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Microorganisms > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

what are the components of the immune system?

A

blood (serum) and lymph (lymph system)

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2
Q

what do cells, proteins, and supporting systems do?

A
  • kill or inactivate invaders

- reacts to chemicals and allergens and monitor every cell in the body for cancer

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3
Q

what are the advantages to the immune system?

A
  • kills bacteria, viruses, fungi, and parasites
  • kills human cells infected with intracellular pathogens
  • neutralizes (inactivates) viruses and toxins produced by bacteria
  • kills altered human cells such as tumor or cancer cells
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4
Q

what are some disadvantages to the immune system?

A
  • may cause hypersensitivity reactions such as allergic reactions and interferes with organ and tissue transplant
  • may cause autoimmune diseases
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5
Q

what are the two types of immunity?

A
  • innate (natural) immunity

- acquired (adaptive) immunity

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6
Q

innate immunity

A

inbuilt immunity to resist infection anatomical defenses, inflammation, fever, phagocytosis, and complement proteins

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7
Q

acquired immunity

A

immunity established to adapt to infection specificity, tolerance, and memory

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8
Q

primary organs and tissues of the immune system

A

bone marrow and thymus

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9
Q

secondary organs and tissues of the immune system

A

lymph nodes, spleen, tonsils, and lymphoid tissues, BALT, MALT, and SALT

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10
Q

SALT

A

skin-associated lymphoid tussues

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11
Q

MALT

A

mucous-associated lymphoid tissue

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12
Q

BALT

A

bronchial-associated lymphoid tissue

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13
Q

RBC

A

no role in immune system, carry oxygen to tissues, platelets are a clotting factor

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14
Q

lymphocytes

A

B, T, and K cells

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15
Q

granulocytes

A

neutrophils, basophils, and eosinophils

- release and degranulate in response to allergic reactions

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16
Q

neutrophils

A

essential blood phagocytes, active engulfers and killers of bacteria; phagocytic, major defense against extra-cellular infections

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17
Q

basophils

A

function in inflammatory events and allergies; granulocytes

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18
Q

eosinophils

A

active in worm and fungal infections, allergy, and inflammatory reactions; against parasites

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19
Q

monocytes

A

blood phagocytes that rapidly leave the circulation; mature into macrophages and dendritic cells

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20
Q

macrophages

A

largest phagocytes that ingest and kill foreign cells, strategic participants in certain specific immune reactions, APC, resides in tissues;

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21
Q

dendritic cells

A

relatives of macrophages that reside throughout tissues, responsible for processing foreign matter and presenting it to lymphocytes; phagocytic cells, APC

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22
Q

lymphocytes

A

primary cells involved in specific immune reactions to foreign matter

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23
Q

T cells

A

perform a number of specific cellular immune responses such as assisting B cells and killing foreign cells (CMI)

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24
Q

B cells

A

differentiate into plasma cells and form antibodies (AMI); main players in AMI

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25
Q

mast cells

A

granulocytes, releases inflammatory compounds

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26
Q

first line of defense

A

Nonspecific defense system that prevents pathogens from
entering the body
• Includes: skin and mucous membranes of the respiratory,
digestive, urogenital tracts

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27
Q

skin defenses

A

-Perspiration (high salt), Sebaceous glands secrete oil (low pH)
• Lysozyme- destroys cell wall of bacteria
– Epidermis, Tightly packed layer of cells, Shedding of dead cells

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28
Q

mucous membrane defenses

A

Line body cavities open to the outside
– Epithelium
• Thin layer composed of tightly packed live cells
• Continual shedding of cells carries attached germs
away

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29
Q

microbial antagonism

A

Normal flora:
– Compete with pathogens for space, nutrients
– Promote overall health by providing vitamins to host

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30
Q

mucociliary blanket

A

mucous secretions that traps microbes

  • once trapped, microbes transported away from the lungs
  • can be expelled by coughing and sneezing
  • salvation washes microbes to stomach
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31
Q

what are the components of the second line of defense?

A
  • Phagocytosis
  • Extracellular killing (NK cells)
  • Inflammation
  • Fever
  • Complement System
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32
Q

phagocytosis

A

process by which monocytes, macrophages, neutrophils, and dendritic cells recognize, ingest, and digest extracellular microbes
• Binds to microbe. Internalize it. Fuse it with lysosome. Digest the microbe

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33
Q

hydrolytic enzymes

A

Lipase, Nuclease, Protease, lysozyme

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34
Q

respiratory burst

A

reactions occur as soon as phagosome is formed

– toxic oxygen products are produced which can kill invading microbe

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35
Q

phagocytic failure

A

Bacteria may survive the killing. Bacteria may prevent fusion of lysosome with phagosome. Or, Bacteria may produce chemicals that kills or inhibit phagocytic cells

36
Q

anti-phagocytic factors

A
  • Capsule (hard to engulf)
  • Carotenoid (antioxidant that neutralizes oxygen)
  • Leukocidine (kills phagocytic cells)
37
Q

inflammation

A

The release of inflammatory mediators from injured tissue cells initiates
a cascade of events which result in the signs of inflammation
• nonspecific response to tissue injury due to infection or physical means
• cardinal signs, redness, warmth, pain, swelling, and altered function

38
Q

acute inflammatory response

A

involves chemical mediators
• Quickly developed, beneficial, promotes healing
– events which result in elimination of invading pathogens
• capillary dilation and increased blood flow
• temperature rise stimulates inflammatory response
• restrict pathogen movement
• Recruit phagocytes to the area

39
Q

chronic inflammation

A

slow process

• Slow and causes permanent tissue damage

40
Q

fever

A

Pyrogens (chemicals) trigger the hypothalamus to increase the body’s core temperature, temperature over
37C (98.6 F)

41
Q

what are the types of pyrogens

A

Bacterial toxins
– Cytoplasmic contents of bacteria released by lysis
– Antibody-antigen complexes (inflammation)
– Interleukins-1 (IL-1)
- Muscle contractions, increased metabolic activity, and constriction of blood vessels/reduced blood flow, raises the temperature

42
Q

pyrogen

A

fever inducing

43
Q

pyogen

A

puss forming

44
Q

serum proteins

A
  • destroy extracellular bacteria and viruses
    -function as chemotactic signals that recruit phagocytes
    -puncture cell membranes causing cell lysis
    -many complement activities unite the nonspecific and specific arms of
    the immune system to destroy and remove invading pathogens
45
Q

complement proteins

A
  • group of 20 or more proteins that bind and destroy infection
  • normally not active, bind to the surface of bacteria and accumulate and poke a hole and kill it
46
Q

antibody

A

identifies bacteria and complement binds

47
Q

MAC

A

membrane attack complex that pokes holes in bacteria to kill it, attracts phagocytes to the area, and aid phagocytes in doing their job

48
Q

classical complement pathway

A

dependent on antigen-antibody interaction

49
Q

lectin complement pathway

A

nonspecific defense against intravascular invasion by bacteria and fungi

50
Q

opsonization

A

coating of microbes by serum proteins, which assist with recognition/ingestion by phagocytic cells
– molecules that carry out above are called opsonins, such as antibody and complement proteins
– bind to microbial cells, coating them for phagocyte recognition

51
Q

acute phase proteins

A

macrophage activation by bacteria  cytokine release liver stimulation Produce acute phase protein
– includes C-reactive protein (CRP), mannan-binding lectin (MBL)
• can bind bacterial surfaces and act as opsonins

52
Q

antigens

A
  • elicit an immune response and B cells and T cells are activated in response to each specific antigen
  • most are large, complex molecules Size restriction
  • can have several antigenic determinant sites (epitopes)
53
Q

how do antigens enter into the body?

A

– Breaks in the skin and mucous membranes
– Via bite or needle (injection)
– Via grafts and organ transplant
– Autoimmunity

54
Q

what can antigens be?

A

– Cell wall, capsule, pili, flagella, and proteins of viruses, fungi,
and protozoa
– Food and dust can also contain antigenic particles

55
Q

haptens

A

small organic molecules
not antigenic by themselves but may become antigenic when bound
to larger carrier molecule e.g., penicillin

56
Q

adjuvents

A

added to vaccine (inactivated microbes) to make them

more antigenic

57
Q

IgG

A

major circulating antibody

58
Q

IgM

A

first to appear after infection

59
Q

IgA

A

major antibody in secretions

60
Q

IgE

A

involved in allergic reactions

61
Q

what are the components of the third line of defense?

A

antibodies

62
Q

what are the consequences of antigen-antibody binding?

A

opsonization, angulation, complement reaction, neutralization, and precipitation

63
Q

cytokines

A

Soluble proteins or glycoproteins that act as mediators
– released by one cell population that act as intercellular mediators or signaling molecules
• Autocrine Function, self
• Paracrine function, nearby
• Endocrine function, systemic

64
Q

what are the classes of cytokines?

A

– Tumor necrosis factor (TNF)
– Interleukins
– colony-stimulating factors (CSFs)
– Interferons (INFs)

65
Q

MHC

A
  • major histocompatibility complex
  • receptor molecules are like fingerprints
  • on all cells except RBC
66
Q

T-independent antigen

A
  • antigen processing
  • Large molecules/Bind to B cells.
    resulted in B cell activation and Ab production, No need to
    APC
67
Q

T-dependent antigens

A

Small molecules, APC
needed to process them and present them to T
helper cells

68
Q

CMI

A
  • cellular mediated immunity

- T cells to memory T cells and effector T cell, the Effector T cell turns into cytokines

69
Q

AMI

A
  • antibody-mediated immunity

- B cells turn into memory B cell and plasma cell, and plasma cell turns into antibody

70
Q

consequences of antigen-antibody binding

A

neutralize toxins

  • neutralize viruses
  • marks invaders for attack by immune system components
  • Activate complement system
  • aids phagocytosis (opsonization)
  • Stimulate inflammation
71
Q

natural immunity

A

acquired through the normal life experiences of a human and is not induced through medical means
- active (infection) and passive(breastmilk) forms

72
Q

artificial immunity

A
  • produced purposefully through medical procedures - immunizations
  • active (vaccination) and passive (immune globulin therapy) forms
73
Q

attenuated vaccines

A

Live/weakened strains/reducing virulence
• Mild infections/no disease, strong immune response/ triggers CMI
• Viral vaccines trigger a cell-mediated immune response
• Results in herd immunity
• Problems: with reversion, with immunosuppressed, with pregnant

74
Q

inactivated vaccines

A

Dead microbes or their fragments
• Problems: May causes inflammatory response and no herd immunity
• Antigenically weak, and needs high or multiple doses, or the incorporation of an
adjuvant, to make the vaccine more effective, (also may produce allergic reactions)

75
Q

toxoid vaccines

A

Chemically or thermally modified toxins
• Useful for some bacterial diseases/ Stimulate antibody-mediated immunity/ Require
multiple doses

76
Q

vaccine safety

A

• Mild toxicity is the most common problem, or may cause disease or allergic reactions
• Anaphylactic shock
• Allegations that certain vaccines against childhood diseases cause or trigger autism,
diabetes, and asthma, Research has not substantiated these allegations

77
Q

donor-recipient matching

A

MHC compatibility between donor and recipient is hard to achieve due
to a high degree of MHC variability among individuals
• Host T helper cells recognizes foreign MHC molecules on the transplanted tissue (graft),
which aid cytotoxic T cells in destroying the graft, OR T-helper cells releases cytokines
which stimulate destruction of graft by macrophages

78
Q

graft-versus-host disease

A

Graft cells attack the recipient tissues
• e.g., in bone marrow transplants
– disease prevented by treating donor with immunosuppressive drugs to deplete marrow of
mature T cells

79
Q

why are fetuses not rejected?

A

– The fetus is not a privileged site but is not rejected
– Rejection is prevented by the many different immunosuppressive mechanisms
• Early embryos do not express MHC class I and II molecules on the placental layer that is in contact with maternal
tissues
• Cytokines that enhance MHC expression have no effect on placental cells
• T cells are prevented from functioning in the placenta to reject the fetus

80
Q

autoimmunity

A

– presence of serum antibodies against self antigens (autoantibodies)
– often benign/natural consequence of aging/induced by infectious organisms, drugs…

81
Q

autoimmune disease

A

– results from activation of self-reactive T and B cells/leads to tissue damage

82
Q

immunodeficiency

A
  • Conditions resulting from defective immune mechanisms
  • failure to recognize and/or respond properly to foreign antigens
  • Opportunistic infections can play an important part of these diseases
83
Q

primary immunodeficiency

A
  • Result from some genetic or developmental defect

* Develop in infants and young children

84
Q

acquired immunodeficiency

A
  • Develop as a direct consequence of some other recognized cause
  • Develop in later life
  • Sever Stress: Excess production of corticosteroids suppresses CMI
  • Malnutrition: Inhibit B cells and T cells development
85
Q

clinical immunology:

A

Serology; study and diagnostic

use of antigen-antibody interactions in serum

Microorganisms (11 decks)

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