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Flashcards in Chapter 16 Deck (74)
1

immunity

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

2

innate immunity

specificity & memory
2 lines of defense

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)

3

adaptive immunity

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

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.

4

describe role of physical factors in the first line of defense

skin
mucous membranes
flush

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.

5

describe role of chemical factors in the first line of defense

low pH
lysozyme
sebum

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.

6

describe role of normal microbiota in the first line of defense

prevent overgrowth of pathogens.

7

2nd line of defense

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

8

components of the 2nd line of defense

plasma, leukocytes (WBC)

9

plasma

involved in blood clotting, inflammation, transporting iron.

10

leukocytes

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

11

granulocytes
NBE

have granules in cytoplasm. Includes neutrophils, basophils, eosinophils

12

neutrophils

numbers
granules stain:
nucleus shape
___cyte
increase during what kind of infection

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

13

basophils

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

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

14

eosinophils

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

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

15

agranulocytes
MDL

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

16

monocytes

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

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

17

dendritic cells

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

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

18

lymphocytes

nucleus shape
includes TBN

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

19

T lymphocytes

cellular immunity

20

B lymphocytes

humoral immunity (produce antibodies)

21

natural killer cells (NK cells)

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))

22

leukocytosis

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

23

leukopenia

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

24

differential WBC count

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

25

phagocytosis

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

26

phagocytes

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

27

steps in phagocytosis

C
A
I
D

chemotaxis, adherence, ingestion, digestion

28

chemotaxis

chemical attraction of phagocytes to microorganisms

29

adherence

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.

30

adherence: toll-like receptors (TLRs)

receptors on surface of microorganisms that phagocytes attach to.

31

adherence: PAMPs

pathogen-associated molecular patterns of microbes, facilitates adherence

32

adherence: opsonin

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

33

adherence: opsonization

coating process

34

ingestion

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

35

ingestion: phagosome

sac covering microorganism

36

digestion

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

37

digestion: phagolysosome

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

38

How do pathogens evade phagocytosis?

Can mary lou see peanut butter?

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

39

M protein & capsules

block adherence

EX: strep. Pneumonia & strep. Pygoenes.

40

Leukocidins & streptolysins

kill phagocyte

EX: staph, strep

41

pore-forming toxins

Secrete ___________ that lyse phagocyte membrane.

Trypanosome cruzi

42

biofilms

very resistant to phagocytosis.

Pseudomonas aeruginosa

43

inflammation

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

acute inflammation

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

EX: response to a boil by S. aureus.

45

chronic inflammation

long lasting, less intense; more destructive.

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

46

signs & symptoms of inflammation

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

47

functions of inflammation

1. to destroy or remove the triggering agent;

2. to confine the injurious agent;

3. to repair or replace the damaged tissues.

48

tumor necrosis factor alpha

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

process of inflammation: vasodilation and increased permeability

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

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

process of inflammation: phagocytic migration and phagocytosis

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

process of inflammation: tissue repair

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

52

vasodilation

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

53

increased permeability

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

edema

accumulation of fluid, causes pressure in area

55

histamine

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

kinins

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

57

prostaglandins

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

leukotrienes

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

59

cytokines

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

60

pus

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

61

abscess

isolated site of infection (pimples, boils, pustules)

62

margination

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

63

diapedesis

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

64

cause of fever

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

65

effect of fever

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

complement system

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

complement activation: classic pathway

antibodies activate complement

68

complement activation: alternative pathway

pathogens or pathogenic products activate complement

69

complement activation: lectin pathway

lectins bind to microbial polysaccharides

70

3 consequences of complement

cytolysis, inflammation, phagocytosis

71

c3

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

cytolysis

extracellular fluid flows into target cell and cell bursts

73

production and function of gamma interferon

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

production and function of alpha & beta interferon

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