Alteration In Hematological Function Flashcards
(139 cards)
1
Q
Alterations of erythrocyte (2)
A
-insufficient or excessive
-normal number of cells, with abnormal components
2
Q
Anemias
A
Conditions of too few erythrocytes or an insufficient volume of them in blood
3
Q
Polycythemias
A
Erythrocyte numbers or volume is excessive
4
Q
Leukocytosis
A
Increased numbers of leukocytes
-in response to infections
5
Q
Example of leukocytosis
A
Proliferation disorder such as leukaemia
6
Q
Function of clotting
A
To stop bleeding
7
Q
Clotting
A
Interaction between endothelium, platelets, and clotting components
8
Q
Terms ending in -cytic
A
Refer to cell size
9
Q
Terms ending in chromic
A
Refer to hemoglobin content
10
Q
Anisocytosis
A
Varying in size
11
Q
Poikilocytosis
A
Assuming various shapes
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
13
Q
Result of blood viscosity decreasing
A
Increased heart rate and stroke volume
14
Q
Hypoxemia
A
Reduced oxygen levels in the blood
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
16
Q
Hypoxemia compensation can result in
A
Heart failure
17
Q
Maccrocytic-normochromic
A
Large stem cells (megaloblasts) in bone marrow that form unusually large RBC
-normal content of hemoglobin
18
Q
Macrocytic-normochromic is caused by
A
Ineffective RBC DNA synthesis
-defective vitamin B and folic acid
19
Q
Result of macrocytic-normochromic
A
Affected RBC die in circulation, decreasing RBC in blood and causing anemia
20
Q
Eryptosis
A
Premature death of damaged erythrocytes
21
Q
Erythroblasts require ___ and ____ for proliferation during their differentiation
A
Folate, vitamins B12
22
Q
What is the most common macrocyclic type caused by vitamin B deficiency
A
Pernicious anemia
23
Q
Pernicious
A
Highly injurious or destructive
24
Q
Look at diagram on slide nine
A
Draw it out
25
Pernicious anemia
Autoimmunity condition
-produce antibodies against parietal cells
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What do parietal cells produce
Intrinsic factor
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What is the purpose for intrinsic factor
It is required for absorption of vitamin B12, which is required for DNA synthesis in RBC
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Pernicious anemia may also be result of
Past infection of H.pylori
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Manifestations of Pernicious anemia
slow developing, usually severe once noticed
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Early symptoms of Pernicious anemia
Often ignored as they are non specific
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Normal Hb levels
>120 g/L
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When Hb levels reach _____ patient experiences classic Pernicious anemia symptoms
70-80 g/L
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Classic Pernicious anemia symptoms
-fatigue
-paresthesia of feet and fingers
-abdominal pain
-nerve demyelination
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Paresthesia
Tingling, prickling feeling
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Symptoms of Pernicious anemia are
Irreversible
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Folate or folic acid
Essential vitamin for RBC RNA and DNA synthesis
-coenzyme
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Folates are coenzymes required for synthesis of
Thymine and purines
-which affect RBC undergoing rapid cell reproduction
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What are humans daily folate requirement (found in diet)
50-200 mg/day
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Manifestations of folate deficiency anemia
-Similar to malnourished appearance
-scales on mouth and burning mouth syndrome
40
Burning mouth syndrome presents as
Red beefy tongue
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TX for folate deficiency anemia
Oral folate administration
-effective administration anaemia will disappear in 1-2 weeks
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Microcytic hypochromic anemias
Abnormally small RBC with reduced amounts of Hb
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What does Microcytic hypochromic anemias cause
-Iron metabolism disorders
-heme synthesis disorders
-globin synthesis disorders
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Result of Microcytic hypochromic anemias
Iron deficiency anemia
-thalassemia
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Thalassemia
Inherited disorder causing reduced hemoglobin
46
Iron deficiency anemia is caused by
Chronic blood loss, or inadequate iron intake
-not related to intrinsic dysfunction of iron metabolism
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Metabolic iron deficiency
Insufficient iron delivery to bone marrow or impaired iron absorption into bone marrow
-dysfunction in iron metabolism
48
What amount of blood loss can cause IDA
2-4 mL/day
49
Can Iron be recycled? what potentially disrupts this balance?
Yes
-blood loss disrupts this balance
50
Iron deficiency anemia: reasons for iron deficiency (four things)
-medications causing GI bleeding (aspirin, NSAIDS)
-surgery decreasing transit time and absorption
-insufficient iron intake
-pica
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Pica
Disorder causing the eating of non nutritional substances
-dirt, chalk, paper
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IDA stage one
Iron stores depleted, RBC production remains normal
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IDA stage 2
Insufficient iron transported to marrow, iron deficient RBC production begins
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Stage 3 IDA
Hemoglobin deficient RBC begin to replace normal RBC that are being destroyed
-anemia occurs
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Iron deficiency anemia is not noticed until (what levels of Hb)
70-80 g/L of Hb
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IDA classic symptoms
-structural changes in epithelial tissue
-koilonychia (finger nails brittle and shaped like spoon)
-glossitis (tongue papillae atrophy)
-dysphasia due to web of mucus
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How do you diagnose IDA (indirect, direct)
Indirect : measurement of serum levels of ferritin, trasnferrin saturation or total iron binding capacity
DIrect: iron stores measure by bone marrow biopsy
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TX for iron deficiency anemia
Eliminate sources of blood loss
-iron replacement therapy until ferritin level reaches 50 ug/L
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Ug/L
millionth of a gram/litre
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Normocytic-normochromic anemias
Characterized by normal size and normal Hb levels, but insufficient in numbers
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Aplastic anemia
Infiltrative disorders of bone marrow
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Posthemorrhagic
Sudden blood loss with normal iron stores
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Acquired hemolytic
Destruction of RBC
-developed after birth
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Hereditary hemolytic
Destruction of RBC
-sickle cell anemia
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Hemolysis
Destruction by eryptossi
-premature death of damaged erythrocytes
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Four normocytic normochromic anemias
1. Aplastic
2. Posthemorrhage
3. Hemolytic
4. Chronic inflammation
67
Draw out diagram on slide 21
Now
68
When are we affected by alterations in quantity of leukocytes
Too many or too few or structurally defective
69
Leukocytosis
WBC count is higher than normal
-due to normal protective response to physiological stressors
70
When is leukocytosis rare vs more common?
Rare: acute bacterial infection
More common: in acute viral infections (especially EBV)
71
Lekopenia
WBC count is lower than normal
-this is never a normal response
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Leukopenia vs normal wbc
L: <4.0 x 10^9/L
Normal: 4.5 to 11 x 10^9/L
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Leukopenia is associated with reduction in
Neutrophils
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Neutrophil count below 1.0 x 10^9/L
Infection increases rapidly
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Neutrophil count below 0.5 x 10^9/L
Life threatening infection
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Infectious mononucleosis
Benign, acute, self limiting
-characterized by infection of B lymphocytes
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Common causes of Infectious mononucleosis
EBV (most likely), HIV, HEP A, Rubella
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____ percent of all humans infected with EBV occurs during childhood
95%
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Early infections are ____ and supply _____ to EBV
-asymptomatic
-immunity
Rarely develops into Infectious mononucleosis
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What is Infectious mononucleosis called in teenagers and YA
Kissing disease since it travels through saliva
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Infectious mononucleosis infection begins with invasion of
B cells which have receptors for EBV
-firstly appears in throat area and then spreads to lymphoid tissues
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Life cycle of EBV (five steps)
1. Infection
2. Transformation and establishment of viral latency
3. Proliferation
4. Lyric cycle and virion release
5. Travel into B cell (repeat)
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Leukaemia
Malignant disorder of bone marrow and usually also blood
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Main features of leukaemia
Uncontrolled proliferation of malignant leukocytes
-decreasing production of hematopoietic cells
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WHO guidlines five categories of leukaemia
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
Hematopoietic cells
Immature cell that can develop into all types of blood cells
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Acute leukaemia
undifferentiated and immature cells (blast cells)
-onset of disease is RAPID
-short survival time
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Chronic leukaemia
More differentiated cells but not functionally normal
-slow progression
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Most lymphoid neoplasms arise from
Arise from B cells and T cells
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Leukaemia are clonal disorders driven by
Genetically abnormal stem like cancer cells
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Leukemic blasts
Abnormal WBC that fills bone marrow and spills into blood
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Normal bone marrow cells cease to function resulting in
Pancytopenia
-reduction in production of all blood cellular components
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Leukaemia mutation occurs in
Philadelphia chromosome translocation
-chromosome 9 and 22
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Pdiledelphia cheomsome translocation percentage
95% in chronic myeloid leukaemia, 30% acute lymphocytic leukaemia
95
Result of leukaemia mutations
Production of a unique protein (BCR-ABL) reduces apoptosis and releases immature cells into circulation
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ALL
Acute lymphocytic leukaemia
-affects B cells, T cells, NK cells
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AML
Acute myeloid leukaemia
-affects RBC, platelets, eosinophils, neutrophils, basophils
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Most cases of ALL are in
Children
1-10 yoa
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Most cases of AML are in
Older adults
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AML has a decreased rate of
Apoptosis
-differentiation in affected cells cause blood to be populated with dysfunctioned blood cells
101
Signs and symptoms of acute leukaemia
Fatigue (anemia)
-bleeding due to lower platelet count
-fever due to infections bc of dysfunctional immune response
102
CLL or chronic lymphocytic leukaemia
Slow growing cancer with too many immature lymphocytes found cells in bone and blood
103
What is the most common leukaemia in adults
Chronic leukaemia
-western world
104
CML or chronic myeloid leukaemia
Slow developing cancer
-too many myeloid cells (RBC and platelets) being made in bone marrow
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CLL main deficit
B cells fail to mature into plasma cells
-inability to synthesize antibodies
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CML main effect
Philadelphia chromosome and presence of BCR-ABL protein (95%)
107
Only known cause of CML
Exposure to ionizing radiation
108
Chronic phase of CML
2-5 years
May be asymptomatic
109
CML Accelerated phase
6-18 months
-proliferation of malignant cells
-splenomegaly (enlarged spleen) develops
-infections
110
CML terminal blast phase
Survival 3-6 months
-rapid and progressive leukocytosis (inc in number of WBC)
111
Spleen controls
Blood level of white blood cells, red blood cells, and platelets
112
Diagnosis of CLL
CLL is characterized by accumulation of of monoclonal B cells in blood
113
Monoclonal B cells
Condition in which a higher than normal number of identical B cells are found in blood
114
Progressive CLL TX
Chemotherapy
-not curative
115
TX for CLL
Stem cell transplant has achieved prolonged disease free survival
116
CML TX
Current modalities do not cure the disease
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Lymphadenopathy is characterized by
Enlarged lymph nodes, due to an inc in lymphocytes and monocytes
-palpable and painful
118
Localized LO
Indicates drainage from an infected area
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Generalized LO
Occurs less often
-generally with occurrence of infection/malignant disease in adults
120
Causes of LO
1. Neoplastic disease
2. Immune or inflammatory conditions
3. Endocrine disorders
4. Lipids storage diseases
121
Basic groups of Hodgkin and Non Hodgkin
B cell, T cell, NK cell neoplasms
122
Malignant lymphomas
Proliferation of malignant lymphocytes in lymph system
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Lymphomas are a result of
Genetic mutation of infection
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Result of malignant lymphomas
Cell with uncontrolled and excsssive growth accumulates in lymph nodes
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Most common blood cancer in Canada
Lymphoma
126
Two classifications of lymphoma
Hodgkin lymphoma, non Hodgkin lymphoma
127
Hodgkin lymphoma
Progresses from one group of lymph node to another
-unique B cells (reed sternberg) used to diagnosis but not always there
128
Hodgkin lymphoma incidence is higher in
Males
Media age: 64 (20-40) (60-70)
129
RS cells
Are the alignment transformed lymphocyte
-binuclaer cells used diagnosis
130
HL appears to be derived from
B cells that have no undergone successful immunoglobulin rearrangement
131
SIR
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
Manifestations of HL
Enlarged painless lymph node on neck
133
Common systemic symptoms HL
-fever without infection
-drenching night sweats
-itchy sin (pruritis)
-weight loss
-combined appearance of these symptoms = poor prognosis
134
Diagnosis of HL
Blood work: complete blood count, sedimentation rate, lymph node biopsy
135
Nonhodgkins lymphoma
Heterogenous group of lymphoid tissue neoplasms with difffering patterns of activity and responses to treatment
136
B cell, T cell, NK cell neoplasms WHO definition
Origination from (B/T/NK cells) at various levels of differentiation
137
NHL cancers are differentiated from
HL primarily by a lack of reed sternberg cells
138
Nonhodgkins lymphoma path physiology
Best described as progressive colonial expansion of B, T and NK cells
-oncogenes activated by translocation
-unpredictable spreading easily
139
Risk factors of Nonhodgkins lymphoma
-old male and white
-autoimmune
-HIV, EBV, Hep C
-organ transplants, immune suppressants
-gastric infection and H. Pylori
