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PoM > Immunology - Type I Hypersensitivity > Flashcards

Immunology - Type I Hypersensitivity Flashcards

1
Q

Antibody

A

IgE

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2
Q

Definition

A

IgE mediated, immediate (reaction within minutes), most allergic reactions (genetic predisposition)

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3
Q

Allergy

A

molecules from outside own body, breathe or take in (foods, mold, donder, drugs/medication, bee stings, pollen), contact with skin (latex, lotions and soaps)

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4
Q

Allergen

A

First exposure = sensitization, subsequent exposure gets serious

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5
Q

First exposure (sensitization)

A

Allergen enters body -> antigen-presenting cell (dendritic cells/macrophages, alongside co-stimulatory molecule) -> naive T-helper -> primed T-helper (T_H_2) -> cytokines (interleukins: IL-4/-5/-10) -> IL-4 interacts with B cell (usually produces IgM too, but only IgE specific to allergen required) -> Il-5 interacts with eosinophils (granulocytes) which degranulate releasing toxic substances -> IgE specific to allergen are cytotropic antibodies that bind to cell surface in this case mast cells (granulocytes) Fc receptors creating Fcε receptors (sensitization)

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6
Q

Second exposure

A

Fcε receptors on mast cells cross-link with antigen -> degranulation (pro-inflammatory mediators = allergic reaction)

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7
Q

Early phase reactions (within minutes)

A

Pro-inflammatory mediators with proteases, eosinophils and histamine (causes blood vessel dilation and increased permeability = edema (swelling) and urticaria (hives), acts on H1 receptors in bronchi = smooth muscle contraction = difficulty breathing

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8
Q

Late phase reactions (8-12 hours)

A
  • Pro-inflammatory mediators IL-4/-5/-10 and leukotrienes LTB4 + LTC4 (facilitate communication) -> T_H_2 cells, basophils (granulocytes), eosinophils
  • Leukotrienes lead to smooth muscle contraction (like histamines) and attract more immune cells (even after allergen is gone, neutrophils, mast cells, eosinophils)
  • mild symptoms = hives (urticaria), eczema, allergic rhinitis, asthma
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9
Q

Large load of allergen

A

Severe symptoms (higher vascular permeability and airway constriction) -> inadequate supply to vital organs -> anaphylactic shock

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10
Q

Medical attention for hypersensitivity

A

Can get better and then worsen, start with antihistamines (lower vascular permeability, bronchoconstriction), corticosteroids (lessen inflammatory response), epinephrine constricts blood vessels (intramuscular injection through epipen/intravenous injection)

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11
Q

First line of treatment in anaphylactic type I hypersensitivity

A

epinephrine

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12
Q

Binding of ______ antibodies to ______ activates…

A

Immunoglobulin E, Fc receptors, granulocytes (mast cells)

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13
Q

Cytokine ______ stimulates the production of ______ which degranulate in type I hypersensitivity reaction

A

Interleukin-5 (IL-5), eosinophiks

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14
Q

In type I hypersensitivity reactions, the first 30-60 seconds of _____ muscle contraction in the _____ and _____ are due to _____ and afterwards to _____ and _____

A

smooth, airways, GI tract, histamine, leukotrienes, prostaglandins

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15
Q

_____ cytokines cause _____ to synthesize IgE antibodies instead of ___ antibodies, which mediate type I hypersensitivity reactions

A

Interleukin-4 cytokines, B cells, IgM

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16
Q

In the second exposure in type I hypersensitivity reactions the _____ cross-link the IgE antibodies in 2 or more interactions

A

antigens

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17
Q

The mainstay of preventing type I hypersensitivity reactions is…

A

avoidance of the allergen

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18
Q

___ ___ test is used to know the specific allergen causing type I hypersensitivity reactions

A

skin prick

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19
Q

In type I hypersensitivity reactions, the degranulation of _____ and _____ induces ____ muscle contraction, increased vascular ____, and vasodilation

A

histamine, heparin, smooth, permeability

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20
Q

Type I hypersensitivity reactions are characterized by their (rapid/delayed) _____ onset

A

rapid

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21
Q

H_ _ s, e _ _ a, allergic ____ and a _ _ _a are all symptoms of a type I hypersensitivity reaction

A

hives, eczema, rhinitis, asthma

22
Q

What are they?

A

exaggerated immune reaction mediated by IgE antibodies (atopy (genetic tendency to develop allergic diseases)) triggered by harmless antigen (allergen)

23
Q

Sensitization phase

A

allergen -> antigen presenting cells (APCs) -> B-cells, Th2 cells assist in IgE production -> bind via Fc region to mast cells which are sensitized

24
Q

Re-exposure/effector phase - general

A

cytotropic/IgE receptor binding, allergens bind to Fab region (one constant and one variable domain of each of the heavy and the light chain) of IgE on sensitized cells -> activates mediator release

25
Q

Re-exposure/effector phase - early phase reactions (within minutes)

A

Primarily mast cell-release of preformed mediators (ie histamine, proteases, chemoactants), causes vasodilation, capillary leak, increased secretions, bronchial smooth muscle contraction

26
Q

Re-exposure/effector phase - late phase reactions (8-12 hrs)

A

Mediators require synthesis (ie interleukins 4+5+10, leukotrienes), increases early downstream effects, prolongs inflammatory response

27
Q

Additional common type I hypersensitivity reactions

A

atopic eczema, eosinophilic esophagitis

28
Q

Diagnosis

A
  • Lab results: skin allergen testing, variable sensitivities, eosinophilia
  • History of symptoms, frequency, triggers
29
Q

Hypo/de-sensitization

A

Escalating doses of allergen subcutaneously injected over course of years, variable effectiveness (more severe reactions = less responsive)

30
Q

Acute rhinitis - pathology and causes

A

IgE-mediated immune response upon re-exposure of airborne allergens to eyes/nose, aka hay fever, local mast cells of eye+ nose mucosa degranulate and release immediate mediators (ie histamine), hay + pollen (seasonal due to flowering plants) + dust + animal hair + mold spores

31
Q

Acute rhinitis - Signs and symptoms

A

Due to increased fluid in eyes and nasal cavity, conjunctival injection, eyelid edema, sneezing, rhinorrhea, nasal obstruction, edematous bluish-red nasal turbinates

32
Q

Acute rhinitis - Diagnosis

A

Skin allergen tests (subdermal introduction of defined amount of allergen to volar surface of forearm, observe for wheal-and-flare reaction at specific site, clinical presentation (history of symptoms, frequency, triggering events)

33
Q

Acute rhinitis - Treatment

A

Medications = oral antihistamine ie H1 blockers and nasal corticosteroids; nasal irrigation, environmental control, when severe hypo/desensitization

34
Q

Anaphylaxis - pathology (general)

A

Generalized, life-threatening allergic response, systemic release of large quantities of immune mediators, symptoms most severe at site of greatest mediator concentration

35
Q

Anaphylaxis - pathology (immune mediators - histamine)

A

Ubiquitous systemic concentration, vasodilator, immune system modulator, H1 receptor -> tachycardia, pruritus, rhinorrhea, bronchospasm, H2 receptor -> flushing, hypotension

36
Q

Anaphylaxis - pathology (immune mediators - tryptase)

A

High skin concentration, activate complement, coagulation pathways, kallikrein-kinin systems, angioedema+hypotension+disseminated intravascular coagulation (DIC)

37
Q

Anaphylaxis - pathology (immune mediators - Leukotriene C4, Prostaglandin D2)

A

In high lung concentration, bronchoconstriction, increased mucus secretion

38
Q

Anaphylaxis - causes

A

Drugs (ie beta-lactam, antibiotics, insulin), food (ie nuts, eggs, seafood), proteins (ie blood transfusions, tetanus), latex

39
Q

Anaphylaxis - signs and symptoms (Generalized, mild-moderate)

A

Flushing, feeling of doom, tachycardia, urticaria, incontinence

40
Q

Anaphylaxis - signs and symptoms (Generalized, severe)

A

Syncope, shock, hypoxia, cardiorespiratory collapse

41
Q

Anaphylaxis - diagnosis

A

Clinical presentation - symptoms indicate allergic reaction

42
Q

Anaphylaxis - treatment (immediate, necessary)

A

Epinephrine (intravenously (IV, 1/10000), intramuscularly (IM, 1/1000)) repeat every 30 minutes with potential epinephrine infusion after bolus(es)

43
Q

Anaphylaxis - treatment (adjunct therapy)

A

H1, H2 receptor blockers, IV corticosteroids, IV fluids, oxygen supplementation

44
Q

Anaphylaxis - treatment (critical care)

A

Intubation, vasopressors if necessary

45
Q

Food allergy - pathology and causes

A

Adverse food reaction is an immune response to ingested antigens, distinct from non-immunologic adverse food reactions (enzyme deficiency ie lactase, toxic ingestions ie staphylococcal toxin, intolerance ie caffeine)

46
Q

Food allergy - types (IgE mediated)

A

rapid onset (minutes to couple hours after ingestion), immune mediator release from tissue mast cells, circulating basophils, common allergens include peanuts+soy+milk+wheat+fish

47
Q

Food allergy - types (Non-IgE mediated)

A

Symptoms subacute to chronic in nature, leukocytosis, local lymphocytic destruction of GI tissue, celiac disease, food protein-induced enterocolitis syndrome (FPIES)

48
Q

Food allergy - types (Mixed IgE/non-IgE-mediated)

A

Variable immune response, acute responses involving IgE-mediation, others favoring leukocytes (ie eosinophils, lymphocytes), atopic dermatitis, eosinophilic gastroenteritis

49
Q

Food allergy - signs and symptoms

A

Dermatologic (ie pruritus, erythema, urticaria), GI (ie nausea, vomiting, abdominal pain, diarrhea), anaphylactic (ie cardiac/respiratory); non-IgE mediated = nonspecific, subacute/chronic GI symptoms, distinct dermatologic vesicular, papular eruptions, dermatitis herpetiforms in celiac disease

50
Q

Food allergy - diagnosis

A

Lab results - skin allergy testing; other diagnostics - food elimination trials

51
Q

Food allergy - treatment

A

Medications: antihistamines (may be of little value unless urticaria and angioedema present), other interventions: elimination of offending food from diet, mild disease may remit with time

PoM (33 decks)

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