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Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Innate immunity

A

Nonspecific, no memory, rapid response, inborn
Leukocytes, TLR, PAMP, iNKT
Skin/inflammatory response

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2
Q

Acquired immunity

A

specific, has memory, slower to respond, 2 branches (cell mediated/humoral)
lymphocytes (b/t) , APC, cytokines, complement

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3
Q

Cell mediated

A

T lymphocytes
antibodies are not involved

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4
Q

Humoral

A

B lymphocytes, plasma cells, antibodies are involved

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5
Q

Types of acquired immunity

A

Active vs passive
natural vs artificial

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6
Q

Active, natural

acquired immunity

A

infection

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7
Q

Active artificial

acquired immunity

A

Vaccination
- immunogens
- live virus

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8
Q

Passive, natural

acquired immunity

A

maternal antibody transfer (IgG)

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9
Q

passive, artificial

acquired immunity

A

Immunoglobulin plasma transfer
- tetanus Ig
- Rho-Gam
- ATGAM
- Thymoglobulin

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10
Q

Immunomodulator

A

can cause both positive/negative fx
bacteria + its byproducts on immune system

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11
Q

Immunostimulants

A

stimulates T cells and macrophages in immune deficiency
- isoprinosine
- bacillus calmette goerin
- levamisole

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12
Q

Immunopotentiator

A

boosts a failing immune system
- IV immunoglobulin
- CMV immunoglobulin

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13
Q

Immunoadjuvants

A

Given with antigen
- muramyl dipeptide (MDP)

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14
Q

Immunosupressants

A

attenuate the immune response
- azathioprine
- glucocorticoids
- calcineurin inhibitors
- antilymphocyte globulin

for organ transplant

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15
Q

Primary immunodeficiency

A

Congenital/genetic
- Severe combined immunodeficency aka SCID (tcell/bcell defect)

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16
Q

Seconday immunodeficiency

acquired

A

Lifetime development, can be caused by other disease/environment
- Drug therapy, cancer, irradiation, malnutrition, old age, chronic disease

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17
Q

3 main ways the immune system can fail

A
  1. Hypersensitivity
  2. Immunodeficiency
  3. Autoimmune disease
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18
Q

Neutrophil count

A

2300-7700 cells/mm3
50-70% (60%)

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19
Q

CD4+ count

A

70-110 (80) cells/mm3
38-46% (42)

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20
Q

CD8+ count

A

50-90 (70) cells/mm3
31-40% (35%)

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21
Q

WBC count

A

4500-11000 (7500) cells/mm3
100%

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22
Q

Leukocytosis

A

high WBC

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23
Q

Leukopenia

A

Low WBC

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24
Q

Neutropenia

A

Low neutrophil
risk of opportunistic infection

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25
Q

Cluster Determination (CD)

A

specific sites on lymphocytes surfaces made of proteins/glycoprotein
Used to monitor disease states
Drug target

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26
Q

CD3

A

on all T lymphocytes

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27
Q

CD4

A

on helper T lymphocytes
TH1 or TH3

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28
Q

CD8

A

Cytotoxic/supressor T lymphocytes

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29
Q

CD20

A

B lymphoctes

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30
Q

CD25

A

Activated T lymphocytes
B lymphocytes
IL2 receptor chain Tac

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31
Q

CD56

A

Natural Killer Cell

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32
Q

Functional assessment of cell mediated immunity of T cells

A

skin test using common recall antigens:
candida, mumps, ppd, trichophyton
Tests for anergy (no response despite prev exposure)

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33
Q

Total immunoglobulins measure

A

Measures B cell function by serum protein (humoral response) electrophoresis w/ 5 fractions
(IgG, IgM, IgA, IgE, IgD)
Assess primary vs secondary immunodeficiency

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34
Q

IgM

A

Pentamer
Primary response
best at fixing complement in monomer form (B cell receptor)
Does not cross placenta

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35
Q

IgG

A

monomer
secondary response
80% in serum
heavy chain binds to phagocyte
crosses placenta/breast milk
neutralizes/opsonizes

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36
Q

IgA

A

dimer
respiratory secretory actions

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37
Q

IgE

A

Monomer
Allergy and parasitic activity (Type 1 hypersensitivity)
Binds to mast cells and basophils

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38
Q

IgD

A

monomer
B cell receptor, homeostasis

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39
Q

Source of cytokines

A

Soluble mediators secreted by various cells to aid in communication between cells

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40
Q

Types of cytokines

A

Proinflammatory
Regulatory
colony stimulating

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41
Q

Proinflammatory cytokines

A

IL-1
TNF
CSF

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42
Q

Regulatory cytokines

A

Interleukins 1,2,4,6
TNFa/b

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43
Q

IL1

A

From macrophages, fibroblasts, endothelial cells
Activates lymphocytes, hematopoetic growth factor, induces inflammation

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44
Q

IL2

A

From CD4 t cells (TH1)
Activates lymphocytes and NK cells

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45
Q

IL4

A

From CD4 T cells (TH2), mast cells, basophils, eosinophils
Activates macrophages, lymphocyte growth factor
Promotes IgE production and bone marrow precursor proliferation

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46
Q

IL6

A

From CD4 T cells (TH2), macrophages, mast cells, fibroblasts
Augments inflammation
Growth factors: lymphocytes and hematopoetic

47
Q

TNF a

A

From macrophages, NK cells, Lymphocytes, mast cells
Activates cells to produce acute phase proteins (WBC, endothelial, lymph/liver cells)

48
Q

TNF b

A

From T lymphocytes
Tumoricidal action

49
Q

Hematopoetic growth factors

A

IL3 (multi-lineage)
EPO (RBC)
G-CSF
GM-CS

50
Q

Interferon alpha

A

From monocytes/other
Antiviral effect: activates NK cells/macrophages, upregulates MHC 1

51
Q

Interferon gamma

A

From T lymphoctes and NK cells
Activates NK cells/macrophages, upregulates MHC 1 & MHC 2

52
Q

G CSF

A

Filgrastim
recombinant DNA
Increases neutrophil count

53
Q

G CSF

A

Filgrastim
recombinant DNA
Increases neutrophil count

54
Q

GM CSF

A

Sargramostim (Leukine)
DNA recombinant
dose dependent prod neutrophils and macrophages

55
Q

Colony stimulating Factor indication

A

Chemo
bone marrow transplant
myelodysplastic syndrome
HIV

56
Q

EPO

A

retacrit, darbepoetin alfa
Binds EPO receptor on erythroid CFU
Stimulates BFU-E and CFU in bone marrow to proliferate/differentiate into mature RBC

57
Q

INF alpha

drug

A

Peginterferon alfa
- 2a = pegasys; 2b=pegintron
- antiviral action, surpess cell cycle, induce apoptosis/anti-angiogenic actions,
immunomodulator, increases phagocytosis
For hepatitis C virus

58
Q

INF beta

A

Peginterferon beta 1a (plegridy)
- INF b1a (Avonex/Refib); INF b1b (Betaseron)
For relapsing multiple sclerosis

59
Q

G-CSF ADR

Filgrastim (neupogen); Pegfilgrastim (neulasta)

A

Bone pain
N/V
marked leukocytosis (high WBC)
increased uric acid
hypersensitivity rxn

59
Q

G-CSF ADR

Filgrastim (neupogen); Pegfilgrastim (neulasta)

A

Bone pain
N/V
marked leukocytosis (high WBC)
increased uric acid
hypersensitivity rxn

60
Q

GM-CSF ADR

sargramostim (leukine)

A

Fever
Diarrhea
N/V
Malaise/weakness
headache/chills
rash

61
Q

EPO ADR

A

HyPERtension
Fever
N/V
headache, rash, itching, joint aches, cough

62
Q

Interferon a ADR

A

Bone pain
myalgia
Fever,fatigue
Neutropenia (low)

63
Q

Monoclonal antibody classes (2)

A
  1. unconjugated (naked)
  2. immunoconjugates (tag toxin, chemo agent, or radioactive particle)
64
Q

Therapeutic use of moab

A

Target:
- surface antigens –> cell death
- growth factor receptors –> stop proliferation

65
Q

HAMA reaction

A

can increase CL of moab and reduce bidning to target (reduce therapeutic effect & cause hypersensitivty/infusion reaction)
Common with murine source

66
Q

HAMA premedication

A

glucocorticoids
diphenhydramine

67
Q

PolyAb

A

When the immune response to antigen is heterogenous. Plasma cells are sensitized to different epitopes and produce multiple different antibodies to the same antigen
1 antigen, many antibodies

68
Q

PolyAb products

A

Gammagard S/D
gamunex
ocagam

for immunodeficiency

69
Q

Limitation of PolyAb

A

batch to batch varability because it’s produced in different animals at different times
High chance of cross-reactivity due to recognition of multiple epitopes

70
Q

IVIG

A

intravenous immunoglobulin = artificial passive immunity
A IV blood product containing at least 90% of pooled IgG antiboides harvested from at least 1000 patients (polyclonal formulation)
DO NOT INTERCHANGE IV and IM !!!

71
Q

SLE treatment

A

pathology: B cells produce autoantibodies = organ damage
Belimumab (benlysta): targets B cell receptor to cause depletion; for lupus nephritis

72
Q

RA treatment

A

Drugs will modify TNF-a, reduce inflammation
1. Etanercept (enbrel): soluble cytokine receptor drug
* fusion proteins bind to TNF-a in circulation, prevent binding to T cell target

  1. Infliximab/adalimumab: chimeric mAb
    * moab binds to circulating TNF-a, prevent interaction with lymphocytes/macrophages + inactivate laready bound TNF-a
73
Q

Cytokine surface receptors

A

on target cell

74
Q

Soluble cytokine receptors

A

endogenous, circulates in blood

75
Q

TNF-a

A

endogenous mediator of inflammation
* increases tissue adhesion molecules
* stimulates pro-inflammatory cytokines (IL2,IL2,IL5,PG)

76
Q

Exudate

A

High protein content

77
Q

Transudate

A

Low protein content

78
Q

Tetanus

A

AKA lockjaw, bacterial infection (clostridium tetani) , non-contagious
Characterized by muscle spasm and back muscle spasms (or opistotonos) which start in the jaw and progress to other body parts

79
Q

Tetanus sx

A

Sx: fever, sweating, headaches, urinary retention, tachycardia, HTN, impaired swallowing

everyone should get vaccinated
Tetanus Ig for tx

80
Q

Type 1 hypersensitivity cells

A

B lymphocytes/plasma cells/mast cells/IgE antibodies

81
Q

Type 2 hypersensitivity cells

A

Macrophage/IgD> antibody/neutrophils/RBC

82
Q

Type 3 hypersensitivity cells

A

IgG or IgM antibodies/basophils/lymphocytes/neutrophils/c3b

83
Q

Type 3 hypersensitivity cells

A

IgG or IgM antibodies/basophils/lymphocytes/neutrophils/c3b

84
Q

Type 4 hypersensitivity cells

A

T lymphocytes, cytokines, macrphages

NO ANTIBODIES – CELL MEDIATED

85
Q

MAb limits

A

potential hypersensitivity reactions
unknown long term effect
limited production
antigenic modulation

86
Q

Abciximab (ReoPro)

A

binds to GP2B3A to inhibit platelet aggregation

87
Q

Muromonab-CD3

A

anti-CD3 antibody prevents or reverses allograft rejection

88
Q

Muromonab-CD3

A

anti-CD3 antibody prevents or reverses allograft rejection

89
Q

Liposomal conjugates (moab)

A

Amphotericin B
Doxorubicin

90
Q

Alemtuzumab (Campath)

A

MoAB against CD52 surface antigen on mature lymphocytes (T cell> B cell), NK cells, macrophages, monocytes, eosinophils, male reproductive tract. FC domain activates complement → ab dependent cellular cytotoxicity (ADCC) → cell lysis

91
Q

Basiliximab (simulect)

A

blocks CD25 to prevent activated T-lymphocyte proliferation (makes Il-2 resistant to stimulation)

92
Q

Inflammation purpose

A
  1. prevent antigen from invading body unchecked
  2. Promotes healing and repair from antigen invasion
  3. limits festering of antigen in body
93
Q

inflammation characteristics

A
  1. Nonspecific, not dependnent on antigen type
  2. Depends on activity of cellular/chemical components
  3. temperature, heat, redness, swelling, loss of function
94
Q

Cells of acute inflammation

A

Primarily neutrophils

95
Q

cells of chronic inflammation

A

lymphocytes and macrophages
granulomatous inflammmation (granulomas) form

96
Q

Treatment of systemic inflammation

A
  1. Fever
  2. assess CBC with differential
    - leukocytosis left shift
    - increased immature WBC bands
    - ANC calculation check neutrophil count
    - Lymphangitis
    - Lymphadenopathy
    - Edema
    - scar like tissue (fibrosis)
97
Q

Type 1 hypersensitivity presentation

A
  1. Reduced blood pressure after allergen exposure
  2. Reduced end organ dysfuncion
  3. Respiratory compromise/skin reaction/persistent GI sx
98
Q

Type 1 Hypersensitivity mechanism

A
  1. allergen exposure
    - immunologic: IgE (food,med,insect bite,latex)
    - non-immunologic (exercise, cold air/water, meds, etc)
  2. sensitized B cells are activated and produce IgE antibodies. Second exposure = mast cell degranulation
  3. Fatality greatest in first 30 min due to anaphylaxis, watch for late phase reactions
  4. Mediators:
    - primary: histamine, chemotactic factors
    - secondary: leukotrienes, prostaglandin
99
Q

Atopy

A

heightened immune response to common allergens – asthma, allergic rhinitis

100
Q

Type 2 hypersensitivity presentation

A

Cytotoxic IgG
Hemolytic anemia of newborn
-Rho negative mother’s B cells make IgG antibodies against Rho positive fetus –> cross placenta and cause RBC lysis
Graves disease (hyperthyroid
- antibodies block TSH receptor on thyroid epithelial cells, constantly stimulate TH release even without TSH present

101
Q

Type 3 hypersensitivity presentation

A

Immune complex mediated IgG
1. serum sickness (fever, rash, swollen joints/lymph, dermatitis
2. arthus reaction (local, not rotating insulin)
3. drug induced lupus (minimal organ involvement)

102
Q

Drug Induced Lupus

Type 3 hypersensitivity

A

Milder/rarer disease than idiopathic SLE
Sx: fever, malaise, myalgia
Occurance: slow acetylators, elevated ANA/SS-DNA/ESR
Drugs: hydralazine, procainamide, isoniazid, quinidine, TNFa inhibitors

103
Q

Type 4 hypersensitivity presentation

A

Cell mediated (t cell); delayed HS that occurs a few days after exposure to an antigen
A. Tuberculosis PPD, contact dermatitis
B. chronic asthma/allergic rhinitis
C. contact dermatitis, SJS, TEN, maculopapular
D. Acute generalized Exanthematous Pustulosis

104
Q

Type 4A

A

TH1 cell activation
Effector: macrophage activation
Antigen presented by cells or by T cell stimulation

contact dermatiitis, TB PPD

105
Q

Type 4B

A

TH2 cell activation
Effector: Eosinophils
Antigen presented by cells or by T cell stimulation

chronic asthma/allergic rhinitis

106
Q

Type 4C

A

Serious life threatening condition: macules rapidly spread and coalesce, leading to epidermal blistering, necrosis, and sloughing– of SKIN and in mucosa (eye, mouth, GI)
TEN more BSA affected than SJS

SJS, TEN, contact dermatitis (again)

107
Q

Type 4D

A

Soluble antigen presented by cells or direct T-cell stimulation
Effector: Neutrophils
Patho unclear, 90% drug association (less so bacterial/viral/parasitic)
Occurs up to 3 weeks after drug exposure

AGEP

108
Q

Contact dermatitis treatment

A

Drugs:
* Topical steroids (HC)
* Oral antihistamines
* Topical immunomodulators (tacrolimus)
* Systemic steroids (if sx do not subside in 7-14 days)
Homeopathic
* cold compress
* for oozing lesions: calamine lotion, colloidal oatmeal
* Mild soap, nonirritating, avoid dye/fragrance
* acoid known triggers, wash skin after exposure

109
Q

Type 4 cell mediated disease manifestations

A
  1. tuberculosis
  2. leprosy
  3. schistosomiasis
  4. sarcoidosis
  5. contact dermatitis
  6. eczema
110
Q

Type 1 hypersensitivity treatment

A
  1. Give epinephrine every 15-20 minutes
    * 1:1000 IM or SQ every 15-20 minutes
    * If bronchospasm doesnt respond to epi, use nebulized albuterol in the ER
  2. Oxygen therapy if needed (8-10L/min)
  3. Treat late phase reactions using (histamine blockers)
    * IV diphenhydramine 25-50mg
    * h2 receptor blocker (cimetidine)
  4. Reduce recurrent risk
    * IV hydrocortisone 5mg/kg or 250mg
    * OR PO prednisone 20mg – taper usually needed
  5. If hypotensive? – give IV fluids isotonic or colloid replacement
111
Q

SJS/TENs drug induced

A

SJS 50%; 95% SJS
* Sulfonamides (bactrim, sulfasalazine)
* Antibiotics (aminopenicillins, fluoroquinolones, cephalosporins)
* Anti-epileptics
* Miscellaneous (allopurinol)

112
Q

AGEP is associated with:

A

drugs (90%)

Immunology (6 decks)

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