Histamine and Antihistamines

Flashcards covering the pharmacology of histamine, including its receptors (H1-H4), physiological roles, and the classifications and clinical uses of antihistamines.

Autacoids

Derived from the Greek words "autos" (self) and "akos" (remedy), these are biologically active amines described as 'local hormones' that are formed in the tissues on which they act rather than in specific endocrine glands.

Histidine decarboxylase

The enzyme responsible for converting the amino acid L-histidine into histamine.

H1 Receptor

Located in smooth muscle, endothelium, and the CNS; its activation leads to vasodilation, bronchoconstriction, and the primary symptoms of allergic rhinitis and motion sickness through the increase of $IP3$ and $DAG$.

H2 Receptor

Located in gastric parietal cells, cardiac muscle, and the brain; it primarily regulates the secretion of hydrochloric acid ($HCl$) and increases heart rate and contractility through protein Gs and increased $AMPc$.

H3 Receptor

Mainly found in the basal ganglia and cerebral cortex, these presynaptic receptors inhibit the release of neurotransmitters such as acetylcholine, norepinephrine, and serotonin by decreasing $AMPc$.

H4 Receptor

Found in the thymus, small intestine, spleen, and colon; they are suggested to be involved in the recruitment of hematopoietic cells like eosinophils and function as immunomodulators.

Triple Response (Histamine)

The characteristic skin reaction to histamine consisting of Edema, Erythema (redness), and Areola (flare).

Physiological Antagonist

A substance like Adrenaline that produces an opposite effect to histamine by acting on different receptors; it is the first-choice treatment for anaphylaxis.

Inverse Agonist

An agent that binds to the same receptor as an agonist but induces a pharmacological response opposite to that of the agonist.

First-Generation Antihistamines

Non-selective H1 antagonists that easily penetrate the blood-brain barrier, resulting in significant side effects such as sedation, somnolence, and increased appetite.

Second-Generation Antihistamines

Selective H1 antagonists that do not cross the blood-brain barrier, making them safer for work and school performance due to their lack of sedative effects.

Third-Generation Antihistamines

Derivatives of second-generation drugs (e.g., Fexofenadine, Desloratadine) designed to increase efficacy against allergic symptoms while minimizing adverse reactions; they can be detected within 30 minutes of administration.

Indirect Antagonists

Drugs categorized as release inhibitors (e.g., Cromolyn, Nedocromil) that prevent mast cell degranulation and are used alongside beta-2 adrenergic agonists for asthma management.

Cinetosis

Motion sickness, commonly treated with H1 antagonists such as Dimenhydrinate, Meclizine, or Scopolamine.

Pizotifen

A drug with polyvalent inhibitory effects on biogenic amines like serotonin, histamine, and tryptamine; it is used for migraine prevention and to stimulate weight gain.

Metabolite conversion: Hydroxyzine

The parent drug that is converted into the active metabolite Cetirizine by the hepatic microsomal system.

Metabolite conversion: Loratadine

The parent drug that is converted into the active metabolite Desloratadine.

H2 Antagonists examples

Medicines used to reduce gastric acid, including Cimetidine (Tagamet), Ranitidine (Ranisen), Famotidine (Facidex), and Nizatidine.

Tioperamide

An experimental H3 and H4 antagonist with high expectations for treating sleep disorders, obesity, and psychiatric issues.

Atropinic effects

Anticholinergic side effects caused by some H1 antagonists, including dry mouth (mucosas secas), blurred vision, and urinary retention.