ABAI flashcards

32 cards. Read the term and the definition here. The deck at the top of this page is optional.

Type I hypersensitivity

IgE-mediated immediate hypersensitivity in which allergen cross-links IgE on mast cells, causing degranulation and release of histamine and tryptase within minutes.

Anaphylaxis epinephrine dose

Intramuscular epinephrine 0.01 mg/kg of 1:1000 concentration, maximum 0.5 mg, injected into the anterolateral thigh as first-line therapy.

Serum tryptase timing

Mast-cell protease that peaks 1 to 2 hours after anaphylaxis onset; an elevated acute level collected during the event supports retrospective diagnosis.

Skin prick test

In vivo IgE test with high sensitivity and lower specificity; antihistamines and extensive skin disease can cause false-negative or uninterpretable results.

Allergic rhinitis first-line

Intranasal corticosteroids are the most effective single maintenance therapy for moderate-to-severe allergic rhinitis; oral antihistamines are adjunctive for mild symptoms.

Asthma reversibility criterion

Post-bronchodilator improvement in FEV1 of at least 12 percent and at least 200 mL supports a diagnosis of reversible airflow obstruction.

Type IV hypersensitivity

T-cell mediated delayed hypersensitivity with onset 48 to 72 hours after exposure; patch testing is read at 48 and 72 to 96 hours.

Penicillin allergy testing

For low-risk immediate reactions, beta-lactam skin testing followed by a graded oral challenge is the standard evaluation strategy.

Beta-2 agonist mechanism

Stimulates beta-2 adrenergic receptors on airway smooth muscle, raising intracellular cAMP and causing bronchodilation for acute symptom relief.

Allergen immunotherapy

Repeated exposure to gradually increasing allergen doses induces tolerance, reducing symptoms and medication need for allergic rhinitis and venom allergy.

Hereditary angioedema

C1 inhibitor deficiency causing recurrent angioedema without urticaria; it is bradykinin-mediated and does not respond to epinephrine or antihistamines.

Food allergy diagnosis

Specific IgE or skin prick testing has high false-positive rates; oral food challenge remains the diagnostic gold standard when history and testing are discordant.

Chronic spontaneous urticaria

Recurrent wheals for more than 6 weeks without an identifiable trigger; second-generation H1 antihistamines are first-line, with up-dosing before biologics.

Aspirin-exacerbated respiratory disease

Triad of asthma, nasal polyposis, and sensitivity to COX-1 inhibitors; symptoms arise from shunting of arachidonic acid to leukotrienes.

IgG characteristics

Most abundant serum immunoglobulin, the only class crossing the placenta via FcRn, and a major activator of the classical complement pathway.

IgM characteristics

Pentameric antibody produced first in a primary response; it is the most efficient immunoglobulin at activating complement and appears in acute infection.

Secretory IgA

Dimeric IgA with J chain and secretory component that neutralizes pathogens at mucosal surfaces; it is the predominant mucosal antibody.

IgE characteristics

Lowest-concentration serum immunoglobulin; binds FcεRI on mast cells and basophils and mediates type I hypersensitivity reactions.

MHC class I presentation

Presents endogenous peptides to CD8+ cytotoxic T cells on the surface of nearly all nucleated cells, enabling detection of intracellular infection.

MHC class II presentation

Presents exogenous peptides to CD4+ helper T cells and is expressed on antigen-presenting cells such as dendritic cells, macrophages, and B cells.

Classical complement pathway

C1q binds IgM or IgG, activating C4 and C2 to form C3 convertase, leading to C3b and the membrane attack complex.

Membrane attack complex

C5b, C6, C7, C8, and C9 assemble to form a pore in target membranes, causing osmotic lysis of pathogens and cells.

X-linked agammaglobulinemia

BTK mutation blocks B-cell maturation, causing absent B cells and low all immunoglobulin classes with recurrent bacterial infections in boys.

SCID presentation

Severe combined immunodeficiency presents in infancy with failure to thrive, chronic diarrhea, and opportunistic infections; live vaccines are contraindicated.

Neutrophil oxidative burst

Phagocytes generate reactive oxygen species via NADPH oxidase; defective burst causes chronic granulomatous disease with catalase-positive organism infections.

Complement C3 deficiency

Low C3 impairs opsonization and predisposes to recurrent infections with encapsulated bacteria such as Streptococcus pneumoniae and Neisseria.

T cell receptor

Alpha-beta heterodimer that recognizes peptide presented on MHC molecules; CD3 transduces the activation signal.

Coombs classification

Hypersensitivity types I through IV: IgE immediate, antibody cytotoxic, immune complex, and delayed T-cell mediated, respectively.

Antibody affinity versus avidity

Affinity is the strength of a single antigen-antibody binding site; avidity is the combined strength of all sites in a multivalent antibody.

Primary immunodeficiency screen

Initial evaluation includes complete blood count with differential and quantitative serum immunoglobulins; abnormal results prompt lymphocyte subsets and functional testing.

DiGeorge syndrome

22q11 deletion causing thymic hypoplasia with low T cells, hypocalcemia from parathyroid hypoplasia, and conotruncal cardiac defects.

Anergy in self-tolerance

Peripheral tolerance mechanism in which mature lymphocytes encountering self-antigen without costimulation become functionally unresponsive rather than activated.