Chapter 16-Exam 3 Flashcards

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1
Q

able to be productively infected

A

susceptibility

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2
Q

unable to allow a productive infection

A

resistance

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3
Q

an active process that prevents establishment or progression of an infection

A

immunity

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4
Q

defenses against any pathogen, present at birth

A

innate immunity

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5
Q

First line of defense in the immune system

A

physical and chemical factors & normal microbiota:

  • intact skin
  • mucous membrane and their secretions
  • lacrimal apparatus
  • ciliary escalator
  • epiglottis
  • saliva
  • urine
  • vaginal secretions
  • peristalsis, defecation, vomiting
  • normal microbiota
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6
Q

Second line of defense in the immune system

A

non-specific physiologic processes:

  • phagocytes such as neutrophils, eosinophils, dendritic cells, and macrophages
  • inflammation
  • fever
  • antimicrobial substances
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7
Q

Third line of defense in the immune system

A

adaptive immunity:

  • specialized B and T cells (lymphocytes)
  • antibodies
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8
Q

specific resistance to a specific pathogen, develops overtime

A

adaptive immunity

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9
Q

physical factors of innate immunity that: block

A

skin, mucous membrane, epiglottis

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10
Q

physical factors of innate immunity that: trap

A

mucus, hairs

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11
Q

physical factors of innate immunity that: wash

A

tears, saliva, urine, vaginal secretions

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12
Q

physical factors of innate immunity that: move

A

cilia, peristalsis, defecation, vomiting

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13
Q

cutaneous membrane

A

skin: covers the body surface and provides a physical barrier to the entrance of microbes

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14
Q

mucous membranes

A

line the body cavities and are open to the exterior of the body

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15
Q

Epidermis

A

consists of tightly packed cells with a thick layer of keratin- containing dead cells

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16
Q

_________ inhibits microbes (Epidermis)

A

dryness

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17
Q

_________ blocks microbes (Epidermis)

A

water-tightness

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18
Q

_________ removes microbes (Epidermis)

A

shedding

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19
Q

inner layer of skin that is made of connective tissue

A

dermis

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20
Q

______ ________ are in the dermis

A

blood vessels

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21
Q

Why can microbes get into the blood stream if they are found in the dermis?

A

Endothelial cells of vessels are not densely packed, and can allow microbes to pass by them

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22
Q

What is the purpose of the keratinized layer in the epithelium?

A

to provide an air-tight barrier

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23
Q

How do mucous membranes differ from cutaneous membranes?

A

They do not have a water- tight keratinized layer above the living cells and instead of having squamous epithelium, they have goblet cells that produce mucous that protects the epidermis.

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24
Q

What systems do the mucus membranes line?

A

mucus membranes are an epithelial layer lining the respiratory, gastrointestinal, urogenital, visual, and auditory
systems.

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25
Q

traps microbes in respiratory and GI tracts

A

mucus

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26
Q

What components make up mucus?

A

a mix of glycoproteins and water

contains many anti-microbial substances

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27
Q

surface projections on cells of the respiratory
tract that move mucus and trapped microbes out of the
upper respiratory tract.

A

cilia

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28
Q

Which is more effective: mucus membranes or the skin?

A

skin

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29
Q

What is the ciliary escalator, and how far does it move the ciliary blanket? What can speed it up?

A

The ciliary escalator is also known as ciliary clearance and it is the self-clearing mechanism of the bronchi.
ciliary escalator moves the mucus blanket 1-3 cm/hr
coughing speeds up the movement

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30
Q

What pathway does tear flow take?

A

Tears flow from lacrimal glands under eyelid to

lacrimal canal

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31
Q

_________ and _________ by tears keeps microbes from settling on eye surface

A

washing; dilution

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32
Q

chemical factors that are part of the first line of defense

A
  • sebum
  • lysozyme
  • saliva
  • gastric juice
  • urine
  • vaginal secretions
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33
Q

What is sebum? What is it made out of?

A

Sebum is the oily secretion of the
sebaceous glands that are embedded in the skin. Sebum is a complex mixture of lipids (many fatty
acids and triglycerides) that have anti-microbial
activity.

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34
Q

______ and ______ also contain many nutrients that bacteria and fungi may use to grow

A

sweat and sebum

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35
Q

what pH inhibits bacteria and fungi?

A

pH of 6 or lower

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36
Q

pH 1.2–3.0

A

gastric juice (hydrochloric acid)

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37
Q

pH (3–5)

A

vaginal secretions and skin

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38
Q

a substance made by saliva or urine that acts as a bacteriostatic or bactericidal for many species

A

urea

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39
Q

What is a lysozyme? Who discovered it?

A

Lysozyme is a small enzyme that attacks the peptidoglycan chains in the cell walls of bacteria, causing the cells to burst. Alexander Flemming (who discovered
penicillin) discovered lysozyme as an antibiotic.

40
Q

What are Hematopoeitic cells and what do they function as in the second line of defense?

A

perform a variety of functions
- red blood cells carry O2 and CO2
- white blood cells function in immunity and injury
travel throughout the body via the circulation
move in and out of the interstitial space (fluid
surrounding all cells of the body) by squeezing
through the endothelial cells of the blood vessels
all develop from a common stem cell

41
Q

three types of granulocytes

A
  • neutrophils
  • basophils
  • eosinophils
42
Q

three types of agraunulocytes

A
  • monocytes (macrophages)

- dendritic cells

43
Q

another term for WBCs

A

leukocytes

44
Q

key features of neutrophils

A

phagocytosis

45
Q

key features of basophils

A

histamine

46
Q

key features of eosinophils

A

kill parasites

47
Q

key features of monocytes

A

phagocytosis (APC)

48
Q

key features of dendritic cells

A

phagocytosis (APC)

49
Q

three types of lymphocytes

A
  • T cells
  • B cells
  • NK cells
50
Q

key features of T cells

A

cell-mediated immunity

51
Q

key features of B cells

A

produce antibodies

52
Q

key features of NK cells

A

destroy target cells (infected or cancerous)

53
Q

non WBCs that are involved in blood clotting

A

platelets

54
Q

Differential White Cell Count (what are the percentages of each?)

A
Neutrophils 60–70%
Basophils 0.5–1%
Eosinophils 2–4%
Monocytes 3–8%
Lymphocytes 20–25%
55
Q

what is the difference between leukocytosis and leukopenia?

A

increase in white cell count = leukocytosis

decrease in white cell count = leukopenia

56
Q

describe the pathway of lymph flow throughout the lymphatic system?

A

blood plasma —> interstitial fluid —> lymph —> blood plasma

57
Q

what type of phagocytic cells live only a short time

and predominate early in infections?

A

neutrophils

58
Q

what type of phagocytic cells last up to several months

and predominate later in infections?

A

macrophages and other wandering phagocytes

59
Q

Describe the seven phases of phagocytosis:

A
  1. chemotaxis and adherence of pseudopod
  2. ingestion of target
  3. formation of phagocytic vesicle or phagosome
  4. fusion with a lysosome, forming phagolysosome
  5. digestion of target by digestive enzymes
  6. formation of residual body
  7. discharge of indigestible material
60
Q

Define Toll-like receptors

A

TLRs are protein molecules on cell surfaces
throughout the body
TLRs are how macrophage pseudopods adhere to
bacteria
TLRs are “pattern recognition receptors,” that is,
they recognize pathogen-associated molecular
patterns, specific signatures in molecules in the
extracellular space.
TLRs that recognize bacterially-produced molecules
(such as LPS, peptidoglycan, flagellin, dsRNA), and
signal the immune system via cytokines (like TNFalpha)
that bacteria are present.

61
Q

microbes that inhibit adherance

A

Streptococcus pyogenes, S. pneumoniae (by using M proteins and capsules)

62
Q

microbes that kill phagocytes

A

Staphylococcus aureus (leukocidins)

63
Q

microbes that lyse phagocytes

A

Listeria monocytogenes (membrane attack complex)

64
Q

microbes that escape the phagosome

A

Shigella, Rickettsia

65
Q

microbes that prevent the formation of phagosome-lysosome fusion

A

HIV, Mycobacterium tuberculosis

66
Q

microbes that survive in the phagolysosome

A

Coxiella burnettii

67
Q

What is the purpose of inflammation in the second line of defense? What are some signs/ symptoms?

A
Purpose: to destroy and remove the injurious agent
limit the agent’s effects by walling it off to repair the damage
Signs and symptoms: 
Redness
Swelling (edema)
Pain
Heat
(Loss of function)
68
Q

describe the process of inflammation

A

cells damaged by infection release histamine,
prostoglandins, and other signaling molecules
blood clot and abscess form
vasodilation, increased vessel permeability
phagocytes (monocytes, neutrophils) migrate
margination
diapedesis
phagocytosis
tissue repair, epidermis and dermis regenerate

69
Q

what is margination?

A

phagocytes stick to endothelium, the blood vessel cells

70
Q

what is diapedesis?

A

phagocytes squeeze between endothelial cells

71
Q

What are the four types of signaling molecules released due to cell damage?

A
  1. histamine
  2. kinins
  3. prostaglandins
  4. leukotrienes
72
Q

Vasodilation triggered by signaling molecules
results in the _______ and _____ we association with
inflammation

A

redness and heat

73
Q

The increased permeability of blood vessels results

in _______ or ________.

A

edema or swelling

74
Q

acute inflammation vs. chronic inflammation

A

Acute inflammation, lasts relatively short time
Chronic inflammation, lasts years due to the accumulation of activated macrophages induces
fibroblasts, which synthesize collagen fibers,
resulting in fibrosis or scarring. Chronic inflammation is also a contributing factor in some cancers

75
Q

what body temperature does the hypothalamus regulate the body at?

A

37 degrees

76
Q

How is fever a second line of defense?

A

intensifies the effects of IFNs, inhibits growth of some microbes, and speeds up body reactions that aid repair

77
Q

Describe the process of fever formation at the cellular level

A

Gram-negative endotoxin cause phagocytes to
release interleukin–1 (IL–1)
Hypothalamus releases prostaglandins that reset
the hypothalamus to a high temperature
Body increases rate of metabolism and shivering
which raise temperature
Vasodilation and sweating: Body temperature falls
(crisis)

78
Q

What are some advantages and disadvantages to having a fever?

A
Advantages
- Increases transferrins
- Increases IL–1 activity
- Produces Interferon
Disadvantages
- Rapid heart beat (tachycardia)
- Acidosis (low blood pH)
- Dehydration 44–46°C (111°F) is fatal!
79
Q

What are the antimicrobial substances that are part of the second line of defense?

A
  1. complement system
  2. IFNs
  3. Iron-binding proteins
  4. antimicrobial peptides
80
Q

What is the complement system? Is it part of the innate or adaptive immune systems?

A

The complement system is an enzyme
cascade that damages bacterial plasma
membranes, increases the ability of antibodies and
phagocytic cells to clear microbes and debris, and
promotes inflammation.
It is part of the innate immune system, but works
with the adaptive immune system (that which
involves antibodies and T cells).

81
Q

Describe the Classical Pathway of Complement

Activation

A

C1 is activated by microbe-antibody complexes
C1 causes C2 to split into C2a + C2b
C1 causes C4 to split into C4a + C4b
C2a* combines with C4b, and together they split
C3
C3a and C3b initiate the complement cascade

82
Q

Once the complement pathway has been activated, what happens during the complement cascade?

A

C3b
binds to microbe and enhances phagocytosis, a
process called opsonization (enhances
phagocytosis)
splits C5
C5b, C6, C7, C8 and multiple C9 fragments form a
membrane attack complex, which punches a hole
in the microbe, causing lysis
C3a and C5a bind to mast cells which release
histamine and other signaling molecules
C5a is a chemotactic factor, which attracts
phagocytes to the infection site

83
Q

What are the key effects of the complement pathway?

A

Opsonization or immune adherence, which
enhances phagocytosis
Formation of membrane attack complex which leads
to cytolysis (cell lysis)
Attraction of phagocytes to the infected area
inflammation stimulated by complement

84
Q

causes opsonization (complement)

A

C3b

85
Q

cause cell lysis (complement)

A

C5b + C6 + C7 + C8 + C9

86
Q

cause inflammation (complement)

A

C3a + C5a

87
Q

Describe the Alternative Pathway of Complement

Activation

A
  1. C3 combines with factors B, D, and P (which are host proteins attracted to the bacterial cell surface) on the surface of the microbe
  2. This causes C3 to split into C3a and C3b
88
Q

Describe the Lectin Pathway of Complement

Activation

A
  1. Lectin binds to an invading cell
  2. Bound lectin splits C2 and C4
  3. C2a and C4b combine to activate splitting of C3
89
Q

What are some of the methods by which bacteria can evade complement?

A
  • Capsules prevent complement activation
  • Some surface lipid-carbohydrates prevent
    membrane attack complex (MAC) formation
  • Some bacterial enzymes digest C5a
    (C5a peptidase), which inhibits the infiltration of
    neutrophils and macrophages to the infection site
90
Q

What is the role of iron in innate immunity?

A
  • bacteria need lots of iron
  • iron is hard to get in the environment
  • siderophores are secreted bacterial proteins that
    sequester iron from their environment and allow the
    microbes to more easily take it up
  • animal hosts have iron binding proteins, such as
    transferrins, that transport and store iron
91
Q

What are some characteristics of antimicrobial peptides?

A
  • extremely small proteins: 12-15 amino acids long
  • very diverse; more than 600 known
  • broad spectrum
  • not specific
  • lyse bacterial cells
  • inhibit cell wall synthesis
  • destroy RNA and DNA
92
Q

What are interferons?

A

Interferons are cytokines, signaling molecules

between cells during an immune response

93
Q

interferons that cause cells to produce

antiviral proteins that inhibit viral replication

A

IFN-alpha and IFN-beta

94
Q

interferons that causes neutrophils and macrophages

to phagocytize bacteria

A

IFN-gamma

95
Q

What is the mechanism by which interferons work?

A

Production of interferons occurs mainly in response to microbes, such as viruses and bacteria, and their products. Binding of molecules uniquely found in microbes by pattern recognition receptors, such as membrane bound Toll like receptors, can trigger release of IFNs.

IFNs released by the virus-infected host cell bind to plasma membrane or nuclear membrane receptors on uninfected neighboring host cells, inducing them to synthesize antiviral proteins (AVPs).

AVPs degrade viral mRNA and inhibit protein synthesis and thus interfere with viral replication