Partial exam Flashcards
(103 cards)
1
Q
Any substance that may be specifically bound by an antibody or TCR
A
Antigen
2
Q
Any antigen capable of eliciting immune response
A
Immunogen
3
Q
Antigens that elicit immediate hypersensitivity reactions
A
Allergen
4
Q
Hapten definition
A
small molecule that stimulates production of antibody molecules only when conjugated to larger molecules
5
Q
Larger molecule that binds to hapten
A
Carrier
6
Q
Initial asymptomatic immune response to an antigen
A
Sensitization
7
Q
Body´s hyperreactivity to a foreign substance
A
Allergy
8
Q
Atopy definition
A
Genetic predisposition to produce IgE after antigen exposure
9
Q
Characteristics of allergens
A
Repeated exposure and does not stimulate responses of Th1 or Th17
10
Q
Top 5 allergens found in patch tests
A
Nickel sulfate, balsam of Peru, fragrance mix I, quaternium-15, neomycin
11
Q
Type of inflammatory response produced by allergen
A
Type 2
12
Q
Mediators of allergic response
A
IL4, IL5, IL13
13
Q
Hallmark of allergic response
A
Production of IgE antibody
14
Q
Role of IL25, IL33 and TSLP in type 2 cytokines
A
Activate ILC2 to upregulate GATA3 → enhances IL5 and IL13
15
Q
Role of Th2 cells and Tfh cells in type 2 allergy
A
Th2 for inflammation and Tfh to help B cells produce IgE
16
Q
Early and late phase reaction
A
Early → vascular changes, dependent on IgE and mast cells (histamine, vasodilation)
Late → accumulation of inflammatory leukocytes
17
Q
ILs secreted by Th2 cells and their roles
A
IL4 → Th2 differentiation
IL5 → enhances eosinophil production and activation
IL13 → stimulates mucus secretion
ILC2 → produce IL5 and IL13
18
Q
What receptor does mast cells and basophils express
A
FcERI
19
Q
Which cell expresses low levels of FcERI
A
Eosinophils
20
Q
Growth factor of mast cells and basophils
A
IL3
21
Q
Action of histamine
A
Increase vascular permeability, stimulate smooth muscle cell contraction
22
Q
Mutation that alters FcERI
A
FCER1A
23
Q
Mutation IL33
A
Association with asthma
24
Q
Mutation on filaggrin
A
Atopic dermatitis
25
Mutation associated with asthma
ADAM33
26
Sex incidence of asthma
Before puberty more in males
After puberty more in females
27
Main metabolite of nicotine
Cotinine
28
Type of second hand smoke
Side stream → smoke given off burning end of cigarette
Main stream → smoke exhaled from lungs of smokers
29
Biomarkers of asthma
FeNO → induced by IL13
Sputum eosinophils → >2%
Airway periostin
Serum IgE
30
Mainstay of asthma tx
Corticosteroids
31
Only biological agent approved for asthma
Omalizumab
32
Clinical manifestations associated with late-onset persistent asthma
Sinusitis and nasal polyps
33
5 phenotypes of asthma
Early onset → childhood and allergic symptoms
Late onset → adult, sinusitis
Exercise induced
Obesity related → lack Th2
Neutrophilic
34
Clinical features of asthma
dyspnea, wheezing (expiratory), chest tightness, cough (night)
35
Lung function tests of asthma
* Spirometry → FEV1/FVC <0.75
* FEV1 after bronchodilator → >12% or 200 mL change
* Peak flow meter → documenting
* PEF >10% (adults) and 13% (children)
36
Characteristics evaluated in asthma control
Symptoms <2 per week
Nighttime awakening <2 per month
Interference normal activity
SABA use <2 per week
Peak flow <80%
37
Tx use in route 1 and 2 of GINA tx
Route 1 → ICS and formoterol
Route 2 → SABA
38
Unresponsiveness to antigen that is induced by exposure to that antigen
Tolerance
39
Where does central tolerance occur
bone marrow and thymus
40
Explain central tolerance of T cells
They mautre in thymus
Positive selection: recognizes MHC molecules to survive
Negative selection: bind strongly to self antigens and undergo apoptosis
Tregs generted during negative selection, help maintain tolerance by suppressing
41
Explain central tolerance of B cells
They mature in bone marrow
Negative selection → if they bind to self antigen they can die by apoptosis, undergo receptor editing or anergy
42
Function of AIRE
Autoimmune regulator critical for central tolerance
Facilitates negative selection by ensuring developing T cells are exposed to self-antigens
43
How does peripheral T cell tolerance work
T cell response needs costimulator
44
Definition of anergy
functional unresponsiveness, no costimulation so no response
45
CD28, CTLA4 and B7 roles in tolerance
CD28 and B7 → costimulation of T cell
CTLA4 and B7 → inhibition of T cell
B7 binds with more affinity to CTLA4
46
In which cell is B7 and CD28
B7 in APCs and CD28 in T cells
47
Characteristics between CTLA4 and PD1
CTLA4 inhibits CD4 and is found in secondary lymphoid organs
PD1 inhibits CD8 and is found in peripheral tissues
48
Critical for function and development of Tregs
FOXP3
49
What is high on Tregs
CD25 (IL2 receptor), FOXP3 and CTLA4
50
IL needed for generation, survival and competence of Tregs
IL2
51
Inhibitory mechasisms of Tregs
TFGb: inhibits proliferation if T cells
IL10: inhibis production of IL12 and expression of costimulators
Binds to B7 to reduce costimulation
Consumption IL2: deprives of growth factor
52
Intrinsic pathway of apoptosis
Mitochondrial: Cell injury activates BIM to bind to Bax and Bak → caspase 9 → death
53
Extrinsic pathway of apoptisis
death receptor: uses Fas and FasL → capsae 8 → death
54
How does receptor editing work in B cell tolerance
B cell recognizes self antigen → change receptors
Immature cells activate RAG1 and 2 genes and initiate new VJ recombination in IG light chian → creased a new BCR with new specificity
55
Main problem of autoimmune disease
defective self-tolerance
56
Genetic susceptibiltiy of ankylosing spondylitis
HLA-B27
57
Molecular mimicry
Microbial antigens cross react with self antigens
58
Immediate hypersensitivity
Type I: IgE antibodies
Allergic
59
Antibody-mediated hypersensitivity
Type 2: IgG and IgM cause injury
Organ specific
60
Diseases of type 2 hypersensitivity
Autoimmune hemolytic anemia, glomerulonephritis, Graves and myasthenia gravis
61
Immune complex-mediated hypersensitivity
Type 3: IgG and IgM cause complexes that deposit in blood vessels
Systemic
62
Diseases of type 3 hypersensitivity
SLE and rheumatoid arthritis
63
Cell-mediated hypersensitivity
Type 4: T lymphocytes
Delayed hypersensitivity
64
Type 4 hypersensitivity diseases
Poison ivy/oak rashes
65
Delayed type hypersensitivity
24-48 hrs after exposure
Can produce granulomas
66
Type of hypersensitivity in allergic rhinitis, allergic conjunctivitis and atopic dermatitis
Type 1
67
Clinical features of allergic rhinitis
Congestions, clear rhinorrea, pruritos of nose/eyes
68
CNS role in allergic rhinitis
Parasymphathetic causes vasodilation (rhinorrhea)
Symphathethic causes sneezing/congestion
69
Evaluation of allergic rhinitis
Allergic salute, shiners, oral breathing, pale nasal mucosa
70
Cobblestone appearance of posterior pharyngeal wall
Allergic rhinitis
71
Classification of allergic rhinitis
Mild → normal
Moderate/severe → abnormal sleep, impairment daily activities, troublesome symptoms
Persistent → >4 days per week for >4 weeks
Intermittent → <4 days per week or <4 weeks
72
Dx of allergic rhinitis, atopic dermatitis and allergic conjunctivitis
Clinical
73
Pharmacotherapy of allergic rhinitis
Intermittent → intranasal antihistamines
Mild → intranasal corticosteroids
Moderate/severe → intranasal corticosteroids + intranasal antihistamines
74
Inflammation of conjunctiva caused by allergy
Allergic conjunctivitis
75
Clinical features of allergic conjunctivitis
Itching, dry eye, blurred vision, excessive tearing, bilateral
76
Tx for allergic conjunctivitis
Avoid exposure to allergen, artificial tears, pharmacological therapy
77
Pharmacotherapy of allergic conjunctivitis
Mild symptoms → naphazoline (vasoconstrictor + antihistamine), azelasine (histamine H1 antagonist)
Uncontrolled symptoms → cetirizine (oral antihistamine) ketorolac (topical NSAID)
Severe/persistent → topical mast cell stabilizers
78
Chronically relapsing inflammatory skin disease
Atopic dermatitis
79
First manifestation of atopic dermatitis
Weeping
80
Onset of atopic dermatitis
3-6 months old
81
Mutation in atopic dermatitis
Filaggrin
82
Principal microorganism to cause problems in atopic dermatitis
Staph aureus
83
Prophylaxis for atopic dermatitis
Oral vitamin D
84
Main trigger of atopic dermatitis
Aeroallergens
85
Principal clinical feature of atopic dermatitis
Severe pruritus
86
Differential for atopic dermatitis
Suborrheic dermatitis and psoriasis
87
Methacoline tests
<4 mg/mL o 100 ug → AHR significativa
4-16 mg/mL o 100-400 ug → borderline
>16 mg/mL o 400 ug → negative
88
Asthma endotypes (4)
T2 high: Th2 and ILC2, E2 stimulation
T2 low: Th17 and ILC3, E1 stimulation
Mixed: E1 and E2 stimulation, high cytokines
Paucigranulocytic: Treg, Breg, chronic stimulation, no cytokines
89
Phenotypes of asthma associated with Th2 and non-associated with Th2
Th2: early onset, late onset, exercise induced
Non Th2: Obesity related, neutrophilic
90
Respiratory infection that is a predisposing factor of asthma
rhinovirus C (HRV-C)
91
Characteristics of Th2 phenotypes of asthma (3)
Early onset: IgE and Th2; responds to corticosteroids and omalizumab; FeNO and sputum eosinophils
Late onset: Adults, more severe, sinusitis and nasal polyps; IL-5 and cysteinyl leukotriene tx; IL-13 and IL-5 biomarkers
Exercise: reactive bronchoconstriction; tx leukotriene supprersor, b agonist, IL9
92
Characteristics of non Th2 phenotypes of asthma (2)
Poor response to corticosteroids
Obesity: women, proinflammatory state
Neutrophilic: more metalloproteinases, Th17, macrolides tx
93
Allergen that activates PAR1 and PAR4 to create allergic reaction
Dust mites
94
Asthma exacerbated by nonspecific stimuli but not caused by it
work-exacerbated asthma
95
Exposure to specific agent in occupational setting
Occupational asthma
96
Characteristic of asthma phenotypes (4)
T2 high → ILC2 and Th2; E2 stimulation
T2 low → ILC3 and Th17; E1 stimulation
Mixed → E2 and E1 stimulation; high cytokines
Paucigranylocytic → chronic, Treg and Breg
97
Genetic predisposition of asthma (chromosome)
Chromosome 2q-related genes (IL33, IL13)
98
Difference of marked allergens and cross reactive allergens
Marker allergen → clearly ids primary sensitizing source
Cross-reactive allergen → have similar epitopes to allergens that cause allergic reaction
99
Primary function of PGD2 during allergic inflammation
Bronchoconstriction and promotion of neutrophil accumulation
100
What does the downregulation of filaggrin produce in atopic dermatitis
Impairment filament aggregation in transitional zone of stratum corneum
101
Most common type of allergic conjunctivitis
Seasonal allergic conjunctivitis (during pollen season)
102
Second most common type of allergic conjunctivitis
Perennial allergic conjunctivitis (persistent all year)
103
Hay fever
Allergic rhinitis
