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1
Q

what are the 4 Type I hypersensitivities

A 
Systemic anaphylaxis
Acute urticaria 
Seasonal rhinoconjuncivitis 
Asthma
Food allerg
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2
Q

what are the symptoms of systemic anaphylaxis

Route of entry?

A 
edema
increased vascular permeability 
laryngeal edema 
Circulatory collapse 
Death

route is intravenous (either directly or following oral absorption into the blood)

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3
Q

what are the symptoms of urticaria and route of entry

A

Local increase in blood flow and vascular permeability

through skin

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4
Q

what are the symptoms and route of entry of seasonal rhinoconjunctivitis

A

edema of nasal mucosa
sneezing

inhalation

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5
Q

what are the symptoms and route of entry of asthma

A

bronchial constriction
increased mucous production
Airway inflammation

inhalation

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6
Q

what are the symptoms and route of entry of food allergy

A 
vomiting
diarrhea
pruitis (itching)
urticaria 
anaphylaxis (rarely)

oral

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7
Q

what are the TH2 cytokines

A

IL-4
IL-5
IL-9
IL-13

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8
Q

where are mast cells most prominent

A

skin and mucosa

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9
Q

what are the preformed proinflammatory mediators (from granules) in the mast cell (4)

A

histamine
serotonin
heparin
serine proteases

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10
Q

what are the newly formed lipid mediators (eicosanoids) of the mast cells

A

prostaglandin D2

leukotrienes

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11
Q

what do prostaglandins and leukotrienes cause

A

smooth muscle contraction
increase vascular permeability
stimulate mucus secretion

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12
Q

what do histamine and heparin do?

A

toxic to parasites
increase vascular permeability
cause smooth muscle contraction

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13
Q

what cells are the major contributor to tissue damage

A

eosinophils

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14
Q

what is the cause of chronic allergic inflammation

A

Eo’s in high numbers

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15
Q

what does major basic protein do?

A

toxic to parasites and mammaian cells

triggers histamine release from mast cells

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16
Q

what are the leukotrienes

A

LTC4, LTD4, LTE4

LTB4 - pro-inflammatory

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17
Q

what is the function of leukotrienes

A

overlapping activities with histamine

BUT have a much slower onset and more powerful, and have a much longer duration than histamine in bronchoconstriction

cause an INCREASE in capillary permeability and mucus production

antagonists against these work much better in the treatment of allergies/asthma

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18
Q

what are the functions of IL-4

A

TH2 cell growth factor

Isotype switching to IgE

Increase VCAM-1

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19
Q

function of IL-13

A

Airway esoinophilia

Mucous gland hyperplasia increased production of mucous in asthma but too much is detrimental

Airway fibrosis & remodeling

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20
Q

what is the function of IL-5

A

regulator of Eo production and survival

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21
Q

what is the function of TNF

A

Recruitment & activation of inflammatory cells

Altered function & growth of airway smooth muscles

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22
Q

what is the early phase allergic response mediated by

A

histamine and lipid mediators (after antigen has bound a mast cell sensitized with IgE)

so smooth muscle response and vascular effects

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23
Q

what is the late phase reaction of IgE mediated allergic responses

A

inflammation due to cytokines

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24
Q

what occurs during the early phase (minutes- hour)

A

cross linking of IgE on mast cells with allergen

Degranulation of mast cells

sneezing, pruritis, rhinorrhea, congestion
(increased mucus secretion and smooth muscle contraction leading to airway obstruction)

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25
what occurs during the late phase chronic allergic response
hours 4-12 influx and activation of eo's neutrophils, basophils and lymphocytes (TH2) TH2's release cytokines increase in mast cells in the area and increased expression of FCe receptors on mast cells
26
what are the systemic symptoms of the last phase response
fatigue, myalgias, asthma
27
what do eosinophils do once recruited in the late phase response?
Proinflammatory mediators Local tissue damage, sinus infections Chronic Hyperplastic eosinophilic sinusitis (CHES)
28
what are some of the systemic responses of mast cell activation
(Histamines) vasodilation vascular leak ``` Lipid mediators (PAF,PGD2,LTC4) Bronchoconstriction Intestinal hypermotility ``` cytokines inflammation enzymes tissue damage
29
what are some of the systemic response of Eo activation in allergic response
tissue damage | killing of parasites and host cells
30
what is the hygiene hypothesis
the more non-hygeniec the less likely a person is to have atopic response
31
what occurs with a high dose of intravenous allergen
general release of histamine | causes systemic anaphylaxis
32
what occurs with low dose of subQ allergen
local release of histamine | causes wheal and flare reaction
33
what occurs with low inhaled dose of allergen
allergic rhinitis (upper airway) caused by increased mucus production and nasal irritation asthma (lower airway) due to contraction of bronchial smooth muscle and increased mucus secretion
34
what occurs with ingestions of allergen
contraction of intestinal smooth muscle which induces vomiting outflow of fluid into gut causes diarrhea antigen diffuses into blood vessels and is widely disseminated causing urticaria (hives) or anaphylaxis
35
what is allergic rhinitis
Paroxysms of sneezing, rhinorrhea, nasal obstruction, and itching of the eyes, nose, and palate Postnasal drip, cough, irritability, and fatigue
36
what are allergic shiners
Both infraorbital edema and darkening due to subcutaneous venodilation and accentuated lines or folds below the lower lids (Dennie-Morgan lines) suggest allergic conjunctivitis.
37
what is the difference between acute and chronic urticaria
Acute urticaria: New onset urticaria that has been present for less than six weeks. Chronic urticaria:  Recurrent urticaria occurring most days of the week for a period of more than six weeks.
38
what is the cause and symptoms of acute urticaria
Mediated by cutaneous mast cells in the superficial dermis. Release mediators upon activation, including histamine, which cause itching, and vasodilatory mediators, which cause localized swelling in the uppermost layers of the skin. A typical urticarial lesion is an intensely pruritic, erythematous plaque. Individual lesions usually appear over the course of minutes, enlarge and coalesce with other lesions, and then disappear within a few hours. Urticaria is sometimes accompanied by angioedema, or swelling deeper in the skin.
39
what are the mediators of the early phase? | what are the mediators of the late phase
early - mast cell mediators late- influx of inflammatory celsl (T's, Eo's Basophils)
40
what are the symptoms of asthma
Airway hyperresponsiveness -intermittent wheezing cough and dyspnea Contraction & relaxation of airway smooth muscle Anywhere in tracheobronchial tree – varying degrees of obstruction variable airflow limitations – reversible
41
what is the early phase of asthma
Bronchoconstriction (minutes) Due to Release of mast cell mediators Contract smooth airway muscles, reflex neural pathways
42
what is the late phase of asthma
Bronchoconstriction (several hours) Influx of inflammatory cells (Ts, Eos, Baso) Contract smooth airway muscles
43
what are the treatments for asthma
corticosteroids to reduce inflammation epinephrine to induce bronchial relaxation leukotriene antagonists to inhibit bronchial constriction
44
what are some of the symptoms of anaphylaxis (exposure by blood route)
Due to systemic mast cell activation: ``` Hypotension: Increased vascular permeability can produce a shift of 35% of vascular volume to the extravascular space within 10 minutes Tachycardia Urticaria Flushing Bronchoconstriction Laryngeal edema Diarrhea Sense of “doom” ```
45
what is the difference between anaphylactic and anaphylactoid ?
anaphylactic is allergy (IgE mediated) anaphylactoid is direct, non immunological release of mediators
46
what are some examples of anaphylactoid reactions
Aspirin Nonsteroidal anti-inflammatory drugs (NSAIDs) Radiopaque contrast media Fluorescein Dextran Thiamine Opiates Complement components: Anaphylatoxins C3a, C4a, & C5a
47
what is the timing of onset of symptoms to fatal cardiac arrests in food, drugs and venom
Food 5-35 minutes Drugs 10-20 minutes Venom 10-15 minutes Early response
48
what are the risk factors for anaphylactic shock
Atopy Route and timing of administration of Ag Asthma is a risk factor for fatal anaphylaxis Delayed epinephrine is a risk factor for fatal outcomes
49
what are some of the treatment methods for treating anaphylactic shock
induce T regulatory T cells to stop TH2 activation block co-stimulation and inhibit TH2 cytokines in order to prevent activation of B cell to produce IgE Inhibit effects of IgE binding to mast cell in order to prevent mast cell activation inhibit effects of mediators and inhibit synthesis of mediators (by using antihistamine) block IL-5 and CCR3 in order to block cytokine and chemokine receptors that mediate eosinophil recruitment and activation
50
what are the effects of SIT (allergen specific immunotherapy) on immune parameters
increase ratio of TH1 to TH2 cytokines Induce T regs Class switching to IgA,IgG which compete with IgE for allegro binding thereby decreasing allergen capture and presenation that is facilitated by IgE in complex with the high-affinity receptor for IgE decrease the number of mast cells and their ability to release mediators decrease recruitment of neutrophils and eosinophils
51
problems in conventional allergen-specific immunotherapy `
long term treatment is required for decrease in specific IgE levels
52
what is allergen sensitization
repeated exposures
53
the TH2 cytokines IL-4 and IL13 do what...
isotype switching to IgE prduction
54
what are the environmental factors for developing type I hypersensitivity
pollution diet allergen burden disease
55
mast cells release what in what response
histamine in the early response
56
eosinophils release what in what response
leukotrienes
57
what do the pulmonary stretch receptors do?
slow and lie in the smooth muscle; reflex effect is a slowing of respiratory frequency due to increased expiratory time (Hering-Breuer inflation reflex); reflex is not evident in adult subjects unless the tidal volume exceeds 1 L. if it is over 1 L they get stretched out and they slow down breathing rate
58
what do irritant receptors do?
lie between airway epithelial cells; stimulated by noxious gases, cigarette smoke, inhaled dusts, and cold air; reflex can include bronchoconstriction and hyperpnea; rapid
59
what do the j receptors do
- ending of non-myelinated C fibers; believed to be located in the alveolar walls, close to capillaries; respond quickly to chemicals injected into the pulmonary circulation; induce rapid shallow breathing; receptors can be triggered by an increase in interstitial fluid volume (linked to respiratory sensation of difficulty in breathing associated with left heart failure and interstitial lung disease)
60
what do bronchial c fibers do
like J receptors but sense changes in the bronchial circulation
61
what are the 3 points in respiratory control that contribute to increased PaCO2 in acute on chronic respiratory failure
Loss of stimulation of the peripheral chemoreceptors leading to reduced ventilation b/c he was given 100% O2 --hypoxemia is partly responsible for driving respiratory rate Worsening of ventilation-perfusion mismatch loss of hypoxic vasoconstriction upon administration of 100% O2 Haldane effect administration of 100% O2 results in a higher release of CO2 from hemoglobin and subsequently higher PaCO2 levels
62
what is hypersensitivity pneumonitis
Group of lung diseases caused by inhalation of exogenous antigenic molecules (usually organic) Transient fever, hypoxemia, myalgias, arthralgias, dyspnea, cough 2-9 hr after exposure Symptoms resolve without treatment provided there is no re-exposure to antigen Examples include bird fancier’s disease and pigeon breeder’s lung
63
what is the immunology associated with hypersensitivty pneumonitis
Prior sensitization is necessary Not associated with IgE or eosinophils Higher prevalence in non-smokers (80-95%) >40% lymphocytes suggestive of HP; higher percentage of neutrophils and degranulated macrophages Cell-mediated immune process TGF-β, IL-1, IL-12, TNF-α, IL-6 IL-2, IFN-γ Disease can be transferred with CD4+ T cells Tx with corticosteroids aids recovery initially, long-term outcome is unaffected

RESP 1 (2 decks)

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