test 5!!!!!! Flashcards

1
Q

etiology

A

study of disease

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2
Q

infection

A

colonization of the body by pathogens

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3
Q

pathogenesis

A

the manner in which a disease develops

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4
Q

disease

A

infection results in any change from a state of health

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5
Q

infectious disease

A

disease in which pathogens invade a susceptible host and carry out at least part of their life cycle in the host

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6
Q

normal microbiota

A

normally don’t cause disease
normally do not cause disease
probiotics: live microorganism ingested

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7
Q

Transient microbiota

A

present for several days, weeks, or months, the disappear

-normally do not cause disease

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8
Q

where do you find normal microbiota?

A

skin, nose and throat, lg intestine, urinary and reproductive system

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9
Q

what are the benefits of microbiota?

A
  1. protects host by microbial antagonism: comets with pathogens to prevent overgrowth and infection
  2. synthesize B vitamins and vitamin K for host
  3. stimulate immune response
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10
Q

microbial synergism

A

2 microbes work together to produce greater effect than either acting alone

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11
Q

how does normal microbiota cause disease?

A

they can act as opportunistic pathogens.

  • if they move outside normal environment
  • increase in number( yeast infection)
  • encounter immunocompromised host
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12
Q

how are we able to tag one specific pathogen to a disease?

A

Robert koch
-developed Koch’s postulates:
have to isolate pathogen from the sick, grow pathogen of pure culture, inject to healthy rat, isolate same pathogen if rat get sick or dies

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13
Q

what are the limitations of Koch’s Postulates ?

A
  1. some cannot be cultured on cmedia
  2. some disease are not clear cut( many organism cause the same signs and symptoms)
  3. some pathogens may cause several disease condition s
  4. can’t infect human with pathogen
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14
Q

symptoms

A

change in body function felt by the patient

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15
Q

sign

A

change in body that can be measured or observed ex; fever, rash

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16
Q

syndrome

A

specific groups of signs and symptoms that accompany a disease

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17
Q

communicable disease

A

can spread from one host to the next

-contagious disease: easily spread from 1 to another

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18
Q

noncommunicable disease

A

not transmitted by one host to another

-lyme disease

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19
Q

sporadic disease

A

occurs only occasionally in a population (typhoid fever )

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20
Q

endemic disease

A

constantly in a population

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21
Q

epidemic disease

A

acquired by many hosts in a given area in a short time (influenza)

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22
Q

pandemic disease

A

worldwide epidemic (AIDS)

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23
Q

severity or duration of disease

A

acute disease, chronic disease, and latent disease

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24
Q

acute disease

A

develop rapidly and last only a short time (flue)

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25
Q

chronic disease

A

develops slowly, less severe but lasts for a long time (TB, hepatitis B)

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26
Q

latent disease

A

period of no-symptoms when the pathogen is inactive (shingles)

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27
Q

local infection

A

limited to a small area of the body

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28
Q

systematic infection

A

microorganism or their products are spread throughout the body or lymph

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29
Q

focal infection (local to systematic)

A

systematic infection that began as local infection

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30
Q

sepsis

A

inflammation fro the spread of microbes and their toxins

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31
Q

blood is normally sterile but,________

A

microbes or their products may be present as a result of disease

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32
Q

toxemia

A

toxins

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33
Q

viremia

A

virus

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34
Q

primary infection

A

acute that causes initial illness

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35
Q

secondary infection

A

opportunistic infection after a primary infection; more serious

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36
Q

subclinical infection

A

no noticeable signs or symptoms (inapparent infections)

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37
Q

predisposing factors (make body more susceptible to disease)

A
  1. short urethra in females
  2. inherited traits
  3. climate and weather
  4. fatigue
  5. age
  6. lifestyle
  7. nutrition
  8. chemotherapy
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38
Q

herd immunity

A

results from vaccination,

acts as barrier to the spread of an infectious disease

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39
Q

events during an infection

A

source of pathogen, transmission, invasion, pathogenesis

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40
Q

graph stages of disease

A
incubation period 
prodromal period 
period of illness 
period of decline 
period of convalescence
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41
Q

components necessary for the spread of disease??

A

reservoir of infection - source of pathogen (continuous)

susceptible host ; to multiply in

route of transmission

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42
Q

living reservoirs of infection

A

human: transmit pathogens to other ; aids
animals: carry pathogens to humans

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43
Q

zoohoses

A

animal disease that can b transferred to human (rabies, lyme disease)

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44
Q

nonliving reservoirs of infection

A

soil
water
food

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45
Q

types of transmission of disease

A

contact

vehicle

vectors

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46
Q

types of contact foe transmission of disease

A

direct (sex, kissing, touching)

indirect ( spread by means of nonliving objects

droplets

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47
Q

vehicle type of transmission of disease

A

transmission by inanimate reservoir

waterborne

food-borne

air borne

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48
Q

vectors as type of transmission of disease

A

carry pathogen from one host to another

mechanical : housefly

biological : mosquito

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49
Q

Healthcare associated infections

A

received in healthcare facility

50
Q

factors to HAI

A

compromised host

microorganism in healthcare (resistant to antibiotics)
-normal microbiota dangerous

chain of transmission

51
Q

endogenous

A

patients on microbiota ..dangerous

52
Q

exogenous

A

staff, visitors, or other patients (transferred microbiota

53
Q

chain of transmission

A

direct contact

indirect contact (formats, airborne)

54
Q

22% surgical infections

A

….

55
Q

emerging infectious diseases

A

new diseases, increase in incidence, showing a potential to increase in the near future

56
Q

zika viral disease

A

stared in Brazil, mosquito transmitted, dangerous to pregnant women,

57
Q

what happens to the fetus if a women is infected with Zika?

A

microcephaly (small head)

Guillain Barre Syndrome (nerve seeks damaged by person’s own immune system ->muscle weakness and paralysis)

58
Q

what contributes to infectious diseases?

A

evolution of microbes

widespread inappropriate use of antibiotics

modern transportation

animal control measures

public health failure

59
Q

epidemiology

A

the study where and when disease occur and how they are transmitted in populations

60
Q

CDC (centers for disease control and prevention)

A

collect and analyze epidemiological info in the US

gives you rate if morbidity(notable disease) and motility (deaths from notable disease)

61
Q

pathogenicity

A

the ability to cause disease

62
Q

virulence

A

the degree if pathogenicity

63
Q

how does a microorganism enter a host?

A
  1. mucus membrane (respiratory tract, GI tract, Genitourinary tract)
  2. skin
  3. parental route : deposited directly into tissues
    - injections, bites, cuts, surgery
  4. placental route: intrauterine infections
64
Q

preferred mode of entry

A

nose

65
Q

ID 50

A

infectious dose

66
Q

LD 50

A

Lethal dose

67
Q

How do organisms attach to the host?

A

adherence: bacteria has adherence factors that attach to the host cell.
- glycoproteins and lipoproteins

68
Q

examples of adherence factors?

A

glycocolyx

frimbrie

Mproteins

69
Q

how does bacteria invade a host cell?

A

invasins : help the bacteria hide within the cell by rearranging actin filaments of the host cytoskeleton (uses actin to move from cell to cell)

capsules: impair phagocytosis

cell wall components: M protein, Opa protein, mycelia acid

enzymes: coagulase(clots blood), kinases(spreads infection) , IgA protease (destroy IgA antibody)

70
Q

cell wall competes that help Bactria invade the host cell???

A

M protein: resists phagocytosis

Opa protein: allow attachment to host cells

Mycolic acids: resists digestion

71
Q

how does a pathogen damage the host cell??

A

using the host nutrients (using their iron= siderophores)

causing direct damage (cell lysis, toxin or waste product)

causing indirect damage via immune response

72
Q

antitoxin

A

antibody against a specific toxin

73
Q

toxoid

A

inactivated toxin used in vaccine

74
Q

exotoxin

A

mostly produced by gram + bacteria

not heat stable

high toxicity (low lethal dose)

specific to a cell structure or function in host

non fever inducing

75
Q

types of exotoxins

A
  • classified by structure and function

- host cell type affected

76
Q

exotoxins by structure and function

A
  1. AB toxin (A: active enzyme, B: binds to cell )
  2. membrane disrupting toxins ( lyse the cell
  3. superantigen (cause a big immune response)
  4. genotoxin ( damage to DNA)
77
Q

exotoxin by host cell type

A
  1. neurotoxin (muscles )
  2. enterotoxin ( disease of GI tract)
  3. cytotoxin (inhibit protein synthesis )
78
Q

exotoxin and phage conversion

A

bacteria infected by virus and have gone lysogenic, are now able to produce toxin, but weren’t before being infected

79
Q

endotoxin :

A

mostly produced by gram (-) bacteria

lipid A of LPS

heat stable

low toxicity (high dose to have an effect)

fever inducing

in order for the endotoxin to have an effect lipid A has to be released

80
Q

lipid A may cause

A

fever and septic shock , release when phagocytosis

81
Q

how does a bacterial cell exit the host??

A

respiratory tract (coughing, sneezing)

GI tract

Genitourinary tract

skin

blood

82
Q

innate immunity:

A

defenses against any pathogen; rapid; present at birth

83
Q

first line of defense physical factors :

A

skin, mucous membranes, ciliary escalator, earwax, hair in nose, epiglottis, vomiting, diarrhea, defecaftion, peristalsis

84
Q

mucus

A

viscous glycoproteins that trap microbes and prevent tact from drying out

85
Q

chemical factors of first line of defense ?

A

sebum in skin, lysozyme, low pH

86
Q

second line of defense?

A

phagocytosis, inflammation, fever , antimicrobial substances

87
Q

white blood cells responsible for second line of defense?

A

Neutrophils, Basophils, Eosinophils

88
Q

neutrophils?

A

phagocytic, work in early stages of infection

89
Q

basophils?

A

release histamine in allergic reaction

90
Q

Eosinophils?

A

phagocytic; toxic against parasites and helminths

91
Q

phagocytosis

A

ingestion of microbe or particle by phagocytes

-macrophages

92
Q

how does phagocytosis work??

A

Toll-like receptors (TLRs) attach to pathogen associated molecular patterns (PAMPS)

93
Q

what’s the purpose of inflammation ?

A

to repair and replace damaged tissue, intent is to limit damage

94
Q

signs of inflammation

A

redness, pain, heat, swelling

95
Q

body’s thermostat

A

hypothalamus

96
Q

how does fever get initiated

A

pyrogens (endotoxins) cause phagocytes to release Interleukin 1 and that causes hypothalamus to release PG, which go to the hypothalamus and raise the temperature

97
Q

advantages of fever

A

speeds up metabolism (faster repair, speeds up other body’s defenses

98
Q

adaptive immunity

A

defenses that target a specific pathogen, acquired though infection or vaccination

99
Q

primary response

A

first Time the immune system combats a particular foreign system

100
Q

secondary response

A

later interactions with the same pathogen; faster and more effective due to “memory”

101
Q

humoral immunity

A

mediated by B Lymphocytes, produce antibodies that combat antigens

B cells —> plasma cells —> antibodies

some B cells produce memory cells which fight extracellular pathogens

102
Q

cell mediated immunity

A

mediated by T lymphocytes, does not involve antibodies
-Tcells: secrete cytokines

destroy intracellular pathogens

103
Q

antigen (ag)

A

substances that cause body to produce specific antibodies

104
Q

antibody (AB)

A

globular proteins (Immunoglobulins)

made in response to antigen

attaches from epitope or antigenic determinants

105
Q

valence

A

number of antigen binding sites on an antibody

-bivalent antibodies gave 2 binding sites

106
Q

antigens

A

foreign material (enzymes, cell surface structures, exotoxins, cell surface marker (blood typing, graphing)

107
Q

epitope

A

antigenic determinants : portion of antigen recognized by lymphocyte receptor

108
Q

antigen-antibody binding function???

A

to recognize, bind to and neutralize antigens (complementary fit )

109
Q

most abundant antibody

A

IgG, protects fetus

110
Q

antibody structure

A

4 protein chains, variable region, constant region

111
Q

antibody in response to a first time infection?

A

IgM and then IgG(memory)

112
Q

summarize clonal selection of antibody producing cells

A

inactivated B cells have receptors that recognize antigens and bind to them, then antigens fragments are displaced on MHC class II molecules, where then a helper T cell attaches to the displayed antigen fragment and releases cytokines, and then B cells are activated and lots of AB are produced

113
Q

T cells

A

-made in bone marrow, but mature in thymus
-nver produce antibodies
-combat intracellular pathogens
have T-cell receptors (TCR) on surfaces that interact with antigen presented by antigen presented cells (APC) on MHC molecules

114
Q

antigen presented cells (APC)

A

centric cells and microphages

115
Q

T cell receptors (TCR)

A

does not react with free antigen

116
Q

Helper T cells (CD4, and Th)

A

bind to MHC class II molecules that present antigens on B cells and APCs

117
Q

TH1:

A

activates macrophages, and stimulates antibody production

118
Q

TH2:

A

activate B cells to produce, IgM (for initial infection) and IgE (allergic Rxn)

119
Q

TH17:

A

contribute to inflammation

120
Q

Macrophages (Tcells)

A

activated by helper T cells, patent mechanism for destruction of Ag

121
Q

Cytotoxin T lymphocytes (CTL) (CD8, Tc)

A

destroys infected or cancerous self cells

-releases perforin and granzymes that induce apoptosis

122
Q

natural killer cells

A

extra cellar killing by the immune system

  • leukocytes destroy cells that don’t express MHC class I self-antigens
  • attack virus infected cells, cancer cells and parasites
  • form poses in these cells which lead to apoptosis