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What is the mainstay treatment for obesity?"<b><span style=""color: rgb(0, 85, 127);"">Increased physical activity coupled with a calorie-restricted diet.</span></b>"
When is drug therapy recommended for obesity treatment?<div>Drug therapy is recommended for:</div><ul><li>BMI &gt; 30 kg/m².</li><li>BMI &gt; 27 kg/m² with two or more comorbidities, such as hypertension and diabetes.</li><li>Used in conjunction with behavioral therapy and lifestyle modifications.</li></ul>
<div>What are the main types of drugs used for obesity treatment?</div><ol><li><strong>Anorexiants:</strong><ul><li>Diethylpropion</li><li>Phentermine</li></ul></li><li><strong>GLP-1 Receptor Agonists:</strong><ul><li>Semaglutide (Wegovy)</li><li>Liraglutide (Saxenda)</li><li>GIP and GLP-1 receptor agonists (e.g., Tirzepatide - Mounjaro)</li></ul></li><li><strong>Lipase Inhibitors:</strong><ul><li>Orlistat (Alli, Xenical)</li></ul></li><li><strong>Combination Drugs:</strong><ul><li>Bupropion/naltrexone (Contrave)</li><li>Phentermine/topiramate (Qsymia)</li></ul></li></ol>
<div>What are the criteria for obesity?</div><ul><li><strong>Calorie consumption exceeds calorie expenditure.</strong></li><li>Associated with increased food intake and sedentary lifestyle.</li></ul>
What is Orlistat (Alli, Xenical), and how does it help in obesity management?<br>"Orlistat is a&nbsp;<b><span style=""color: rgb(0, 85, 127);"">lipase inhibitor&nbsp;that prevents fat absorption</span></b>, aiding in weight management."
What comorbidities are associated with obesity?<div>Obesity is linked to:</div><ul><li>Hypertension</li><li>Cardiovascular disease</li><li>Type 2 diabetes mellitus</li><li>Nonalcoholic fatty liver disease</li><li>Osteoarthritis</li><li>Sleep apnea</li><li>GERD</li><li>Chronic kidney disease</li></ul>
<div><strong>What are anorexiants for appetite suppression?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 255);""><b>Diethylpropion</b></span></li><li><span style=""color: rgb(170, 0, 255);""><b>Phentermine</b></span></li><li><span style=""color: rgb(170, 0, 255);""><b><em>Classified as a controlled substance due to potential for abuse.</em></b></span><br></li></ul>"
<div><strong>What is the mechanism of action (MOA) of anorexiants?</strong></div>"<ul><li><b>Increases <span style=""color: rgb(170, 0, 255);"">norepinephrine and dopamine</span></b> release.</li><li><b>Inhibits reuptake of these neurotransmitters.</b></li><li>Results in <span style=""color: rgb(170, 0, 255);""><b>""fight-or-flight"" signaling, reducing appetite.</b></span></li></ul>"
<div><strong>What are the pharmacokinetics (PK) of Phentermine?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 255);""><b>Duration depends on formulation.</b></span></li><li>Excreted primarily via the <b>kidneys</b>.</li></ul>"
"<div><strong>What are the pharmacokinetics (PK) of <span style=""color: rgb(170, 0, 255);"">Diethylpropion</span>?</strong></div>""<ul><li>Rapid absorption with <span style=""color: rgb(170, 0, 255);""><b>extensive first-pass metabolism.</b></span></li><li>Active metabolites; half-life: <b><span style=""color: rgb(170, 0, 255);"">4–8 hours.</span></b></li><li>Excreted mainly via the kidneys.</li></ul>"
<div><strong>What are the common side effects of anorexiants?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 255);""><b>Dry mouth</b></span></li><li>Headache</li><li>Insomnia</li><li>Constipation</li><li>Increased heart rate (HR) and blood pressure (BP)</li><li><b><span style=""color: rgb(170, 0, 255);"">**think fight or flight**</span></b></li></ul>"
<strong>What are the contraindications of anorexiants?</strong><br>"<div>Avoid in patients with:</div><ul><li><b><span style=""color: rgb(170, 85, 127);"">Cardiac history</span></b> (uncontrolled hypertension, arrhythmias, heart failure, stroke).</li><li>Use of <span style=""color: rgb(170, 85, 127);""><b>MAOIs or other sympathomimetics.</b></span></li></ul>"
<div><strong>What happens with long-term use of anorexiants?</strong></div>"<ul><li><span style=""color: rgb(255, 85, 255);""><b>Tolerance develops within weeks → weight loss plateaus.</b></span></li><li>Increasing dose is ineffective; medication is discontinued once plateau is reached.</li></ul>"
<div><strong>What are examples of GLP-1 receptor agonists?</strong></div><ul><li>Liraglutide (Saxenda)</li><li>Semaglutide (Wegovy)</li></ul>
<div><strong>What is the MOA of GLP-1 receptor agonists?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 127);""><b>Increase glucose-dependent insulin release.</b></span></li><li><span style=""color: rgb(170, 0, 127);""><b>Decrease glucagon secretion</b></span>.</li><li>Slow gastric emptying → Increases satiety.</li></ul>"
<div><strong>What are the indications for GLP-1 receptor agonists?</strong></div><ul><li><b>Adults with BMI ≥27 (with comorbid conditions) or BMI ≥30</b> (obesity).</li><li><b>Children</b> (Saxenda): <b>12–17 years with obesity and ≥60 kg.</b></li></ul>
<div><strong>What are the PK features of GLP-1 receptor agonists?</strong></div><ul><li><b>Metabolized like proteins</b>; no specific organ elimination.</li></ul>
<div><strong>What are the adverse effects of GLP-1 receptor agonists?</strong></div>"<ul><li>Nausea, vomiting, diarrhea, constipation.</li><li><span style=""color: rgb(170, 0, 127);""><b>Hypoglycemia, acute gallbladder disease.</b></span></li><li><span style=""color: rgb(170, 0, 127);""><b>Pancreatitis: avoid with chronic pancreatitis</b></span>.</li><li><span style=""color: rgb(209, 0, 0);""><b>Contraindicated in medullary thyroid disease or multiple endocrine neoplasia Type 2.</b></span></li></ul>"
<div><strong>What is Tirzepatide (Zepbound)?</strong></div><ul><li>Dual GIP/GLP-1 receptor agonist.</li></ul>
<div><strong>What is the MOA of Tirzepatide?</strong></div><ul><li>Activates GIP and GLP-1 receptors.</li><li>Enhances insulin secretion and sensitivity.</li><li>Reduces calorie intake by delaying gastric emptying.</li></ul>
<div><strong>What are the indications for Tirzepatide?</strong></div><ul><li><b>Adjunct to a reduced-calorie diet and increased physical activity for chronic weight management.</b></li></ul>
<div><strong>What are the contraindications for Tirzepatide?</strong></div>"<ul><li><span style=""color: rgb(255, 85, 255);""><b>Personal/family history of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2.</b></span></li><li>Known hypersensitivity.</li><li>Use caution with:<ul><li><span style=""color: rgb(255, 85, 255);""><b>Severe GI disease</b></span></li><li><span style=""color: rgb(255, 85, 255);""><b>Acute kidney, gallbladder, pancreatitis issues</b></span></li><li><span style=""color: rgb(255, 85, 255);""><b>Hypoglycemia</b></span></li><li><span style=""color: rgb(255, 85, 255);""><b>Diabetic retinopathy</b></span></li><li><span style=""color: rgb(255, 85, 255);""><b>Suicidal behavior</b></span></li></ul></li></ul>"
<div><strong>What are the adverse effects of Tirzepatide?</strong></div>"<ul><li>Most common: GI symptoms, hair loss, <b>eructation</b> (belching).</li><li><b><span style=""color: rgb(170, 0, 127);"">Avoid in pregnancy.</span></b></li></ul>"
<div><strong>What is the Black Box Warning (BBW) for GLP-1 receptor agonists and Tirzepatide?</strong></div>"<ul><li>Risk of <span style=""color: rgb(170, 0, 127);""><b>thyroid C-cell tumors.</b></span></li></ul>"
<div><strong>What is Orlistat (Xenical, Alli) used for?</strong></div><ul><li>Weight loss.</li><li>Chronic weight maintenance.</li></ul>
<div><strong>What are the available forms of Orlistat?</strong></div><ul><li>Xenical® (120 mg): Prescription.</li><li>Alli® (60 mg): Over-the-counter.</li></ul>
<div><strong>What is the MOA of Orlistat?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 127);""><b>Pentanoic acid ester</b></span> that <b><span style=""color: rgb(170, 0, 127);"">inhibits gastric and pancreatic lipases in the gut.</span></b></li><li><b>Blocks the breakdown and absorption of dietary fat by ~30%</b>.</li><li>Weight loss occurs through calorie reduction due to decreased fat absorption.</li></ul>"
<div><strong>What are the PK features of Orlistat?</strong></div>"<ul><li><b>Route:<span style=""color: rgb(170, 0, 255);"">&nbsp;Oral, taken with meals containing fat</span></b>.</li><li>Minimal systemic absorption; <span style=""color: rgb(170, 0, 255);""><b>excreted in feces.</b></span></li><li>No dose adjustments for renal or hepatic impairment.</li><li>Effectiveness: <span style=""color: rgb(170, 0, 255);""><b>3–5% weight loss with lifestyle changes.</b></span></li></ul>"
<div><strong>What are the adverse effects (AE) of Orlistat?</strong></div>"<ul><li><strong>Common GI Effects:</strong><ul><li><span style=""color: rgb(255, 85, 255);""><b>Oily spotting.</b></span></li><li><span style=""color: rgb(255, 85, 255);""><b>Flatulence with discharge.</b></span></li><li><span style=""color: rgb(255, 85, 255);""><b>Fecal urgency.</b></span></li><li><span style=""color: rgb(255, 85, 255);""><b>Increased defecation.</b></span></li><li><span style=""color: rgb(255, 85, 255);""><b>Minimized with a low-fat diet or cholestyramine.</b></span></li></ul></li><li><strong>Rare:</strong> Pancreatitis, liver injury.</li></ul>"
<div><strong>What are the contraindications for Orlistat?</strong></div>"<ul><li><span style=""color: rgb(212, 0, 0);""><b>Pregnancy.</b></span></li><li><span style=""color: rgb(212, 0, 0);""><b>Chronic malabsorption syndrome or cholestasis.</b></span></li></ul>"
<div><strong>What are the special considerations for Orlistat?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 255);""><b>Interferes with absorption of fat-soluble vitamins (A, D, E, K) and beta-carotene</b></span>.<ul><li><strong>Recommendation:</strong>&nbsp;Take multivitamins at least 2 hours apart from Orlistat.</li></ul></li><li><b>Interferes with absorption of medications</b> like:<ul><li><span style=""color: rgb(170, 0, 255);""><b>Amiodarone.</b></span></li><li><span style=""color: rgb(170, 0, 255);""><b>Cyclosporine.</b></span></li><li><span style=""color: rgb(170, 0, 255);""><b>Levothyroxine.</b></span></li><li><b>Separate doses of levothyroxine by 4 hours and monitor clinical response.</b></li></ul></li></ul>"
<div><strong>What is the use of Bupropion/Naltrexone (Contrave)?</strong></div><ul><li>Chronic weight management.</li></ul>
<div><strong>What is the mechanism of action for Bupropion/Naltrexone (Contrave)?</strong></div>"<ul><li><b>Bupropion:</b>&nbsp;<span style=""color: rgb(255, 85, 255);""><b>Stimulates CNS POMC neurons, promoting appetite suppression.</b></span></li><li><b>Naltrexone:</b>&nbsp;<span style=""color: rgb(255, 85, 255);""><b>Blocks auto-inhibitory feedback on the hypothalamic melanocortin system.</b></span></li><li><b>Combo effect:</b>&nbsp;<span style=""color: rgb(255, 85, 255);""><b>Regulates the mesolimbic reward system, reducing cravings.</b></span></li></ul>"
<div><strong>What are the pharmacokinetics of Bupropion/Naltrexone (Contrave)?</strong></div>"<ul><li><strong>Bupropion:</strong>&nbsp;Metabolized in the liver via <b><span style=""color: rgb(170, 0, 255);"">CYP2D6</span></b>.</li><li><strong>Naltrexone:</strong>&nbsp;Excreted through <b><span style=""color: rgb(170, 0, 255);"">kidneys</span></b>.</li></ul>"
<div><strong>What are the adverse effects of Bupropion/Naltrexone (Contrave)?</strong></div><ul><li>Nausea.</li><li>Headache.</li><li>Dry mouth.</li><li>Dizziness.</li><li>Constipation.</li><li><strong>Risk of suicidal ideation.</strong></li></ul>
<div><strong>What is the use of Phentermine/Topiramate (Qsymia)?</strong></div><ul><li>Long-term weight loss.</li><li>Combo effect for appetite suppression and increased satiety.</li></ul>
<div><strong>What is the dosing for Phentermine/Topiramate (Qsymia)?</strong></div><ul><li>Gradual dose escalation every 2 weeks.</li><li><b>Discontinue if &lt;5% weight loss after 12 weeks on the highest dose.</b></li><li><b>Taper off to prevent seizures when stopping treatment</b></li></ul>
<div><strong>What is the mechanism of action for Phentermine/Topiramate (Qsymia)?</strong></div>"<ul><li><strong>Phentermine:</strong><ul><li>CNS: <span style=""color: rgb(170, 0, 255);""><b>Increase in norepinephrine</b></span> (NE) and <b><span style=""color: rgb(170, 0, 255);"">dopamine release and reuptake inhibition.</span></b></li><li><b><span style=""color: rgb(170, 0, 255);"">Acts as a stimulant</span></b> to promote weight loss and <span style=""color: rgb(170, 0, 255);""><b>counteracts sedative effects of topiramate</b></span>.</li></ul></li><li><strong>Topiramate:</strong><ul><li>CNS: <span style=""color: rgb(0, 170, 255);""><b>Increases GABA.</b></span></li><li><span style=""color: rgb(0, 170, 255);""><b>Anticonvulsant with observed weight loss effects.</b></span></li></ul></li></ul>"
<div><strong>What are the pharmacokinetics of Phentermine/Topiramate (Qsymia)?</strong></div><ul><li>Excreted primarily via kidneys.</li><li>Limited hepatic metabolism.</li></ul>
<div><strong>What are the adverse effects of Phentermine/Topiramate (Qsymia)?</strong></div>"<ul><li><strong>Phentermine:</strong><ul><li>Paresthesia.</li><li><b>Altered taste.</b></li><li>Insomnia.</li><li>Dry mouth.</li><li>Constipation.</li><li>Dizziness.</li><li><span style=""color: rgb(170, 85, 127);""><b>Hypokalemia</b></span>.</li></ul></li><li><strong>Topiramate:</strong><ul><li><span style=""color: rgb(170, 85, 127);""><b>Reduced efficacy of oral contraceptives.</b></span></li><li><span style=""color: rgb(170, 85, 127);""><b>Increases kidney stone risk due to weak carbonic anhydrase inhibition.</b></span></li></ul></li></ul><div><strong>Contraindications:</strong></div><ul><li>Pregnancy (<span style=""color: rgb(170, 85, 127);""><b>risk of birth defects: cleft palate</b></span>).</li></ul>"
<div><strong>What is osteoporosis?</strong></div><ul><li>Progressive loss of bone mass, leading to skeletal fragility.</li></ul>
<div><strong>What are the risks associated with osteoporosis?</strong></div><ul><li>Increased fracture risk.</li><li>Common in postmenopausal women and older adults.</li></ul>
<div><strong>What causes osteoporosis?</strong></div><ul><li>Imbalance in bone resorption and formation.</li></ul>
<div><strong>What is Paget's disease?</strong></div><ul><li>Disorder of bone remodeling leading to disorganized, enlarged, or misshapen bones.</li></ul>
<div><strong>What are the symptoms and involvement of Paget's disease?</strong></div><ul><li>Symptoms: <b>Bone pain, deformity, or fractures.</b></li><li>Involvement: <b>Typically affects one or a few bones.</b></li></ul>
<div><strong>What is osteomalacia?</strong></div><ul><li>Softening of bones due to vitamin D deficiency.</li><li>In children, it is called rickets.</li></ul>
<div><strong>What is the role of osteoclasts in the bone remodeling process?</strong></div><ul><li>Cells that break down and resorb bone.</li></ul>
<div><strong>What is the role of osteoblasts in the bone remodeling process?</strong></div>"<ul><li><b>Build</b> and mineralize new bone (<span style=""color: rgb(170, 0, 127);""><b>deposit hydroxyapatite</b></span>).</li></ul>"
<div><strong>What is the bone remodeling cycle and its significance?</strong></div><ul><li>~10% of the skeleton is replaced annually to maintain calcium balance.</li><li>Imbalance (Bone Loss) = Bone resorption &gt; Bone formation.</li></ul>
<div><strong>What are the types of calcium supplements used to prevent osteoporosis, and how should they be taken?</strong></div><ul><li><strong>Calcium Carbonate:</strong>&nbsp;40% elemental; take with food.</li><li><strong>Calcium Citrate:</strong>&nbsp;21% elemental; better tolerated; can be taken with or without food.</li></ul>
<div><strong>Why is Vitamin D important in osteoporosis prevention, and what are the forms available?</strong></div><ul><li>Vitamin D is critical for calcium absorption.</li><li>Forms: D2 (ergocalciferol) or D3 (cholecalciferol).</li></ul>
<div><strong>What are the side effects associated with calcium supplementation?</strong></div><ul><li>Gas and bloating.</li></ul>
<div><strong>What are the common drug interactions with calcium supplements?</strong></div>"<ul><li>Iron preparations.</li><li>Thyroid replacement therapy.</li><li><span style=""color: rgb(170, 0, 127);""><b>Antibiotics such as fluoroquinolones and tetracycline.</b></span></li></ul>"
<div><strong>What is the recommended timing for taking calcium supplements to avoid drug interactions?</strong></div><ul><li>Take calcium supplements several hours apart from other medications.</li></ul>
<div><strong>What lifestyle modifications can help prevent osteoporosis?</strong></div><ul><li>Engage in weight-bearing exercise.</li><li>Stop smoking.</li><li>Reduce alcohol intake.</li></ul>
<div><strong>What type of medication should be avoided to prevent increased bone loss, and why?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 127);""><b>Avoid long-term glucocorticoid use (&gt;3 months) as it increases bone loss.</b></span></li></ul>"
<div><strong>What are some drugs used to treat osteoporosis?</strong></div><ul><li>Abaloparatide (TYMLOS)</li><li>Alendronate (FOSAMAX, BINOSTO)</li><li>Calcitonin (MIACALCIN)</li><li>Denosumab (PROLIA)</li><li>Ibandronate (BONIVA)</li><li>Raloxifene (EVISTA)</li><li>Risedronate (ACTONEL, ATELVIA)</li><li>Romosozumab (EVENITY)</li><li>Teriparatide (FORTEO)</li><li>Zoledronic acid (RECLAST, ZOMETA)</li></ul>
<div><strong>What are some drugs used for disorders of bone remodeling?</strong></div>"<ul><li><b><span style=""color: rgb(170, 0, 255);"">Etidronate</span></b> (Generic only)</li><li><b><span style=""color: rgb(170, 0, 255);"">Pamidronate</span></b> (AREDIA)</li><li>""Easy Bones Remodel""</li></ul>"
<div><strong>Which drugs contribute to bone loss or fracture risk?</strong></div><ul><li>Aluminum antacids</li><li>Anticonvulsants (e.g., phenytoin)</li><li>Aromatase inhibitors</li><li>Furosemide</li><li>Glucocorticoids</li><li>Heparin</li><li>Medroxyprogesterone acetate</li><li>Proton pump inhibitors</li><li>Selective serotonin reuptake inhibitors</li><li>Thiazolidinediones</li><li>Thyroid (excessive replacement)</li></ul>
What are bisphosphonates used to treat?<ul><li>Osteoporosis</li><li>Paget's disease</li><li>Bone metastases</li><li>Hypercalcemia of malignancy</li></ul>
<div><strong>Which drugs are considered bisphosphonates?</strong></div><ul><li>Etidronate</li><li>Ibandronate</li><li>Pamidronate</li><li>Alendronate (Fosamax)</li><li>Zoledronic acid (Reclast)</li><li>Risedronate</li><li>Tiludronate</li></ul>
<div><strong>What are the specific uses of certain bisphosphonates?</strong></div>"<ul><li>Etidronate: <span style=""color: rgb(170, 0, 127);""><b>Paget's disease, heterotopic ossification</b></span></li><li>Ibandronate: Osteoporosis</li><li>Pamidronate: <b><span style=""color: rgb(170, 0, 127);"">Hypercalcemia of malignancy</span></b></li><li>Alendronate (Fosamax): <b><span style=""color: rgb(170, 0, 127);"">Postmenopausal osteoporosis</span></b></li><li>Zoledronic acid (Reclast): <b>IV option for patients intolerant to oral bisphosphonates</b></li></ul>"
<div><strong>What is the mechanism of action (MOA) of bisphosphonates?</strong></div>"<ul><li>Binds to <span style=""color: rgb(170, 0, 255);""><b>hydroxyapatite crystals in bone</b></span></li><li><span style=""color: rgb(170, 0, 255);""><b>Reduces osteoclastic activity</b></span>, decreasing bone resorption and turnover</li><li><b>Slightly increases bone mass and reduces fracture risk</b></li></ul>"
<div><strong>What are the pharmacokinetics (PK) of bisphosphonates?</strong></div>"<ul><li>Oral absorption: <b><span style=""color: rgb(170, 0, 127);"">Poor (&lt;1% of dose), greatly affected by food and medications</span></b></li><li>Plasma clearance: <b>Rapid; binds avidly to hydroxyapatite in bone</b></li><li>Distribution: Binds to bone</li><li>Excretion: Via kidneys; avoid in severe renal impairment</li></ul>"
<div><strong>What are the common adverse effects of bisphosphonates?</strong></div><div></div>"<ul><li>Diarrhea</li><li>Abdominal pain</li><li>Musculoskeletal pain</li><li><b>Esophagitis and esophageal ulcers (<span style=""color: rgb(170, 85, 127);""><i>important to remain upright after oral formulations like alendronate, ibandronate, risedronate, and zoledronic acid)</i></span></b></li></ul>"
<div><strong>What are the severe adverse effects of bisphosphonates?</strong></div><ul><li>Osteonecrosis of the jaw (risk increases with long-term use)</li><li>Atypical femur fractures</li></ul>
<div><strong>What are the recommendations for long-term bisphosphonate use?</strong></div>"<ul><li><b>Drug holidays </b>after:<ul><li><span style=""color: rgb(170, 0, 255);""><b>5 years of oral bisphosphonates</b></span></li><li><span style=""color: rgb(170, 0, 255);""><b>3 years of IV zoledronic acid</b></span></li></ul></li></ul>"
<div><strong>Which bisphosphonates are available in IV formulations?</strong></div><ul><li>Ibandronate</li><li>Zoledronic acid</li></ul>
<div><strong>What is the antiresorptive activity of bisphosphonates?</strong></div><ul><li><b>Etidronate</b>: 1</li><li><b>Tiludronate</b>: 10</li><li><b>Pamidronate</b>: 100</li><li><b>Alendronate</b>: 1,000</li><li><b>Risedronate</b>: 5,000</li><li><b>Ibandronate</b>: 10,000</li><li><b>Zoledronic acid</b>: 10,000</li></ul>
<div><strong>What is the mechanism of action (MOA) of Denosumab?</strong></div><ul><li>Monoclonal antibody targeting receptor activator of nuclear factor kappa-B ligand (RANKL).</li><li>Inhibits osteoclast formation and function, reducing bone resorption.</li></ul>
<div><strong>What are the indications for Denosumab?</strong></div><ul><li>Approved for the treatment of postmenopausal osteoporosis in women at high risk for fracture.</li></ul>
<div><strong>How is Denosumab administered?</strong></div><ul><li>Subcutaneous injection every 6 months.</li></ul>
<div><strong>What is the clinical use of Denosumab?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 127);""><b>First-line agent for osteoporosis in patients at higher risk of fracture.</b></span></li></ul>"
<div><strong>What are the adverse effects (AEs) of Denosumab?</strong></div>"<ol><li>Increased risk for infection.</li><li>Dermatological reactions (e.g., rashes).</li><li><b>Hypocalcemia</b>.</li><li>Rare but severe:<ul><li><span style=""color: rgb(209, 0, 0);""><b>Necrosis of the jaw.</b></span></li><li><span style=""color: rgb(209, 0, 0);""><b>Atypical femur fractures.</b></span></li></ul></li></ol>"
<div><strong>What are Parathyroid Agents?</strong></div><ol><li><strong>Teriparatide (Forteo):</strong>&nbsp;Recombinant form of human parathyroid hormone (PTH).</li><li><strong>Abaloparatide (Tymlos):</strong>&nbsp;Analog of parathyroid hormone-related peptide (PTHrP).</li></ol>
<div><strong>What is the Mechanism of Action (MOA) of Parathyroid Agents?</strong></div><ul><li>Act as agonists at the parathyroid hormone receptor.</li><li>Stimulate osteoblastic activity, increasing bone formation and bone strength.</li></ul>
<div><strong>How are Parathyroid Agents administered?</strong></div><ul><li>Subcutaneous (SQ) injection once daily.</li></ul>
<div><strong>What are the indications for Parathyroid Agents?</strong></div><ul><li>Patients at high risk of fracture.</li><li>Patients who failed or cannot tolerate other therapies.</li></ul>
<div><strong>What are the adverse effects of Parathyroid Agents?</strong></div><ol><li>Hypercalcemia.</li><li>Orthostatic hypotension.</li><li>Increased risk of osteosarcoma (observed in preclinical rat studies).</li></ol>
<div><strong>What is the limitation for using Parathyroid Agents?</strong></div><ul><li>Not recommended for use <b>beyond 2 years</b> in a patient’s lifetime.</li></ul>
<div><strong>What is the Mechanism of Action (MOA) of Romosozumab?</strong></div><ul><li><b>Monoclonal antibody that inhibits sclerostin.</b></li><li>Sclerostin is a key regulator in bone remodeling that inhibits bone formation.</li><li>By binding to and blocking sclerostin, it:<ul><li>Promotes osteoblast activity and bone formation.</li><li>Decreases bone resorption.</li></ul></li></ul>
<div><strong>What are the indications for Romosozumab?</strong></div><ul><li>Approved for use in postmenopausal women with osteoporosis at high risk of fractures.</li></ul>
<div><strong>How is Romosozumab administered?</strong></div><ul><li>Once-monthly subcutaneous injection for 12 months.<ul><li>Note: Two injections are required to deliver the full dose.</li></ul></li></ul>
<div><strong>What are the adverse effects of Romosozumab?</strong></div><ol><li>Arthralgias (joint pain).</li><li>Headache.</li><li>Injection site reactions.</li></ol>
<div><strong>What are the contraindications for Romosozumab?</strong></div><ul><li>Avoid in patients with a history of:<ul><li>Myocardial infarction (MI).</li><li>Stroke.</li></ul></li><li>Clinical trials noted a small but significant increase in these events.</li></ul>
<div><strong>What is a key treatment consideration for Romosozumab?</strong></div><ul><li>After 12 months of therapy, transition to another antiresorptive agent is recommended to maintain benefits.</li></ul>
<div><strong>What is the purpose of Raloxifene (Evista)?</strong></div><ul><li>Prevention and treatment of osteoporosis.</li></ul>
<div><strong>What makes Raloxifene an alternative to bisphosphonates?</strong></div><ul><li>It is considered an alternative for patients <b>who cannot tolerate bisphosphonates.</b></li><li>However, it has<b> not been shown to reduce nonvertebral or hip fractures.</b></li></ul>
<div><strong>What is the Mechanism of Action (MOA) of Raloxifene?</strong></div>"<ul><li><span style=""color: rgb(170, 0, 127);""><b>Mimics estrogen's effects</b></span> on bone (agonist action).</li><li><span style=""color: rgb(170, 0, 127);""><b>Antagonizes estrogen’s effects in breast and endometrial tissues.</b></span></li></ul>"
<div><strong>What are the key benefits of Raloxifene?</strong></div><ul><li>Increases bone density.</li><li>Does not increase the risk of endometrial cancer.</li><li>Decreases the risk of invasive breast cancer.</li></ul>
<div><strong>What are the adverse effects of Raloxifene?</strong></div>"<ul><li><strong>Common side effects:</strong><ul><li><b><span style=""color: rgb(170, 0, 127);"">Weight gain (10% of women)</span>.</b></li><li>Hot flashes.</li><li>Leg cramps.</li></ul></li><li><strong>Significant risks:</strong><ul><li><span style=""color: rgb(170, 0, 127);""><b>Increased risk of venous thromboembolism (VTE).</b></span></li><li>Pulmonary embolism.</li><li>Stroke.</li></ul></li></ul>"
<div><strong>Why is estrogen replacement therapy no longer recommended for postmenopausal osteoporosis?</strong></div><ul><li>It increases the risks of:<ul><li><b>Endometrial cancer (when combined with progestin in women with an intact uterus).</b></li><li>Breast cancer.</li><li>Stroke.</li><li>Venous thromboembolism (VTE).</li><li>Coronary events.</li></ul></li></ul>
<div><strong>What are the indications for Calcitonin (Salmon Calcitonin)?</strong></div><ul><li>Osteoporosis treatment in postmenopausal women who are at least 5 years postmenopausal.</li><li>Pain relief in patients with recent painful vertebral fractures.</li></ul>
<div><strong>What is the mechanism of action (MOA) of Calcitonin?</strong></div><ul><li><b>Reduces bone resorption by inhibiting osteoclast activity.</b></li><li>Less effective than other osteoporosis treatments.</li><li>Not routinely recommended due to <b>limited efficacy</b>.</li></ul>
<div><strong>What is the clinical use of Calcitonin?</strong></div><ul><li>Primarily used for <b>short-term relief of fracture pain</b>.</li><li>Administered via <b>intranasal formulation, which is the most commonly used route</b></li></ul>
<div><strong>What are the adverse effects (AEs) of Calcitonin?</strong></div><ul><li><b>Rhinitis</b>.</li><li>Other nasal symptoms such as congestion or irritation.</li></ul>