The Histamine Story
Immune Response 101
Hypersensitivity Junction
The "Anti" Drugs
Emergency & Clinical Care
100

This amino acid is the direct chemical precursor converted into histamine by the enzyme histidine decarboxylase

Histidine

100

This generic, non-specific acute response is a "first-line" defense that lacks immunologic memory

Innate Immune Response

100

Use this four-letter mnemonic to recall the four distinct types of hypersensitivity responses

Allergic 

Cytotoxic 

Immune Complex

Delayed (T-cell mediated) 

100

Most H1 antihistamines are technically classified as these because they stabilize receptors in their inactive state

inverse agonists

100

This is considered the pathognomonic hallmark symptom of an ocular allergy

itch

200

This specific receptor type predominantly mediates immediate hypersensitivity reactions, leading to vascular permeability and smooth muscle contraction.

H1 receptor

200

Unlike the innate system, this acquired response features specificity and memory, meaning subsequent responses are amplified.

Adaptive Immune Response

200

This specific immunoglobulin is the primary mediator of Type I "Immediate" hypersensitivity reactions

IgE

200

First-generation antihistamines cause dry mouth and blurred vision by non-specifically binding to these receptors

muscarinic receptors

200

Unlike viral infections that produce follicles, ocular allergies are known to produce these on the conjunctiva

papillae

300

These are the two primary routes for the inactivation of histamine in the tissues

HMT and DAO

300

These cells stimulate T-cells to mature into Helper T's, which then cause B-cells to transform into plasma cells.

Dendritic cells (or APCs)

300

This type of hypersensitivity is uniquely T-cell based, antibody-independent, and takes 48–96 hours to develop.

Type IV

300

Second and third-generation antihistamines produce fewer CNS effects because they stay largely outside of this

blood-brain barrier

300

This is the immediate drug of choice for treating a systemic anaphylactic reaction.

epinephrine

400

This is the primary receptor type responsible for promoting gastric acid production and certain immune cell activations

H2 receptor

400

This humoral defense mechanism is activated by microbe surface interaction in the innate system and by antigen-antibody complexes in the adaptive system.

complement cascade

400

Graves disease and Myasthenia Gravis are examples of this "cytotoxic" hypersensitivity type.

Type II

400

This class of drugs works by blocking the calcium influx that stimulates mast cell degranulation.

mast cell stabilizers

400

This is the name of the first FDA-approved non-injectable, intranasal epinephrine spray

Neffy

500

Histamine-induced vasodilation can lead to hypotension and this compensatory heart rate response.

reflex tachycardia

500

These specific B-cells are responsible for secreting antibodies rapidly upon re-exposure to a known antigen.

Memory B-cells

500

Type III hypersensitivity is characterized by the deposition of these into tissues, leading to local inflammation.

immune complexes

500

This specific mast cell stabilizer is 2500 times more potent than cromolyn and is effective at reducing eosinophil migration.

Lodoxamide

500

These are the four "cardinal signs" of inflammation that may indicate a need for combination anti-inflammatory therapy

redness, heat, swelling, and pain