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AII Week 3 > Basic Science > Flashcards

Basic Science Flashcards

1
Q

Exogenous

A

Infectious agent is not normally found on or in the body

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2
Q

Endogenous

A

Infectious agent that can be routinely found on the body but does not normally cause disease

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3
Q

How do exogenous agent cause disease

A

When it enters the host from the environment

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4
Q

How do endogenous agents cause disease

A

Overcomes innate host immunity to cause disease

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5
Q

Vector

A

Insects and other carriers that transmit disease

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6
Q

Zoonotic hosts (reservoirs)

A

Animals that harbor infectious agents

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7
Q

Nosocomial infections

A

Hospital acquired infections. Happens when the normal flora is colonized with other bacteria

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8
Q

What is a physical barrier

A

Something that impedes the entry of bacteria from the external environment into sterile areas of the body

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9
Q

Examples of physical barriers

A

Skin, mucous membranes, secretions, perspiration, nose hairs, hair on arms/legs, gastric acids (pH)

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10
Q

Commensals

A

Organisms that live symbiotically on or within the human host but rarely causes disease

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11
Q

Where are the normal flora of the body located

A
  1. Skin - staph
  2. Oropharynx - strep
  3. LI - enterococci, enteric bacilli
  4. Vagina - lactobacilli
  5. Colon - bacteroides
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12
Q

What do commensal bacteria secrete

A

TLR ligands, which bind to TLR on surface of normal intestinal tissue. This stimulates basal signaling which protects the cells of the intestine from injury (i.e., when abx are introduced)

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13
Q

Carrier

A

Anything that carries and transfers bacteria to a susceptible individual

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14
Q

Opportunistic infections

A

Infections that result from normal flora (commensals) or from environment that usually do not cause disease (not considered human pathogens). immunocompromised hosts

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15
Q

Colonization

A

When normal flora is overgrown by endogenous or exogenous organisms. (i.e. broad spectrum abx will kill lactobacilli in the vagina, which will then allow for the colonization of candida).

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16
Q

3 host defense mechanism to inhibit colonization of bacteria

A
  1. Mechanical clearance
  2. Phagocytic killing
  3. Depriving organism of nutrients
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17
Q

What site is usually easier for colonization

A

Sterile areas of the body because there are fewer microbes. However the immune system will be vigorous

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18
Q

Congenital infections

A

Acquired in utero

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19
Q

The complement system is part of which immunity

A

Innate immunity

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20
Q

What are the major cytokines involved in an inflammatory reaction when a microbe enters the body

A

Interleukin-1, 6, TNF, and interferon-y. Secreted by macrophages

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21
Q

What are the acute-phase reactants

A

Rheumatoid factor
C-reactive protein
Ferritin
Proteinase inhibitors

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22
Q

What is the complement system composed of

A

Plasma proteins and cell membrane receptors (the C proteins, produced by the liver)

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23
Q

What are the two pathways of the complement system

A

Classic and alternative. Mostly mediated by C3 and terminal components C5-C9

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24
Q

What activates the complement system

A

Antigen-antibody complexes. Directly activate C1

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25
Q

What activates the alternative pathway

A

Mechanisms independent of antibodies, usually interactions with bacterial surface carbohydrates (“nonspecific).. Microbe binds directly to C3

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26
Q

What do both pathways ultimately proceed towards

A

Creation of a MAC, which results in target cell lysis. C3 and C5-C9 must be activated, which then makes C3 convertase enzyme, then MAC.

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27
Q

Opsonization

A

Complement system facilitates phagocytosis through proteins called opsonins. Coat invading organism making them susceptible to engulfment (destruction by neutrophils/macrophages). Controlled by C3b

28
Q

MAC

A

The membrane attack complex inserts itself into the target organism = increased permeability/lysis. Formed by C5b-C9

29
Q

Indirect action of complement system (anaphylotoxins

A

Produces substances that are chemotactic for WBC which then promotes (amplifies) an inflammatory response - vasodilation, increased perm of caps, histamine release.
Controlled by C3-C5a

30
Q

3 functions of the complement system

A
  1. opsonization
  2. MAC = lysis
  3. Induction of inflammation (anaphylotoxins - vasodilation, increased perm of caps)
31
Q

Pts with a C3 deficiency have increased susceptibility to what

A

Encapsulated bacteria (S. pneumoniae and haemophilus influenza)

32
Q

Pts with C5-C9 deficiency have increased susceptibility to what

A

Neisseria group because they are unable to form a MAC and therefore cannot lyse the organism

33
Q

What are the phagocytic cells

A

Neutrophils
Monocytes
macrophages

34
Q

How does phagocytosis work

A

The bacteria attaches to the cell surface of neutrophil or macrophage, which then triggers extension of pseudopod to enclose the bacteria and engulf it

35
Q

How are neutrophils activated

A

Via chemoattractants (located at the site of infection, usually in the tissue)

36
Q

How is infection established

A
  1. Organism encounters host
  2. Gains entry into host
  3. Multiplication and spread
  4. Cause injury
37
Q

Severity of infection

A

Acute, subacute, or chronic

38
Q

Outcomes of infection

A
  1. resolution
  2. chronic active infection
  3. Prolong asymptomatic excretion of agent
  4. Latency of agent within host
  5. Death
39
Q

Modes of encounter

A

Endogenous (normal flora)
Exogenous (colonization)
Host immune state

40
Q

Modes of entry

A

Inhalation, ingestion (ingression), mucous, penetration from insect bite or cut (direct entry)

41
Q

Factors that influence multiplication and spread

A
  1. Inoculum size
  2. Nutrition for microbe
  3. Anatomic location
  4. Environment for microbe
  5. Virulence
42
Q

Ways that microbes cause injury

A
  1. mechanical obstruction ie bowel obstruction
  2. cell death
  3. inflammation
  4. Humoral/cellular immunity
43
Q

Infection

A

When microorganism multiplies at a normal sterile site. Different from colonization!

44
Q

3 types of chronic infections

A

Saprophytic - organism does not cause adverse affects
Parasitic - causes tissue damage
Latency - Herpes

45
Q

Contamination

A

When an organism is in a location that it is not normally found in

46
Q

What do type I interferons do

A

Made up of several proteins that nonspecifically inhibit viral replication inside host cell. When a cell is exposed to a virus they secrete interferons into the EC fluid, then bind to plasma membrane receptor. Triggers antiviral secretion and prevents virus from replicating in all cells of surrounding area

47
Q

What do TLRs do

A

They recognize and bind to highly conserved molecular features on pathogens called PAMPs

48
Q

PAMPs

A

Pathogen associated molecular patterns. Site on bacteria that is usually made up of lipopolysaccharides or lipids or carbs. TLR bind to these through recognition. ACTIVATE THE INNATE IMMUNE

49
Q

What happens once a TLR binds with a PAMP (ligand)

A

2nd messengers are generated which leads to secretion of IL-1 and IL-2 and TNF, which in turn stimulates the activity of immune cells (innate response)

50
Q

2 functions of the TLRs

A
  1. Induction of 2nd messenger leading the secretion of IL-2 and IL-1
  2. Induce attachment of a microbe to a macrophage which in turn causes phagocytosis
51
Q

What are PRR’s (pattern-recognition receptors)

A

Proteins that recognize and bind to a variety of pathogen ligands or PAMPS (TLRs belong to the PRR family)

52
Q

DAMPs

A

Molecules that initiate the immune response in noninfectious ways. Many are nuclear or cytosolic proteins. They are usually released from the cell following tissue injury

53
Q

Targets of NK cells

A

Virus and cancer cells. And can attack directly without specific antigen recognition

54
Q

How does innate Immune activation lead to cytokine secretion

A

Bacteria enters body binds with macrophage. Macrophage is then activated and secretes cytokines, cheekiness, and TNFa.

55
Q

What is the function of IL-1b

A

Stimulate helper T cells to secrete IL-2 which stimulates T cell proliferation. FEVER!!!!!

56
Q

Function of TNFa

A

Induces fever, apoptotic cell death, inflammation response to injury/infection, and inhibits viral replication

57
Q

What happens when you get too much cytokine (IL-1B and TNFa) release

A

They start to destroy healthy tissue around the bacteria which can lead to septic shock, microglia neuron destruction (alzheimers), asthma, gout, IBS

58
Q

Chronic inflammatory disease

A

When you have too much cytokine release and causes disease in the absence of a pathogen (noninfectious)

59
Q

Examples of chronic inflammatory disease

A 
IBS
RA
Asthma
Alzheimers
Atherosclerosis 
Gout
60
Q

Why is the epithelial lining so good at being a physical barrier

A

Because of the tight junctions

61
Q

Which phagocyte is the most abundant

A

Neutrophils (60-70%)

62
Q

Which phagocyte is normally found in healthy tissue

A

Macrophages

63
Q

Which phagocyte is mostly associated with pus

A

Neutrophils

64
Q

Which phagocyte has a longer life span

A

Macrophages

65
Q

2 modes by which NK cells destroy

A
  1. Release of cytotoxins (performs/granules)
  2. Produce interferons that promote unit-viral responses
    ATTACK AND LYSE ABNORMAL CELLS
66
Q

What causes the activation of NK cells to lyse target cells

A

The lack of MHC 1 expressed on all cells (minus RBC). They need this MHC 1 in order to NOT kill the cell

67
Q

What do inflammasomes do

A

Cleaves the pro-form of IL-1B to its smaller and active form of IL-1B that is secreted from cells

AII Week 3 (5 decks)

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