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OU Immunology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What steps are involved in diagnosis of allergy?

A
  • comprehensive history
  • physical exam
  • non-immunologic tests
  • immunologic tests
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2
Q

What is the purpose of a physical exam when diagnosing allergy?

A

rule out other causes

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3
Q

examples of immunologic diagnostic tests for allergy

A
  • in-vivo: allergy skin test
  • in-vitro: IgE antibody
  • provocative and elimination tests
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4
Q

types of skin tests

A
  • cutaneous: prick, puncture, scratch
  • intradermal
  • in-vivo
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5
Q

skin test: cutaneous

A
  • put a drop of allergen on pt’s skin

- scratch with needle

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6
Q

sensitivity of skin test

A
  • depth of puncture
  • amount of langerhans present
  • presence of B and T cells in epidermis
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7
Q

risks of intradermal skin test

A

may hit a capillary with an allergen that pt is allergic to

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8
Q

What are positive results of skin tests?

A
  • wheal
  • flare
  • happens within 15-30 minutes
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9
Q

How common is testing for immune complex disease done?

A

Not common; reactions don’t happen until after 2-4 hours and are similar to late phase reactions that occur following positive IgE-mediated reaction

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10
Q

Limitations to skin tests

A
  • not good for food and drugs

- pt should not be on antihistamines or topical corticosteroids when taking skin test

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11
Q

skin test: in-vivo

A
  • reaction may occur up to 48-72 hours

- for delayed hypersensitivity (associated with T cells)

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12
Q

What is an examples of skin tests done in-vivo?

A
  • tuberculin: positive read out: erythema

- patch test: contact dermatitis

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13
Q

examples of in-vitro allergy tests

A
  • IgE testing in blood
  • eosinophil count
  • blood differential
  • serum ig electrophoresis
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14
Q

examples of tests of IgE testing in blood

A
  • RAST (Radioallergosorbent)
  • MAST (Multiple allergosorbent)
  • FAST (Fluorescent Allergosorbent)
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15
Q

principle of IgE testing in blood

A
  • allergen stuck to a solid phase
  • pt’s IgE from serum is exposed to allergen
  • anti-human IgE sticks on pt’s IgE
  • imaging substrate attached to anti-human IgE
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16
Q

provocative allergen test

A

challenge with increased dose of allergen

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17
Q

elimination allergen test

A

get rid of antigen and see if allergic response goes away

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18
Q

Therapies to allergy

A
  • eliminate exposure to allergen
  • treat symptoms
  • immunotherapy with allergy extracts
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19
Q

other names for immunotherapy

A
  • desensitization

- hyposensitization

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20
Q

mechanism for immunotherapy

A

administering a small dose of allergen to induce an immune response against the allergen but not large enough of a dose to induce the allergic response itself

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21
Q

route of administration for immunotherapy

A
  • subq

- sublingual

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22
Q

Examples of FDA approved sublingual therapy

A
  • grass pollen: Oralair, Grastek
  • ragweed pollen: Ragwitek
  • dust mite: Odactra
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23
Q

What are standardized allergenic extracts?

A
  • allergenic extracts that fall within FDA standards

- 19 available

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24
Q

quantity of allergenic extracts

A
  • 900 diagnostic

- 600 therapeutic

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25
Q

Why would a panel of allergic extracts be useful?

A

because different geological areas are exposed to different allergens

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26
Q

With respect to the perspectives of infection, what are the emphasis on?

A
  • parasite and parasite-drug interaction

- host and host-parasite interaction

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27
Q

opportunistic infections

A
  • immunocompromised patients getting attacked by their normal flora
  • happens when there is not enough CD4
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28
Q

virulence factors

A
  • allow parasite to take advantage of host

- ex. capsule, LPS

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29
Q

causes of disease

A

when tissue damage is caused by pathogen directly or by the host response to the parasite

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30
Q

What are the top three infections that cause cancer?

A
  • Hep B and C
  • Human papillomavirus
  • H. pylori
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31
Q

What are the general approaches to an ID?

A
  • immune status of host
  • characteristic of parasite
  • type of host-parasite interaction
  • management
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32
Q

What are the types of host-parasite interaction?

A
  • toxigenic
  • extracellular
  • facultative intracellular
  • obligate intracellular
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33
Q

What are the phases of the host immune response?

A
  • innate immunity
  • inflammation
  • adaptive immunity
  • protective response
  • immunological memory
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34
Q

What are ideal goals to manage ID?

A
  • prevent establishment of infection
  • eradicate parasite
  • prevent tissue damage; recover tissue
  • establish lifelong immunity
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35
Q

toxigenic infection

A
  • infectious agent produces toxins

- endo (LPS) or exo

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36
Q

exotoxins

A
  • soluble protein excreted if infectious agent

- each is distinctive in their property

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37
Q

What are ways in which exotoxin can cause infection?

A
  • intoxication
  • toxigenic infetion
  • toxin involvement + virulence factors
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38
Q

antitoxin

A

toxin neutralizing IgG

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39
Q

How can you protect against toxin?

A
  • active immunization with toxoids

- passive immunixation with antitoxins

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40
Q

septic shock

A
  • lipid A (toxin) induce release of pro-inflammatory cytokines (IL-1beta, TNFalpha)
  • sepsis if live bacteria is present
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41
Q

What is the antibody for lipid A?

A

IgM

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42
Q

What is IgG’s role in toxin infection?

A
  • toxin neutralization
  • binds to toxin
  • gets taken up in APC
  • eliminated from body
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43
Q

examples of extracellular organisms that cause infections

A
  • gram + / - bacteria
  • spirochetes
  • mycoplasma
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44
Q

Anti-infectives are most susceptible to which type of infection?

A

extracellular infection

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45
Q

What is an important virulence factor for bacteria?

A
  • anti-phagocytic capsule

- without this, pathogen can be phagolysosomed

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46
Q

What are the phases of infection with respect to extracellular infections?

A
  • attachment to epithelial receptors
  • penetration of epithelium
  • acute inflammatory response
  • lymphatic spread
  • efferent phase of immune response
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47
Q

What is present in the gut and lung that prevents infectious bacteria colonization?

A

sIgA

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48
Q

How does pathogens fight sIgA?

A

they have proteases that can cleave these IgA

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49
Q

What is a hallmark of bacterial infection? (per lecture)

A

presence of neutrophil

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50
Q

What are components of efferent phase of immune response (for extracelllar infection)?

A
  • IgG, IgM
  • Complement
  • Neutrophil
  • try to minimize amount of bacteria circulating
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51
Q

How does neutrophil kill microbial pathogens?

A
  • neutrophils have cell surface receptors which help engulfs pathogen
  • when pathogen is inside the cell, it is destroyed via neutrophil’s toxic contents (slides pg 31)
  • release ROS to kill bacteria and phagolysosome (lec 4-13 @ 20:05)
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52
Q

What advantage does facultative intracellular organisms have?

A

they can survive best either intracellular or extracellular environment

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53
Q

examples of facultative intracellular organisms that cause infection

A
  • mycobacteria (ex TB)
  • actinomycetes
  • fungi (ex Coccidioides)
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54
Q

phases of facultative intracellular infection

A
  • attachment to epithelial receptors
  • penetration of epithelium
  • acute inflammatory response
  • monocyte / macrophage involvement
  • efferent phase of immune response
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55
Q

Which pathogen is neutrophil not efficient in killing?

A
  • facultative intracellular organisms

- can be engulfed and live in neutrophil

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56
Q

What are components of efferent phase of immune response (for facultative intracellular infection)?

A
  • cell mediated immunity

- IFNgamma works through its receptors on macrophages and facilitate phagocytosis

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57
Q

obligate intracellular organisms

A

survive best when they are withing our own cells

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58
Q

examples of obligate intracellular organisms

A
  • viruses
  • Chlamydia
  • Rickettsia
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59
Q

tissue tropism (virus)

A

virus have a preferable site of infection

60
Q

What does the body do to protect against viral infection?

A
  • IFN - NK, T cells
  • CD8 cytotoxic T cells
  • sIgA and serum IgG to prevent reinfection
61
Q

Why is CD8 the best to fight against viral infection?

A

will recognize infected host cell and kill it

62
Q

What is best to fight off facultative intracellular infections?

A
  • IFNgamma

- CD4

63
Q

What is best to fight off extracellular infections?

A
  • neutrophil

- antibody

64
Q

What is best to fight off toxigenic infections?

A
  • antibodies

- antitoxins

65
Q

What is best to fight off obligate intracellular infections?

A
  • CD8+ cytotoxic T cells
66
Q

primary immunodeficiency

A
  • hereditary / genetic

- gene missing that is not translating a protein

67
Q

X-linked Agammaglobulinemia

A

body is deficient of anti-bodies

68
Q

primary immunodeficiency consists of what being deficient?

A
  • B cell
  • T cell
  • neutrophil
  • macrophage
  • complement
69
Q

SCID

A
  • person does not have B or T cells
  • most susceptible to facultative and obligate
  • RAG1 or RAG2 affected
70
Q

What are factors that can lead to secondary immunodeficiency?

A
  • poor lifestyle choices
  • virus infections
  • neoplasms
  • trauma
  • iatrogenic
71
Q

How is immunodeficiency diagnosed? What are the steps taken to diagnose immunodeficiency?

A
  • phagocytosis
  • complement measurement
  • NK cell #
  • antibody-mediated immunity
  • cell-mediated immunity
  • evaluation of organ systems
72
Q

In testing immunodeficiency, what consists of phagocytosis tests?

A
  • CBC and differential; WBC and neutrophil count

- neutrophil function tests | chemotaxis

73
Q

In testing immunodeficiency, what consists of antibody-mediated immunity tests?

A
  • total serum Ig, IgG, IgA, IgM, IgE
  • presence of specific antibody after immunization (titer)
  • isohemagglutinins; IgM function
74
Q

In testing immunodeficiency, what consists of cell-mediated immunity tests?

A
  • CBC and differential; lymphocyte count
  • T cell subsets | CD4:CD8 ratio
  • delayed hypersensitivity tests
75
Q

If you lack antibody, complement, neutrophil, what infection are you susceptible to?

A

common pyogenic bacteria

76
Q

If you lack cell-mediated immunity, what infection are you susceptible to?

A
  • virus
  • parasite
  • intracellular bacteria
77
Q

If you lack antibody, what infection are you susceptible to?

A
  • virus
  • parasite
  • intracellular bacteria
78
Q

If you lack mucosal immunity, this may or may not lead to increased infections in mucous membrane. Why?

A

because other antibody types compensate for IgA deficiency

79
Q

What is the main cause of immunodeficiency?

A

infection

80
Q

If you lack IgA, what happens to suffice for it?

A
  • IgG, IgM, and IgD will go up

- but since IgG goes up, lyses will go up because IgG induce phagocytosis

81
Q

Therapy of immunodeficiency

A
  • symptomatic and supportive therapy
  • Ig (passive immunization)
  • bone marrow transplant
  • cytokines
  • thymus derived factors
  • gene therapy
82
Q

What is the FDA and CDC’s role in vaccination?

A
  • FDA oversees manufacturing process

- CDC published guidelines

83
Q

What is the main goal of active immunization?

A

to have memory B and T cells stay in the body for a long period of time for protective response

84
Q

passive immunization

A

preformed antibodies

85
Q

Why do we need vaccines?

A
  • serious enough
  • contagious
  • cannot control
  • cost-risk-benefit
  • where anti-infectives are useless
86
Q

incubation period

A

time when person gets exposed to when infection manifests itself

87
Q

Which immunization is most common? (pre or post exposure) And why?

A
  • pre-exposure aka phophylactic

- because incubation period is short

88
Q

What can post-exposure immunization be useful for?

A
  • aka therapeutic
  • pathogens with long incubation periods
  • Rabies, Hep B
89
Q

herd immunity

A

immunizing everyone in the region in which the pathogen will most likely strike

90
Q

types of active immunizing agents

A
  • toxoids
  • live attenuated
  • inactivated
  • this list is not inconclusive
91
Q

toxoid immunization

A
  • modified toxin

- reduce toxicity without altering immunogenicity

92
Q

live attenuated immunization

A
  • modified pathogen with reduced pathogenicity but same immunogenecity
  • must produce infection and proliferate to trigger immunity
93
Q

inactivated immunization

A

pathogen killed and cannot proliferate but still immunogenic

94
Q

subunit vaccine

A

contains purified or recombinant antigens of infectious organism

95
Q

combined vaccine

A

consists of 2 or more immunogens physically combined into a separate product

96
Q

conjugate vaccine

A

attaching poor immunogen to carrier protein

97
Q

When you see a number at the end of a vaccine, what does that mean?

A

valency; how many strains it targets

98
Q

storage of vaccines

A

most products are stored at 2-8°C and dated for about 2 years

99
Q

Which vaccines are administered subq?

A
  • most live virus vaccines

- fluid toxins

100
Q

Which vaccines are administered IM?

A

killed vaccines

101
Q

Why are vaccines never given IV?

A
  • if you already have antibodies for that particular vaccine, it will bind to and clear it before it can be presented to T cell
  • immune complex syndrom may occur
102
Q

What are hazards of active immunization?

A
  • direct toxicity
  • allergy
  • infectious
103
Q

What can antibodies lead to with respect to immunization?

A
  • no effect
  • protective to host
  • pathologic
  • block pathogenesis of pathogen
104
Q

What are potential risks of live virus vaccines?

A
  • integrated infection
  • oncogenic
  • teratogenic
105
Q

What are contraindications for active immunization?

A
  • serious febrile illness
  • pregnancy
  • immunodeficiency
  • passive immunization within past 6 weeks
  • children under one year
106
Q

Hep B

A
  • should be given to baby before baby leaves hosptial

- if baby’s mom is hep +, baby should be given antibodies within 12 hours of birth and then give vaccine

107
Q

influenza: quantity of doses

A

6 months to 6 years: two annual doses

108
Q

poliomyelitis vaccine

A
  • oral vaccine has live attenuated

- there is also an inactivated form

109
Q

pneumococcus vaccine

A

13 valent

110
Q

DTaP

A

initial 5 doses, boosters in the form of of TDap (@ 11 years) or Td (every 10 years)

111
Q

Gardisil

A
  • human papillomamvirus vaccine

- 4 and 9 valent

112
Q

Vaccines for 0-2 year olds

A
  • Hep B
  • Rotavirus
  • DTap
  • Haemophilus influenzae type B (Hib)
  • Pneumococcal conjugate
  • Polio inactivated
  • Influenza
  • MMR
  • Varicella
  • Hep A
113
Q

Vaccines for 3-18 year olds

A
  • Tdap
  • Polio inactivated
  • Influenza
  • MMR
  • Varicella
  • HPV
  • Meninogococcal
114
Q

Pneumococcal polysaccharide

A

administer to patients 2 years and older for high risk individuals

115
Q

Vaccines for 19 years and older

A
  • influenza
  • Td / Tdap
  • Varicella
  • HPV
  • HZV (zoster)
  • MMR
  • Pneumococcal
116
Q

Vaccines for 19 years and older (high risk individuals)

A
  • Meningococcal
  • Hep A
  • Hep B
  • Haemophilus influenzae type B (Hib)
  • Pneumococcal
117
Q

heterologous immunoglobulin

A

comes from animals

118
Q

homologous immunoglobulin

A

comes from humans

119
Q

potential problems of homologous immunoglobulin

A
  • presence of infectious organisms that causes latent infections
  • blood clot formation
120
Q

onset of action of IGIM, IGIV, IGSC

A
  • IGIM: 2-5 days
  • IGIV: almost immediately
  • IGSC: 2.5 days
121
Q

IgA content in IGIM, IGIV, IGSC

A

Relative to each other:

  • IGIM: max
  • IGIV: intermediate
  • IGSC: low
122
Q

IGIV most beneficial for which conditions?

A
  • AIDS
  • bone marrow transplant
  • premature babies
  • B cell insufficiency
123
Q

What are disease for which we need hyperimmune immunoglobulins?

A
  • Hep B
  • rabies
  • CMV
  • small pox
  • tetanus
  • botulism
  • anthrax
124
Q

How are mab produced?

A
  • mouse immunized against certain antigen
  • spleen cells are isolated
  • B cells from spleen are fused with myeloma cells
  • hybridoma formed
  • hybridoma produce antibodies specific to anigen used to immunize mouse
125
Q

What is the solution to allergy sickness with respect to mabs?

A
  • chimeric or humanized ab

- administer lower dose

126
Q

forms of mab

A
  • mostly IgG
  • can be complete ig
  • can be FAB fragment
127
Q

administration of mab

A
  • IV

- subQ

128
Q

What are the ways in which mab interacts with cell receptor?

A
  • agonist
  • antagonist
  • cell damage
129
Q

How does mab cause cell damage?

A
  • complement fixation
  • ab-dependent cell cytotoxicity
  • apoptosis
130
Q

What is a side effect of targetting tumor cells via mab?

A

kidney obstruction trying to clear all the lysed cells

131
Q

Define cytokine

A

Soluble intercellular mediators of immunity that regulate cell-cell interactions

132
Q

How are cytokines categorized?

A
  • interleukins
  • interferon
  • growth factors
133
Q

characteristics of cytokines

A
  • MW of 5k-75k
  • weakly immunogenic
  • produced by our own immune cells
  • can be produced by non-immune epithelial cells
  • can act as autocrine / paracrine manner
134
Q

Pleiotropy

A

cytokine that can work on multiple types of cells

135
Q

Redundancy

A

multiple cytokines that overlap in their action but binds to its own receptors

136
Q

How can you lengthen half life of cytokine?

A

Pegylate it!

137
Q

What are mechanisms of cytokines inhibitors?

A
  • neutralizing antibodies

- cytokine antagonists

138
Q

What are interferons used for?

A
  • viral infection

- cancer

139
Q

What are IL2 and IL11 used for?

A
  • cancer

- thrombocytopenia

140
Q

Hematopoietic Growth Factors

A
  • G-CSF
  • GM-CSF
  • Epoetin
141
Q

G-CSF

A

promotes neutrophil and granulocytes reconstitution from stem cells

142
Q

GM-CSF

A

promotes myeloid (macrophages and dendritic) cells reconstitution from stem cells

143
Q

Epoetin

A

stimulates erythropoiesis

144
Q

Alpha interferon type I

A
  • anti-viral

- anti-neoplastic

145
Q

Beta interferon type I

A

MS

146
Q

Gamma interferon type II

A

infections associated with chronic granulomatous disease (lack of NADPH oxidase)

OU Immunology (7 decks)

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