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Uncategorized > Chapter 16 > Flashcards

Chapter 16 Flashcards

1
Q

immunity

A

ability to ward off disease, aka RESISTANCE. Lack of immunity: susceptibility

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2
Q

innate immunity

specificity & memory
2 lines of defense

A

presented at birth, prior to encounter with disease-causing agents.

Nonspecific, does not involve specific recognition or memory.

Readily protects against all diseases.

Includes 2 lines of defense:

1st: physical barrier – skin, mucous membranes.
2nd: internal, composed of protective cells, cellular agents, and processes that inactivate the disease-causing agents (phagocytes, interferons, inflammation, fever)

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3
Q

adaptive immunity

line of defense
slower to response because it has to activate what?

A

3rd line of defense; specific and has memory.

Defenses elicited upon encounter with the disease-causing agent.

Slower to respond because it has to activate the T lymphocytes and the B lymphocytes.

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4
Q

describe role of physical factors in the first line of defense

skin
mucous membranes
flush

A

Skin - as a physical barrier, blocks entrance of microbes. Outer epidermis and underlying dermis. Dryness and shedding of skin, thickness, and abundance of keratin are protective barriers.

Mucous membranes: block entrance of microbes. Consists of epithelial layer and underlying connective tissue layer. Lines gastro, respiratory, and genitourinary tracts.

LAST: tears, saliva, urine, mucous, vag secretion help flush microbes away.

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5
Q

describe role of chemical factors in the first line of defense

low pH
lysozyme
sebum

A

low pH either destroys or inhibits growth of microbes.

Lysozyme (in perspiration, tears, saliva, nasal secretions, tissue fluids, urine) can break chemical bonds on peptidoglycan; more effective against gram (+) vs gram (-).

Sebum - functions as protectant.

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6
Q

describe role of normal microbiota in the first line of defense

A

prevent overgrowth of pathogens.

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7
Q

2nd line of defense

A

composed of cells (Phagocytes), antimicrobial chemicals (complement system, interfereon, iron-binding proteins, antimicrobial peptides, processes (inflammation, fever)

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8
Q

components of the 2nd line of defense

A

plasma, leukocytes (WBC)

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9
Q

plasma

A

involved in blood clotting, inflammation, transporting iron.

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10
Q

leukocytes

A

WBCs, 2 groups based on granules in cytoplasm–granulocytes and agranulocytes

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11
Q

granulocytes

NBE

A

have granules in cytoplasm. Includes neutrophils, basophils, eosinophils

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12
Q

neutrophils

numbers
granules stain:
nucleus shape
\_\_\_cyte
increase during what kind of infection
A

most numerous WBC. Granules stain pink, have multi-lobed nucleus, are phagocytes (able to leave blood), numbers increase during acute infection

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13
Q

basophils

granules stain:
have a _____ shaped nucleus
release:
involved in:

A

granules stain blue-purple, have a U or S shaped nucleus, release histamine, involved in inflammation and allergic response

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14
Q

eosinophils

granules stain:
nucleus shape
can they leave blood? (word)
increase during what kind of infection
involved in what kind of reaction
A

granules stain red or orange, have a bi-lobed nucleus; phagocytic; able to leave blood; number increases during parasitic worm infections; involved in allergic reactions

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15
Q

agranulocytes

MDL

A

no granules visible, includes monocytes, dendritic cells, and lymphocytes

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16
Q

monocytes

nucleus shape
mature to what
become what in tissues
increase during what kind of infection (ex)

A

kidney-shaped nucleus; mature to macrophages and become actively phagocytic in the tissues; numbers increase during chronic infections, such as tuberculosis

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17
Q

dendritic cells

derived from
abundant in what locations
functions are to (2)
senses
bridges
A

derived from monocytes,

abundant in the epidermidis of skin, mucous membranes, thymus, lymph nodes;

function is to destroy microbes by phagocytosis (nonspecific),

initiate adaptive immunity (specific)–

dendritic cells sense the signals from innate immunity and trigger T cell activation, sort of bridging innate immunity and adaptive immunity

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18
Q

lymphocytes

nucleus shape
includes TBN

A

have a spherical nucleus, includes T lymphocytes, B lymphocytes, and natural killer cells

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19
Q

T lymphocytes

A

cellular immunity

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20
Q

B lymphocytes

A

humoral immunity (produce antibodies)

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21
Q

natural killer cells (NK cells)

A

function in innate immunity–kill infected host cells and tumor cells, and release perforin (poke a hole in the plasma membrane, causing cytolysis) and granzymes (induces apoptosis (self destruction))

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22
Q

leukocytosis

A

total # of WBC increases during infections (meningitis, infectious mono, appendicitis, pneumococcal pneumonia, gonorrhea)

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23
Q

leukopenia

A

decrease in leukocyte count, may be caused by salmonellosis, brucellosis, some viral and rickettsial infections

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24
Q

differential WBC count

A

count the % of leukocytes (percentage of each white cell in total WBC); serve as an indicator of disease

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25
Q

phagocytosis

A

ingestion of a microorganism or other substance by a cell. 2nd line of defense.

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26
Q

phagocytes

A

cells that perform phagocytosis, all are WBCs or derived from WBCs.

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27
Q

steps in phagocytosis

C
A
I
D

A

chemotaxis, adherence, ingestion, digestion

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28
Q

chemotaxis

A

chemical attraction of phagocytes to microorganisms

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29
Q

adherence

A

attachment of phagocytes (via receptors, such as Toll-like receptors) to the microorganism (through pathogen-associated molecular patterns, PAMPs), or other materials. Microbes are more readily phagocytized when coated with certain antimicrobial proteins called opsonins such as complements or antibodies. Coating process is called opsonization.

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30
Q

adherence: toll-like receptors (TLRs)

A

receptors on surface of microorganisms that phagocytes attach to.

31
Q

adherence: PAMPs

A

pathogen-associated molecular patterns of microbes, facilitates adherence

32
Q

adherence: opsonin

A

serum protein that coats microorganism to promote attachment of the microorganism to the phagocyte

33
Q

adherence: opsonization

A

coating process

34
Q

ingestion

A

plasma membrane of phagocyte engulfs the microbe through pseudopods; enclose the microbe in phagosome, which is acidic

35
Q

ingestion: phagosome

A

sac covering microorganism

36
Q

digestion

A

phagosome fuses with lysosome to form a phagolysosome, in which contents are digested.

37
Q

digestion: phagolysosome

A

larger structure, when phagosome and lysosome membranes fuse, digests items brought in by ingestion

38
Q

How do pathogens evade phagocytosis?

Can mary lou see peanut butter?

A

capsules & M protein, leukocidins or streptolysins, pore-forming toxins, biofilms

39
Q

M protein & capsules

A

block adherence

EX: strep. Pneumonia & strep. Pygoenes.

40
Q

Leukocidins & streptolysins

A

kill phagocyte

EX: staph, strep

41
Q

pore-forming toxins

A

Secrete ___________ that lyse phagocyte membrane.

Trypanosome cruzi

42
Q

biofilms

A

very resistant to phagocytosis.

Pseudomonas aeruginosa

43
Q

inflammation

A

second line of defense, local, defensive response triggered by damage to the body’s tissues resulting from microbial infection, physical or chemical agents.

Includes acute & chronic.

44
Q

acute inflammation

A

quick & intense, may result in elimination of the cause and tissue repair, very beneficial.

EX: response to a boil by S. aureus.

45
Q

chronic inflammation

A

long lasting, less intense; more destructive.

EX: response to tuberculosis in a chronic infection of M. tuberculosis.

46
Q

signs & symptoms of inflammation

A

redness, pain, heat, swelling, sometimes loss of function

47
Q

functions of inflammation

A
  1. to destroy or remove the triggering agent;
  2. to confine the injurious agent;
  3. to repair or replace the damaged tissues.
48
Q

tumor necrosis factor alpha

A

a cytokine.

In response to TNF-a in the blood, the liver synthesizes a group of proteins called acute-phase proteins;

other acute-phase proteins are present in the blood in an inactive form, and are converted to an active form during inflammation

49
Q

process of inflammation: vasodilation and increased permeability

caused by
vasodilation responsible for
increased permeability responsible for
both help deliver

A
  1. caused by chemicals released by damaged cells; chemicals include histamines, kinins, prostaglandins, leukotrienes, cytokines;
  2. vasodilation responsible for redness (erythema) and heat;
  3. increased permeability responsible for edema (accumulation of fluid);
  4. vasodilation and increased permeability help deliver clotting factors to injured/infected area and wall off the injurious microbes or agents
50
Q

process of inflammation: phagocytic migration and phagocytosis

A
  1. chemotactic factors (complements, leukotrienes, microbial components, toxins) attract phagocytes to the site of infection;
  2. Phagocytes squeeze between endothelial cells via diapedesis to reach site of infection;
  3. neutrophils often arrive first, monocytes follow;
  4. once monocytes leave blood into tissue, they change to be free macrophages (wandering macrophage); Neutrophils are involved in early stages of infection. Macrophages are larger and more phagocytic than neutrophils; macrophages usually involved in later stage of infection.
  5. Both neutro & macrophages destroy microbes by phagocytosis.
  6. They themselves eventually die and become part of the pus.
51
Q

process of inflammation: tissue repair

A

Replaces dead or damaged cells. Tissues with stem cells can be restored; tissues where cells do not replicate cannot be repaired (cardiac & brain)

52
Q

vasodilation

A

dilation of blood flow which increases blood flow to damaged area, responsible for redness (erythema) and heat associated inflammation

53
Q

increased permeability

A

permits defensive substances normally retained in blood to pass through walls of blood vessels and enter injured area. Permits fluid to move from blood into tissue spaces, responsible for edema

54
Q

edema

A

accumulation of fluid, causes pressure in area

55
Q

histamine

A

causes vasodilation - present in mast cells in connective tissue, circulating basophils, blood platelets–released in direct response to the injury of cells that contain it, also released in response to stimulation by certain components of the complement system.

56
Q

kinins

A

causes vasodilation - present in blood plasma, attracts neutrophils to the injured area

57
Q

prostaglandins

A

causes vasodilation - intensify effects of histamine and kinins; help phagocytes move through capillary walls; associated w/ pain related to inflammation; pain killers inhibit production of prostoglandins

58
Q

leukotrienes

A

causes permeability - produced by mast cells and basophils, help attach phagocytes to pathogens in addition to increased permeability of blood vessels.

59
Q

cytokines

A

produced by activated macrophages, bring about vasodilation and increased permeability.

60
Q

pus

A

mixture of dead tissue cells, leukocytes, pathgoens, and body fluids in a walled-off area

61
Q

abscess

A

isolated site of infection (pimples, boils, pustules)

62
Q

margination

A

process when phagocytes (monocytes & neutrophils) arrive, they stick to the lining of the blood vessels

63
Q

diapedesis

A

migration of phagocytes squeezing between endothelial cells to reach site of infection (ameboid-like movement)

64
Q

cause of fever

A

second line of defense; systemic response; most frequent cause is infection from bacteria or virus

65
Q

effect of fever

A

abnormally high body temperature,

helps step up the production of T cells
intensifies effect of antiviral interferons
increases production of transferrins that decrease iron available to microbes.
High temp also speeds up body’s reactions and helps body tisues to repair themselves more quickly.

66
Q

complement system

A

defensive system consisting of over 30 cascading proteins produced by liver and found circulating in blood serum within tissues throughout body.

Complements the immune system in destroying microbes.

Not adaptable and does not change over person’s lifetime. Innate immune system.

Can be recruited and brought into action by adaptive immune system.

kills by cytolysis, inflammation and phagocytosis, also prevents excessive damage to host tissues.

67
Q

complement activation: classic pathway

A

antibodies activate complement

68
Q

complement activation: alternative pathway

A

pathogens or pathogenic products activate complement

69
Q

complement activation: lectin pathway

A

lectins bind to microbial polysaccharides

70
Q

3 consequences of complement

A

cytolysis, inflammation, phagocytosis

71
Q

c3

A

complement protein, activation starts a cascade of cytolysis, inflammation, and phagocytosis.

Inactive C3 splits into activated C3a and C3b.

C3b binds to surface of microbe, and receptors of phagocytes attach to the C3b–enhances phagocytosis by coating microbe (opsonization).

C3b also initiates series of reactions that result in cytolysis.

C3a and C5a bind to mast cells and cause them to release histamine and other chemicals that increase blood vessel permeability during inflammation.

72
Q

cytolysis

A

extracellular fluid flows into target cell and cell bursts

73
Q

production and function of gamma interferon

A

produced by lymphocytes; induces neutrophils and macrophages to kill bacteria; causes macrophages to produce nitric oxide that inhibits ATP production, thus kills bacteria and tumor cells; increases expression of class I and class II molecules that increases antigen presentation.

74
Q

production and function of alpha & beta interferon

A

produced by virus-infected host cells, induce the uninfected cells to express antiviral proteins

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