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Semestre 6: bloque 2 > Final Immune disorders > Flashcards

Final Immune disorders Flashcards

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1
Q

Classification of anaphylaxis

A

Immunologic
Idiopathic
Non-immunologic

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2
Q

Pathophysiology of IgE mediated anaphylaxis

A

Type I hypersensitivity with mast cell activation

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3
Q

Pathophysiology of non-IgE mediated anaphylaxis

A

Substances (ex. opioids) can release histamin directly without IgE involvement

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4
Q

Most common cause of anaphylaxis

A

Foods

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5
Q

Most fatal cause of anaphylaxis

A

Drugs

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6
Q

Most common symptom of anaphylaxis

A

Generalized urticaria (hives)

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7
Q

Diagnosis for anaphylaxis

A

At least 2 symptoms from different systems
Measurement of blood beta-tryptase

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8
Q

Medicine given for anaphylaxis

A

Epinephrine

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9
Q

How must an epinephrine injection be given in anaphylaxis

A

Intramuscular injection in mid-outer thigh

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10
Q

Mechanisms of epinephrine in anaphylaxis tx

A

a1: increase peripheral vascular resistance
b1: increase myocardial contractility
b2: bronchodilation

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11
Q

Type of hypersensitivity reaction in serum sickness

A

Type III hypersensitivity reaction

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12
Q

Main cause of serum sickness

A

Vaccines

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13
Q

Clinical manifestations of serum sickness

A

Malaise, rash, fever, arthralgias, lymphadenopathy

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14
Q

Characteristics of serum sickness-like reactions

A

Px do not have vasculitis involvement

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15
Q

Pathophysiology of serum sickness

A

IgM antibodies develop 7 days after primary inoculation with antigen to form immune complexes that cause tissue damage

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16
Q

3 types of immune complex mediated end organ damage

A

IgG: activators of macrophages and phagocytes
IgG and IgM: activate classical complement
IgA: activate alternative complement

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17
Q

Classic complement proteins that are anaphylotoxins

A

C3a and C5a

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18
Q

When do signs and symptoms of serum sickness appear

A

1-3 weeks after admin of medication

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19
Q

Skin disorder caused by contact with exogenous substance that elicits an allergic/irritant response

A

Contact dermatitis

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20
Q

Mutation in contact dermatitis

A

Loss of function of R501x and 2282del4 in filaggrin gene

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21
Q

Types of contact dermatitis

A

Allergic: T cell delayed response
Irritant: no prior sensitization, direct injury

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22
Q

Characteristics of irritant contact dermatitis

A

Clinical presentation restricted to skin in direct contact with irritants

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23
Q

Most common form of contact dermatitis

A

Irritant dermatitis

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24
Q

Key effector cells in irritant contact dermatitis

A

Epidermal keratinocytes

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25
Why does irritant contact dermatitis has a higher prevalence in women
Because irritants like nickels, essential oils, makeup or soaps are more used by women
26
Diagnosis of contact dermatitis
Patch testing
27
Symptomatic therapy of contact dermatitis
Topical corticosteroids
28
Common chronic, relapsing immune-mediated disease involving skin and small joints in genetically predisposed px
Psoriasis
29
Onset of psoriasis
Onset in first 3 decades of life
30
Main event in psoriasis
Formation of demarked erythematous plaques with large scaling
31
How are the layers of the skin in psoriasis
Epidermis: thickened Granular layer: reduced Dermis: inflammatory infiltrate
32
Genetic factor of psoriasis
PSORS1 (Chromosome 6p)
33
Pathogenesis of psoriasis
Trigger causes DC activation  activation T cells  release cytokines  keratinocyte hyperproliferation and inflammation  formation of plaques
34
What is the main difference between plasmacytoid DCs and myeloid DCs
pDCs: main inducers mDCs: main amplifiers
35
Characteristics of plasmacytoid DCs
Infiltrate psoriatic skin and initiated expansion of autoimmune T cells Produce massive amounts of type 1 IFN
36
Chemokine responsible for the recruitment of plasmacytoid DCs
Chemerine
37
Characteristics of myeloid DCs
Amplifiers of local inflammation Found in dermal-epidermal junction and dermis
38
Key event in psoriasis
T-cell migration from dermis into epidermis
39
Characteristics of Tregs in psoriasis
Increased in number but less functional due to IL-6
40
Most common clinical feature of psoriasis
Plaques
41
Difference between seasonal and perennial allergy
Seasonal: during specific times of the year, by outdoor allergens Perennial: year-round, by indoor allergens
42
Characteristic of IgE diagnostic tests for allergy and asthma
Elevated levels associated with atopic disorders Low levels support dx of non allergic asthma Presence confirms sensitization
43
Characteristics of skin tests
Administer allergens/histamine control solutions to skin Wheal and flare reaction followed by late-phase reaction
44
Characteristics of puncture skin testing
Placing allergen drops in skin and introducing them into epidermis by needle puncture 15-20 minutes for reaction
45
Characteristics of intradermal skin test
Inject allergen into skin intracutanously using tubercullin sytinge 15-20 minutes for reaction
46
Function of conjunctival, nasal and bronchial provocation test
Used primarily for research to study allergen exposure and physiological changes
47
Characteristics of bronchoprovocation and nasal provocation
Bronchoprovocation: with methacholine or histamine via nebulizer Nasal provocation: controlled administration of buffer or allergen into nasal passage
48
Minimal detectable concentration of IgE
0.5-1 ug/L
49
Use of component-resolved diagnostic (CRD)
To distinct between sensitization to genuine and cross-reactive allergens
50
Proteinase released during mast cell degranulation
Tryptase
51
Tryptase levels detected in anaphylaxis
>11.4 ug/L
52
Marker for activation of basophils
CD63
53
Properties of corticosteroid tx
Inhaled: severe asthma Oral: severely uncontrolled asthma and acute exacerbations Topical: eczema
54
Properties of B2-agonist bronchodilators
SABA: short acting, por rapid relief of bronchial obstruction LABA: long acting, effective when combined with ICS-formoterol
55
Properties of antihistamines
Blocks histamine H1 receptor 2nd generation most preferable since it does not cause sedation 1st line for urticaria and itching
56
Properties of decongestants
Temporary relief for congestion Constricts blood vessels to reduce swelling
57
Properties of leukotriene antagonists
Prevent leukotrienes from binding to their receptor CysLT1 Reduces bronchoconstriction and inflammation Montelukast*
58
Properties of anticholinergics
Useful for exacerbations when added to SABA Not recommended for long-term
59
Properties of theophylline
Asthma symptoms reliever (short acting) Antiinflammatory effects Alternative for low-income countries
60
Properties of chromoline
Mast cell stabilizers Most effective for ocular symptoms
61
Properties of epinephrine
1st line for anaphylaxis
62
Characteristic of allergen-specific immunotherapy
Shift from Th2 to Th1 immune responses Increased allergen-specific IL-10 production
63
Tx of choice for Hymenoptera venom
Subcutaneous immunotherapy
64
Anti-IgE biological agent for asthma and allergy
Omalizumab
65
Components of asthma self-management
Asthma education: informational Asthma control: training
66
Non-pharmacological recommendations for asthma tx
Avoid active and passive smoking Occupational asthma: strictly avoid sensitizing allergens Normal pediatric vaccination Respiratory exercises
67
Scoring of ACT Questionnaire
20-25 → controlled 16-19 → partial <15 → uncontrolled
68
Extent to which a person's behavior corresponds with agreed recommendations from a health care provider
Adherence
69
Disease factors involved in adherence
Chronic Asymptomatic periods Prophylactic tx Lack of perception of physiologic compromise
70
Treatment factors involved in adherence
Cost Adverse effects Incomplete benefit Requirement of complex behavior Delayed benefit
71
Patient factors involved in adherence
Life distractions Stress Depression Comorbidities Limited literacy
72
Most effective therapy interventions to reduce adherence
Simplified, once-daily asthma therapies
73
How are patient-focused interventions for asthma
Direct education and behavioral interventions
74
Risk factors for death in asthma
Asthma history: severe exacerbations, hospitalizations, ED visits Social history: low socioeconomic status, illicit drug use, inner-city residence Comorbidities: cardiovascular, chronic lung and chronic psychiatric diseases
75
Characteristics of good response, incomplete response and poor response to asthma management of exacerbations
*Good: No wheezing or dyspnea, PEF >80% *Incomplete: Persistent wheezing and dyspnea, PEF 50.79% *Poor: Marked wheezing and dyspnea, PEF <50%
76
What to do when there is a good response to asthma management exacerbations
Contact clinician for follow-up instructions Consider short course of oral systemic corticosteroids
77
What to do when there is an incomplete response to asthma management exacerbations
Add oral systemic corticosteroid Continue inhaled SABA Contact clinician this day for further instruction
78
What to do when there is a poor response to asthma management exacerbations
Add oral systemic corticosteroid Repeat inhaled SABA If distress severe & non responsive to initial tx: call your doctor and proceed to ED
79
Track 1 steps
Step1 & 2: as needed low dose Step 3: low dose maintenance Step 4: medium dose maintenance Step 5: Add-LAMA and high dose maintenance
80
Track 2 steps
Step 1: ICS when SABA taken Step 2: Low dose ICS Step 3: low dose ICS-LABA Step 4: medium/high dose ICS-LABA Step 5: Add LAMA and high dose
81
Steps for asthma and their clinical presentation
*Step 1: symptoms <1-2 d/w *Step 2: symptoms <3-5 d/w with normal lung function *Step 3: symptoms most days or waking once a week, low lung function *Step 4: daily symptoms, waking at night, low lung function *Step 5: acute exacerbation
82
Diagnostic of anaphylaxis (symptoms)
Option 1: Skin/mucosal + respiratory or low BP/end-organ Oprtion 2: 2+ of skin, low BP or end organ, respiratory, GI Option 3: low BP after exposure

Semestre 6: bloque 2 (10 decks)

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