Lecture 11 Flashcards

(104 cards)

1
Q

Plasma

A

Fluid component of blood

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2
Q

Blood composition and function

A

Red cells, leukocytes, and platelets; carries antibodies, oxygen, nutrients, hormone , and CO2 plus other waste products

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3
Q

Red blood cell function

A

Oxygen/Carbon Dioxide exchange
(the more red blood cells the more oxygen you can carry); Most numerous cells in the blood

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4
Q

Leukocytes (WBC) function and types

A

Immune functions; Neutrophils (Most numerous – first line), Monocytes (Phagocytic Macrophages), Eosinophils (Allergy, parasitic infections), Lymphocytes (Adaptive Immunity), and Basophils (Parasitic infections)

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5
Q

Platelet function

A

Hemostasis

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6
Q

Stem cells

A

Precursor cells in bone marrow that differentiate to form red cells, white cells, and platelets (any cell) - Hematopoietic stem cells differentiate into any blood cell type

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7
Q

Erythroblast

A

Precursor cells in bone marrow

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8
Q

Hemoglobin

A

An oxygen-carrying protein formed by the developing red cell

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9
Q

Ganulocytes/ Polymorphpnucleargraulocytes

A

PMN - Eosinophils, Basophils, Neutrophils

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10
Q

Where are Lymphocytes produced?

A

Mainly in lymph nodes and spleen; some are produced in bone marrow

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11
Q

Neutrophils

A

The first line of defence (Most numerous in adults,
Makeup 60-70% of total circulating WBC, Actively phagocytic, Predominant in inflammatory reactions)

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12
Q

Monocytes

A

3-5% of leukocytes (Increased in certain types of chronic infection, Circulate to sites of inflammation, Transition to Macrophages (APC), Infection/tissue repair)

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13
Q

Eosinophils/Basophils

A

Present in low numbers (Increased in allergic reactions and Increased in presence of animal–parasite infections)

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14
Q

Lymphocytes

A

15-20% of leukocytes (T/B cells, seen predominantly in children, Mostly located in lymph nodes, spleen, and lymphoid tissues (some in circulation plus lymphatic system), cell-mediated and humoral defence reactions)

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15
Q

Platelets

A

Essential for blood coagulation, Much smaller than leukocytes, Represent bits of the cytoplasm of megakaryocytes, the largest precursor cells in bone marrow, Short survival, about 10 days

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16
Q

Hematopoiesis

A

Formation and development of blood cells; bone marrow replenishes blood cells (damage/age)

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17
Q

Substances necessary for hematopoiesis

A

Protein, Folic Acid, Vitamin B12 (required for DNA synthesis), Iron (Decreased RBC production if any of these are lacking)

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18
Q

How is RBC production regulated

A

Oxygen content in blood which stimulates hormone (epo) release from kidneys

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19
Q

True or False: High reticulocyte count indicates the body is creating a lot of RBC

A

True, they leave bone marrow and differentiate into RBC in circulation

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20
Q

Red cell production

A

Regulated by oxygen content of the arterial blood – stimulated by erythropoietin

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21
Q

White cell production

A

Regulated by Interleukin levels/ response to infection – complex

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22
Q

Heme

A

Porphyrin ring that contains an iron atom

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23
Q

Globin

A

The largest part of hemoglobin; forms different chains designated by Greek letters such as alpha, beta, gamma, delta, and epsilon

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24
Q

Porphyrin ring

A

Produced by the mitochondria; iron is inserted to form heme

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25
Reticulocyte
A young red cell without a nucleus, but retains some organelles; identified by special strains found in bone marrow (matures in 24-48)
26
Globin chains
Produced by ribosomes; joined to heme to form a hemoglobin unit (4 subunits to complete hemoglobin tetramer)
27
Red blood cell degradation
Worn-out red cells are removed in the spleen, Hemoglobin is degraded and excreted as bile by the liver, The porphyrin ring cannot be salvaged, Globin chains break down and are used to make other proteins, and Iron is extracted and saved to make new hemoglobin
28
Reduced oxygen supply stimulates
Erythropoiesis (erythropoietin)
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High partial pressure oxygen in lungs
Promotes binding
30
Low partial pressure oxygen in tissues
Promotes release
31
Methemoglobin Iron
Fe 3+, not in ferrous state, can't bind oxygen, inherited disorder or response to toxic agents
32
Carboxyhemoglobin
Binds CO with high affinity (200x stronger than oxygen), blocks oxygen binding, products of incomplete combustion
33
Where are Iron reserves stored?
Liver, bone marrow, and spleen
34
What do Duodenal cells produce?
Hepcidin to block uptake by duodenal cells and interferes with iron transport
35
Hemochromatosis
Common genetic disease transmitted as an autosomal recessive trait – chronically absorbs too much iron
36
Reasons for Iron overload
Patients who take iron supplements chronically, or have blood disorders where there is a loss of RBC destruction (sickle cell), overload due to inability to reduce iron levels
37
Treatment for Hemochromatosis
Periodic removal of blood (phlebotomy) until iron stores are depleted, and use of iron chelation treatment to remove iron
38
Anemia causes
Insufficient raw materials (Iron deficiency, vitamin B12 deficiency, Folic acid deficiency), Inability to deliver adequate red cells into circulation due to marrow damage or destruction (aplastic anemia), excessive loss of red cells
39
Hemorrhage
External blood loss
40
What do Sickle cell and thalassemia cause?
Shortened survival of red cells in circulation
41
Hereditary hemolytic anemia
Defective red cells
42
Normocytic anemia
Normal size and appearance
43
Macrocytic anemia
Cells larger than normal impaired (folic acid and Vitamin B12 deficiency)
44
Microcytic anemia
smaller cells (thalassemia)
45
Hypochromic anemia
Reduced hemoglobin content
46
Hypochromic microcytic anemia
Smaller than normal and reduced hemoglobin content
47
Iron-deficiency Anemia
The most common type; Hypochromic microcytic anemia (not enough iron);
48
When does Iron-deficiency Anemia happen
This happens when there are a lack of iron in the diet, rapids periods of growth in infants, inadequate reutilization of iron, chronic infection/inflammation, cancers, and loss of blood (GI tract, excessive menstrual bleeding, too frequent blood donations)
49
Laboratory tests in blood for iron deficiency
Serum ferritin (low), Serum iron (low), and Serum iron-binding capacity (high)
50
Iron-Deficiency Anemia Treatment
Learning the cause of anemia, treatment on cause than symptoms, administering supplementary iron
51
Vitamin B12 deficiency anemia
Those who are vegetarian are at risk; found in meat, milk, and foods rich in animal proteins; For structural and functional integrity of the nervous system; deficiency may lead to neurologic disturbances
52
Folic acid
Green leafy vegetables and animal protein foods; are required for normal hematopoiesis and normal maturation of many other types of cells
53
Absence or deficiency of vitamin B12 or folic acid
Mature red cells are larger than normal or macrocytes; corresponding anemia is called macrocytic anemia, Leukopenia (low WBC), thrombocytopenia (low platelets), Abnormal red cell maturation or megaloblastic erythropoiesis
54
Folic Acid Deficiency Anemia Pathogenesis
Inadequate diet: Encountered frequently in chronic alcoholics Poor absorption caused by chronic intestinal disease Occasionally occurs in pregnancy with increased demand for folic acid
55
Pernicious Anemia (macrocytic anemia)
Lack of intrinsic factor (B12); causes included gastric mucosal atrophy, Autoantibodies directed against gastric mucosal cells and intrinsic factor, Surgery to remove sections of the stomach, and Chronic intestinal diseases (Crohn’s, IBD)
56
Pernicious Anemia treatment
Increased oral dose (B12 supplements) or Intramuscular injections
57
Conditions that depress bone marrow function
Anemia of chronic disease: Mild suppression of bone marrow function (parvoirus B19), Aplastic anemia (Marrow injured by radiation, anticancer drugs or chemicals, Autoantibodies, CTL autoimmunity)
58
What does bone marrow suppression affect?
WBC and platelets - Pancytopenia (anemia, leukopenia, thrombocytopenia)
59
Bone marrow treatment
Depends on the cause; Blood and platelet transfusions, Immunosuppressive drugs, Hemopoietic stem cell transplant in highly selected cases of aplastic anemia, or no specific treatment
60
Hereditary hemolytic anemia
Genetic abnormality prevents normal survival, Abnormal shape (Hereditary spherocytosis; These cells have no central pallor), Abnormal hemoglobin (Hemoglobin S (sickle hemoglobin) or hemoglobin C), Defective hemoglobin synthesis (Thalassemia minor and major; globin chains are normal, but synthesis is defective)
61
Thalassemia
Defective synthesis of alpha or beta globulin causing a lack of hemoglobin production
62
Alpha – (4 genes)
1- no change 2 -trait with mild disease, 3 severe disease, 4 – incompatible with life (hydrops fetalis)
63
Unstable Beta tetramers
Defective Oxygen exchange; formed by lack of alpha and excess beta chains
64
Beta – (2 genes)
Heterozygous-mild, homo-severe
65
Sickle cell
Hemoglobin S (beta Hgb point mutation); Present in areas where Malaria is/was common; Constant sickling wears out cells and sickled cells are targeted for early destruction by the spleen, cells can also form blockages, chronic joint pain also occurs
66
Sickle cell trait vs. Sickle cell disease
Trait: heterozygous, generally asymptomatic, Disease: homozygous, chronic health problems
67
Vaso-occlusive crisis
Severe, abdominal pain (kidney, liver spleen infarction)
68
Acquired Hemolytic Anemia
Normal red cells that are unable to survive due to a hostile environment; Attacked and destroyed by antibodies and Destruction of red cells by mechanical trauma
69
Clotting Disorders
Disseminated intravascular Coagulation (DIC), Thrombotic Thrombocytopenic Purpura TTP –clots form in small blood vessels damaging RBC
70
Diagnostic Evaluation of Anemia
History and physical examination, Complete blood count to assess the degree of anemia, leukopenia, and thrombocytopenia, Blood smear to determine if normocytic, macrocytic, or hypochromic microcytic, Reticulocyte count to assess the rate of production of new red cells, lab tests, bone marrow study, and evaluation of blood loss
71
Secondary polycythemia
Common, Reduced arterial oxygen saturation leads to a compensatory increase in red blood cells (increased erythropoietin production)
72
Primary or polycythemia vera
Rare, Manifestation of diffuse marrow hyperplasia of unknown etiology (cause), an overproduction of red cells, white cells, and platelets; can evolve into granulocytic leukemia
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Polycythemia Complications
Clot formation due to increased blood viscosity and platelet count
74
Polycythemia Treatment (both types)
Primary polycythemia: Treated with drugs that suppress marrow function Secondary polycythemia: Periodic removal of excess blood
75
Secondary thrombocytopenic purpura
Damage to bone marrow from drugs or chemicals; Bone marrow infiltrated by leukemic cells or metastatic carcinoma
76
Primary/ Immune thrombocytopenic purpura (ITP)
Associated with platelet antibodies where the bone marrow produces platelets, but they are rapidly destroyed, chronic in adults (immune suppression for treatment)
77
Lymphatic System function
Provide immunologic defenses against foreign material via cell-mediated and humoral defense mechanisms and provides return of lost circulatory volume to vascular system
78
Lymph nodes
Bean-shaped structures consisting of a mass of lymphocytes supported by a meshwork of reticular fibers that contain scattered phagocytic cells
79
Where is lymphoid tissue
Present in thymus, tonsils, adenoids, lymphoid aggregates in intestinal mucosa, respiratory tract, and bone marrow
80
Thymus
Overlies base of the heart; large during infancy and childhood; undergoes atrophy in adolescence (essential in the prenatal development of the lymphoid system and in the formation of body’s immunologic defence mechanisms ( T cell development/ selection))
81
Spleen
Specialized to filter blood (Macrophages, antibodies, lymphocytes and sinusoids to detect and remove pathogens in blood)
82
Reasons for splenectomy
Traumatic injury: To prevent fatal hemorrhage Blood diseases: Excessive destruction of blood cells in the spleen (hereditary hemolytic anemia) Prevent chronic splenomegaly Cancer – Leukemia, Lymphoma
83
Effects/risks of a splenectomy
Less-efficient elimination of bacteria (especially if blood-borne) Impaired production of antibodies Predisposed to systemic infections Risk of increased platelet/RBC
84
Which infections are splenectomy patients at risk of?
Streptococcus pneumoniae, Haemophilus influenzae, and meningococcus infections
85
Treatment for Splenectomy
Vaccines and antibiotic prophylaxis
86
Infectious mononucleosis
Lymphatic System disease; usually caused by Epstein-Barr virus (EBV-B-cell 90%) or CMV – Tcell/macrophages (5-7%) Risk: spleen may rupture during high-contact sports and in those with compromised immune systems (give rise to B cell lymphoma)
87
Enlarged LN cancers
Metastatic tumors: Breasts, lung, colon, other sites, Malignant lymphoma (Hodgkin lymphoma and Non-Hodgkin lymphoma), and Lymphocytic leukemia
88
Leukemia
A neoplasm (Cancer) of hematopoietic tissue; Leukemic cells diffusely infiltrate the bone marrow and lymphoid tissues, spill over into the bloodstream, and infiltrate throughout various organs of the body
89
Aleukemic leukemia
Condition in which white cells are confined to the bone marrow such that their number in the peripheral blood is normal or decreased
90
Myelodysplasia (Preleukemia)
A disturbed growth and maturation of marrow cells; 3 types: Anemia (Reduced number of erythrocytes), Leukopenia (Reduced number of white cells), Thrombocytopenia (Reduced number of platelets) Not all patients develop leukemia
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Common types of hematopoietic cells that give rise to leukemia
Granulocytic, Lymphocytic, and Monocytic
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CLL, CML, ALL, AML
chronic lymphocytic leukemia, chronic myelogenous leukemia, acute lymphocytic leukemia, and acute myeloid leukemia
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Splenomegaly
Enlarged spleen
94
Hepatomegaly
Enlarged liver
95
Lymphadenopathy
Enlarged lymph nodes
96
Bone pain in Leukemia
Expansion of cells in bone marrow
97
Chronic leukemia
The evolution of disease proceeds at a relatively slow pace and often can be controlled
98
Acute leukemia
A rapidly progressive disease, more difficult to control
99
Diagnosis Leukemia
flowcytometry (phenotyping) bone marrow biopsy, Karyotyping (numbers, disease-specific risk genes – BCR/ABL fusion)
100
Lymphoma
When cancerous cells form solid tumors in LN; mostly diseased B-cells or some T-cells which disrupt immune function
101
Hodgkin Lymphoma
young adults, start in single LN and spreads to others and eventually other parts of the body. Usually detected early as a single or group of enlarged LN
102
Reed-Steinberg cells
(large atypical B-cells) that act as nucleus of tumor and secrete cytokines to attract other tumor cells
103
Non-Hodgkin
Older adults, variable in appearance an progression, often not detected until widespread dissemination has occurred
104
Treatment of Leukemia and Lymphoma + survival rate
Destruction of malignant cells by chemotherapy or radiation to produce remission (3 phases: Induction/Consolidation/Maintenance) Other treatments: - Hematopoietic Stem Cell Therapy (BMT, peripheral, cord blood): replaces malignant cells (must use immune suppression drugs) 50% 5 year survival rate if HLA match is found