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HLSC 222 Pathophysiology 🧫 > Chapter 8 > Flashcards

Chapter 8 Flashcards

1
Q

What factors influence infection?

A

Communicability
Infectivity
Virulence
Toxigenicity
Portal of entry

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2
Q

Communicability

A

Ability to spread from one individual to others and cause disease

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3
Q

Infectivity

A

Pathogen ability to invade and multiply in host
-Attachment, escape of phagocytes, dissemination (spread)

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4
Q

Virulence

A

Severity or harmfulness of a disease or poison

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5
Q

Toxigenicity

A

Ability to produce toxins
-influences virulence

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6
Q

Portal of entry

A

Route by which a pathogen infects a host
-Direct contact, inhalation, ingestion
-Animal/insect bite

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7
Q

What are bacteria?

A

Prokaryotes (lack nucleus)
Aerobic or aerobic
Gram-positive or negative

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8
Q

What are the 2 main factors that make gram-negative more difficult to defeat than gramp-positive?

A

Outer membrane
Porin channels

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9
Q

What is a major cause of nosocomial infections?

A

Staphylococcus aureus

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10
Q

Where is Staph. aureus commonly found in body?

A

Normal skin and nasal passages

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11
Q

What are S. aureus virulent abilities?

A
  1. Produce protein that blocks compliment attack
  2. Avoid innate immunity by producing inhibitors that avoid recognition
  3. When engulfed by phagocyte, they resist lysosome by changing the chemistry of their cell walls
  4. Resist many antibiotics
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12
Q

What are exotoxins?

A

Enzymes released from inside of pathogen

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13
Q

What do exotoxins do?

A

Damage host cell plasma membrane or inactivate enzymes critical to protein synthesis

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14
Q

What are endotoxins?

A

Released from outer capsule

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15
Q

What do endotoxins do?

A

Activate inflammatory response and produce fever

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16
Q

What systems do endotoxins activate?

A

Compliment and clotting systems

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17
Q

How do endotoxins cause Hypotension?

A

They increase capillary permeability and large volumes of plasma enter surrounding tissue causing hypotension

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18
Q

Bacteremia

A

Presence of bacteria

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19
Q

Septicemia

A

Growth of bacteria

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20
Q

Bacteremia and septicaemia are results of?

A

result of defence mechanisms failure

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21
Q

What is the most common affliction of humans?

A

Viral diseases

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22
Q

What does virus replication require?

A

Entry into host cell

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23
Q

Describe the simple organism of a virus

A

DNA/RNA surrounded by a capsid and sometimes an envelope

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24
Q

Do all viruses require medication treatment?

A

Not all, some are self-limiting

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25
Q

How are viruses transmitted?

A

Aerosol
Infected blood
Sexual contact
Vector (ticks, mosquitoes)

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26
Q

Cytopathic

A

Causing damage to living cells

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27
Q

Viruses inhibit host cell?

A

DNA or RNA synthesis

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28
Q

What do viruses cause the release of?

A

Lysosomes
-Kill host cell

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29
Q

What do viruses fuse host cell into?

A

Multicellular giant cell

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30
Q

What happens when a virus alters host cells antigen properties?

A

Immune system attacks own cells

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31
Q

How do viruses cause uninhibited growth?

A

Transform host cells into cancerous cells

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32
Q

What do viruses utilise to cause damage to the host?

A

Host cell’s resources

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33
Q

Influenza

A

Highly contagious viral infection of respiratory passages with antigenic variation

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34
Q

Antigenic variation

A

Ability to change viral antigen (spikes) yearly causing dysfunction of Adaptive immune response (B/T cells)
e.g; SARS-CoV-2 virus is responsible for COVID-19

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35
Q

What are fungi?

A

Large eukaryotes with thick, rigid cell walls

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36
Q

What do fungal infections resist?

A

Penicillin

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37
Q

What ways can fungi exist?

A

Single-celled yeasts
Multi-cellular moulds
or both

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38
Q

How do fungi reproduce?

A

Simple division or budding

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39
Q

Mycoses

A

Diseases caused by fungi

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40
Q

Dermatophytes

A

Fungi that invade skin, hair or nails

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41
Q

Diseases produced by dermatophytes are called?

A

Tineas
e.g: Tinea capitis (scalp)

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42
Q

What do fungi adapt to?

A

Host environment
-Wide temperature variations, low oxygen…

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43
Q

What do fungal infections suppress?

A

Immune defences

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44
Q

What promotes fungal infection?

A

Low WBC count

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45
Q

What is the most common cause of fungal infection?

A

Candida albicans

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46
Q

Where is Candidia albicans found in individuals?

A

Normal skin microbiome
GI tract
Vagina

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47
Q

What is the most common fungal infection in cancer patients and transplantation?

A

Candida albicans

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48
Q

Who experiences dissemination of Candida albicans?

A

Immunocomprimised
-deep infection, high mortality

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49
Q

What is the death rate of disseminated candidiasis?

A

30-40%

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50
Q

What are parasites?

A

Unicellular protozoa to large worms (helminths)
e.g, flukes, nematodes, tapeworms

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51
Q

How are parasites spread?

A

Human to human via vectors
e.g; ticks, mosquitoes
or Ingestion of contaminated food or water

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52
Q

What is parasitic tissue damage caused by?

A

Toxin damage or inflammatory/immune response

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53
Q

Where does Plasmodium(malaria) occur?

A

In RBC

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54
Q

What occurs within 48-72 hours of having malaria?

A

Anemia

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55
Q

What do RBC release in malaria infection?

A

Cytokines
TNF-a and IL-1

56
Q

What do the cytokines released by RBC in malaria infections cause?

A

Fever, chills and vommiting

57
Q

What are antibiotics?

A

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

58
Q

What are the types of antimicrobials?

A

Bactericidal
Bacteriostatic

59
Q

Bactericidal

A

Agent that kills other microorganisms

60
Q

Bacteriostatic

A

Agent that inhibits growth of other microorganisms

61
Q

What are some safeguards to infectious diseases that are poorly implemented?

A

-Hand hygiene
-proper sanitary disp[osal
-Water treatment
-Sanitary food transportation, prep and serving
-Control of insect vectors
-Support of research`

62
Q

Describe the changes to antibiotic resistance over the years

A

1944: Penicillin effective at treating infection in British Hospital
1946: 14% of all Staphylococcus aureus penicillin resistant
1950: 59% resistant
1990: 89% resistant

63
Q

What has caused a rise in antibiotic resistance?

A

Lack of compliance with therapeutic regimen
Overuse of antibiotics

64
Q

What are vaccines?

A

Biological preparations of weakened (attenuated) or dead (inactivated) pathogens

65
Q

How long does adaptive response take to activate after getting a vaccine?

A

2 weeks

66
Q

what is the beneficial end result of a vaccine?

A

When infection by virus occurs, adaptive immunity is already prepared
-No delay

67
Q

What is an example of a vaccine mixture?

A

DTap
-Diptheria, tetanus and pertussis

68
Q

What does HERD immunity require?

A

85% of population immunised

69
Q

What are toxoids?

A

Chemically altered pathogen toxin injected into the body so the body can learn to defeat it

70
Q

What is passive immunotherapy?

A

Performed antibodies against a pathogen are given to an individual

71
Q

Where are the antibodies used for passive immunotherapy obtained from?

A

Human immunoglobulin obtained from pathogen survivor

72
Q

what is becoming the focus after a rise in antibiotic resistance?

A

Passive immunotherapy

73
Q

What causes primary congenital immunodeficiency?

A

Genetic defect

74
Q

What causes secondary acquired immunodeficiency?

A

Another illness
e.g; cancer

75
Q

What kind of genetic defect causes primary deficiencies?

A

Single gene defect

76
Q

Describe the mutations of primary deficiencies

A

Sporadic not inherited
Occur before birth, symptoms appear early or late in life

77
Q

How many in Canada have primary deficiencies?

A

1/200
70% undiagnosed

78
Q

How are primary deficiencies categorised into groups?

A

based on what aspect of immune system is defective
eg: antibody deficient

79
Q

What are some combined deficiencies?

A

SCID
DiGeorge syndrome
Hypogammaglobulinemia

80
Q

What is Severe combined immunodeficiency (SCID)?

A

Underdeveloped thymus causing an absence of T cells
-few detectible lymphocytes

81
Q

What is Digeorge syndrome?

A

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

82
Q

What is Hypogammaglobulinemia?

A

defect in B cell maturation or function causing lower levels of circulating immunoglobulins (antibodies) in the blood

83
Q

What deficiencies are more common?

A

Secondary deficiencies

84
Q

What is an example of a severe secondary deficiency?

A

AIDS, cancer

85
Q

What is CBC (complete blood count)?

A

Total numbers of RBC, WBC and platelets

86
Q

What is differential?

A

Individual numbers of lymphocytes, granulocytes and monocytes

87
Q

What determines subpopulations of immunogloblins?

A

Quantitative determination of immunoglobulins

88
Q

What is total complement assay?

A

Total number of complements in blood

89
Q

What are some replacement therapies for immune deficiencies?

A

Stem cell transplants
mesenchymal stem cell injection
Gene therapy

90
Q

Where are stem cells obtained from for stem cell transplants?

A

Bone marrow
Umbilical cord
-temporary improves

91
Q

What is mesenchymal stem cell injection?

A

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

92
Q

What is gene therapy?

A

Insertion of normal genes into individuals genetic material to reconstitute the immune system

93
Q

What is a potential complication associated with gene therapy?

A

leukaemia

94
Q

What causes AIDS?

A

HIV

95
Q

What cells are depleted in AIDS patients?

A

Helper T cells

96
Q

What are Helper T cells necessary for?

A

Activation of both T and B cells

97
Q

How does HIV progress to AIDS?

A

HIV causes dysfunctional Adaptive immune system which increases susceptibility to disease

98
Q

AIDS most common transmission route?

A

heterosexual activity

99
Q

What percent of people infected with AIDS are women?

A

50%

100
Q

How can children contract AIDS from their mothers?

A

Via placenta, breastfeeding

101
Q

Why is HIV vaccine difficult to develop?

A

It is genetically and antigenic ally variable.
Individuals have high levels of antibodies that aren’t protective so if a vaccine creates antibodies they might not work

102
Q

How is HIV treated/prevented?

A

Anti-retroviral therapy

103
Q

Retroviral

A

Virus with RNA not DNA

104
Q

Where are the ART sites?

A

Entrance inhibitors
Rever transcriptase inhibitors
Integrase inhibitors
Protease inhibitors
-Not curative, decreases death

105
Q

Hypersensitivity

A

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

106
Q

Examples of hypersensitivity?

A

Allergy
Autoimmunity
Alloimmunity

107
Q

Allergy

A

Harmful effects of hypersensitivity to environment (exogenous) entigens
e.g; pollen, bee sting

108
Q

Autoimmunity

A

Disturbance in immunological tolerance of self-antigens (immune system doesn’t recognise own antigens)
-Autoimmune diseases

109
Q

Alloimmunity

A

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

110
Q

What are the 4 types of hypersensitivity mechanisms?

A

Type I
Type II
Type III
Type IV

111
Q

What is Type I immune mechanism?

A

mediated by antigen specific IgE and products of mast cells (histamine)

112
Q

What are immediate hypersensitivity reactions?

A

Reaction that occurs within minutes or hours

113
Q

Example pf immediate hypersensitivity reaction?

A

Anaphylaxis
-most rapid and severe

114
Q

Anaphylaxis symptoms?

A

Pruritis
Erythema
Vominting, diarrhoea, breathing difficulties

115
Q

Pruritis

A

Severe itching

116
Q

Erythema

A

Red patches on skin

117
Q

What is delayed hypersensitivity reactions?

A

reaction occurs after several hours and are at maximal days later

118
Q

What is the most common hypersensitive reaction?

A

Type I

119
Q

What are Type I against?

A

Environmental antigens = allergic

120
Q

What happens when allergen is initially exposed (Type I)?

A

IgE binding to mast cell receptors and person become sensitised

121
Q

What happens after a subsequent exposure to an allergen (type I)?

A

Mast cells release cytokines and cause a hypersensitive reaction

122
Q

What tissues are most affected by Type I?

A

Tissues with more mast cells
Skin, GI tract, pulmonary tract

123
Q

Atopic

A

Individuals predisposed to developing allergies

124
Q

If one parent has allergies?

A

40% of offspring will

125
Q

If both parents have allergies?

A

Up to 80% of offspring will

126
Q

What is Type II hypersensitivity?

A

Tissue specific or cytotoxic
-Antibody mediated destruction of healthy host cells (specific cell or tissue)

127
Q

What are tissue-specific antigens?

A

Attach only to plasma membranes of certain cells
e.g; platelets have antigens found on no other cell in body

128
Q

What are the 5 mechanism of Type II?

A

A, B, C, D, E

129
Q

What does each Type II mechanism begin with?

A

Antibody binding to tissue-specific antigens

130
Q

Type II A mechanism?

A

Cell is destroyed by antibodies and complements (Membrane attack complex)

131
Q

Type II B mechanism?

A

Cell destruction through phagocytosis by macrophage

132
Q

Type II C mechanism?

A

tissue damage caused by toxic products produced by neutrophils
Soluble antigens from infectious agents or host’s own cells bind to cell surface.
Neutrophils are attracted and release their granules into healthy cells= damage cells

133
Q

Type II D mechanism?

A

Antibody- dependent cell mediated cytotoxicity (ADCC)
-Binding of IgG antibodies attracts NK cells that release toxins to destroy cell

134
Q

Type II E mechanism?

A

Target cell malfunction (not destruction) because antibody prevents cells from interacting with normal molecule
e.g; Grave’s disease targets thyroid

135
Q

What is Type III hypersensitivity?

A

Immune complex
- ˜antigen–antibody immune complexes are formed in circulation and later deposited in vessel walls or extravascular tissues

136
Q

What is Type IV hypersensitivity?

A

Cell mediated (T cells activated–> macrophages –> cell destroyed)
-NO ANTIBODIES
Example: graft rejection, allergy to poison ivy, metals

HLSC 222 Pathophysiology 🧫 (16 decks)

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