This document summarizes several classes of antihypertensive drugs, including their mechanisms of action and effects. It discusses diuretics, ACE inhibitors, angiotensin receptor blockers, beta-blockers, calcium channel blockers, alpha-blockers, centrally acting drugs, and vasodilators. For each class, it describes their advantages and disadvantages in treating hypertension, as well as recommendations for use.
Drugs used in treatment of rheumatoid arthiritisPravin Prasad
This document summarizes drugs used to treat rheumatoid arthritis. It discusses disease-modifying antirheumatic drugs (DMARDs) which are used to modify disease progression, including conventional synthetic DMARDs like methotrexate and sulfasalazine, as well as biological DMARDs like TNF-alpha inhibitors. It provides details on the mechanisms of action, pharmacokinetics, uses, and adverse effects of various DMARDs. Nonsteroidal anti-inflammatory drugs are used for symptom relief while corticosteroids can provide prompt anti-inflammatory effects but do not alter disease progression. The document concludes that methotrexate is preferred as initial treatment and certain drugs should not be combined.
Pharmacology of Ethyl and Methyl AlcoholManoj Kumar
This document provides information on ethyl and methyl alcohol. It discusses that alcohols are produced by fermenting sugars and starches and the major commercial source is molasses. It then describes different types of alcoholic beverages and their alcohol contents. Key differences between ethanol and methanol are highlighted, including that ethanol is safe for consumption in moderation while methanol is highly toxic.
Introduction to CNS Pharmacology, with Anatomy and physiology of CNS, mode of neuro-transmission via action potential and role of major neurotransmitter in the brain with drug design pharmacology of CNS drugs.
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This document discusses drugs used to treat Parkinson's disease. It begins by describing the signs and symptoms of Parkinsonism including rigidity, tremor, bradykinesia, and impaired balance. It then discusses the pathophysiology involving degeneration of dopamine neurons in the substantia nigra and resulting dopamine deficiency in the striatum. The document covers various drug classes used to treat Parkinson's including levodopa, dopamine agonists like bromocriptine and pramipexole, MAO-B inhibitors like selegiline, and COMT inhibitors like entacapone. It provides details on the mechanisms of action, pharmacokinetics, benefits and adverse effects of these antiparkinsonian drugs.
This document summarizes several classes of antihypertensive drugs, including their mechanisms of action and effects. It discusses diuretics, ACE inhibitors, angiotensin receptor blockers, beta-blockers, calcium channel blockers, alpha-blockers, centrally acting drugs, and vasodilators. For each class, it describes their advantages and disadvantages in treating hypertension, as well as recommendations for use.
Drugs used in treatment of rheumatoid arthiritisPravin Prasad
This document summarizes drugs used to treat rheumatoid arthritis. It discusses disease-modifying antirheumatic drugs (DMARDs) which are used to modify disease progression, including conventional synthetic DMARDs like methotrexate and sulfasalazine, as well as biological DMARDs like TNF-alpha inhibitors. It provides details on the mechanisms of action, pharmacokinetics, uses, and adverse effects of various DMARDs. Nonsteroidal anti-inflammatory drugs are used for symptom relief while corticosteroids can provide prompt anti-inflammatory effects but do not alter disease progression. The document concludes that methotrexate is preferred as initial treatment and certain drugs should not be combined.
Pharmacology of Ethyl and Methyl AlcoholManoj Kumar
This document provides information on ethyl and methyl alcohol. It discusses that alcohols are produced by fermenting sugars and starches and the major commercial source is molasses. It then describes different types of alcoholic beverages and their alcohol contents. Key differences between ethanol and methanol are highlighted, including that ethanol is safe for consumption in moderation while methanol is highly toxic.
Introduction to CNS Pharmacology, with Anatomy and physiology of CNS, mode of neuro-transmission via action potential and role of major neurotransmitter in the brain with drug design pharmacology of CNS drugs.
This document discusses various haematinics including iron, vitamin B12, folic acid, and erythropoietin. It covers their roles in red blood cell formation, daily requirements, dietary sources, absorption and transport, deficiency states, preparations used to treat deficiencies, and therapeutic uses to treat conditions like iron deficiency anemia and megaloblastic anemia. It provides details on the pharmacokinetics and pharmacology of administering these substances.
This document discusses drugs used to treat Parkinson's disease. It begins by describing the signs and symptoms of Parkinsonism including rigidity, tremor, bradykinesia, and impaired balance. It then discusses the pathophysiology involving degeneration of dopamine neurons in the substantia nigra and resulting dopamine deficiency in the striatum. The document covers various drug classes used to treat Parkinson's including levodopa, dopamine agonists like bromocriptine and pramipexole, MAO-B inhibitors like selegiline, and COMT inhibitors like entacapone. It provides details on the mechanisms of action, pharmacokinetics, benefits and adverse effects of these antiparkinsonian drugs.
This document provides an overview of opioids including their pharmacology, mechanisms of action, classifications, and clinical uses. It discusses how opioids bind to receptors in the central and peripheral nervous systems to produce analgesic and other effects. Opioids are classified based on their receptor activities and include pure agonists, partial agonists, mixed agonist-antagonists, and pure antagonists. The document reviews the central and peripheral effects of opioids as well as their indications, contraindications, and interactions. It also discusses opioid tolerance, dependence, overdose, and withdrawal.
Summary of thyroid and antithyroid drugs
-Introduction
-Synthesis
-Pharmacological Action
-Mechanism of action
-Drugs in Hypothyroidism
-Thyroid Inhibitors
-Drugs in Hyperthyroidism
This ppt discusses pharmacological actions, toxic effects and clinical applications of corticosteroids. It also mentions precations to be taken while using steroids
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This document discusses various antimycobacterial drugs used to treat tuberculosis and leprosy. It describes the mechanisms of action, development of resistance, and importance of drug combinations for isoniazid, rifampin, ethambutol, pyrazinamide, streptomycin, fluoroquinolones, linezolid, bedaquiline, and dapsone. Resistance develops rapidly if these drugs are used alone rather than in combination regimens.
Methimazole and propylthiouracil are the major drugs used to treat thyrotoxicosis. Methimazole is more potent and can be given once daily, while propylthiouracil is dosed more frequently. Both drugs inhibit thyroid hormone production and propylthiouracil also blocks peripheral conversion of T4 to T3. Iodide salts like Lugol's solution rapidly reduce hormone synthesis and release within a week. Radioactive iodine is used to ablate the thyroid gland and provide long-term control of Graves' disease, with effects seen over months. Propranolol provides symptomatic relief by blocking sympathetic overactivity in thyrotoxicosis.
This document discusses anti-thyroid drugs used to treat hyperthyroidism. It covers the history of anti-thyroid drug development beginning with thiourea derivatives. It classifies anti-thyroid drugs and describes their sites of action and structure-activity relationships. Specific drug classes discussed include thiamides, iodine, radioactive iodine, and ionic inhibitors. Adverse effects, uses, and pharmacokinetics are described for individual drugs. Treatment of hyperthyroidism in pregnancy and thyroid storm are also covered.
Histamine is a chemical messenger that mediates allergic and inflammatory reactions. It is synthesized and stored in mast cells and basophils before being released in response to stimuli. Histamine binds to H1, H2, H3, and H4 receptors, with the H1 and H2 receptors being clinically relevant drug targets. Antihistamines are used to treat allergic conditions by blocking H1 receptors, and H2 receptor blockers inhibit gastric acid secretion. First-generation antihistamines have greater sedative and anticholinergic side effects than second-generation drugs due to interactions with other receptors.
This document discusses various sedative-hypnotic drugs that act on the central nervous system. It begins by distinguishing drugs that produce sedation from those that induce sleep. It then describes normal sleep cycles and the stages of sleep. The rest of the document details different classes of sedative-hypnotic drugs including benzodiazepines, barbiturates, antihistamines, and others. It provides information on their mechanisms of action, pharmacological effects, clinical uses, and important considerations regarding administration and withdrawal.
This document discusses haematinics, which are substances required for blood formation and used to treat anaemias. It focuses on iron, vitamin B12, and folic acid. Iron is essential for haemoglobin synthesis and is absorbed in the small intestine. Deficiencies can cause anaemia. Vitamin B12 and folic acid are also essential for red blood cell formation and preventing megaloblastic anaemia. The document provides details on the metabolism, deficiencies, and treatments of these important haematinics.
This document discusses hematinics, which are agents used to treat anemia and increase red blood cell counts or hemoglobin levels. It provides details on normal red blood cell production, the indications and adverse effects of oral and parenteral iron therapy, iron absorption and transport, and iron poisoning. It also covers folic acid sources and roles, causes of folate deficiency, and indications for folic acid supplementation. Finally, it discusses vitamin B12 structure and sources, pharmacokinetics, and nutritional deficiency.
The document discusses opium and its derivatives that are used as pain medications. It begins by explaining that opium is obtained from the poppy plant and describes the basic process of pain signaling in the nervous system. It then focuses on opioids like morphine, codeine, heroin, and other synthetic opioids. It covers topics like how opioids work in the body by binding to opioid receptors, their uses as analgesics, side effects, dependence and withdrawal, important terminology, and interactions with other drugs.
This document discusses insulin and antidiabetic drugs. It begins by describing the pancreatic axis and role of insulin and glucagon in maintaining glucose homeostasis. It then defines diabetes mellitus and describes the main types, Type 1 and Type 2 diabetes. It discusses treatment approaches for both types, including lifestyle changes and various drug classes. The mechanisms and preparations of insulin are outlined in detail. Finally, it reviews common oral antidiabetic drugs like sulfonylureas, meglitinides, biguanides, thiazolidinediones, and alpha-glucosidase inhibitors.
Hematinics are substances used to treat and prevent anemia. Megaloblastic anemias are caused by vitamin B12 or folate deficiencies and are characterized by large, abnormal red blood cells. Vitamin B12 is essential for two metabolic reactions and acts as a coenzyme. It is absorbed in the ileum with intrinsic factor and stored in the liver. Deficiencies can be detected using the Schilling test which evaluates vitamin B12 absorption. Treatment involves cyanocobalamin injections or oral methylcobalamin supplements.
This document provides information about anti-psychotic drugs. It discusses psychosis and its symptoms like hallucinations and delusions. Schizophrenia is described as the most common psychotic disorder. First and second generation (atypical) anti-psychotics are outlined, including their mechanisms of action primarily involving dopamine receptor blockade. Advantages of atypicals include ability to treat negative symptoms with fewer side effects like extrapyramidal symptoms. Common atypical drugs discussed are clozapine, olanzapine, risperidone, and quetiapine.
Cephalosporins are a class of beta-lactam antibiotics that inhibit bacterial cell wall synthesis. They include first, second, third, fourth, and fifth generation drugs with varying spectra of coverage. They have concentration-dependent bactericidal activity and are excreted renally. Common side effects include diarrhea, rash, and nephrotoxicity. Vancomycin and polymyxins have activity against gram-positive and highly resistant gram-negative bacteria, respectively. Tetracyclines have broad-spectrum coverage including MRSA and are bacteriostatic.
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
This document provides an overview of various drugs that affect the nervous system, organized by drug class. It discusses analgesics like opioids and NSAIDs; anesthetics like general gases and local anesthetics; anti-anxiety drugs like benzodiazepines and barbiturates; anti-seizure medications; CNS stimulants; antipsychotics; antidepressants; Parkinson's disease medications; and drugs that affect the autonomic nervous system, including cholinergic and anticholinergic drugs. Mechanisms of action, effects, and side effects are described for many of these drug classes and examples.
This document provides information on anti-anemic drugs, focusing on iron and vitamins B12 and folate. It defines different types of anemia based on red blood cell size and describes the manifestations and causes of megaloblastic anemia from deficiencies in B12 or folate. It outlines the dietary sources, absorption, transport, storage and excretion of iron as well as indications, preparations, dosages and adverse effects of oral and parenteral iron therapy for iron deficiency anemia. The roles and therapeutic uses of vitamins B12, folate and erythropoietin in various clinical conditions are also summarized.
Thyroid hormones are essential for normal development and metabolic homeostasis. Their synthesis involves iodine uptake, oxidation and coupling reactions catalyzed by thyroid peroxidase. T4 and T3 are stored and released from the thyroid gland under TSH influence. Levothyroxine is the preferred treatment for hypothyroidism as it has a longer half-life. Antithyroid drugs like methimazole and propylthiouracil inhibit thyroid peroxidase to treat hyperthyroidism. Radioactive iodine is also used which is taken up and destroys the thyroid gland. Symptomatic treatments include beta blockers.
The document summarizes key information about the thyroid gland, including its location, hormones produced, and synthesis of thyroid hormones. It describes the transport and iodination of tyrosine in the gland and the formation of T3 and T4. It also discusses the transport and relationship of T3 and T4, diseases of the thyroid gland like hyperthyroidism and hypothyroidism, and treatments including synthetic levothyroxine, radioactive iodine, antithyroid drugs, iodides, and management of thyroid storm.
This document provides an overview of opioids including their pharmacology, mechanisms of action, classifications, and clinical uses. It discusses how opioids bind to receptors in the central and peripheral nervous systems to produce analgesic and other effects. Opioids are classified based on their receptor activities and include pure agonists, partial agonists, mixed agonist-antagonists, and pure antagonists. The document reviews the central and peripheral effects of opioids as well as their indications, contraindications, and interactions. It also discusses opioid tolerance, dependence, overdose, and withdrawal.
Summary of thyroid and antithyroid drugs
-Introduction
-Synthesis
-Pharmacological Action
-Mechanism of action
-Drugs in Hypothyroidism
-Thyroid Inhibitors
-Drugs in Hyperthyroidism
This ppt discusses pharmacological actions, toxic effects and clinical applications of corticosteroids. It also mentions precations to be taken while using steroids
This document summarizes different types of central nervous system stimulants and cognition enhancers. It discusses convulsants, analeptics, psychostimulants like amphetamines and caffeine. It also covers what cognition is, types of dementia like Alzheimer's disease, and cognition enhancers like cholinergic activators like donepezil and rivastigmine, as well as memantine and Ginkgo biloba. The document provides information on their mechanisms of action and therapeutic uses.
This document discusses various antimycobacterial drugs used to treat tuberculosis and leprosy. It describes the mechanisms of action, development of resistance, and importance of drug combinations for isoniazid, rifampin, ethambutol, pyrazinamide, streptomycin, fluoroquinolones, linezolid, bedaquiline, and dapsone. Resistance develops rapidly if these drugs are used alone rather than in combination regimens.
Methimazole and propylthiouracil are the major drugs used to treat thyrotoxicosis. Methimazole is more potent and can be given once daily, while propylthiouracil is dosed more frequently. Both drugs inhibit thyroid hormone production and propylthiouracil also blocks peripheral conversion of T4 to T3. Iodide salts like Lugol's solution rapidly reduce hormone synthesis and release within a week. Radioactive iodine is used to ablate the thyroid gland and provide long-term control of Graves' disease, with effects seen over months. Propranolol provides symptomatic relief by blocking sympathetic overactivity in thyrotoxicosis.
This document discusses anti-thyroid drugs used to treat hyperthyroidism. It covers the history of anti-thyroid drug development beginning with thiourea derivatives. It classifies anti-thyroid drugs and describes their sites of action and structure-activity relationships. Specific drug classes discussed include thiamides, iodine, radioactive iodine, and ionic inhibitors. Adverse effects, uses, and pharmacokinetics are described for individual drugs. Treatment of hyperthyroidism in pregnancy and thyroid storm are also covered.
Histamine is a chemical messenger that mediates allergic and inflammatory reactions. It is synthesized and stored in mast cells and basophils before being released in response to stimuli. Histamine binds to H1, H2, H3, and H4 receptors, with the H1 and H2 receptors being clinically relevant drug targets. Antihistamines are used to treat allergic conditions by blocking H1 receptors, and H2 receptor blockers inhibit gastric acid secretion. First-generation antihistamines have greater sedative and anticholinergic side effects than second-generation drugs due to interactions with other receptors.
This document discusses various sedative-hypnotic drugs that act on the central nervous system. It begins by distinguishing drugs that produce sedation from those that induce sleep. It then describes normal sleep cycles and the stages of sleep. The rest of the document details different classes of sedative-hypnotic drugs including benzodiazepines, barbiturates, antihistamines, and others. It provides information on their mechanisms of action, pharmacological effects, clinical uses, and important considerations regarding administration and withdrawal.
This document discusses haematinics, which are substances required for blood formation and used to treat anaemias. It focuses on iron, vitamin B12, and folic acid. Iron is essential for haemoglobin synthesis and is absorbed in the small intestine. Deficiencies can cause anaemia. Vitamin B12 and folic acid are also essential for red blood cell formation and preventing megaloblastic anaemia. The document provides details on the metabolism, deficiencies, and treatments of these important haematinics.
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The document discusses opium and its derivatives that are used as pain medications. It begins by explaining that opium is obtained from the poppy plant and describes the basic process of pain signaling in the nervous system. It then focuses on opioids like morphine, codeine, heroin, and other synthetic opioids. It covers topics like how opioids work in the body by binding to opioid receptors, their uses as analgesics, side effects, dependence and withdrawal, important terminology, and interactions with other drugs.
This document discusses insulin and antidiabetic drugs. It begins by describing the pancreatic axis and role of insulin and glucagon in maintaining glucose homeostasis. It then defines diabetes mellitus and describes the main types, Type 1 and Type 2 diabetes. It discusses treatment approaches for both types, including lifestyle changes and various drug classes. The mechanisms and preparations of insulin are outlined in detail. Finally, it reviews common oral antidiabetic drugs like sulfonylureas, meglitinides, biguanides, thiazolidinediones, and alpha-glucosidase inhibitors.
Hematinics are substances used to treat and prevent anemia. Megaloblastic anemias are caused by vitamin B12 or folate deficiencies and are characterized by large, abnormal red blood cells. Vitamin B12 is essential for two metabolic reactions and acts as a coenzyme. It is absorbed in the ileum with intrinsic factor and stored in the liver. Deficiencies can be detected using the Schilling test which evaluates vitamin B12 absorption. Treatment involves cyanocobalamin injections or oral methylcobalamin supplements.
This document provides information about anti-psychotic drugs. It discusses psychosis and its symptoms like hallucinations and delusions. Schizophrenia is described as the most common psychotic disorder. First and second generation (atypical) anti-psychotics are outlined, including their mechanisms of action primarily involving dopamine receptor blockade. Advantages of atypicals include ability to treat negative symptoms with fewer side effects like extrapyramidal symptoms. Common atypical drugs discussed are clozapine, olanzapine, risperidone, and quetiapine.
Cephalosporins are a class of beta-lactam antibiotics that inhibit bacterial cell wall synthesis. They include first, second, third, fourth, and fifth generation drugs with varying spectra of coverage. They have concentration-dependent bactericidal activity and are excreted renally. Common side effects include diarrhea, rash, and nephrotoxicity. Vancomycin and polymyxins have activity against gram-positive and highly resistant gram-negative bacteria, respectively. Tetracyclines have broad-spectrum coverage including MRSA and are bacteriostatic.
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
This document provides an overview of various drugs that affect the nervous system, organized by drug class. It discusses analgesics like opioids and NSAIDs; anesthetics like general gases and local anesthetics; anti-anxiety drugs like benzodiazepines and barbiturates; anti-seizure medications; CNS stimulants; antipsychotics; antidepressants; Parkinson's disease medications; and drugs that affect the autonomic nervous system, including cholinergic and anticholinergic drugs. Mechanisms of action, effects, and side effects are described for many of these drug classes and examples.
This document provides information on anti-anemic drugs, focusing on iron and vitamins B12 and folate. It defines different types of anemia based on red blood cell size and describes the manifestations and causes of megaloblastic anemia from deficiencies in B12 or folate. It outlines the dietary sources, absorption, transport, storage and excretion of iron as well as indications, preparations, dosages and adverse effects of oral and parenteral iron therapy for iron deficiency anemia. The roles and therapeutic uses of vitamins B12, folate and erythropoietin in various clinical conditions are also summarized.
Thyroid hormones are essential for normal development and metabolic homeostasis. Their synthesis involves iodine uptake, oxidation and coupling reactions catalyzed by thyroid peroxidase. T4 and T3 are stored and released from the thyroid gland under TSH influence. Levothyroxine is the preferred treatment for hypothyroidism as it has a longer half-life. Antithyroid drugs like methimazole and propylthiouracil inhibit thyroid peroxidase to treat hyperthyroidism. Radioactive iodine is also used which is taken up and destroys the thyroid gland. Symptomatic treatments include beta blockers.
The document summarizes key information about the thyroid gland, including its location, hormones produced, and synthesis of thyroid hormones. It describes the transport and iodination of tyrosine in the gland and the formation of T3 and T4. It also discusses the transport and relationship of T3 and T4, diseases of the thyroid gland like hyperthyroidism and hypothyroidism, and treatments including synthetic levothyroxine, radioactive iodine, antithyroid drugs, iodides, and management of thyroid storm.
This document discusses thyroid hormones, their functions, and drugs used to treat thyroid disorders. It provides details on:
1. The metabolic functions of thyroid hormones including increasing glucose and fat metabolism and basal metabolic rate.
2. Drugs used to treat hyperthyroidism like thioamides which inhibit thyroid hormone synthesis, iodides which inhibit hormone release, beta blockers, and radioactive iodine.
3. Drugs used for hypothyroidism replacement like synthetic levothyroxine which has high stability and allows for laboratory monitoring of serum levels.
4. Potential adverse effects and considerations for use of these drugs during pregnancy and nursing.
Thyroid hormones regulate metabolism and are essential for growth, development, and maintaining body temperature and energy levels. Levothyroxine and liothyronine are used to treat hypothyroidism by replacing deficient hormones, while thioamides, iodides, radioactive iodine, and beta blockers are used to treat hyperthyroidism by inhibiting hormone synthesis or action. Specifically, thioamides inhibit thyroid peroxidase and deiodination of hormones, while iodides suppress hormone synthesis and release; radioactive iodine damages the thyroid through beta particle emission; and beta blockers alleviate hyperthyroidism symptoms.
The document discusses the thyroid gland and thyroid hormones. It covers the normal circulating thyroid hormones, which are thyroxine (T4), triiodothyronine (T3), and reverse T3 (rT3). It also discusses the metabolism and mechanisms of action of thyroid hormones. Additionally, it provides details on the treatment of hyperthyroidism and hypothyroidism, including the drugs used to treat hyperthyroidism such as propylthiouracil, methimazole, potassium iodide, radioactive iodine, and beta blockers.
THE THYROID GLAND AND DRUGS USED IN THYROID.pdfHarunMohamed7
The document discusses thyroid hormones, thyroid abnormalities, and associated drugs. It covers:
1. Thyroid hormones T4 and T3, their functions, and regulation by TSH.
2. Hyperthyroidism causes like Graves' disease and their symptoms. Diagnosis involves T4, TSH tests.
3. Drugs for hyperthyroidism - Radioactive iodine destroys thyroid tissue. Thioamides like methimazole and propylthiouracil block hormone synthesis. Beta blockers reduce symptoms.
Antithyroid agents are hormone antagonists that inhibit thyroid hormone synthesis. Common antithyroid drugs include propylthiouracil, methimazole, and carbimazole. These drugs act by inhibiting the thyroid peroxidase enzyme, blocking the production of thyroid hormones. Antithyroid drugs are quickly absorbed orally and distributed throughout the body. They reduce thyroid hormone levels by 30-40% in treated patients but can cause side effects like hypothyroidism or agranulocytosis with long-term use.
The thyroid gland produces thyroid hormones triiodothyronine (T3) and thyroxine (T4) which increase metabolism. Too little hormone causes hypothyroidism with symptoms like bradycardia and weight gain, while too much causes hyperthyroidism with symptoms like tachycardia and weight loss. Hypothyroidism is treated with levothyroxine replacement therapy. Hyperthyroidism treatments include anti-thyroid medications to block hormone synthesis, radioactive iodine ablation of the thyroid gland, or surgery.
Thyroid gland - disordesa , symptomes and treatment Areej Abu Hanieh
The thyroid gland produces thyroid hormones that regulate metabolism. Hypothyroidism occurs when hormone levels are too low, causing slowed functions, while hyperthyroidism is when levels are too high, speeding functions up. Thyroid disorders are treated by replacing hormones (levothyroxine) or inhibiting hormone production/release (propylthiouracil, methimazole, iodide). Precautions must be taken with medications due to potential side effects on heart, liver and other organs.
Thyroid Hormone Disorders lecture :-
-Thyroid gland & Thyroid hormones.
-How does Thyroid hormone is formed ?
-Regulation of secretion.
-Hypothyroidism.
-Treatment of hypothyroidism .
-Administration of Levothyroxin.
-Levothyroxin interactions.
-Levothyroxin cautions.
-Hyperthyroidism .
-Symptoms & treatment of Hyperthyroidism.
-Removal of part or all of the thyroid.
-Blockade of hormone release .
-Inhibition of thyroid hormone synthesis.
-Mechanism of action of antithyroid.
-Administration of antithyroid drugs.
-Antithyroid drugs interactions.
-Antithyroid drugs cautions.
-General notes.
-Practical notes on levothyroxin.
-Practical notes on antithroid drugs.
-Rapid review.
-Test yourself.
The document discusses the physiology of the thyroid gland and thyroid hormones such as T3 and T4. It describes how the pituitary-thyroid axis controls thyroid hormone production and discusses different types of thyroid enlargement including simple goiter, diffuse hyperplastic goiter, toxic nodular goiter, and Graves' disease. The principles and advantages/disadvantages of different treatment approaches for hyperthyroidism are provided, including anti-thyroid drugs, surgery, and radioiodine therapy. Potential postoperative complications of thyroid surgery are also listed.
1. Antithyroid drugs like methimazole, carbimazole, and propylthiouracil are used to treat hyperthyroidism by inhibiting thyroid hormone synthesis. Iodine and iodide salts can also be used to inhibit hormone release and synthesis.
2. Radioactive iodine is commonly used to destroy thyroid tissue through beta particle emission, providing a permanent treatment for hyperthyroidism.
3. Beta-blockers like propranolol are used to rapidly alleviate sympathetic overactivity symptoms of hyperthyroidism while other treatments take effect. They also reduce peripheral thyroid hormone conversion.
The document discusses thyroid hormones and thyroid inhibitors. It describes the synthesis and actions of thyroid hormones T3 and T4. It then outlines different classes of thyroid inhibitors including antithyroid drugs, iodine/iodides, and radioactive iodine. Antithyroid drugs like methimazole and propylthiouracil inhibit hormone synthesis while iodine/iodides inhibit hormone release. Radioactive iodine is used therapeutically to destroy the thyroid gland in conditions like Graves' disease.
The document discusses thyroid hormones and thyroid inhibitors. It describes the synthesis and actions of thyroid hormones T3 and T4. It then outlines different classes of thyroid inhibitors including antithyroid drugs, iodine/iodides, and radioactive iodine. Antithyroid drugs like methimazole and propylthiouracil inhibit hormone synthesis while iodine/iodides inhibit hormone release. Radioactive iodine is used therapeutically to destroy the thyroid gland in conditions like Graves' disease.
This document provides an overview of drugs used to treat hyperthyroidism. It begins by outlining the learning objectives which are to describe drug classes, mechanisms of action, clinical uses, and adverse effects for treating hyperthyroidism. It then discusses the thyroid gland and regulation before explaining the various causes of hyperthyroidism and thyrotoxicosis. The main drug classes for treatment include thioamides, iodides, radioactive iodine, and beta blockers. Specific drugs like propylthiouracil, methimazole, and radioactive iodine are examined in depth regarding their mechanisms of action, pharmacokinetics, uses, and adverse effects. Special considerations for treatment during pregnancy and for thyroid
This document discusses how various drugs can interfere with thyroid function. It begins by defining primary and central hypothyroidism. It then explains how drugs can disrupt thyroid hormone synthesis, alter thyroid autoimmunity, and affect follicular cell activity. Specific drugs like amiodarone, lithium, and cytokines are highlighted. The document also discusses how drugs can interfere with T4 metabolism and conversion to T3. It provides examples of medications that can alter thyroid function tests or T4 binding. Finally, it emphasizes the importance of recognizing drug interactions to correctly interpret thyroid tests and treat patients.
This document discusses thyroid disorders, including the physiology of thyroid hormone production and regulation. It describes the causes, signs and symptoms, and treatment approaches for hyperthyroidism (thyrotoxicosis). The major causes of hyperthyroidism include Graves' disease, toxic multinodular goiter, and subacute thyroiditis. Treatment options discussed include antithyroid medications, beta-blockers, iodine, surgery, and radioactive iodine. The goal of treatment is to normalize thyroid hormone levels, minimize symptoms, and individualize therapy based on the patient and disease characteristics.
Thyroid hormones like triiodothyroxine (T3) and thyroxine (T4) are synthesized in the thyroid gland and regulated by thyroid stimulating hormone (TSH). Anti-thyroid drugs work by inhibiting thyroid hormone synthesis, iodine trapping, or hormone release. Common anti-thyroid drugs include propylthiouracil, methimazole, carbimazole, iodine, and radioactive iodine. These drugs are used to treat hyperthyroidism and can control overactive thyroid function by various mechanisms of action like inhibiting thyroid peroxidase or iodide uptake into the thyroid gland.
This document discusses the physiology, drugs, and management of hyperthyroidism and hypothyroidism. It covers the thyroid hormones T3 and T4, their biosynthesis and metabolism. It describes drug therapies for hyperthyroidism including thioamides, iodides, radioactive iodine, and anion inhibitors. It discusses the management of Graves' disease, subacute thyroiditis, thyroid storm and hyperthyroidism in pregnancy. It also covers therapies for hypothyroidism including levothyroxine and liothyronine, management of myxedema coma, and subclinical hypothyroidism.
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This document provides an overview of pharmacology of laxatives and anti-diarrheal drugs. It describes various classes of laxatives including bulk forming, stool softeners, stimulant purgatives, and osmotic purgatives. Specific laxatives discussed include bran, psyllium, docusate, bisacodyl, senna, magnesium and sodium salts. It also covers anti-diarrheal drugs, describing management of diarrhea, oral rehydration therapy, zinc supplementation, antimicrobial therapy, probiotics, and non-specific drugs like racecadrotil, loperamide. The document provides details on mechanisms of action, indications, and side effects of various laxatives
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This document provides an overview of basic principles of drugs affecting the central nervous system (CNS). It discusses the cellular organization of the brain including neurons and supporting cells. It describes the blood-brain barrier and how it impacts drug delivery to the CNS. It also outlines neuronal excitability and ion channels, processes involved in synaptic signaling, and various central neurotransmitters including amino acids, acetylcholine, monoamines, peptides, purines, and neuromodulatory lipids.
This document discusses various classes of cell wall inhibiting antibiotics, including beta-lactams such as penicillins, cephalosporins, carbapenems, and monobactams. It describes their mechanisms of action, spectra of activity, uses, and side effects. Specifically, it provides details on the discovery and uses of penicillin, outlines various penicillin derivatives including natural, acid resistant, and extended spectrum versions, and discusses resistance and pharmacokinetics.
This document discusses pharmacodynamic principles including what drug targets are and how drugs act on the body. It describes the main drug targets as enzymes, ion channels, transporters, and receptors. It explains how drugs can increase or decrease enzymatic activity and block or modulate ion channels. Transporters are also discussed. The document outlines how ligands can be agonists, antagonists, partial agonists, or inverse agonists when interacting with receptors. It further discusses concepts such as dose-response curves, potency, efficacy, therapeutic index, synergism, and antagonism.
The document discusses drug metabolism and biotransformation. It notes that the liver is the primary site of biotransformation, which converts non-polar compounds to polar ones for excretion. Biotransformation can inactivate drugs, produce active metabolites, or activate inactive prodrugs. It occurs in two phases: phase I involves oxidation, reduction, and hydrolysis; phase II involves conjugation. Cytochrome P450 enzymes, especially CYP3A4, are responsible for many phase I reactions. Drug metabolism determines a drug's half-life, clearance, and affects dosing. Therapeutic drug monitoring measures drug concentrations to optimize dosing for drugs with a narrow therapeutic index.
This document discusses adverse drug effects including classification, severity, and types such as side effects, toxicity, idiosyncrasy, allergy, dependence, withdrawal, teratogenicity, mutagenicity, carcinogenicity, and drug-induced diseases. It classifies adverse drug reactions into types A through E based on factors like pharmacological action and duration of use. It also defines terms like side effects, toxicity, idiosyncrasy, allergy, dependence, withdrawal reactions and discusses various organ-specific drug induced diseases.
This document discusses essential medicines, rational drug use, and fixed dose combinations (FDCs). It defines essential medicines as those that meet priority healthcare needs based on efficacy, safety, and cost-effectiveness. Each country publishes its own essential medicines list, which is updated every two years by the WHO. Rational drug use means using the right drug for the right indication in the right manner at the lowest cost. Irrational drug use can lead to adverse effects and increased costs. FDCs combine drugs to increase effectiveness, reduce side effects, and improve compliance, but can also increase costs and side effects if not properly formulated.
This document discusses various routes of drug administration including local and systemic routes. Local routes deliver drugs directly to the site of action and include topical application to the skin, eyes, ears etc. Deeper local routes use injections into joints, the spine or arteries. Systemic routes administer drugs through the entire body and include oral, sublingual, rectal, transdermal, inhalation, nasal and parenteral routes like subcutaneous, intramuscular, intravenous and intradermal injections. Each route has advantages and disadvantages related to onset of action, side effects, patient convenience and drug properties.
Process of new drug development & approvalDr. Marya Ahsan
The development of a new drug is a long, complex, and costly process taking at least 10 years and $500-1000 million. It involves pre-clinical studies in animals, followed by clinical trials in four phases with humans. Phase I establishes safety, Phase II establishes efficacy and side effects, Phase III tests efficacy in larger groups, and Phase IV monitors long-term safety after approval. After successful clinical trials, approval is sought from regulatory authorities like the FDA by submitting a New Drug Application before marketing.
Pharmacological management of irritable bowel diseaseDr. Marya Ahsan
A 40-year-old nurse complains of gastrointestinal issues including nausea, abdominal pain, bloating, constipation, and left lower quadrant pain with bowel movements for the past 4 years. Examinations and tests were negative. Her symptoms are consistent with irritable bowel syndrome (IBS). IBS is diagnosed based on recurrent abdominal pain associated with changes in stool frequency or form. It can be caused by issues with intestinal motility, perception, or microbiota. Treatment focuses on controlling symptoms and may include diet, lifestyle changes, psychotherapy, and various drug therapies depending on the IBS subtype.
This document provides an overview of pharmacokinetic principles related to absorption and distribution of drugs. It defines key terms like pharmacokinetics, bioavailability, and apparent volume of distribution. The factors that determine absorption like pH, blood flow, surface area, and P-glycoprotein expression are described. Distribution is affected by regional blood flow, plasma and tissue protein binding, and lipid solubility. Apparent volume of distribution indicates what volume the drug appears to be distributed in based on plasma concentration.
This document provides an overview of antihypertensive agents (blood pressure medications). It discusses the types and classes of antihypertensives, including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and alpha blockers. It describes the mechanisms of action, therapeutic uses, and potential side effects of each class. The document is intended to teach healthcare providers about selecting and utilizing different antihypertensive drugs to treat hypertension.
Antiarrhythmic drugs are classified according to their mechanism of action and effects on cardiac electrophysiology. Class I drugs block sodium channels, while Class II are beta blockers, Class III block potassium channels, and Class IV block calcium channels. The main classes used are Class Ia (quinidine, procainamide), Class Ic (flecainide, propafenone), Class III (amiodarone, sotalol), and calcium channel blockers (verapamil, diltiazem). Each drug has therapeutic uses for specific arrhythmias as well as adverse effects that must be considered.
This document provides information on antirheumatic drugs used to treat rheumatoid arthritis (RA). It describes the pathophysiology of RA involving inflammatory cytokines like TNF, IL-6, IL-1. NSAIDs provide initial symptomatic relief but DMARDs like methotrexate, hydroxychloroquine, leflunomide, and sulfasalazine suppress disease progression. Biological DMARDs targeting TNF or non-TNF pathways like abatacept are used when traditional DMARDs are ineffective. The goals of treatment are to reduce symptoms, prevent joint damage, and maintain function. Adverse effects of various drugs are also outlined.
This document discusses antipsychotic drugs, including their classification, mechanisms of action, uses, and side effects. It describes how antipsychotics are primarily used to treat schizophrenia and other psychotic disorders by blocking dopamine receptors. It distinguishes typical/first generation antipsychotics that are more likely to cause extrapyramidal side effects from atypical/second generation antipsychotics that have a lower risk of these motor side effects but a higher risk of metabolic adverse effects like weight gain and diabetes. The document provides details on various antipsychotics and their mechanisms, pharmacokinetics, therapeutic uses, and important adverse effects and cautions.
Migraine is a severe headache accompanied by nausea, vomiting, light and sound sensitivity. It is caused by vasodilation of cranial blood vessels. Treatment includes acute medications like triptans and ergot alkaloids to constrict vessels and relieve symptoms. Prophylactic drugs like beta-blockers, antidepressants, and anticonvulsants are used to reduce migraine frequency. Triptans are the most effective acute treatment but can have cardiovascular side effects, while ergot alkaloids are less tolerated but more specific vasoconstrictors. Prophylaxis is recommended for those with frequent or severe migraines.
Pharmacological agents in bronchial asthma and copdDr. Marya Ahsan
This document provides an overview of pharmacological agents used to treat bronchial asthma and chronic obstructive pulmonary disease (COPD). It discusses the classification, mechanisms of action, and side effects of various drugs including bronchodilators, corticosteroids, leukotriene modifiers, mast cell stabilizers, methylxanthines, monoclonal antibodies, and other agents. Treatment guidelines are also presented, outlining a stepwise approach for asthma management and algorithms for acute asthma exacerbations.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
2. Thyroid hormones
• Thyroid hormone is essential for normal
development, especially of the CNS.
• In the adult, thyroid hormone maintains
metabolic homeostasis and influences the
functions of virtually all organ systems
• Serum concentrations of thyroid hormones are
precisely regulated by the pituitary hormone
TSH in a negative-feedback system
4. Synthesis & Release
• Iodide uptake:
Iodine is actively taken up by the follicular cells under the influence of TSH
• Oxidation and iodination of tyrosine
Iodide is oxidised to iodinium ion (I+) by thyroid peroxidase.
I+ combines with tyrosine (on surface of thyroglobulin) to form MIT and DIT
• Coupling reaction
MIT + DIT = T3
DIT + DIT = T4
These reactions are catalysed by thyroid peroxidase
5. Synthesis & Release
• Storage & release
T3 and T4 formed on surface of thyroglobulin is transported to inner side of
follicle for storage as thyroid colloid
They are released by proteolysis and exocytosis under influence of TSH
• Peripheral conversion of T4 to T3
More T4 is released than T3 (4:1)
Circulating T4 is converted to T3 by iodothyronine 5’-deiodinase
7. Transport, Metabolism & Excretion
• T3 is 5 times more active than T4
• t ½ of T4 = 6-7 days t ½ of T3 = 1-2 days
• Thyroid hormones are bound to:
Thyroxine binding globulin (TBG)
Thyroxine binding prealbumin
Albumin
• Inactivation occurs by deiodination , decarboxylation and conjugation
mainly in the liver
9. Drugs for hypothyroidism
• Levothyroxine (T4)
• Liothyronine (T3)
• Liotrix (T4/T3 combination)
Levothyroxine (T4) is preferred over T3
(liothyronine) or T3/T4 combination
products (liotrix) for the treatment of
hypothyroidism.
It is better tolerated than T3 preparations
and has a longer half-life
10. Levothyroxine (T4)
• Well absorbed from the stomach and
small intestine (80% absorption)
• Absorption increases on taking on an
empty stomach
• Available as tablets and liquid-filled
capsules for oral administration and as a
lyophilized powder for injection
• Levothyroxine is dosed once daily, and
steady state is achieved in 6 to 8 weeks.
• Toxicity is directly related to T4 levels and
manifests as nervousness, palpitations
and tachycardia, heat intolerance, and
unexplained weight loss.
11. Liothyronine (T3)
• Liothyronine is available as tablets
and an injectable form.
• Liothyronine absorption is nearly
100%, with peak serum levels 2–4
h following oral ingestion.
• Liothyronine may be used when a
more rapid onset of action is
desired, such as myxedema coma
• Liothyronine is less desirable for
chronic replacement therapy:
More-frequent dosing (t1/2 = 18–24
h)
Higher cost
Risk of arrhythmia
12. Uses of thyroxine
Mainly used as a supplement in hypothyroidism in:
• Children – Cretinism
• Adult hypothyroidism
• Myxoedema
• Simple or non-toxic goitre
• Myxoedema coma
• Subclinical hypothyroidism
• Nodular goitre
• Papillary carcinoma of thyroid
13. Drugs for hyperthyroidism: Thyroid Inhibitors
I. Hormone Synthesis Inhibitors
(Antithyroid drugs)
Propyltiouracil, Carbimazole,
Methimazole
II. Hormone Release Inhibitors
Iodides (Lugol’s iodine, Sodium
iodide, potassium iodide)
III. Destruction of thyroid tissue
Radioactive iodine
IV. Ionic inhibitors
Thiocynates, perchlorates, nitrates
14. Antithyroid drugs
• Inhibits the synthesis of thyroid hormones.
• They inhibit the enzyme thyroid peroxidase.
Thus inhibit:
Oxidation & Iodination of tyrosine residue
Coupling reaction
• Propylthiuracil also inhibits the peripheral conversion of T4 to T3
15. Pharmacokinetics of antithyroid drugs
• Rapidly absorbed orally
• Readily cross placenta and enter
milk
(so, they should be avoided in
pregnancy, except propylthiuracil
because it crosses less readily)
• The drugs are excreted in urine as
inactive conjugated form
16. Uses of antithyroid drugs
• To achieve spontaneous remission and control in:
Grave’s disease
Toxic nodular goitre
• Used prior to radioactive iodine
• Pre-operative control of hyperthyroidism
• Thyroid storm
(PTU is preferred because it can
inhibit peripheral conversion)
Methimazole is
preferred over PTU
because of
once daily dosing
(longer t ½ )
Lower incidence of
adverse effects
[Except in pregnancy: PTU
is preferred]
17. Adverse effects of antithyroid drugs
Adverse effects:
Skin rashes (most
common)
Nausea, headache
Pain & stiffness in the
joints
Loss or greying of
hair
PTU is associated
with hepatotoxicity
and agranulocytosis
(rare)
Patients should be instructed to
immediately report the
development of sore throat or fever
and should discontinue their
antithyroid drug and
obtain a granulocyte count
18. Iodine and iodides
• It is the fastest acting agent
• Inhibits the release of thyroid hormones
• The gland shrinks in size and becomes firm and less vascular
The maximal effect occurs after 10–15 days of continuous therapy.
On continuous treatment there is loss of therapeutic effect!!
(thyroid constipation and thyroid escape)
Iodide is the oldest
remedy for disorders of
the thyroid gland. In
high
concentration, iodide
limits its own transport
and acutely and
transiently inhibits the
synthesis of thyroid
hormones.
(the Wolff-Chaikoff
effect)
19. Iodides
Uses:
• Pre-operative preparation before subtotal thyroidectomy
……given 7-10 days pre-operatively to shrink the gland, make it firm and
less vascular
• Thyroid storm (in conjunction with antithyroid drugs and propranolol)
(Lugol solution) consists of 5% iodine
and 10% potassium iodide
Typical doses include 16–36 mg (2–6 drops) of
Lugol solution
Adverse effect:
Hypersensitivity to iodine: angioedema and laryngeal oedema
Chronic intoxication causes ‘iodism’
20. Radioactive iodine
I-127: stable isotope
I-131, I-123, I-125: radioactive isotopes
I-131: t ½ = 8 days
• Commonly used iodine isotope for therapeutic and diagnostic purposes
• Emits γ and β particles.
• Taken as sodium salt by oral route
21. Radioactive iodine
• The radioactive iodine is actively taken up by the follicular cells
• It emits β particles which destroys thyroid parenchyma (up to 0.5-2 mm)
• There is negligible damage to adjacent tissue
Uses:
Grave’s disease
In patients who cannot undergo thyroidectomy (elderly patients)
Patients with existing heart disease
Toxic nodular goitre
22. Radioactive iodine
Advantages
• Risk of complications of surgery is
avoided
No Surgical scar
No injury to recurrent laryngeal nerve
No damage to parathyroid gland
• Cure is permanent
Disadvantages
• Permanent hypothyroidism
• Delayed onset
• Can not be used during pregnancy
• Avoided in young patients
23. Adjuvant therapy: Symptomatic treatment
• β- blockers (Propranolol):
Antagonize the sympathetic/adrenergic effects of thyrotoxicosis—
Reduce the tachycardia, tremor, and stare—and relieve palpitations,
anxiety, and tension.
24. Thyroid storm
Thyroid storm is an uncommon but life-threatening
complication of thyrotoxicosis
in which a severe form of the disease is usually
precipitated by an intercurrent medical problem
Treatment:
Supportive measures
Antithyroid drugs - PTU is preferred
(PTU impairs peripheral conversion of T4
→ T3)
Oral iodides
β -blockers
Treatment of the underlying
precipitating illness
26. Parathormone
• Parathyroid hormone (PTH) plays a key role in the regulation of calcium
and phosphate homeostasis and vitamin D metabolism
• When serum ionised calcium levels fall, PTH secretion rises
• Parathormone (PTH) acts on:
Skeleton increases osteoclastic bone resorption and bone formation
Renal tubules promotes reabsorption of calcium and reduce
reabsorption of phosphate
promotes the conversion of 25-hydroxyvitamin D to the active metabolite
enhances calcium absorption from the gut
27. • Primary hyperparathyroidism is caused by autonomous secretion of PTH,
usually by a single parathyroid adenoma
• Presents with hypercalcemia with a raised PTH level
• Reduced bone mineral density (osteopenia or osteoporosis): most
common skeletal manifestation hyperparathyroidism
Treatment of life-threatening hypercalcemia in primary
hyperparathyroidism:
IV fluids
Bisphosphonates
Calcitonin
Cinacalcet
Primary Hyperparathyroidism
28. Hypoparathyroidism
• The most common cause of hypoparathyroidism is damage to
the parathyroid glands (or their blood supply) during thyroid
surgery.
• Treatment:
Oral calcium salts
Vitamin D analogues
PTH analogues
29. Calcitonin
• Calcitonin lowers plasma Ca2+ and phosphate concentrations in patients
with hypercalcemia.
• Calcitonin causes direct inhibition of osteoclastic bone resorption
• Calcitonin is administered through subcutaneous injection or nasal spray.
Uses:
• Hypercalcemia
• Disorders of increased skeletal remodeling, such as Paget disease
30. Calcimimetics: Cinacalcet
• Calcimimetics are drugs that mimic the stimulatory effect of Ca2+
• They act on the Calcium-sensing receptor (CaSR) to inhibit PTH secretion
by the parathyroid glands.
• Cinacalcet is the first and only approved drug in the class currently
• Uses:
• Secondary hyperparathyroidism
• Hypercalcemia due to primary hyperparathyroidism or parathyroid
carcinoma (as an alternative treatment to surgery)
31. Bisphosphonates
• Bisphosphonates are analogues of pyrophosphate
MOA:
• Bisphosphonates act by direct inhibition of bone resorption
• Bisphosphonates concentrate at sites of active remodeling released in
the acid environment of the resorption lacunae induce apoptosis in
osteoclasts
33. Bisphosphonates
Oral bisphosphonates can cause heartburn, esophageal
irritation, or esophagitis!!
Take with a full glass of water at least 30 min before
breakfast, and don’t lie down…..Remain upright!
34. PTH analogues
Teriparatide: synthetic PTH analogue
Recombinant human parathormone
Abaloparatide: synthetic PTHrP
• These agents are peptides: given by subcutaneous injection
• Teriparatide and abaloparatide are the only agents currently available that
increase new bone formation.
• Uses:
Severe osteoporosis in patients at a high risk for fracture
Hypocalcemia in patients with hypoparathyroidism (when not controlled by
calcium and Vit D)
35. Calcium
• Calcium is used in the treatment of calcium deficiency states and as a
dietary supplement
• Calcium chloride
• Calcium gluconate
• Calcium carbonate
• Calcium acetate
For control of milder hypocalcemic
symptoms, oral medication suffices,
frequently in combination with vitamin D or
one of its active metabolites
Given intravenously in the
treatment of severe hypocalcemic
tetany.
36. Vitamin D
• Cholecalciferol (vitamin D3)
• Calcitriol (1,25-dihydroxycholecalciferol)
• Ergocalciferol (calciferol) is vitamin D2: used typically in doses of 50,000–
200,000 units/d in conjunction with calcium supplements
• Doxercalciferol (1α-hydroxyvitamin D2), a prodrug: Used for secondary
hyperparathyroidism
Analogues of calcitriol used for secondary hyperparathyroidism:
• Calcipotriene
• Paricalcitol
• Maxacalcitol
Suppress PTH secretion by the parathyroid glands but
have less or negligible hypercalcemic activity.
They are a safer and more effective means of
controlling secondary hyperparathyroidism
The conversion of T4 to T3 in the periphery is blocked by propythiouracil, high dose of propranolol and glucocorticoids
The ionic inhibitors are substances that interfere with the concentration of
iodide by the thyroid gland. These agents are anions that resemble iodide:
thiocyanate, perchlorate, and fluoroborate, all monovalent hydrated anions
of a size similar to that of iodide.
Lithium decreases secretion of T4 and T3, which can cause overt hypothyroidism
in some patients taking Li+ for the treatment of mania
The severity of symptoms of chronic intoxication with iodide (iodism) is related to the dose.
The symptoms start with an unpleasant brassy taste and burning in the mouth and throat as well as soreness of the teeth and gums. Increased salivation, coryza, sneezing, and irritation of the eyes with swelling of the eyelids commonly occur. Mild
Sodium iodide 131I is available as a solution or in capsules for oral administration.
Sodium iodide 123I is available for scanning procedures.
Supportive measures such as intravenous fluids, antipyretics, cooling blankets, and sedation
Prolonged exposure of bone to high levels of PTH is associated with increased osteoclastic activity and new bone formation, but the net effect is to cause bone loss with mobilisation of calcium into the extracellular fluid.
In contrast, pulsatile release of PTH causes net bone gain, an effect that is exploited therapeutically in the treatment of osteoporosis
The classic symptoms of primary hyperparathyroidism are
described by the adage ‘bones, stones and abdominal groans’,
but few patients present in this way nowadays and the disorder
is most often picked up as an incidental finding on biochemical
testing. About 50% of patients with primary hyperparathyroidism
are asymptomatic while others have non-specific symptoms
such as fatigue, depression and generalised aches and pains.
Some present with renal calculi
Hypertension is a
common feature of hyperparathyroidism
The four parathyroid glands lie behind the lobes of the thyroid