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A&P 2 > Unit 10 > Flashcards

Unit 10 Flashcards

1
Q

Nonspecific (Innate) Defense System

A
  • FIRST line of defense- skin & mucous membranes prevent microbe entry
  • SECOND line of defense- antimicrobial proteins, phagocytic cells, etc.
  • Inhibit spread of ALL invaders
  • Rapid response time
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2
Q

Innate Defense (Surface Barriers)

A

-Skin & Mucous Membrane

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3
Q

Innate Defense (Internal Defenses)

A
  • Phagocytes
  • Fever
  • NK Cells
  • Antimicrobial Proteins
  • Inflammation
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4
Q

Surface Barriers

A

Keratin (skin) & mucous membranes

  • Physical Barrier
  • Resistant to: acids & bases, bacterial enzymes & bacterial toxins
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5
Q

Epithelial Chemical Barriers

A

Epithelial membranes secrete chemicals

  • Skin acidity (pH 3-5): ↓bacterial growth
  • Sebum & cerumen: toxic to bacteria
  • Stomach (pH = 2.0): HCl
  • Protein digesting enzymes
  • Lysozyme: Saliva & lacrimal fluid
  • Mucus: traps microorganisms & dirt
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6
Q

Respiratory Tract

A 
Mucus-coated nasal hairs (vibrissae): 
-Trap dirt 
-Trap microbes
-Trap pollen
-Trap mold spores
Upper respiratory tract:
-Cilia move contaminants trapped in mucus away from the lungs
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7
Q

Nonspecific Cells & Chemicals

A
  • Phagocytes
  • Natural killer (NK) cells
  • Antimicrobial proteins: blood & tissue fluid
  • Inflammatory response activates macrophages, WBCs, & chemicals
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8
Q

Phagoctyes

A 
Macrophages:
--Free macrophages 
      Move throughout the body
-Fixed macrophages
      Kupffer cells (liver)  
      Microglia (brain)
Neutrophils: 
-Phagocytic for bacteria
Monocytes: 
-Phagocytic for bacteria
-Monocytes → macrophages
Eosinophils: 
-Phagocytic for parasitic worms
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9
Q

Phagocytosis Steps

A
  • Microbe adheres to phagocyte
  • Phagocyte pseudopods engulf microbe (antigen) into a phagosome (sac)
  • Phagosomes fuse w/ a lysosome to form a phagolysosome
  • Microbe inside phagolysosome is digested by enzymes
  • Nondigestible material is removed by exocytosis
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10
Q

Phagocytosis

A

SLIDE 12, review the picture

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11
Q

Natural Killer (NK) Cells

A
  • Large lymphocytes
  • React nonspecifically
  • Kill cancer cells
  • Kill virus-infected cells
  • Kill their target cells by releasing:
    - Perforins
    - Cytolytic chemicals
    - Chemicals ↑inflammatory response
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12
Q

Inflammatory Response

A
  • Begins when body tissues are injured
    - Prevents the spread of damaging chemicals
    - Disposes of cell debris & pathogens
    - Sets the stage for repair
  • Signs of acute inflammation:
    - Redness, heat, swelling & pain
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13
Q

Inflammatory Chemicals

A
  • Released by injured tissues & WBCs into cell spaces:
    - Prostaglandins
    - Complement
    - Histamine
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14
Q

Vascular Permeability

A
  • Inflammatory chemicals cause:
    - ↑Capillary wall permeability
    - Vasodilation
  • Fluid containing plasma proteins & antibodies leaks into the tissue spaces
    - Causes edema
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15
Q

Vasoconstriction vs. Vasodilation

A
  • Vasoconstriction
    • Normal permeability & blood flow
  • Vasodilation
    • Increased blood flow and permeability of blood vessels with vasodilation
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16
Q

Edema

A
  • Accumulation of fluid in the tissue spaces:
    - Contributes to sensation of pain
    - Dilutes harmful substances
    - Brings in ↑oxygen & ↑nutrients (repair)
    - Allows entry of clotting proteins to wall-off the infection (prevents bacterial movement)
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17
Q

Phagocytic Mobilization Phases (know the definitions)

A
  • Leukocytosis – neutrophils released from bone marrow in response to chemicals released by injured cells
  • Margination – neutrophils cling to capillary walls at the injured area
  • Diapedesis – neutrophils squeeze through capillary walls
  • Chemotaxis – inflammatory chemicals attract neutrophils to the infection site & neutrophils begin phagocytosis
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18
Q

Antimicrobial Proteins

A
  • Interferon & complement:
    • Enhance nonspecific (innate) defenses
      • Attack microorganisms directly
      • Prevent microorganism reproduction
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19
Q

Interferon

A
  • Interferon synthesis is activated when a cell is invaded by a virus
  • Interferon molecules leave infected cell & enter nearby (un-invaded) cells
  • Interferon stimulates neighboring cells to activate their genes for antiviral protein production
  • Blocks viral reproduction
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20
Q

Interferon Action

A

SLIDE 24, know the picture

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21
Q

Interferon Family

A
  • All related immuno-proteins
  • WBCs also secrete interferon
  • Interferons can activate macrophages & NK cells
  • FDA-approved interferon (antiviral drug)
    - Used against hepatitis viruses & herpes virus
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22
Q

Complement

A
  • Proteins (C1-C9)
  • Circulate in blood as inactive proteins
  • ↑Inflammatory response
  • Kill bacteria
  • Body cells are immune to complement
  • ↑Effectiveness of both nonspecific & specific defenses
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23
Q

Complement Pathways

A
  • Complement activation:
    • Binding of antibodies to invading organisms (antigen)
    • Binding of complement to the antigen-antibody complex (complement fixation)
    • Activated in a sequence w/ each step catalyzing the next & forms →
      • Membrane Attack Complex (MAC)
      • Causes cell lysis
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24
Q

C-Reactive Protein (CPR)

A
  • Produced (liver) during inflammation
  • CPR:
    - Targets damaged cells for disposal
    - Activates complement
    - Used to detect acute infections
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25
Q

Fever

A
  • ↑Body temperature in response to invading microorganisms
  • Body’s thermostat is reset upwards in response to pyrogens
    - Pyrogens: chemicals made by WBCs exposed to foreign substances
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26
Q

Fever Effects

A
  • High fevers can denature enzymes
  • Moderate fevers cause:
    - Liver & spleen to store iron (needed by microorganisms)
    - ↑Metabolic rate → ↑tissue repair
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27
Q

Steroid Hormones

A
  • Hydrocortisone, cortisone, cortisol
    - ↓Inflammation (anti-inflammatory)
  • Vasoconstrict: ↓blood flow, ↓edema, ↓redness
  • Used clinically to treat inflammatory diseases (rheumatoid arthritis, etc.)
  • Side effects: Cushing’s syndrome (↑visceral fat, moon-face, buffalo-hump, ↓memory storage/retrieval)
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28
Q

Specific (Adaptive) Defense Systems

A
  • Third line of defense
    • Mounts attack against specific foreign substances
    • Slower to react than nonspecific (innate) system
  • Works with nonspecific (innate) system
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29
Q

Specific (Adaptive) Defense (Humoral Immunity)

A

-B Cells

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30
Q

Specific (Adaptive) Defense (Cellular Immunity)

A

-T Cells

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31
Q

Specific (Adaptive) Defense Immune System

A
  • Recognize specific foreign substances (antigens) & has a memory
  • Neutralize or destroy foreign substances
  • ↑Inflammation & activate complement
  • Two (overlapping) parts:
    • Cellular (cell-mediated) immunity
    • Humoral (antibody-mediated) immunity
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32
Q

Antigens

A

-Activate immune system
-Stimulate an immune system
-Large & complex molecules not normally found in the body (non-self)
Molecules found on cells membranes
-Antigens associated with a foreign cell stimulate an immune response

33
Q

Complex Antigens

A
  • Properties:
    - Immunogensis:
    - ↑Lymphocyte production
    - ↑Antibody production
    - Reactivity – react w/ antibodies
  • Includes foreign: proteins, nucleic acids, lipids & carbohydrates
34
Q

Incomplete Antigens

A
  • Are not immunogenic
  • Are reactive w/ antibodies
  • Specific (adaptive) immune system may recognize them as foreign & mount an attack (allergic response)
  • Found in:
    • Poison ivy, animal dander, dyes, detergents, cosmetics
35
Q

Antigenis Determinants

A
  • Only certain parts of an antigen are immunogenic
  • Lymphocytes form antibodies against the antigen
  • Antibodies only bind to the antigenic determinants of an antigen
  • Naturally occurring antigens have many antigenic determinants
36
Q

Self-Antigens

A
  • Body cells have protein molecules (self-antigens) that are not antigenic to us but are antigenic to other humans
  • MHC (Major Histocompatibility Complex) proteins mark a body cell as self
37
Q

MHC Proteins

A
  • Unique to an individual
  • Each MHC molecule displays a self-antigen
  • In infected cells, MHC proteins bind to fragments of non-self antigens
  • MHC proteins play a role in mobilizing the immune system
38
Q

Specific (Adaptive) Immune System

A
  • Lymphocytes:
    - T lymphocytes – do not make antibodies (control cellular immunity)
    • B lymphocytes – make antibodies (control humoral immunity)
  • Antigen-presenting cells (APCs):
    • Do not respond to specific antigens
    • Play auxiliary roles in immunity
39
Q

Lymphocyte Maturation

A
  • Immature lymphocytes released from bone marrow are all identical
  • Whether a lymphocyte becomes a B cell or a T cell depends on where in the body it matures (immunocompetent)
    • B cells mature in Bone Marrow
    • T cells mature in the Thymus
40
Q

Immunocompetent B or T cells

A
  • Have receptors that respond to specific antigens
  • Become immunocompetent before they encounter antigens
  • Are exported to lymphoid tissue where they encounter antigens
  • Mature into antigen-activated cells upon binding w/ their recognized antigen
41
Q

Lymphocyte Maturation

A

SLIDE 50, know the picture.

42
Q

Antigen-Presenting Cells (APCs)

A
  • Functions:
    • Engulf foreign matter
    • Present fragments of antigens on their surfaces to be recognized by T cells
  • APCs: macrophages
43
Q

Antigen-Presenting Cells (APCs) Macrophages

A
  • Macrophage engulfs foreign cells
  • Attaches foreign antigens (yellow) onto their MHC proteins (green)
  • APC presents antigens to Helper T-cells which activate the Helper T-cells
44
Q

Activated Helper T-Cells

A

Release Chemicals:

 - Stimulate macrophages to become activated macrophages
 - Activated macrophages secrete bactericidal chemicals
45
Q

Helper T-Cell Function

A

SLIDE 56, be able to draw and label picture. ESSAY QUESTION

46
Q

Cytokines Chemicals (three)

A
  • Chemicals used in cellular immunity:
    • Interleukin I
    • Interleukin II
    • Perforin
47
Q

Cytokines (Interleukin I)

A
  • Produced by macrophages (APC cells)

- Stimulates (activates) Helper T-cells

48
Q

Cytokines (Interleukin II)

A
  • Produced by Helper T-cells
  • Stimulates (activates) Cytotoxic T-cells
  • Stimulates (activates) B-cells
49
Q

Cytokines (Perforin)

A
  • Produced by cytotoxic T cells

- Causes lysis (punches holes) in target cells membranes

50
Q

Cytotoxic T-Cells (Killer T-Cells)

A
  • Stimulated by Helper T-Cells
  • Destroy body cells infected with viruses
  • Destroy cancer cells
51
Q

Memory Cells

A
  • T-Cells & B-Cells “remember” an antigen

- React to a second invasion of an antigen more rapidly

52
Q

Regulatory Cells

A

-Stop T-Cell & B-Cell activity after an infection has been conquered

53
Q

Specific (Adaptive) Immunity: Summary

A
  • Two-part defensive system
  • Uses B-lymphocytes, T-lymphocytes & APCs to identify & destroy nonself substances
  • Recognizes foreign substances (antigens)
  • Cells communicate w/ one another so entire immune system mounts a response specific to those antigens
54
Q

Humoral Immunity Response

A
  • Antigen challenge – 1st encounter between antigens & naive immunocompetent cells
  • 1st encounter happens in lymphoid organs
  • If the lymphocyte is a B-cell:
    • Antigen stimulates a humoral immune response
    • Antibodies are made against the antigen by the B-cell
55
Q

Clonal Selection

A
  • B-cells form clones with the same antigens specific receptors
  • Immuocompetent B-cells activate when antigens bind to their receptors
56
Q

B Cell: Summary

A
  • B-Lymphocytes react directly w/ antigens
  • Require stimulation from Helper T-Cells
  • Offspring become Plasma Cells & Memory B-Cells
  • Humoral Immunity
57
Q

Primary & Secondary Responses

A

SLIDE 70, know the picture.

58
Q

B Cells Clones

A
  • Most B-cell clones become antibody-secreting plasma cells
    • Plasma cells make 2000 antibodies/sec
    • Secreted antibodies bind to antigens & mark antigens for destruction
    • Some B-cell clones become memory cells
    • Memory cells mount an immediate response if future exposures to same antigen occurs
59
Q

Lymphocyte Summary

60
Q

Primary Immune Response

A
  • Primary immune response:
    • 1st exposure to a specific antigen
    • Delay period: 3-6 days after antigen challenge
    • Peak levels of antibody are reached in 10 days & then decline
61
Q

Secondary Immune Response

A
  • Secondary immune response: re-exposure to same antigen
    • Memory cells respond quickly
    • Delay period: hours after antigen challenge
    • Antibody levels peak in 2-3 days at higher levels than primary response
    • Antibody levels remain high for weeks to months
62
Q

Active Humoral Immunity

A
  • B cells encounter antigens & produce antibodies against the antigens
    • Natural Active – response to a bacterial or viral infection
    • Artificial Active – response to a vaccine of dead or attenuated pathogens
  • Vaccines – spare us the symptoms of a disease
    • Weakened antigens provide antigenic determinants & are immunogenic
63
Q

Passive Humoral Immunity

A
  • Differs from active immunity in antibody source & level of protection
    • B cells are not challenged by antigens
    • Immunological memory does not occur
    • Ends when antibodies degrade
  • Natural Passive – mother to fetus via placenta
  • Artificial Passive – injection of antibodies (gamma globulin)
64
Q

Acquired Immunity- Naturally Acquired

A
  • Active
    • Infection; contact with pathogen
  • Passive
    • Antibodies pass from mother to fetus via placenta; or to infant in her milk
65
Q

Acquired Immunity- Artificially Acquired

A
  • Active
    • Vaccine; dead or attenuated pathogens
  • Passive
    • Injection of immune serum (gamma globulin)
66
Q

Antibodies

A
  • Also called immunoglobulins
    • Made by activated B cells & plasma cells in response to an antigen
    • Capable of binding only w/ that antigen
  • Five classes of antibodies: IgM, IgA, IgD, IgG, IgE (MADGE)
67
Q

Antibody Classes

A
  • IgM: made by plasma cells
  • IgA: prevents pathogen attachment to cell surface; in lactiferous secretions (passive immunity)
  • IgD: activates B-cells
  • IgG: most abundant/diverse antibody; crosses placenta (passive immunity)
  • IgE: activate mast cells & basophils to release histamine
68
Q

Basic Antibody Structure

A
  • Antibodies: 4 protein chains
    • 2 identical Heavy (H) chains
    • 2 identical Light (L) chains
  • Each chain has a constant (C) region at one end
  • Each chain has a variable (V) region at the other end
    • Variable regions form antigen-binding site
69
Q

Antibody Targets

A
  • Antibodies don’t destroy an antigen (they inactivate it or tag it for destruction)
  • Plasma cells can make a billion different antibody types
  • Antibody mechanisms: complement fixation/activation, neutralization, agglutination, precipitation
70
Q

Complement Fixation & Activation

A
  • Complement fixation:
    • Used against cell antigens
    • Antibodies attach to cell (promote cell lysis)
  • Complement activation:
    • ↑Inflammation
    • ↑Phagocytosis
71
Q

Neutralization

A
  • Neutralization:
    • Antibodies block active sites on viruses or bacteria
    • Prevents antigens from binding to body cells
72
Q

Agglutination & Precipitation

A
  • Agglutination: antigen-antibody complexes cause clumping

- Precipitation: small soluble molecules → large insoluble complexes

73
Q

Antibody Action

74
Q

Immunodeficiencies

A
  • Function of immune system is abnormal
    • Acquired immunodeficiency
    • Congenital immunodeficiency
75
Q

Acquired Immunodeficiencies

A
  • Acquired immune deficiency syndrome (AIDS)
  • Characteristics:
    • Weight loss
    • Swollen lymph nodes
    • Opportunistic infections occur (pneumonia)
76
Q

AIDS

A
  • Caused by human immunodeficiency virus (HIV) transmitted via body fluids
  • HIV enters the body through blood transfusions, contaminated needles, unprotected sex
  • Dates back to 1880’s & is descended from a chimpanzee virus in Africa – Nature
  • HIV: Destroys helper T cells (↓Cell-mediated immunity)
  • HIV multiplies in lymph nodes-no symptoms
  • Symptoms: months to years…or never!
  • HIV’s surface protein attaches to the CD4 receptor on the helper T cell
  • HIV enters the cell
  • HIV reverse transcriptase produces DNA from viral RNA
  • DNA directs the cell to make new viruses
  • Viruses reproduce & infect other cells
  • HIV reverse transcriptase is not accurate & produces frequent errors (mutations)
    • High mutation rate causes drug resistance
  • Treatments:
    • Reverse transcriptase inhibitors (AZT)
    • Drugs are currently being developed to block HIV’s entry into T-cells (CD4 receptor)
77
Q

Autoimmune Diseases

A
  • Immune system cannot distinguish self from nonself
  • Body produces autoantibodies that destroy body tissues
  • Examples:
    - Multiple Sclerosis, Myasthenia Gravis, Graves’ disease, Lupus, Type I diabetes mellitus, rheumatoid arthritis, glomerulonephritis (Bright’s disease
78
Q

Autoimmune Disease Mechanisms

A
  • New self-antigens appear:
    • 1) Gene mutations generate new self-antigens
    • 2) Infectious damage changes original self-antigens
  • If determinants on foreign antigens resemble self-antigens:
    • Antibodies made against foreign antigens cross-react w/ self-antigens
79
Q

Practical Aspects

A
  • Immune system is impaired by:
    • Stress
    • Depression
    • ↓Protein diets
    • Sleep deprivation
  • With ↑age…the immune system becomes less efficient

A&P 2 (7 decks)

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