Beta 2 Receptor Agonists Overview

Beta 2 receptor agonists stimulate relaxation of smooth muscle in the airway leading to bronchodilation, which is mediated through the cyclic AMP pathway. They also inhibit the release of inflammatory mediators from mast cells.

Short-acting beta agonists (SABAs) like albuterol provide 4-6 hours of bronchodilation and are typically used for quick relief of symptoms. Long-acting beta agonists (LABAs) like salmeterol offer 12 hours of bronchodilation and are prescribed for maintenance treatment. Ultra-long acting beta agonists (ULABAs) like indacaterol provide 24 hours of symptom relief.

Theophylline is a methylxanthine that inhibits phosphodiesterases, leading to increased cyclic AMP and subsequent bronchodilation and pulmonary vessel relaxation.

Inhaled corticosteroids (ICS) such as fluticasone and budesonide reduce airway inflammation by inhibiting the release of inflammatory mediators like leukotrienes and cytokines, thereby suppressing the late-phase allergic reaction.

Montelukast, a leukotriene receptor antagonist, specifically blocks the cysteinyl leukotriene receptor, preventing the action of LTD4, a mediator of bronchospasm. Zileuton, a 5-lipoxygenase pathway inhibitor, blocks the formation of leukotrienes from arachidonic acid.

First-generation antihistamines, like diphenhydramine, are non-selective and can bind to both central and peripheral H1 receptors. Second-generation antihistamines, such as cetirizine, exhibit selectivity for peripheral H1 receptors, minimizing central nervous system effects.

Intranasal antihistamines, such as azelastine and olopatadine, provide symptom relief in seasonal allergic rhinitis and vasomotor rhinitis by blocking histamine from binding to H1 receptors in the nasal mucosa.

Decongestants, like pseudoephedrine and phenylephrine, work by activating alpha-adrenergic receptors in the nasal mucosa, resulting in vasoconstriction and reduced nasal congestion.

Nonopioid antitussives, including dextromethorphan and benzonatate, suppress cough by different mechanisms. Dextromethorphan acts centrally in the medulla to increase the cough threshold. Benzonatate exerts a local anesthetic effect on cough receptors in the lungs.

Guaifenesin is the only FDA-approved expectorant that reduces the viscosity of thick sputum by decreasing mucin production from goblet cells and indirectly stimulating vagal nerve activity, leading to increased hydration of the mucus layer.

Inhaled anticholinergics block muscarinic cholinergic receptors by antagonizing acetylcholine, leading to decreased cyclic GMP and reduced contractility of smooth muscle in the lungs. This results in bronchodilation.

Short-acting muscarinic antagonists (SAMAs) like ipratropium bromide provide relief for 4-6 hours. Long-acting muscarinic antagonists (LAMAs) like tiotropium bromide offer 24 hours of bronchodilation, providing long-term control of symptoms.

Beta 2 receptor agonists have some beta 1 receptor activity, which can lead to side effects such as tachycardia and tremors.

Inhaled corticosteroids can cause side effects such as xerostomia, hoarseness, mouth irritation, dysgeusia, and oral candidiasis, especially with frequent use. Long-term use, especially in high doses, can suppress the hypothalamic-pituitary-adrenal (HPA) axis and may inhibit growth in children.

A potent antidiarrheal medication that works by slowing down the movement of the intestines. It's often used for chronic diarrhea, especially in cases of irritable bowel syndrome (IBS).

A medication for chronic diarrhea in irritable bowel syndrome (IBS). It works by interacting with opioid receptors in the gut to reduce intestinal motility and secretions.

A prescription medication for chronic diarrhea in women with diarrhea-predominant irritable bowel syndrome (IBS), especially when other treatments don't work. It helps by slowing down the intestines by blocking a specific type of serotonin receptor.

A class of medications used to prevent and treat nausea and vomiting. They work by blocking dopamine receptors in the brain, specifically in the area that controls nausea, called the chemoreceptor trigger zone (CTZ). Examples include prochlorperazine, perphenazine, and promethazine.

A common antiemetic (anti-nausea) medication used to prevent and treat nausea and vomiting caused by motion sickness. It works by blocking histamine receptors and central cholinergic receptors in the brain.

A medication often used for chemotherapy-induced nausea and vomiting, as well as to stimulate appetite. It works by activating cannabinoid receptors in the brain, which are involved in appetite and mood.

A class of medications that are often used to prevent chemotherapy-induced nausea and vomiting. They work by blocking serotonin receptors in the brain and other parts of the body.

A medication that can prevent and treat motion sickness. It works by blocking acetylcholine receptors in the brain.

One medication class used to prevent and treat nausea and vomiting. It works by blocking a specific type of receptor in the brain that is involved in the feeling of nausea.

A medication that is used to treat nausea and vomiting. It works by blocking dopamine receptors in the chemoreceptor trigger zone, a brain area that influences nausea and vomiting.

A class of medications that are used to help calm the stomach and intestines, especially when there is excessive movement or contractions. These drugs often work by blocking acetylcholine, a chemical messenger in the nervous system that helps control muscle movement.

A serious condition that affects the large intestine, causing inflammation and potentially leading to life-threatening complications.

A group of medications that aim to lessen nausea and vomiting by working on different parts of the brain and body.

A class of medications used to treat nausea and vomiting. They often work by blocking histamine receptors, which can affect the area of the brain that regulates nausea and vomiting.

A medication commonly used for motion sickness and other conditions. It works by blocking histamine receptors and central cholinergic receptors in the brain, helping reduce nausea and vomiting.

Expectorants help to loosen and thin mucus in the respiratory tract, making it easier to cough up.

Gastrointestinal upset, including nausea (n/v) and diarrhea, are potential side effects of expectorants. These drugs should not be used in individuals with coughs related to asthma, chronic obstructive pulmonary disease (COPD), heart failure, or ACE inhibitor therapy.

Diuretics are drugs that increase urine production by the body, primarily used to manage high blood pressure (HTN) and heart failure (HF). They work by promoting increased sodium and water excretion.

Diuretics, especially those used in the initial stages of treatment, can initially lower cardiac output by decreasing plasma volume. This leads to a reduction in peripheral resistance, resulting in lower afterload and blood pressure (BP). Over time, these effects tend to lessen.

Carbonic anhydrase inhibitors, osmotic diuretics, aldosterone antagonists/potassium-sparing diuretics, loop diuretics, and thiazide diuretics are the main classes of diuretics, each with a distinct mechanism.

Diuretics, particularly loop and thiazide diuretics, can lead to glucose intolerance, potentially linked to potassium levels. High sodium intake exacerbates potassium loss, which can cause metabolic alkalosis. Other potential side effects include electrolyte imbalances, hyperuricemia (elevated uric acid levels), and hypotension related to fluid volume reduction.

Loop diuretics like furosemide and bumetanide act primarily in the ascending loop of Henle, inhibiting sodium reabsorption and promoting potassium excretion. They are potent diuretics with short duration but offer a significant increase in sodium excretion.

Thiazide diuretics such as chlorthalidone, hydrochlorothiazide, indapamide, and metolazone target the distal renal tubule, inhibiting sodium reabsorption and increasing potassium excretion. They are longer-acting than loop diuretics and less potent in terms of diuresis.

Thiazide diuretics, unlike other diuretic types, have the unique ability to enter intracellular spaces. This makes them suitable for treating persistent edema (fluid build-up).

Aldosterone antagonists, also called potassium-sparing diuretics, prevent aldosterone from promoting sodium reabsorption and potassium excretion in the distal tubules. These drugs are generally weak diuretics but often used in combination with thiazide diuretics to reduce potassium loss.

Side effects of aldosterone antagonists include gynecomastia in about 50% of patients taking spironolactone and impotence.

Laxatives are medications used to relieve constipation by facilitating bowel movements. They work by various mechanisms, including stimulating the bowels, increasing fluid in the intestines, or softening stool.

Stimulant laxatives, like cascara, senna, bisacodyl, and castor oil, directly stimulate the intestinal muscles to promote bowel movements. This class is often used for chronic constipation, particularly in situations of immobility or reduced bowel motility.

Osmotic laxatives, such as magnesium hydroxide, magnesium citrate, sodium phosphate, and polyethylene glycol (PEG) 3350, draw water into the intestines, increasing stool volume and facilitating bowel movements.

Bulk-producing laxatives, including psyllium, methylcellulose, and polycarbophil, absorb water to increase stool volume and bulk. These are generally considered safe for long-term use and are often recommended for chronic constipation.

The aim of GERD treatment is to reduce or eliminate symptoms, heal esophageal inflammation, prevent complications such as esophageal cancer, and stop symptoms from coming back.

Avoid eating or drinking anything that triggers symptoms, don't overeat, and avoid bending over or strenuous exercise for three hours after eating.

Don't lie flat for at least three hours after you eat or drink, and raise the head of your bed when you sleep.

Losing extra weight can significantly improve GERD symptoms.

Stopping smoking can significantly benefit GERD.

Antacids provide temporary symptom relief by neutralizing stomach acid.

Antacids are often used alongside other GERD medicines for frequent or occasional symptoms, but are not a primary treatment for severe GERD.

Antacids can cause constipation (aluminum and Calcium based), diarrhea (magnesium based), or alkalosis, especially in patients with kidney disease.

PPIs are considered the first-line therapy for most GERD patients, particularly those with frequent symptoms or complications like esophagitis.

PPIs suppress stomach acid production by blocking a key enzyme called H+/K+-ATPase.

PPIs can cause GI symptoms, dizziness, drowsiness, and more serious complications with long-term use, such as nutrient deficiencies, bone fractures, and kidney problems.

H2RAs are used for GERD, but PPIs are generally the preferred choice for most patients.

These drugs strengthen the lower esophageal sphincter (LES) and help prevent stomach acid from flowing back into the esophagus.

Prokinetic agents help speed up stomach emptying, reducing the time acid is in contact with the esophagus. However, their use is limited due to potential side effects.

These agents protect the stomach lining but are primarily used for peptic ulcer disease (PUD).

H2RAs block the histamine-2 receptor on gastric parietal cells, reducing the production of hydrochloric acid (HCl) and increasing gastric juice pH toward a more alkaline state.

Cimetidine, an H2RA, can cause gynecomastia and erectile dysfunction due to its antiandrogenic effects.

H2RAs are not well-studied in pregnancy, so their use during this time should be carefully considered, weighing the potential risks against the benefits.

Metoclopramide is used for lower tiers of GERD therapy but carries a risk of extrapyramidal symptoms (EPS), especially in younger patients.

Antacids improve lower esophageal sphincter (LES) tone and increase gastric pH, making them helpful in managing GERD.

The primary goal of therapy for peptic ulcer disease (PUD) is to eradicate Helicobacter pylori, the main cause of the condition.

Proton pump inhibitors (PPIs) are much more effective than H2RAs at suppressing gastric acid secretion and are therefore the preferred treatment for PUD.

Long-term use of H2RAs can lead to vitamin B12 deficiency, potentially causing anemia and neurologic deficits.

H2RAs do not block histamine-1 receptors, meaning they do not have anticholinergic properties.

Bethanechol, a prokinetic agent, is used in lower tiers of GERD therapy and for gastroparesis but does not heal esophageal lesions.