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Pathophysiology > Chapter Eight - Infection And Defects In Mechanisms Of Defense > Flashcards

Chapter Eight - Infection And Defects In Mechanisms Of Defense Flashcards

1
Q

Communicability

A

Ability to spread from one individual to others and cause disease

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2
Q

Infectivity

A

Pathogen ability to invade and multiply in host
-involves attachment, escape of phagocytes, dissemination

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3
Q

Virulence

A

Severity or harmfu;ness of a disease or poison

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4
Q

Toxigenicity

A

Ability to produce toxins
-greatly influence pathogens virulence

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5
Q

Portal of entry

A

Route by which a pathogen infects host
-direct contact, inhalation or ingestion

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6
Q

Prokaryote cell

A

Nucleoide, pilus, flagellum, cell wall

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7
Q

Eukaryote cell

A

Nucleus, Golgi apparatus, ER, mitrochondrion, lysosome

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8
Q

Bacteria

A

Prokaryotes - lack discrete nucleus
-aerobic or anaerobic
-gram positive or negative

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9
Q

Two main factors that make GN more difficult to defeat than GP

A

outer membrane and porin channels

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10
Q

Porin

A

Gateway
-very few doors that are well guarded can only enter through porin

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11
Q

Staphylococcus aureus

A

-life threatening
-major cause of nosocomial infections
-common on normal skin and nasal passages

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12
Q

Virulent abilities of S.aureus

A

1.produce protein that blocks compliment attack
2. Avoid innate immunity by producing inhibitors that avoid recognition
3. When engulfed, they can resist lysosome by changing chemistry of cell walls
4. Resist actions of antibiotics

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13
Q

Exotoxins

A

Released from inside of pathogen
-enzymes that damage host cell plasma membranes or inactivate enzymes critical to protein synthesis

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14
Q

Endotoxins

A

Released from outer capsule
-activate inflammatory response and produce fever

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15
Q

Bacteremia

A

Presence

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16
Q

Septicaemia

A

Growth

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17
Q

What toxin activates complement and clotting systems

A

Endotoxins

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18
Q

Endotoxins =

A
  1. Inc capillary permeability
  2. Large volumes of plasma into surrounding tissue
  3. Resulting hypotension
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19
Q

If either bacteremia or septicaemia exists that means

A

Defense mechanisms failure

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20
Q

What is the most common affliction of humans

A

Viral diseases

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21
Q

Replication of viruses requires

A

Entry into host cell

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22
Q

Simple structure of virus

A

DNA and RNA surrounded by capsi and perhaps envelope

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23
Q

Viruses are self limiting (true or false)

A

True

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24
Q

Viruses transmitted via

A

-aerosol
-infected blood
-sexual contact
-vector (ticks, mosquitos)

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25
Q

Cytopathic

A

Causing damage to living cells

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26
Q

Cytopathic inhibit

A

Host cell DNA or RNA synthesis

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27
Q

Cytopathic release

A

Lysosomes into host cell, killing cell

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28
Q

Cytopathic: fusion of host cells into

A

Multicellular giant cell

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29
Q

Cytopathic: alteration of host cells antigen properties =

A

Uninhibited growth

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30
Q

Cytopathic: utilization of

A

Host cell resources

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31
Q

Influenza

A

Highly contagious viral infection of respiratory passages

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32
Q

Antigenic variation

A

Ability to change viral antigen (spikes) yearly
-antigens utilized to activate adaptive immune response

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33
Q

Ability to change =

A

Dysfunction adaptive immune response
-B or T cells

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34
Q

SARS-CoV-2 virus’s

A

Responsible for COVID 19

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35
Q

Fungal infections

A

-large eukaryotes with, thick rigid cell walls
-resist penicillin
-exist as single called yeasts, multi cellular, molds or both

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36
Q

Fungal reproduction

A

Simple division or budding

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37
Q

Moulds

A

Filamentous fungi grow as multinucleate, branching hyphae, forming a mycelium

-ringworm

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38
Q

Yeasts

A

Yeasts grow as ovoid or spherical, single cells multiply by budding and division
-histoplasma

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39
Q

Mycoses

A

Diseases caused by funhi

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40
Q

Dermatophytes

A

Fungi that invade skin, hair or nails

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41
Q

Diseases dermatophytes produce are called

A

Tineas

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42
Q

Pathogenicity of fungus

A

Adapt to host environment —> wide temp variations, low oxygen

-suppress immune defences

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43
Q

low white blood cell count promotes

A

fungal infection

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44
Q

Most common cause of fungal infections

A

Candida albicans

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45
Q

Candida albicans is found

A

In normal skin micro biome, GI tract, and vagina of many individuals

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46
Q

Candida albicans is most commonly found in

A

Cancer patients and transplantations
-higher risk of deep infection and higher mortality rates

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47
Q

Death rate of disseminated candidiasis

A

30-40%
-immunocompromised, and spreading

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48
Q

Parasitic infections can vary from

A

Unicellular Protozoa to large worms

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49
Q

How do parasitic infections spread

A

Spread human to human via vectors
-ticks, mosquitos
Or ingestion of contaminated food or water

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50
Q

Parasitic infection causes

A

Tissue damage due to toxin or inflammatory immune response

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51
Q

Plasmodium malaria occurs in RBC

A

Continual infection of RBC
-anemia in 48-72 hours
-RBC release cytokines = fever chills and vomiting

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52
Q

What cytokines do RBC release in plasmodium malaria

A

TNF-a and IL-1

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53
Q

Antibiotics

A

Natural products of fungi, bacteria or other microorganisms that affect growth of specific microorganisms

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54
Q

Antimicrobials (2)

A

-bactericidal
-bacteriostatic

55
Q

Bacterial

A

Agent that kills other microorganisms

56
Q

Bacteriostatic

A

Agent that inhibits growhrt of other microorganisms

57
Q

1944

A

Penicillin effective at treating infection in British hospital

58
Q

1946

A

14% of all S.aureus are penicillin resistant

59
Q

1950

A

59% of S.aureus are resistant

60
Q

1990

A

89% s.aureus are resistant

61
Q

What has caused rise in antibiotic resistance

A

-lack of compliance with therapeutic duration
-overuse of antibiotics

62
Q

Lack of compliance with therapeutic regimen

A

Not using antibiotics iotas for prescribed duration

-results in strongest microbes are left alive and repopulation within pathogens are resistant to specific antibiotic

63
Q

Overuse of antibiotics

A

Destruction of normal micro biome = opens space for more infectious and resistant pathogens

64
Q

Vaccines

A

Biological preparations of weakened or dead pathogens

65
Q

Adaptive response of vaccine usually requires

A

Two weeks to activate

66
Q

Vaccine allows this two week period to be performed against a

A

Non viral pathogen

67
Q

When infection by viral pathogen occurs….

A

Adaptive immunity is already prepared (no two week delay)

68
Q

Vaccine mixture

A

DTaP (diphtheria, tetanus, pertussis

69
Q

HERD immunity requires

A

85 percent of population to be immunized

70
Q

Toxoids

A

Chemically altered pathogen toxin injected into body
-allows body to learn to defeat pathogens toxin

71
Q

Passive immunotherapy

A

Performed antibodies (against pathogen) are given to individual

72
Q

Human immunoglobulin antibodies are obtained from

A

Pathogen survivor

73
Q

Passive immunotherapy is becoming focus after rise of

A

Antibiotic resistance

74
Q

Primary (congenital) immunodeficiency is caused by

A

A genetic defect

75
Q

Secondary (acquired) immunodeficiency is caused by

A

Another illness
-cancer

76
Q

Most primary deficiencies result of a

A

Single gene defect

77
Q

Mutations are

A

Sporadic, and not inheritited
-occurs before birth, but symptoms appear early or late in life

78
Q

Statistics for primary deficiencies in Canada

A

1 in 200 have condition
70% undiagnosed

79
Q

Severe combined immunodeficiency

A

Underdeveloped thymus
-a serene of T cells
-few detectable lymphocytes

80
Q

DiGeorge syndrome

A

Thymus and parathyroid gland dysfunction
-inadequate T cell production and management of plasma calcium

81
Q

Hypogammaglobulinemia

A

Results from defect in B cell maturation or function
-lower levels of circulating immunoglobulins (antibodies) in blood

82
Q

Secondary deficiencies are

A

Acquired deficiencies
-far more common than primary definitives but not as clinically relevant

83
Q

severe examples of secondary deficiencies

A

AIDS or cancer

84
Q

CBC or complete blood count

A

Total numbers of RBC, WBC and platelets

85
Q

Differential

A

Individual numbers and lymphocytes, granulocytes and monocytes

86
Q

Quantitative determination of immunoglobulins

A

Determine sub populations of immunoglobulins

87
Q

Total complement assay

A

Total number of complements in blood

88
Q

Stem cell transplantation from

A

Bone marrow, umbilical cord cells
-most cases improvement is temporary

89
Q

Mesenchymal stem cell injection

A

-undifferentiated stem cells found in bone marrow
-undergo differentiation into other cell types
-have potent immunosuppressive properties

90
Q

Gene therapy

A

Two girls received first therapeutic replacement of defective genes
-inserted normal genes into genetic material

-caused reconstitution of immune system
-some recipients develop leukaemia

91
Q

AIDS

A

-depletes helper T cells that are necessary for activation of both T and B cells

92
Q

Results of HIV

A

-dysfunctional adaptive immune system
-inc susceptibility to disease
-AIDS

93
Q

Epidemiology of AIDS

A

-Heterosexual acuity is most common transmission route worldwide
-women constitute more than 50% of people infected
-children contract via placenta or breastfeeding

94
Q

Difficulties with vaccine development of HIV

A

-HIV genetically and antigenically variable
-individuals with HIV have high levels of antibodies but don’t appear to be protective
-therefore, even if vaccine creates antibodies they might not function effectively

95
Q

Antiretroviral therapy

A

Treatment and prevention of HIV
-retroviral means virus with RNA not DNA

96
Q

Treatment of HIV is not

A

Curative but death is reduced significantly

97
Q

Hypersensitivity

A

Altered immunological response to an antigen that results in disease or damage to host

98
Q

Allergy

A

Harmful effects of hypersensitivity to environmental antigens
-pollen, bee stings

99
Q

Autoimmunity

A

Disturbance in immunological tolerance of self antigens
-immune system doesn’t recognize bodies own antigens
-clinical disorders are called autoimmune diseases

100
Q

Alloimmunity

A

Immune reaction to tissues of another individual
-transfusions, transplants or fetus during pregnancy

101
Q

Type I

A

IgE mediated
-hay fever

102
Q

Type II

A

Tissue specific reactions
-hemolysis in medication allergies

103
Q

type III

A

Immune complex mediated
-gluten allergy

104
Q

Type IV

A

Cell mediated
-poison ivy

105
Q

Most hypersensitive reactions include more than one

A

Type

106
Q

Immediate hypersensitivity reactions

A

Reaction that occurs within minutes or hours

107
Q

Anaphylaxis

A

Most rapid and severe immediate reaction
-within minutes

108
Q

Symptoms of anaphylaxis

A

-pruritis (severe itching)
-erythema (red patches on skin)
-vomiting, diarrhea, breathing difficulties

109
Q

Delayed hypersensitivity reactions

A

Reaction occurs after several hours and are at maximal several days alter

110
Q

What is the most common hypersensitive reactions

A

Type I

111
Q

Type I is mediated by

A

Mast cells and IgE
-primarily histamine

112
Q

Type I: against environmental antigens :

A

Therefore = allergic

113
Q

Type I: initial exposure to allergen =

A

IgE binding to mast cell receptors = person now considered sensitized

114
Q

Type I: subsequent exposure to allergen =

A

Mast cells relapse of cytokines = hypersensitive reaction

115
Q

Type I: tissues with high

A

Mast cells are msot commonly affected
-skin, GI tract, pulmonary tract

116
Q

Atopic

A

Individuals predisposed to developing allergies
-one parent has allergies = 40% offspring will
-both parents have allergies = as high as 80%

117
Q

Initial exposure to allergen =

A

IgE binding to mast cell receptors = person now considered sensitized

118
Q

Re exposure to allergen =

A

Mast cells release of cytokines = hypersensitive reaction

119
Q

Type II : tissue specific

A

-cytotoxic hypersensitivity
-immune reactions against a specific cell or tissue

120
Q

Cytotoxic hypersensitivity

A

Antibody mediated destruction of healthy host cells

121
Q

Type II: tissues specific antigens

A

Because they attach only on plasma membranes of certain cells

122
Q

Example of type II

A

Platelets have antigens found on no other cell in body

123
Q

Type II has five mechanisms

A

A,B,C,D,E
-each mechanisms begins with antibody binding to tissue specific antigens

124
Q

Type II: A

A

Cell is destroyed by antibodies and complements

125
Q

(A) Antibody binding to cell =

A

Activation of complement system = formation of membrane attack complex = disintegration or rupture of cell wall

126
Q

Type II: B

A

Cell destruction through phagocytosis by macrophages

127
Q

(B) antibody binding to cell =

A

Macrophage recognition of a cell to be phagocytize

128
Q

Type II: C

A

Tissue damage caused by toxic products produced by neutrophils

-soluble antigens from infectious agents or hosts own cells binds to cell surface
-neutrophils are attracted and release their granules into healthy cells = damage cells

129
Q

Type II: D

A

Antibody dependant cell mediated cytotoxicity
-binding of igG antibodies to antigens
-attracts NKC that release toxic sutbances that destroy cell

130
Q

Type II: E

A

Target cell malfunction
-Graves’ disease, targets thyroid

131
Q

(E) mechanism doesn’t destroy cell but

A

Causes cell to malfunction
-antibody prevents cells interaction with normal molecule

132
Q

Type III

A

Antigen antibody immune complexes are formed in circulation and later deposited in vessel walls or extra vascular tissues

133
Q

Type IV hypersensitivity : cell mediated

A

Does not involve antibody
-is mediated by T cells

134
Q

Examples of IV hypersensitivity

A

-graft rejection
-allergic reactions from poison ivy or metals = T cell activation = macrophage activation = tissue damage

Pathophysiology (20 decks)

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