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pathophysiology > immunology/infection > Flashcards

immunology/infection Flashcards

1
Q

factors for infection

A

mechanism of action, infectivity, pathogenicity, virulence, toxigenicity

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2
Q

infectivity

A

ability to replicate and infect

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3
Q

pathogenicity

A

ability to produce disease

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4
Q

virulence

A

measurement of pathogen’s ability to kill host

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5
Q

toxigenicity

A

ability to produce toxins/endotoxins which further cause cell death

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6
Q

treatment for chickenpox/shingles

A

acyclovir – may be given prophylactically

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7
Q

stages of infection

A

portal of entry, spread of infection (colonization), invasion, multiplication, spread of disease (portal of exit)

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8
Q

spread of infection (colonization)

A

pathogen attacks cells, adheres to them, and releases enzymes to destroy cell’s protective barrier

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9
Q

fever

A

results from cytokines released, causing inflammation

caused by exogenous & endogenous pyrogens which act directly on hypothalamus

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10
Q

stages of infection

A

incubation, prodromal, acute, convalescent

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11
Q

prodromal stage

A

can last for several weeks – infected individual may be asymptomatic but then begins to suffer from nonspecific flu-like symptoms

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12
Q

myalgia

A

muscle ache

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13
Q

acute stage

A

individual begins to feel better but appears more ill because of body’s immune response

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14
Q

convalescent stage

A

recovery is characterized by gradual return of energy & sense of well-being

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15
Q

diagnostics for infection

A

culture – blood, urine, stool, sputum, body fluids

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16
Q

risks of antibiotics

A

kill normal flora – can lead to resistance, requiring more potent drugs which may damage liver, kidneys

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17
Q

inflammation

A

provides rapid, nonspecific response to injury/invasion that removes/confines injurious agents, stimulates immune response, promotes healing

a vascular, cellular, chemical process

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18
Q

symptoms of inflammation

A

redness, swelling, heat, pain, loss of function

result from increased blood flow (hyperemia), increased vascular permeability, movement of WBC to area of injury

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19
Q

first line of defenses

A

natural immunity, natural barriers (skin, ear wax, mucus) – kill bacteria before it enters body

tight junctions between epithelial cells, mechanical clearance of pathogens, body surface temperature (too low for most microorg.)

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20
Q

second line of defenses

A

inflammation and mast cell degranulation

complex process requires vascular, cellular, chemical activity

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21
Q

third line of defenses

A

adaptive immunity (B&T cells)

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22
Q

biochemical barriers

A

chemicals produced by host cells & normal bacterial flora to prevent pathogen invasion (first line of defense)

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23
Q

sebum barrier

A

contains antibacterial/antifungal fatty acids that can kill bacteria

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24
Q

normal flora as barrier

A

on skin & mucous membranes – can protect against invasion by pathogens through production of chemicals that are toxic to pathogenic microorganisms

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25
Q

mast cell

A

releases chemicals in degranulation that initiate a vascular response: vasoconstriction, vasodilation, increased vascular permeability in area of injury

originate in bone marrow, granulated – release chemicals in response to physical injury, chemical agents, immunological mechanisms

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26
Q

acute inflammatory response

A

vascular changes allow cells & proteins to move out of vessels into injured tissues

vascular response complemented by cellular (neutrophils, macrophages)

coordinated by plasma proteins & cytokines

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27
Q

vasoactive cytokines

A

histamine & serotonin

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28
Q

function of histamine

A

contributes to inflammatory response by interacting with histamine 1 (H1) receptors

stimulation of these receptors causes brief vasoconstriction followed by vasodilation to promote acute inflammatory vascular response

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29
Q

process of mast cell degranulation

A

histamine released, causes vascular effects

chemotactic factors attract neutrophils & eosinophils

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30
Q

3 plasma protein systems

A

complement system (cytokines), clotting system, Kinin system (pain)

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31
Q

complement system

A

composed of plasma proteins

can be activated by lysosomal enzymes released by neutrophils, but most often activated by antigen-antibody complexes & bacterial waste products (toxins)

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32
Q

actions of complement components

A

opsonization; chemotaxis; induce mast cell degranulation, cell lysis & death (membrane attack complex)

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33
Q

opsonization process

A

works on capsules of bacteria – strengthens adherence of phagocyte to pathogen

opsonins include complement & antibodies

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34
Q

phagocytosis process

A 
recognition & adherence
engulfment/endocytosis
formation of phagosome
formation of phagolysosome
destruction by lysosomal enzymes
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35
Q

interleukins

A

important cytokines to both innate and acquired immunity – regulate inflammatory & immune responses

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36
Q

IL-1

A

interleukin that causes fever & activates phagocytes

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37
Q

pyrogen

A

causes fever

38
Q

IL-6

A

interleukin produced by macrophages & lymphocytes, stimulates proteins of inflammation

39
Q

IL-10

A

anti-inflammatory interleukin that balances inflammatory & immune responses by reducing production of inflammatory cytokines

40
Q

interferons

A

protect against viral infections

produced & released by virally infected host cells in response to viral double-stranded RNA

41
Q

types of interferons

A

IFN-alpha, IFN-beta, IFN-gamma

42
Q

IFN-alpha & IFN-beta

A

induce production of antiviral proteins

43
Q

IFN-gamma

A

increases microbiodical activity of macrophages

44
Q

types of exudative fluids

A

serous,fibrinous, purulent, hemorrhagic exudates

45
Q

serous exudate

A

watery – indicates inflammation (i.e. fluid inside blister)

46
Q

fibrinous exudate

A

thick, clotted – indicates more advanced infection than serous, occurs prior to pus formation

fibers visible under microscope

47
Q

purulent exudate

A

pus – indicates bacterial infection

48
Q

hemorrhagic exudate

A

contains blood, indicates bleeding

49
Q

leukocytosis

A

increased numbers of circulating leukocytes

50
Q

acute-phase reactants

A

plasma proteins produced by liver in response to inflammation

fibrinogen & c-reactive protein

51
Q

C-reactive protein

A

elevated in cardiac disease – plaque buildup causes swelling before occlusion & death of tissue

52
Q

chronic inflammation

A

lasts 2 wks or longer

often related to unsuccessful acute inflammatory response

formation of granuloma

53
Q

granuloma

A

wall of epithelioid cells surrounding foreign body or infectious agent, often has necrotic tissue at core

54
Q

sarcoidosis

A

idiopathic autoimmune disorder characterized by granuloma formation, especially in lungs & on skin

55
Q

adaptive immunity

A

each pathogen is “remembered” by a signature antigen – if a pathogen invades again, the memory cells (B & T cells) are able to eliminate it

56
Q

antigen presentation

A

body cells capture foreign antigens and enable their recognition/memory by T cells

57
Q

passive immunity

A

babies receive maternal IgG through the placenta and breast milk – temporary protection, because the baby/fetus does not create its own antibodies/memory cells

can also be transferred artificially via serum transfusion, IVIG, monoclonal antibodies (MAb)

58
Q

risks of passive immunization

A

hypersensitivity reactions, serum sickness

59
Q

monoclonal antibodies (MAb)

A

cloned in lab to attack specific antigens – all drugs that end in “-mab” – often used in cancer therapy, but causes risk of immune response

60
Q

humoral immunity

A

mediated by secreted antibodies produced by B cells, which bind to antigens on pathogens to flag them for destruction

61
Q

immunoglobulins

A

Y-shaped glycoproteins that function as antibodies – found in blood & tissue fluids as well as secretions

synthesized by plasma cells (derived from B cells)

62
Q

5 types of antibodies

A

IgA, IgD, IgE, IgG, IgM

63
Q

IgG

A

most abundant – present in body fluids & enters tissues

only antibody to cross placenta

protects against bacteria, toxins, viruses, & activates complement system

64
Q

IgM

A

first antibody to appear in response to an antigen & first made by newborn – presence suggests current infection

65
Q

IgA

A

found in saliva, tears, colostrum, and bronchial, GI, prostatic, vaginal secretions

primary defense against local infections of mucosal tissues by preventing pathogen attachment to epithelial cells

66
Q

IgE

A

involved in inflammation, allergic responses, and combating parasitic infections

binds to mast cells and basophils, triggering release of histamine – can cause anaphylaxis

67
Q

functions of antibodies

A

neutralization of bacterial toxins & viruses, opsonization of encapsulated bacteria

68
Q

opsonization

A

antibodies & complement bind to capsule of bacteria to make it more easily phagocytized

69
Q

secretory immune system

A

B lymphocytes in lacrimal and salivary glands as well as lymphoid tissue of breast, bronchi, intestines, genitourinary tract prevent invaders from entering body through these areas

70
Q

cell-mediated immunity

A

involves activation of macrophages, NK, antigen-specific cytotoxic T lymphocytes, and release of cytokines

71
Q

antigen-specific cytotoxic T lymphocytes

A

cause apoptosis in body cells displaying foreign antigens

72
Q

major histocompatability complex (MHC) antigens

A

enable the immune system to recognize its own antigens/cells – called HLA (human leukocyte antigen) in humans

73
Q

types of T lymphocytes

A

T cytotoxic, T helper, lymphokine-producing, memory, NK

74
Q

natural killer cells (NK)

A

provide cellular immunity through nonantigenic recognition of abnormal cells (detects chemical changes on cell surface, binds to the cell, and kills it)

type of T lymphocyte

75
Q

T-cell receptor complex (TCR)

A

surface receptor that can recognize and bind antigens

each T lymphocyte has TCR for a specific antigen

76
Q

CD cells

A

CD molecules on T lymphocytes – include CD3, CD4, CD8

77
Q

CD3

A

active in TCR

78
Q

CD4

A

on T helper cells – binds to MCH II molecules on antigen-presenting cells – disabled in HIV

79
Q

CD8

A

on T cytotoxic cells – binds to MHC I molecules

80
Q

T cytotoxic cells

A

aka CD8 cells because they have a CD8 receptor – directly kill infected/malignant cells through production of toxins

81
Q

lymphokine-activated killer activity

A

NK cell activity is enhanced in vitro by exposure to IL-2

82
Q

B lymphocytes

A

mature in bone marrow by acquiring BCRs – each cell has unique antigen receptor

83
Q

B-cell receptors (BCRs)

A

specific membrane-bound antigen receptors on the surface of B cells

84
Q

clonal selection

A

B cell finds and binds to its unique antigen – the B cell becomes activated to proliferate and differentiate into plasma cells and memory cells

85
Q

plasma cells

A

excrete antibodies

86
Q

memory cells

A

remain in system for long periods in order to confer long-lasting immunity to an antigen

87
Q

cytokines

A

low-molecular-weight proteins made by cells that affect behavior of other cells

88
Q

functions of cytokines

A

mediate inflammation & attract/activate phagocytes

maturation factor for WBC/RBC

89
Q

complement system

A

mediator of innate and adaptive immunity that enables body to produce inflammatory response, lyse foreign cells, increase phagocytosis

consists of group of proteins that are normally present but inactice in circulation – activation is initiated by antibody bound to antigens on surface of microbes

90
Q

functions of complement system

A

opsonization, chemotaxis, triggers assembly of MAC

91
Q

membrane attack complex (MAC)

A

leads to lytic destruction of many kinds of cells, including RBC, platelets, bacteria, lymphocytes

pathophysiology (7 decks)

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