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Patho > Week 13: Blood, Immunity > Flashcards

Week 13: Blood, Immunity Flashcards

1
Q

Define neutropenia, causes, consequences

A

abnormally low number of neutrophils
Causes: may be due to reduced production in the bone marrow or destruction of neutrophils elsewhere in the body
Consequences: inability to respond to bacterial infections

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2
Q

What is the infectious agent of mononucleosis?

A

Epstein-barr virus - replicates in epithelial cells then within B lymphocytes which stimulates T cytotoxic cells to target the infected B lymphocytes

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3
Q

Transmission, S/S (6) and prognosis of mononucleosis

A

Transmission: person to person by saliva
S/S: flu-like, fever, sore throat, fatigue; spleen enlargement, lymphadenopathy
Prognosis: self-limiting and does not usually require treatment

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4
Q

Define myelogenous leukemia

A

involves pluripotent myeloid stem cells in bone marrow, interferes with maturation of all blood cells including granulocytes, erythrocytes and thrombocytes

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5
Q

Define lymphocytic leukemia

A

immature lymphocytes and their progenitors that originate in bone marrow but infiltrate spleen, lymph nodes, CNS and other tissues

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6
Q

Define acute vs. chronic leukemia

A

Acute leukemia: rapid increase in # of immature blood cells, most common form in children
Chronic leukemia: buildup of relatively mature but abnormal WBC, generally takes months or years

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7
Q

Characteristics of ALL (3)

A
  • Most common type in young children, but can affect adults usually over age 65
  • Precursor B or T lymphoblasts, with most being pre-B
  • Structural and numerical changes in chromosomes within leukemic cells such as translocations, deletions, hyperploidy or polyploidy that alter ability to regulate normal hematopoiesis
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8
Q

Characteristics of CLL (3)

A
  • Clonal malignancy of B lymphocytes that most often affects adults over age 55 and does not affect children
  • Most common form in adults and 2/3 of all cases are men
  • See change in immunoglobulin gene resulting in low levels of CD markers like CD38 and zeta-associated protein (ZAP-70) involved in signaling T cells and natural killer cells do better, while individuals with higher levels of markers tend to do worse
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9
Q

Characteristics of AML (3)

A
  • Occurs more commonly in adults than children and more commonly in men than women
  • Diverse set of leukemias affecting myeloid precursors in the bone marrow and are most often associated with acquired genetic changes that inhibit myeloid cell differentiation
  • Undifferentiated blast cells replace normal cells within bone marrow causing anemia, neutropenia and thrombocytopenia
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10
Q

Characteristics of CML (6)

A
  • Mainly in adults, may be seen in a small # of children
  • Pluripotent hematopoietic progenitor cell
  • Characterized by excessive proliferation of marrow granulocytes, erythroid precursors and megakaryocytes
  • Philadelphia chromosome
  • Begins in a chronic phase that over several years progresses to an accelerated phase that ultimately enters a blast crisis phase = terminal phase where CML acts like AML
  • CML treated with tyrosine kinase inhibitor drugs that have improved survival rates to over 95%
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11
Q

2 forms of CLL

A
  1. long term survival and eventual death from other causes

2. Rapidly fatal disease despite aggressive therapy

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12
Q

What happens in the formation of the Philadelphia chromosome?

A

creates a new fusion gene that acts like a tyrosine kinase

Activates the cell cycle - cell division rates increased, inhibition of DNA repair

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13
Q

What cells are affected in non-Hodgkin lymphoma, causes (5)?

A

Either B-cell or T-cell neoplasms, may originate from any lymphoid tissues but commonly from lymph nodes

Causes largely unknown, may include infection (EBV, HTLV-1, HIV), chemicals, medical treatment, genetic diseases, autoimmune diseases

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14
Q

What is the characteristic cell formation in Hodgkin Lymphoma? Where is it believed these cells originate from?

A

Reed-Sternberg cells - multinucleated cells

B cells within the germinal centers of the lymph node

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15
Q

Peaks of incidence for Hodgkin Lymphoma, treatment (3)?

A

Two peaks of incidence - age 15-35 and over 55

Treatment: radiation, chemo, hematopoietic stem cell transplantation

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16
Q

Define multiple myeloma; why it is called a “myeloma”?

A

B-cell cancer of the plasma cells that normally produce antibodies

Name comes from impact on all different kinds of cells - generates losses of myeloid function due to infiltration of bone marrow

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17
Q

What are Bence Jones proteins and which disease process do they accompany?

A

cells release protein part of the immunoglobulins

Multiple myeloma

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18
Q

Risk factors (4) and manifestations of multiple myeloma (6)

A

Risk factors: chronic immune stimulation, autoimmune disorders, exposure to ionizing radiation, occupational exposure to pesticides

Manifestations: anemia, neutropenia, thrombocytopenia, infection, renal failure, neurologic symptoms

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19
Q

Explain why liver dysfunction; vessel defects; and platelet defects can give rise to coagulation pathology

A

Liver dysfunction: clotting factor synthesis, bile synthesis and clearing of clotting factors disrupted
Vessel defects: exposure to subendothelial lining triggers the clotting pathway
Platelet defects: clotting factor reactions normally take place on the surface of platelets

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20
Q

What are examples of vessel defects (4) and platelet defects (3)

A

Vessel defects: marfan’s syndrome, vitamin C deficiency, inflammatory responses, atherosclerosis
Platelet defects: thrombocytopenia, splenomegaly, platelet destruction

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21
Q

What are examples of clotting disorders (5)

A
  1. Hemophilia
  2. DIC
  3. Vit K deficiency
  4. Fibrinolytic defects: increased circulating clotting factors, plasmin inhibitor deficiencies
  5. Inherited prothrombic disorders: AT III deficiency, protein C defects
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22
Q

What are the clotting dysfunction tests (3)?

A
  • Platelet count
  • aPTT (activated partial thromboplastin time): measures effectiveness of intrinsic pathway
  • PT (prothrombin time): measures extrinsic pathway
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23
Q

How do aspirin, warfarin and heparin impact blood clotting?

A

Aspirin: inhibits cyclooxygenase
Warfarin: competes with vitamin K
Heparin: interacts with AT III to bind coagulation factors including thrombin and prevent hemostasis

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24
Q

Define DIC

A

complication of diseases that accelerate clotting, causing small blood vessel occlusion, organ necrosis, depletion of circulating clotting factors and platelets, activation of fibrinolytic system and consequent severe hemorrhage

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25
Q

Causes of DIC (4)

A
  • disorders that produce necrosis - burns, trauma, hepatic necrosis, transplant rejection
  • Infection - septicemia, fungal, protozoal, viral infection
  • Neoplastic disease
  • Other conditions - cardiac arrest, cirrhosis, shock
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26
Q

Patho of DIC

A

excessive clotting and consumption of clotting components, excessive circulating thrombin activates fibrinolytic system which dissolves clots

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27
Q

Define thrombocytopenia

Most common cause of what?

A

relative decrease in thrombocytes or platelets

Hemorrhagic disorders

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28
Q

Causes of thrombocytopenia (4)

A
  • Blood loss
  • Decreased platelet production - leukemia, aplastic anemia, drug toxicity
  • Increased platelet destruction - liver cirrhosis, DIC, severe infection
  • Sequestration - increased blood in limited vascular area like spleen
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29
Q

Define idiopathic thrombocytopenia

A

deficiency of platelets as a result of immune system destroying own platelets

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30
Q

What populations does idiopathic thrombocytopenia affect?

A

Acute: children ages 2-4
Chronic: adults under age 50, particular women between 20-40

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31
Q

Define Von Willebrand disease

Inheritance pattern

A

hereditary bleeding disorder characterized by prolonged bleeding time
Autosomal dominant

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32
Q

Consequences of Von Willebrand disease on clotting

A

Deficiency of Von Willebrand’s factor which stabilizes clotting factor VIII

33
Q

Define anemia

How is it diagnosed?

A

reduction in total RBC mass leads to decreased O2 carrying capacity
Assess Hct, Hgb, total RBC

34
Q

Causes of anemia

A

Reduced RBC production: reduced Hgb or DNA synthesis, bone marrow suppression
Enhanced RBC destruction: hemolysis, chronic disease

35
Q

Symptoms of anemia (7)

A

Headache, fatigue, dyspnea, poor exercise tolerance, pallor, syncope, tachycardia

36
Q

3 most common types of anemia

A
  1. Microcytic hypochromic: reduced hemoglobin synthesis d/t iron deficiency, thalassemia, sideroblastic anemia
  2. Macrocytic normochromic: altered DNA synthesis, megaloblastic anemia, vitamin B12 deficiency
  3. Normocytic normochromic: compromise to hematopoiesis (bone marrow suppression) or enhanced RBC destruction
37
Q

Define the following terms related to anemia: aplastic; folic acid or iron deficiency; pernicious; and sideroblastic.

A

aplastic: loss of stem cells or bone marrow matrix causing pancytopenia
folic acid deficiency: common, slowly progressive megaloblastic anemia; folate required for DNA synthesis
iron deficiency: iron required for Hgb and O2 binding
pernicious: malabsorption of B12 - most common megaloblastic anemia
sideroblastic: heterogenous disorders with common defect preventing use of iron in Hgb synthesis even though there are sufficient iron stores

38
Q

General cause of: sickle cell disease, thalassemia, glucose-6-phosphate deficiency

A

sickle cell disease: genetic disorder where genetic change in beta-globin causes sickling, especially in low levels of O2
Thalassemia: genetic disorders causing defect in globin chains that comprise hemoglobin
Glucose-6-phosphate deficiency: genetic disorder that limits the amount of oxidative stress that can be protected against in erythrocytes, resulting in hemolysis

39
Q

What does thalassemia give rise to?

A

hemolytic anemia

40
Q

What triggers oxidative stress in glucose-6- phosphate deficiency (4)

A

Triggered by infections, severe stress, certain foods (fava beans) or certain medicines (antimalarial drugs)

41
Q

Define ABO and Rh incompatibility

A

ABO incompatibility: exposure to blood group antigens that are foreign initiates formation of antibodies
Rh incompatibility: exposure to Rh factor

42
Q

How does ABO and Rh incompatibility occur?

A

woman who is Rh negative develops antibodies against an Rh-positive fetus (not an issue until 2nd pregnancy)

43
Q

What are the risks for ABO/Rh incompatibility to fetal development (2)

A

Erythroblastosis fetalis: refers to a hemolytic disease of the fetus and neonate based upon incompatibilities between fetal and maternal blood

Hydrops fetalis: severe form of erythroblastosis fetalis associated with profound anemia or edema

44
Q

How does RhoGAM work?

A

medicine containing IgG antibodies that attack Rh-D found on fetal RBCs to prevent isoimmunization

45
Q

Define polycythemia

A

increase in RBC mass

46
Q

Define primary polycythemia
What age does this occur?
Causes?

A

chronic disorder characterized by increased RBC mass, erythrocytosis, leukocytosis, thrombocytosis, increased hemoglobin levels
Occurs between ages 40-60
Cause unknown likely related to stem cell defect

47
Q

Define secondary polycythemia
Causes?
What is another name?

A

excessive RBC production due to hypoxia, tumor or disease
Causes: prolonged tissue hypoxia or increased production of erythropoietin
Reactive polycythemia

48
Q

Define spurious polycythemia

causes?

A

increased hematocrit with a normal or low RBC mass

Causes: dehydration, hypertension, elevated serum cholesterol, uric acid levels

49
Q

What happens during the cellular injury, vascular phase, cellular phase of wound healing and what are consequences of acute inflammation?

A

Cellular injury: initiates inflammatory response

Vascular phase: includes vasodilation and increased vascular permeability

Cellular phase: leukocytes enter the injured tissue to destroy infective organisms, remove damaged cells and release inflammatory mediators

Consequences: an exaggerated response may be harmful and process is nonspecific so it may be difficult to control.

50
Q

What is the general patho behind the cardinal signs of inflammation: heat, redness, swelling

A

mediators increase vasodilation and vascular permeability

51
Q

What are mast cells and mast cell degranulation?

A

Mast cells: activation results in release of preformed contents of granules, synthesis of lipid mediators derived from cell membrane precursors and stimulation of cytokine and chemokine synthesis by other inflammatory cells

Mast cell degranulation: allergy antibody IgE present, results in release of inflammatory mediators

52
Q

What is histamine?

A

one of the first mediators to be released from mast cell granules during an acute inflammatory reaction; causes vasodilation and increases permeability

53
Q

Define: chemotactic factor, leukotriene, prostaglandin

A

Chemotactic factor: substances that stimulate cellular movement - eg. Chemokines, complement system

Leukotriene: induces smooth muscle contraction, constricts pulmonary airways, increases microvascular permeability

Prostaglandin: induces vasodilation and bronchoconstriction, inhibits inflammatory cell function

54
Q

Define complement

A

effector mechanism of innate and adaptive immunity that allows body to localize infection and destroy invading microorganisms; 3 different pathways: classical, alternative and lectin

55
Q

Classical vs. alternative pathways of complement system

A

Classical: initiated by an antigen-antibody complex, reactive site on the antibody uncovered and binds to the C1 molecule in the complement system

Alternative: inactive circulating complement proteins activated when exposed to microbial surface molecules, complex polysaccharides

56
Q

Define membrane attack complex, opsonization, chemotaxis

A

Membrane attack complex: assembled during the complement pathway, penetrates microbial cell membrane allowing the passage of ions, small molecules and water into the cell causing cell lysis

Opsonization: coating of an antigen with antibody or complement to enhance binding

Chemotaxis: directed cell migration - inflammatory mediators directed to the site of injury by chemoattractants

57
Q

Define the clotting & kinin system, bradykinin

A

Clotting and kinin system: blood proteins that play a role in inflammation, BP control, coagulation and pain

Bradykinin: increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels and pain

58
Q

Define interleukin, lymphokine, interferon

A

Interleukin: produced by macrophages and lymphocytes in the presence of an invading microorganism or when inflammatory process initiated; enhance the acquired immune response or regulate through suppression or enhancement the inflammatory process

Lymphokine : substance produced by lymphocytes that acts upon other cells of the immune system

Interferon: cytokines that protect the host against viral infections and play a role in the modulation of the inflammatory response

59
Q

Define fever, leukocytosis and acute-phase reactants in relation to inflammation

A

Fever: cytokines affect the thermoregulatory center in the hypothalamus and produces fever

Leukocytosis: increased white blood cells - sign of inflammatory response, usually caused by bacterial infection

Acute-phase reactants: liver dramatically increase the synthesis of acute-phase proteins

60
Q

What are the acute-phase reactants (3)

A

fibrinogen, C-reactive protein, serum amyloid A protein

61
Q

How do granulomas form in chronic inflammation?

A

Macrophages unable to protect against host tissue damage, the body tries to wall off the site by forming a granuloma

62
Q

Basic characteristics of Type I hypersensitivity disorders

A

I: IgE mediated response leads to inflammatory mediators from sensitized mast cells

63
Q

Describe how sensitization, primary response and secondary response occur in allergic reactions

A

Sensitization of mast cell/basophil results in priming the reaction
Primary response: results from degranulation and release of mediators
Secondary response: membrane phospholipids and recruitment of inflammatory cells that release cytokines

64
Q

Clinical consequences of local vs. systemic allergic reaction

A

local: allergic rhinitis characterized by sneezing, itching, water discharge from eyes and nose
systemic: affects the areas in the body where mast cells are located - skin, GI tract and respiratory system

65
Q

Define anaphylaxis

A

systemic life-threatening hypersensitivity reaction with widespread edema, difficulty breathing, vascular shock s/t vasodilation

66
Q

What are the 3 types of grafts?

A

Autologous - donor and recipient are the same
Syngeneic - donor and recipient are identical twins
Allogenic - share similar HLA types

67
Q

Define rejection, what are the phases?

A

immune responses that occur as the recipient’s immune system sees the graft as foreign and begins attacking it immunologically

Hyper acute reaction: occurs immediately after transplant and involves existing recipient antibodies to grant antigens
Acute rejection: within months of transplantation, involves cytotoxic T cells and activation of inflammatory responses that attack the graft
Chronic rejection: prolonged period of time - caused by fibrotic processes mediated by cytotoxic T cells

68
Q

Define graft-versus-host disease

A

Immune competent cells attack tissues in recipient and may manifest as skin lesions, involvement of the GI tract that can become life-threatening

69
Q

Define SCID (severe combined immunodeficiency)

A

primary immunodeficiency characterized by lack of all T and B cell function, sometimes missing NK cells

70
Q

Define primary vs. secondary immunodeficiency

A

Primary: congenital or inherited
Secondary: acquired

71
Q

What are the three forms of wound healing?

A

Resolution: minimal tissue damage, tissue returns to normal in short period of time

Regeneration: healing process occurs in damaged tissue in which cells are capable of mitosis, damaged tissue replaced by identical tissue from proliferation of nearby cells

Replacement: replaced by connective tissue when extensive damage or when cells are incapable of mitosis, chronic inflammation or complications results in fibrosis

72
Q

What are the phases of wound healing?

A

Inflammatory phase: phagocytes eliminate debris

Proliferative phase: building new tissue, including fibroblasts that secrete collagen and growth factors for angiogenesis and stimulation of endothelial cells

Contraction and remodeling phase: development of fibrous scar that is remodeled to become stronger and smaller

73
Q

Define cicatrization, debridement

A

Cicatrization: contraction of fibrous tissue formed at a wound site by fibroblasts
Debridement: cleaning the site of infection

74
Q

Define first-intention vs. second-intention wound healing

A

First-intention: scar tissue laid down across a clean wound with edges in close approximation

Second-intention: parallels first-intention but occurs in wounds in which large sections of tissue have been lost or in wounds complicated by infection

75
Q

Explain how the following relate to compromised wound healing: use of anti-inflammatory drugs; scurvy; infection; and, dehiscence

A

Anti-inflammatory drugs: inhibits wound healing

Scurvy (impaired collagen synthesis): compromises wound healing

Infection: may result in compromised wound healing/prevents epithelialization

Dehiscence: results in bursting open or a previously closed wound

76
Q

Basic characteristics of Type II hypersensitivity disorders

A

II: antibody mediated responses against cell surface or extracellular matrix antigens that result in complement-mediated phagocytosis, inflammation and cell injury or abnormal physiological responses without cell injury

77
Q

Basic characteristics of Type IIi hypersensitivity disorders

A

III: generated by immune complexes that activate complement resulting in activation of inflammatory cells that release tissue-damaging products

78
Q

Basic characteristics of Type IV hypersensitivity disorders

A

IV: tissue damage in which cell-mediated immune response with sensitized T lymphocytes cause cell and tissue injury

Patho (14 decks)

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