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

Micro Exam 4- Chapter 16 & 17 Flashcards

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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
Chemicals Released by Damaged Cells
26
Process of Inflammation
27
Process of Inflammation
28
Process of Inflammation
29
Fever
▪ 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
Fever Advantages
▪ Increases transferrins-which decrease iron availability for microbes ▪ Increases IL-1 activity-which can increase T cells ▪ Produces interferon-protection against viruses
31
Fever Disadvantages
* Tachycardia- increased heart rate * ▪ Acidosis ▪ Dehydration ▪ Seizures ▪ 44–46C (112-114 F) fatal
32
Antimicrobial substances
▪ Complement (antibacterial & antiviral) ▪ Interferons (antiviral)
33
The Complement System
Serum proteins produced that are activated in a cascade Complements the immune system Destroy microbes by cytolysis, inflammation, and phagocytosis
34
**Cascade-**
one reaction triggers the next reaction and so on…
35
**Activated by Antigen**-Antibody binding;
Complement proteins-pathogen binding
36
The Complement System
37
The third line of defense
Adaptive Immunity
38
**Adaptive immunity:**
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
The Lymphatic System
▪ 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
Dual Nature of Adaptive Immune System
41
Dual Nature of Adaptive Immunity
* **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
Dual Nature of Adaptive Immunity
* **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
▪ **Antigens (Ag)**
▪ Cell markers ▪ Protein or polysaccharide that are considered to be foreign and stimulate an immune response.
44
**Epitope:**
Specific portion of the antigen recognized by the antibody
45
**Antibodies(Ab)-**
produced by our bodies in response to a foreign antigen ▪ Globular proteins called **immunoglobulins (Igs)** **When the antibody and antigen combine, clumping occurs.**
46
Functions of Antibodies
47
**IgG Antibodies**
▪ 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
**IgM Antibodies**
▪ 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
**IgA Antibodies**
▪ 10–15% of serum antibodies ▪ Most abundant in secretions ▪ Mucosal protection ▪ Half-life = 6 days
50
**IgD Antibodies**
▪ 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
**IgE Antibodies**
▪ 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
Activation of B Cells
▪ B cells differentiate into: ▪ Antibody-producing **plasma cells** ▪ **Memory cells**
53
Antigen–Antibody Binding
▪ 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
T Cells and Cellular Immunity
* 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
T Helper Cells
▪ recognize Ags on APC ▪ T cells produce cytokines and differentiate into: − T-cells − Memory cells
56
Activation of CD4+T helper cells
57
**T Cytotoxic Cells**
▪ or **TC** cells ▪ Activated into **cytotoxic T lymphocytes (CTLs)** ▪ Induce **apoptosis** in target cell
58
T Regulatory Cells
▪ Suppress T cells against self ▪ Suppress an immune response
59
Natural Killer (NK) Cells
▪ Kill virus-infected and tumor cells ▪ Attack parasites
60
Immunological Memory
▪ **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
Types of Adaptive Immunity ## Footnote ▪ Naturally acquired active immunity
▪ Resulting from infection
62
▪ Naturally acquired passive immunity
▪ Transplacental or via colostrum
63
▪ Artificially acquired active immunity
▪ Injection of Ag (vaccination)
64
▪ Artificially acquired passive immunity
▪ Injection of Ab
65
▪ Serology:
the study of reactions between antibodies and antigens
66
▪ Antiserum:
the generic term for serum because it contains Ab
67
▪ Globulins:
serum proteins
68
▪ Gamma () globulin:
serum fraction containing the most Ab
69
▪ Immunoglobulins:
antibodies

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