α-Glucosidase inhibitors cause dose-related malabsorption, flatulence, diarrhea, and abdominal bloating.
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MOA of Nitroglycerine Nitroglycerine converted to NO (Active Metabolite) NO bonds with Guanylyl cyclase and catalyzes the conversion of GTP to cyclic GMP. cGMP induces the enzyme Myosin LC phosphatase Myosin-LC phosphatase dephosphorylates the phosphorylated myosin-LC (Contraction) to Myosin-LC (Relaxation) Reducing Preload : Vasodilation promotes peripheral pooling of blood and decreases venous return to the heart , reducing preload. This results in decreased myocardial oxygen demand. Reducing Afterload : Arteriolar relaxation reduces systemic vascular resistance and arterial pressure, also known as afterload. This decreases the resistance the heart must overcome to eject blood, which reduces the workload of the heart.
Mechanism of Action of Angiotensin II Type- 1 (AT1) Receptor Blockers Angiotensin II receptor blockers (ARBs) are a class of medications that work by blocking the effects of angiotensin II, a powerful hormone that constricts blood vessels and raises blood pressure. ARBs do this by binding to and blocking the angiotensin II type 1 receptor (AT1 receptor) , which is found in many tissues throughout the body, including the heart, blood vessels, and kidneys. When angiotensin II binds to the AT1 receptor, it causes a number of effects, including: Vasoconstriction (narrowing of blood vessels) Aldosterone release (a hormone that causes the kidneys to retain sodium and water) Catecholamine release (adrenaline and noradrenaline, which also raise blood pressure) Hypertrophic response (thickening of the heart muscle) By blocking the AT1 receptor, ARBs prevent these effects from occurring, which leads to a lowering of blood pressure. ARBs are also known to have other beneficial effects, such as
Classify antithyroid agents in terms of their mechanism of actions. Thyroid hormone synthesis inhibitors : These drugs inhibit the enzyme thyroid peroxidase, decreasing iodide oxidation, iodination of tyrosyl residues in thyroglobulin, and coupling of iodotyrosyl and iodothyronyl residues. EXAMPLES : thioamides, which include propylthiouracil , methimazole , and its prodrug carbimazole. Iodide uptake inhibitors/ ionic Inhibitors : They decrease the uptake of iodide ions into follicular cells of the thyroid gland. EXAMPLES : potassium perchlorate, pertechnetates, thiocyanates, and nitrates. Thyroid hormone release inhibitors : They inhibit the release of thyroid hormones by the thyroid gland. EXAMPLES : The most studied drug in this class is lithium . Thyroid hormone receptor antagonists : These drugs block the action of thyroid hormones at the cellular level. They do this by binding to thyroid hormone receptors and preventing thyroid hormones from exerting their effects. Examples in
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