Pharmacology: H1 and H2 Receptor Blockers Quiz

Naturally occurring compounds that act locally, as hormones, at the site of synthesis and release.

Synthesized from L-histidine by L-histidine decarboxylase and stored in mast cells, basophils, and enterochromaffin-like cells.

Histamine plays a crucial role in allergic reactions, inflammation, and gastric acid secretion.

A paracrine effect means a substance is secreted by one cell affecting neighboring cells.

An autocrine effect means a substance is secreted by a cell and acts on the same cell.

These are drugs that bind to and activate autacoid receptors, mimicking the actions of naturally occurring autacoids.

These drugs either block the synthesis of autacoids or inhibit their interaction with receptors, reducing their effects.

They are a type of autacoid classified by their chemical structure as biogenic amines. They can be agonists that activate receptors or antagonists that block receptors.

A potentially fatal, rapid, life-threatening generalized or systemic hypersensitivity reaction triggered by the release of histamine.

A type of receptor in the body that responds to histamine, involved in various physiological processes.

A type of histamine receptor that is coupled with the G protein 'Gs' and primarily responsible for mediating various effects, including gastric acid secretion, increased heart rate and contractility, and acting as autoreceptors on histaminergic neurons.

A type of histamine receptor that is coupled with the G protein Gs and is found on presynaptic histaminergic neurons, where it acts as an autoreceptor to inhibit the release of histamine.

A group of drugs that block the effects of histamine at the H1 receptor, primarily used to treat allergic reactions.

A group of H1 blockers that are more lipid soluble, allowing them to cross the blood-brain barrier, which can lead to sedative effects. They are generally short-acting.

A group of H1 blockers that are less lipid soluble and, therefore, less likely to cause sedative effects. They have a longer duration of action, typically requiring once-a-day dosing.

The primary mechanism of action for H1 blockers. They compete with histamine for binding sites on the H1 receptor, preventing histamine from activating the receptor.

A class of medications that block the effects of histamine at H1 receptors, mainly used to treat allergies and motion sickness.

First generation H1 blockers have effects on other receptors in the body, leading to side effects such as dry mouth, drowsiness, and urinary retention.

Second generation H1 blockers primarily target H1 receptors, minimizing side effects and improving patient tolerability.

H1 blockers, both first and second generation, are effective in managing allergic symptoms like rhinitis, urticaria, and conjunctivitis.

First generation H1 blockers can help control motion sickness by blocking receptors in the vestibular pathway and the CTZ.

H1 blockers are not effective in treating bronchial asthma.

First generation H1 blockers have sedative properties, but they are not the first choice for insomnia because of their potential for side effects.

Second generation H1 blockers have no sedative properties.

Histamine H2 receptor antagonists, also known as H2 blockers, are medications that block the actions of histamine at H2 receptors in the parietal cells of the stomach, reducing gastric acid secretion.

Cimetidine, ranitidine, famotidine, and nizatidine are examples of histamine H2 receptor blockers.

Serotonin, also known as 5-hydroxytryptamine (5-HT), is a neurotransmitter synthesized from the amino acid L-tryptophan.

Approximately 90% of the body's serotonin is found in the gastrointestinal tract (GIT), mainly in enterochromaffin cells, where it regulates intestinal motility and secretion.

Platelets actively take up and store serotonin in storage granules. When platelets are activated, they release serotonin, which causes vasoconstriction and platelet aggregation, leading to blood clotting.

A class of drugs that activate serotonin receptors, leading to various effects like pain relief, vasoconstriction, and regulating mood, appetite, and intestinal motility.

A class of drugs that block serotonin receptors, preventing its normal activity and leading to various effects like anti-psychotic action or reduction in nausea and vomiting.

A strong vasoconstrictor peptide produced and released by endothelial cells in blood vessels. It plays a role in blood pressure regulation and may be implicated in pulmonary hypertension.

A peptide involved in inflammation, vasodilation, pain transmission, and bronchoconstriction. It is associated with hereditary angioedema.

A potent vasoconstrictor peptide produced from angiotensin I by angiotensin-converting enzyme (ACE). It plays a role in blood pressure regulation and is a target for hypertension treatment.

An enzyme responsible for converting inactive angiotensin I into active angiotensin II, which is a potent vasoconstrictor.

A drug that blocks the activity of angiotensin-converting enzyme (ACE), preventing the production of angiotensin II and leading to lower blood pressure.

A peptide that is converted from inactive angiotensin I into active angiotensin II by angiotensin-converting enzyme (ACE).

Angiotensin II, a potent vasoconstrictor, binds to the Angiotensin type 1 receptor (AT1) leading to increased aldosterone synthesis in the adrenal cortex. Aldosterone further promotes renal sodium reabsorption, resulting in elevated blood volume.

ACE inhibitors are a class of drugs that inhibit the conversion of Angiotensin I to Angiotensin II. This reduces vasoconstriction and aldosterone production, ultimately lowering blood pressure.

NO, a gas molecule, acts as a signaling molecule that regulates various physiological processes. It's synthesized from L-arginine by nitric oxide synthase (NOS), an enzyme found in different tissues.

Inducible NOS (iNOS) is not expressed under normal conditions. It is activated in response to inflammatory signals such as cytokines, while endothelial NOS (eNOS) and neuronal NOS (nNOS) are present under normal physiological conditions.

NO is a potent vasodilator that acts by activating guanylyl cyclase, an enzyme that converts GTP to cyclic GMP (cGMP). cGMP is a 'second messenger' that activates protein kinase G (PKG), leading to smooth muscle relaxation and vasodilation.

Epinephrine binds to its receptor, activating adenylyl cyclase which converts ATP to cAMP, a second messenger that regulates various cellular processes. In contrast, norepinephrine acts on different receptors and utilizes a different signaling pathway involving phospholipase C, IP3, and DAG.

Calcium ions (Ca2+) trigger smooth muscle contraction by binding to calmodulin, activating myosin light-chain kinase. This enzyme phosphorylates myosin, enabling its interaction with actin and resulting in muscle contraction.

Calcium channel blockers are drugs that inhibit the entry of calcium ions into smooth muscle cells, thus preventing muscle contraction. This mechanism leads to vasodilation and reduced blood pressure.