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Micro > Micro Exam 4- Chapter 16 & 17 > Flashcards

Micro Exam 4- Chapter 16 & 17 Flashcards

1
Q

Immunity:

A

ability to ward off disease

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2
Q

Susceptibility:

A

lack of resistance to a disease

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3
Q

Two types of immunity

A
  1. Innate immunity:
  2. Adaptive immunity:
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4
Q

Innate immunity

A

: defenses against any pathogen

First & Second Line of Defense

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5
Q

Adaptive immunity:

A

immunity or resistance to a specific
pathogen

3rd Line of Defense

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6
Q

An overview of the body’s defenses

A
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7
Q

The Concept of Immunity

A

Responses of the innate system are activated by protein
receptors (Toll like receptors; TLRs) in the plasma
membranes of defensive cells

TLRs attach to components on pathogens known as
pathogen associated molecular patterns (PAMPS)

Host receptors induce cytokines(proteins) that regulate the
intensity and duration of immune responses

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8
Q
  1. Physical Factors
    ▪ Include barriers to entry and processes that remove microbes from the body’s surface
A

SKIN

Epidermis consists of tightly packed epithelial cells with

Keratin, a protective protein

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9
Q

MUCOUS MEMBRANES

A

▪ Mucous membranes line GI, respiratory, and reproductive tracts and contain mucus
▪ Mucus: traps microbes
▪ Ciliary escalator: transports microbes trapped in mucus away from the lungs

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10
Q

Mucous membrane examples

A

▪ Lacrimal apparatus: Tears, washes eye
▪ Saliva: washes microbes off
▪ Mucus: coated hairs of nose
▪ Urine: flows out
▪ Vaginal secretions: flow out
▪ Defecation, vomiting and diarrhea

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11
Q
  1. Chemical Factors
A

▪ Unsaturated (Fungistatic) fatty acid in sebum
▪ Secreted by sebaceous glands of skin
▪ Inhibit growth of some bacteria
▪ Keep pH of skin low
▪ Lysozyme in perspiration, tears, saliva, and urine
▪ Low pH (1.2–3.0) of gastric juice
▪ Low pH (3–5) of skin
▪ Low pH (3–5) of vaginal secretions
▪ Low pH (6) of urine

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12
Q
  1. Normal Microbiota and Innate Immunity
A

▪ Microbial antagonism/competitive exclusion: normal microbiota compete with pathogens or alter the environment
▪ Commensal microbiota: one organism (microbe) benefits, and the other (host) is unharmed
▪ May be opportunistic pathogens

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13
Q

SECOND LINE OF DEFENSE

A

Phagocytosis

▪ Phago: from Greek, meaning eat
▪ Cyte: from Greek, meaning cell

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14
Q

Phagocytosis:

A

Ingestion of microbes or particles by a cell, performed by phagocytes
▪ Phagocytes of the white blood cell system are
“professional phagocytes”

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15
Q

Neutrophils:

A

numbers increase in a bacterial infection

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16
Q

▪ Macrophages:

A

dominate in later stages of infection
• Fixed macrophages
• Wandering macrophages

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17
Q

Formed Elements in Blood

A

Polymorphonuclear neutrophils (PMNs)

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18
Q

Formed Elements in Blood

A
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19
Q

Differential White Cell Count
Percentage of each type of white cell in a sample of 100 white blood cells

A
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20
Q

Mechanism of Phagocytosis

A
  1. Chemotaxis- chemical attraction of phagocytes to microbe
  2. Adherence- the binding of a bacterium to a phagocyte
    ▪ Capsule and M protein prevent adherence
    ▪ Opsonins (antibodies and complement factor) promote adherence and hence phagocytosis
  3. Ingestion- Pseudopods extend and engulf microbe inside a phagosome
  4. Digestion- Phagosome and lysosome fuse together and the enzymes break down the microbe
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21
Q

The Phases of Phagocytosis

A
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22
Q

Inflammation

A

▪ Redness
▪ Swelling (edema)
▪ Pain
▪ Heat

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23
Q

Stages of Inflammation

A
  1. Vasodilation
    • blood vessels dilate and become more permeable
    • Release histamine, kinins, prostaglandins, and leukotrienes
  2. Phagocyte Migration and Phagocytosis

An hour after inflammation starts, phagocytes appear.

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24
Q

Phagocyte Migration and Phagocytosis

A
  1. Margination- Neutrophils and monocytes stick to the lining of the blood vessels.
  2. Diapedesis- Phagocytes squeeze between the cells in the lining of the vessels out into the tissue.
  3. Phagocytosis begins.
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25
Q

Chemicals Released by Damaged Cells

A
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26
Q

Process of Inflammation

A
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27
Q

Process of Inflammation

A
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28
Q

Process of Inflammation

A
29
Q

Fever

A

▪ Abnormally high body temperature
▪ Hypothalamus is normally set at 37C
▪ Gram-negative endotoxins cause phagocytes to release interleukin-1 (IL-1)
▪ IL-1 causes hypothalamus to release prostaglandins that reset the hypothalamus to a high temperature.
▪ Temperature will stay raised until all IL-1 is gone.
▪ In response, body increases rate of metabolism, and shivering occurs, which raise temperature
▪ When hypothalamus is reset, vasodilation and sweating occur dropping body temperature (crisis)

30
Q

Fever Advantages

A

▪ Increases transferrins-which decrease iron availability for microbes
▪ Increases IL-1 activity-which can increase T cells
▪ Produces interferon-protection against viruses

31
Q

Fever Disadvantages

A
  • Tachycardia- increased heart rate
  • ▪ Acidosis
    ▪ Dehydration
    ▪ Seizures
    ▪ 44–46C (112-114 F) fatal
32
Q

Antimicrobial substances

A

▪ Complement (antibacterial & antiviral)
▪ Interferons (antiviral)

33
Q

The Complement System

A

Serum proteins produced that are activated in a cascade

Complements the immune system

Destroy microbes by cytolysis, inflammation, and phagocytosis

34
Q

Cascade-

A

one reaction triggers the next reaction and so on…

35
Q

Activated by Antigen-Antibody binding;

A

Complement proteins-pathogen binding

36
Q

The Complement System

A
37
Q

The third line of defense

A

Adaptive Immunity

38
Q

Adaptive immunity:

A

induced resistance to a specific pathogen Is achieved by Lymphocytes

T-Cells: Cellular immunity

B- Cells: Humoral immunity
• Immunity brought about by antibody production

39
Q

The Lymphatic System

A

▪ Lymph fluid
▪ Lymphatic vessels- one directional flow
▪ Lymph nodes- bean shaped
▪ Lymph tissue- tonsils, spleen, thymus, mucous membranes
▪ Red bone marrow- stem cells developing into blood cells

40
Q

Dual Nature of Adaptive Immune System

A
41
Q

Dual Nature of Adaptive Immunity

A
  • Humoral immunity

Due to antibodies

B cells- are responsible for producing antibodies

− B cells mature in the bone marrow
− Plasma cells: activated B cells that produce the antibodies
− Memory cells: activate on subsequent exposures.

42
Q

Dual Nature of Adaptive Immunity

A
  • Cellular immunity
  • Due to T cells
  • T cells- are responsible for producing cytokines which will send instructions to other cells (like B cells)

− T cells mature in the thymus
− Are activated by macrophages that have engulfed a bacteria and presented its antigen on its cell membrane

43
Q

▪ Antigens (Ag)

A

▪ Cell markers
▪ Protein or polysaccharide that are considered to be foreign and stimulate an immune response.

44
Q

Epitope:

A

Specific portion of the antigen recognized by the antibody

45
Q

Antibodies(Ab)-

A

produced by our bodies in response to a foreign antigen
▪ Globular proteins called immunoglobulins (Igs)

When the antibody and antigen combine, clumping occurs.

46
Q

Functions of Antibodies

A
47
Q

IgG Antibodies

A

▪ 80% of serum antibodies
▪ Triggers complement system
▪ In blood, lymph, and intestine
▪ Cross placenta (passive immunity)
▪ Enhance phagocytosis; neutralize toxins and viruses; protect fetus and newborn
▪ Half-life = 23 days indicates there has been an immune response

48
Q

IgM Antibodies

A

▪ 5–10% of serum antibodies
▪ Mainly stays In blood
▪ Responds to blood group antigens
▪ Agglutinate microbes; first Ab produced in response to infection
▪ Half-life = 5 days (better detection of current infection)

49
Q

IgA Antibodies

A

▪ 10–15% of serum antibodies
▪ Most abundant in secretions
▪ Mucosal protection
▪ Half-life = 6 days

50
Q

IgD Antibodies

A

▪ 0.2% of serum antibodies
▪ In blood, in lymph, and on B cells
▪ On B cells, initiate immune response
▪ No well know function
▪ Half-life = 3 days

51
Q

IgE Antibodies

A

▪ 0.002% of serum antibodies
▪ On mast cells, on basophils, and in blood
▪ Respond to Allergic reactions and of parasitic worms
▪ Half-life = 2 days

52
Q

Activation of B Cells

A

▪ B cells differentiate into:
▪ Antibody-producing plasma cells
▪ Memory cells

53
Q

Antigen–Antibody Binding

A

▪ Agglutination
▪ Opsonization: coating with antibodies
▪ Activation of complement:(IgG or IgM)
▪ Antibody-dependent cell-mediated cytotoxicity
▪ Destruction is achieved by other cells besides antibody secreting cells
▪ Neutralization – prevents attachment to other host cells

54
Q

T Cells and Cellular Immunity

A
  • T cells mature in the thymus
  • T cells respond to Ag by T-cell receptors
  • T cells require antigen-presenting cells (APC) which digest antigen
55
Q

T Helper Cells

A

▪ recognize Ags on APC
▪ T cells produce cytokines and differentiate into:
− T-cells
− Memory cells

56
Q

Activation of CD4+T helper cells

A
57
Q

T Cytotoxic Cells

A

▪ or TC cells
▪ Activated into cytotoxic T lymphocytes (CTLs)
▪ Induce apoptosis in target cell

58
Q

T Regulatory Cells

A

▪ Suppress T cells against self
▪ Suppress an immune response

59
Q

Natural Killer (NK) Cells

A

▪ Kill virus-infected and tumor cells
▪ Attack parasites

60
Q

Immunological Memory

A

▪ Antibody titer is the amount of Ab in serum
▪ Primary response occurs after initial contact with Ag
▪ Secondary (memory or anamnestic) response occurs after second exposure

61
Q

Types of Adaptive Immunity

▪ Naturally acquired active immunity

A

▪ Resulting from infection

62
Q

▪ Naturally acquired passive immunity

A

▪ Transplacental or via colostrum

63
Q

▪ Artificially acquired active immunity

A

▪ Injection of Ag (vaccination)

64
Q

▪ Artificially acquired passive immunity

A

▪ Injection of Ab

65
Q

▪ Serology:

A

the study of reactions between antibodies and antigens

66
Q

▪ Antiserum:

A

the generic term for serum because it contains Ab

67
Q

▪ Globulins:

A

serum proteins

68
Q

▪ Gamma () globulin:

A

serum fraction containing the most Ab

69
Q

▪ Immunoglobulins:

A

antibodies

Micro (7 decks)

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