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HSS 3305 > Lecture 11 > Flashcards

Lecture 11 Flashcards

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
Q

Reticulocyte

A

A young red cell without a nucleus, but retains some organelles; identified by special strains found in bone marrow (matures in 24-48)

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26
Q

Globin chains

A

Produced by ribosomes; joined to heme to form a hemoglobin unit (4 subunits to complete hemoglobin tetramer)

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27
Q

Red blood cell degradation

A

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

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28
Q

Reduced oxygen supply stimulates

A

Erythropoiesis (erythropoietin)

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29
Q

High partial pressure oxygen in lungs

A

Promotes binding

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30
Q

Low partial pressure oxygen in tissues

A

Promotes release

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31
Q

Methemoglobin Iron

A

Fe 3+, not in ferrous state, can’t bind oxygen, inherited disorder or response to toxic agents

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32
Q

Carboxyhemoglobin

A

Binds CO with high affinity (200x stronger than oxygen), blocks oxygen binding, products of incomplete combustion

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33
Q

Where are Iron reserves stored?

A

Liver, bone marrow, and spleen

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34
Q

What do Duodenal cells produce?

A

Hepcidin to block uptake by duodenal cells and interferes with iron transport

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35
Q

Hemochromatosis

A

Common genetic disease transmitted as an autosomal recessive trait – chronically absorbs too much iron

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36
Q

Reasons for Iron overload

A

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

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37
Q

Treatment for Hemochromatosis

A

Periodic removal of blood (phlebotomy) until iron stores are depleted, and use of iron chelation treatment to remove iron

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38
Q

Anemia causes

A

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

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39
Q

Hemorrhage

A

External blood loss

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40
Q

What do Sickle cell and thalassemia cause?

A

Shortened survival of red cells in circulation

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41
Q

Hereditary hemolytic anemia

A

Defective red cells

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42
Q

Normocytic anemia

A

Normal size and appearance

43
Q

Macrocytic anemia

A

Cells larger than normal impaired (folic acid and Vitamin B12 deficiency)

44
Q

Microcytic anemia

A

smaller cells (thalassemia)

45
Q

Hypochromic anemia

A

Reduced hemoglobin content

46
Q

Hypochromic microcytic anemia

A

Smaller than normal and reduced hemoglobin content

47
Q

Iron-deficiency Anemia

A

The most common type; Hypochromic microcytic anemia (not enough iron);

48
Q

When does Iron-deficiency Anemia happen

A

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
Q

Laboratory tests in blood for iron deficiency

A

Serum ferritin (low), Serum iron (low), and Serum iron-binding capacity (high)

50
Q

Iron-Deficiency Anemia Treatment

A

Learning the cause of anemia, treatment on cause than symptoms, administering supplementary iron

51
Q

Vitamin B12 deficiency anemia

A

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
Q

Folic acid

A

Green leafy vegetables and animal protein foods; are required for normal hematopoiesis and normal maturation of many other types of cells

53
Q

Absence or deficiency of vitamin B12 or folic acid

A

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
Q

Folic Acid Deficiency Anemia Pathogenesis

A

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
Q

Pernicious Anemia (macrocytic anemia)

A

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
Q

Pernicious Anemia treatment

A

Increased oral dose (B12 supplements) or Intramuscular injections

57
Q

Conditions that depress bone marrow function

A

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
Q

What does bone marrow suppression affect?

A

WBC and platelets - Pancytopenia (anemia, leukopenia, thrombocytopenia)

59
Q

Bone marrow treatment

A

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
Q

Hereditary hemolytic anemia

A

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
Q

Thalassemia

A

Defective synthesis of alpha or beta globulin causing a lack of hemoglobin production

62
Q

Alpha – (4 genes)

A

1- no change 2 -trait with mild disease, 3 severe disease, 4 – incompatible with life (hydrops fetalis)

63
Q

Unstable Beta tetramers

A

Defective Oxygen exchange; formed by lack of alpha and excess beta chains

64
Q

Beta – (2 genes)

A

Heterozygous-mild, homo-severe

65
Q

Sickle cell

A

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
Q

Sickle cell trait vs. Sickle cell disease

A

Trait: heterozygous, generally asymptomatic, Disease: homozygous, chronic health problems

67
Q

Vaso-occlusive crisis

A

Severe, abdominal pain (kidney, liver spleen infarction)

68
Q

Acquired Hemolytic Anemia

A

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
Q

Clotting Disorders

A

Disseminated intravascular Coagulation (DIC), Thrombotic Thrombocytopenic Purpura TTP –clots form in small blood vessels damaging RBC

70
Q

Diagnostic Evaluation of Anemia

A

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
Q

Secondary polycythemia

A

Common, Reduced arterial oxygen saturation leads to a compensatory increase in red blood cells (increased erythropoietin production)

72
Q

Primary or polycythemia vera

A

Rare, Manifestation of diffuse marrow hyperplasia of unknown etiology (cause), an overproduction of red cells, white cells, and platelets; can evolve into granulocytic leukemia

73
Q

Polycythemia Complications

A

Clot formation due to increased blood viscosity and platelet count

74
Q

Polycythemia Treatment (both types)

A

Primary polycythemia: Treated with drugs that suppress marrow function
Secondary polycythemia: Periodic removal of excess blood

75
Q

Secondary thrombocytopenic purpura

A

Damage to bone marrow from drugs or chemicals; Bone marrow infiltrated by leukemic cells or metastatic carcinoma

76
Q

Primary/ Immune thrombocytopenic purpura (ITP)

A

Associated with platelet antibodies where the bone marrow produces platelets, but they are rapidly destroyed, chronic in adults (immune suppression for treatment)

77
Q

Lymphatic System function

A

Provide immunologic defenses against foreign material via cell-mediated and humoral defense mechanisms and provides return of lost circulatory volume to vascular system

78
Q

Lymph nodes

A

Bean-shaped structures consisting of a mass of lymphocytes supported by a meshwork of reticular fibers that contain scattered phagocytic cells

79
Q

Where is lymphoid tissue

A

Present in thymus, tonsils, adenoids, lymphoid aggregates in intestinal mucosa, respiratory tract, and bone marrow

80
Q

Thymus

A

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
Q

Spleen

A

Specialized to filter blood (Macrophages, antibodies, lymphocytes and sinusoids to detect and remove pathogens in blood)

82
Q

Reasons for splenectomy

A

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
Q

Effects/risks of a splenectomy

A

Less-efficient elimination of bacteria (especially if blood-borne)
Impaired production of antibodies
Predisposed to systemic infections
Risk of increased platelet/RBC

84
Q

Which infections are splenectomy patients at risk of?

A

Streptococcus pneumoniae, Haemophilus influenzae, and meningococcus infections

85
Q

Treatment for Splenectomy

A

Vaccines and antibiotic prophylaxis

86
Q

Infectious mononucleosis

A

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
Q

Enlarged LN cancers

A

Metastatic tumors: Breasts, lung, colon, other sites, Malignant lymphoma (Hodgkin lymphoma
and Non-Hodgkin lymphoma), and Lymphocytic leukemia

88
Q

Leukemia

A

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
Q

Aleukemic leukemia

A

Condition in which white cells are confined to the bone marrow such that their number in the peripheral blood is normal or decreased

90
Q

Myelodysplasia (Preleukemia)

A

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

91
Q

Common types of hematopoietic cells that give rise to leukemia

A

Granulocytic, Lymphocytic, and Monocytic

92
Q

CLL, CML, ALL, AML

A

chronic lymphocytic leukemia, chronic myelogenous leukemia, acute lymphocytic leukemia, and acute myeloid leukemia

93
Q

Splenomegaly

A

Enlarged spleen

94
Q

Hepatomegaly

A

Enlarged liver

95
Q

Lymphadenopathy

A

Enlarged lymph nodes

96
Q

Bone pain in Leukemia

A

Expansion of cells in bone marrow

97
Q

Chronic leukemia

A

The evolution of disease proceeds at a relatively slow pace and often can be controlled

98
Q

Acute leukemia

A

A rapidly progressive disease, more difficult to control

99
Q

Diagnosis Leukemia

A

flowcytometry (phenotyping) bone marrow biopsy, Karyotyping (numbers, disease-specific risk genes – BCR/ABL fusion)

100
Q

Lymphoma

A

When cancerous cells form solid tumors in LN; mostly diseased B-cells or some T-cells which disrupt immune function

101
Q

Hodgkin Lymphoma

A

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
Q

Reed-Steinberg cells

A

(large atypical B-cells) that act as nucleus of tumor and secrete cytokines to attract other tumor cells

103
Q

Non-Hodgkin

A

Older adults, variable in appearance an progression, often not detected until widespread dissemination has occurred

104
Q

Treatment of Leukemia and Lymphoma + survival rate

A

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

HSS 3305 (21 decks)

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