-diphenhydramine- - -KINGDOM OF JOGA-

-as of [16 MARCH 2024]–

“di fen HI dra meen”

*MIXTURES* —>

*DRAMAMINE*

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*BENEFITS*

*’euphoria’*

*SIDE EFFECTS*

“blurry vision”

(because it is an ‘anti-cholinergic’)

(meaning it inhibits the signaling of ‘cholinergic nerves’)

(meaning it suppresses ‘acetylcholine’)

“diphenhydramine hydrochloride”
(as in “dissolved in hydrochloride salt”)

(‘diphenhydramine’ is an ‘inverse agonist’ of the “histamine H₁ receptor”)

(it is a member of the ethanolamine class of antihistaminergic agents)

(by reversing the effects of histamine on the capillaries, it can reduce the intensity of allergic symptoms)

(it also crosses the ‘blood–brain barrier’ and inversely agonizes the H₁ receptors centrally)

(its effects on central H₁ receptors cause drowsiness)

potent anticholinergic agent
(which results in dry mouth)

(like many other 1st-generation anti-histamines, diphenhydramine is also a potent ‘antimuscarinic’ (a ‘competitive antagonist’ of ‘muscarinic acetylcholine receptors’) and, as such, at high doses can cause ‘anti-cholinergic syndrome’)

(the utility of diphenhydramine as an ‘anti-parkinson agent’ is the result of its blocking properties on the muscarinic acetylcholine receptors in the brain)

(diphenhydramine also acts as an intracellular sodium channel blocker, which is responsible for its actions as a local anesthetic)

(diphenhydramine has also been shown to inhibit the reuptake of serotonin)

(it has been shown to be a potentiator of analgesia induced by morphine, but not by endogenous opioids, in rats)

(allergy medication)

(first-generation antihistamine)

(deliriant)

(discovered in 1943 by ‘george rieveschl’)

(in 1946 it became the first prescription antihistamine approved by the US FDA)

Diphenhydramine mainly works through antagonizing the H1 (Histamine 1) receptor,

(although it has other mechanisms of action as well)

The H1 receptor is located on

*respiratory smooth muscles,

vascular endothelial cells,

the gastrointestinal tract (GIT),

cardiac tissue,

immune cells,

the uterus,

and the central nervous system (CNS) neurons

When the H1 receptor is stimulated in these tissues it produces a wide variety of actions including

increased vascular permeability,

promotion of vasodilation causing flushing,

decreased atrioventricular (AV) node conduction time,

stimulation of sensory nerves of airways producing coughing,

smooth muscle contraction of bronchi and GIT,

and eosinophilic chemotaxis promoting the allergic immune response

Diphenhydramine acts as an inverse agonist at the H1 receptor, thereby reversing effects of histamine on capillaries, reducing allergic reaction symptoms.

Given that diphenhydramine is a first-generation antihistamine, it readily crosses the blood-brain barrier and inversely agonizes the H1 CNS receptors, resulting in drowsiness, and suppressing the medullary cough center

The H1 receptor is similar to muscarinic receptors.

Therefore, diphenhydramine also acts as an antimuscarinic;

it is a competitive antagonist of muscarinic acetylcholine receptor, resulting in its use as an antiparkinson medication

Lastly, diphenhydramine acts as an intracellular sodium channel blocker, resulting in local anesthetic properties.

The liver metabolizes diphenhydramine via CYP450.

It is excreted in the urine, unchanged,

and has a half-life of 3.4-9.2h.

(its time to peak, serum is 2 hours)

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