Pharmacology Chapter 2.1

Beta 3 selective agonists (Mirabegron, Vibegron) are drugs that prevent voiding and help those with overactive bladder and urinary incontinence.

Non-selective beta-blockers, such as Propranolol, block both beta 1 and beta 2 receptors in the body.

Beta 1 selective blockers, such as Atenolol, primarily target beta 1 receptors mainly found in the heart.

Beta 1 blockers with intrinsic sympathomimetic activity (ISA), such as Pindolol, partially activate beta receptors while blocking them.

Beta 1 blockers with membrane stabilizing activity (MSA), such as Labetalol, have additional effects on cell membranes.

Diuretics are drugs that increase urine flow by eliminating sodium (natriuretic) and water (aquaretic).

Diuretic braking refers to mechanisms that counterbalance diuretic effects, bringing sodium excretion in line with sodium intake.

Drugs that increase the rate of urine flow through the excretion of sodium (natriuretic) and water (aquaretic).

A disorder characterized by excess antidiuretic hormone (ADH) secretion, leading to water retention, diluted blood (hyponatremia), and low blood osmolarity. It can cause symptoms like lethargy, nausea, and seizures.

This condition occurs when the body holds on to too much water, diluting the blood and making it difficult for the kidneys to remove excess water.

Commonly observed in individuals with malignancies, pulmonary diseases, CNS injuries, or those undergoing surgery.

Medications like certain antidepressants (SSRIs), antipsychotics (haloperidol), and anti-diabetic drugs (sulfonylureas) can trigger SIADH.

Common treatments involve water restriction, intravenous hypertonic saline to restore blood sodium, diuretics to enhance water excretion, and drugs that block ADH's action.

A synthetic analog of vasopressin primarily used for its V2 receptor agonistic activity, which helps with water reabsorption in the kidneys.

A medication that blocks the action of vasopressin, specifically targeting the V2 receptor, which plays a crucial role in water reabsorption in the kidneys.

A natural hormone responsible for vasoconstriction and promoting water reabsorption. It is administered intravenously, subcutaneously, intramuscularly, intra-arterially or intranasally.

A condition where the kidneys are unable to concentrate urine, leading to excessive water loss and causing dehydration.

A type of diabetes insipidus where the kidneys do not respond properly to vasopressin.

A type of diabetes insipidus where the pituitary gland does not produce enough vasopressin.

A condition where the blood sodium levels are abnormally low, often caused by excess water in the body.

A condition where there is excessive water loss from the body, typically due to a lack of vasopressin or a failure of the kidneys to respond to it correctly.

Carbonic anhydrase inhibitors are a class of diuretics that primarily target the proximal convoluted tubule (PCT) of the nephron. They potently inhibit the enzyme carbonic anhydrase, causing a reduction in bicarbonate reabsorption and leading to increased urine output.

Acetazolamide, dorzolamide, dichlorphenamide, and methazolamide are examples of carbonic anhydrase inhibitors.

Carbonic anhydrase inhibitors can be used to treat a variety of conditions, including open-angle glaucoma, high altitude sickness, epilepsy, and metabolic alkalosis. They can also be used in combination with other diuretics for resistance to diuretic monotherapy.

Osmotic diuretics are a group of diuretics that work primarily in the proximal convoluted tubule and the loop of Henle. They increase the osmotic pressure within the tubules, preventing water reabsorption and promoting excretion of water and electrolytes.

Glycerin, isosorbide, mannitol, and urea are examples of osmotic diuretics.

A genetic disorder characterized by mutations in the SLC12A3 gene, leading to impaired reabsorption of sodium, chloride, and potassium in the distal convoluted tubule of the kidney. This results in hypokalemia, hypomagnesemia, and metabolic alkalosis.

Osmotic diuretics are commonly used to reduce intracranial pressure, cerebral edema, and manage dialysis disequilibrium syndrome. They can also be used in the treatment and prevention of acute kidney injury (AKI).

A class of diuretics that block the sodium-chloride symporter (NCC) in the distal convoluted tubule of the kidney, reducing sodium reabsorption and increasing urine output. They are commonly used to treat hypertension and edema.

Loop diuretics, also known as high-ceiling diuretics, are potent diuretics primarily targeting the thick ascending limb (TAL) of the nephron. They inhibit the Na+-K+-2Cl− symporter, drastically reducing salt reabsorption in that segment and causing significant diuresis.

A class of diuretics that work by directly blocking the epithelial sodium channels (ENaC) in the collecting tubule of the kidney, reducing sodium reabsorption and increasing potassium retention. They are used to treat conditions like Liddle syndrome, cystic fibrosis, and lithium-induced nephrogenic diabetes insipidus.

Furosemide, bumetanide, ethacrynic acid, and torsemide are examples of loop diuretics. These drugs share common structural features, such as a sulfonamide moiety or other similar chemical groups.

These agents block aldosterone receptors in the collecting tubule, reducing sodium reabsorption and potassium excretion. They are used to treat conditions like hyperaldosteronism, edema, hypertension, and hepatic cirrhosis.

Thiazide diuretics may reduce the effectiveness of uricosuric agents, sulfonylureas, insulin, NSAIDs, COX-2 inhibitors, and bile acid sequestrants.

Thiazide diuretics may increase the effectiveness of anesthetics, diazoxide, digitalis, lithium, loop diuretics, vitamin D, and arsenic trioxide.

Thiazide diuretics can increase the risk of hypokalemia when used with amphotericin B, corticosteroids, quinidine, and dofetilide.

A rare but potentially life-threatening adverse effect of thiazide diuretics, characterized by a rapid decline in blood pressure, electrolyte imbalance, and kidney failure.

Loop diuretics are commonly used to treat acute pulmonary edema, a condition where fluid builds up in the lungs. They are also effective in other edematous conditions, drug overdose, hypercalcemia (with normal saline solution), and hyponatremia (with hypertonic saline).

Loop diuretics are not the first-line choice for treating hypertension, despite their effectiveness in reducing fluid volume. Other classes of drugs, like ACE inhibitors or beta-blockers, are typically preferred.

Loop diuretics can cause hyperglycemia, hyperlipidemia, and hyperuricemia. They also lead to significant depletion of total-body sodium, which can result in hypovolemia. Ototoxicity is another potential side effect, especially with ethacrynic acid.

Loop diuretics should be avoided in postmenopausal women, patients with severe volume depletion, anuria (absence of urine production), and individuals allergic to sulfonamides.

Loop diuretics can interact with other drugs, increasing the risk of side effects or altering their efficacy. This includes aminoglycosides, carboplatin, paclitaxel, cisplatin, digitalis glycosides, lithium, propranolol, sulfonylureas, NSAIDs, probenecid, thiazide diuretics, and amphotericin B.

Thiazide diuretics, like hydrochlorothiazide, block the reabsorption of sodium and chloride in the distal convoluted tubule of the kidney. This leads to increased urine production and reduced blood pressure.

Thiazide diuretics have a broad range of uses, including edema treatment, hypertension management, heart failure management, preventing kidney stones due to excessive calcium excretion, treating nephrogenic diabetes insipidus, and addressing bromide intoxication.