and two heavy chains of antibody
-proper SIR would induce proper apoptosis
-EBV factors and expand tissue growth

132
Q

Manifestations of HL

A

Enlarged painless lymph node on neck

133
Q

Common systemic symptoms HL

A

-fever without infection
-drenching night sweats
-itchy sin (pruritis)
-weight loss
-combined appearance of these symptoms = poor prognosis

134
Q

Diagnosis of HL

A

Blood work: complete blood count, sedimentation rate, lymph node biopsy

135
Q

Nonhodgkins lymphoma

A

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

136
Q

B cell, T cell, NK cell neoplasms WHO definition

A

Origination from (B/T/NK cells) at various levels of differentiation

137
Q

NHL cancers are differentiated from

A

HL primarily by a lack of reed sternberg cells

138
Q

Nonhodgkins lymphoma path physiology

A

Best described as progressive colonial expansion of B, T and NK cells
-oncogenes activated by translocation
-unpredictable spreading easily

139
Q

Risk factors of Nonhodgkins lymphoma

A

-old male and white
-autoimmune
-HIV, EBV, Hep C
-organ transplants, immune suppressants
-gastric infection and H. Pylori

Pathophysiology (20 decks)

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