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.
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
Introduction.
Biosynthesis
Types of Thyroid diseases
Thyroid Drugs
Antithyroid Drugs
Mechanism of action
Structure
Adverse Drug Reactions and Uses.
Reference
Summary of thyroid and antithyroid drugs
-Introduction
-Synthesis
-Pharmacological Action
-Mechanism of action
-Drugs in Hypothyroidism
-Thyroid Inhibitors
-Drugs in Hyperthyroidism
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
Introduction.
Biosynthesis
Types of Thyroid diseases
Thyroid Drugs
Antithyroid Drugs
Mechanism of action
Structure
Adverse Drug Reactions and Uses.
Reference
Summary of thyroid and antithyroid drugs
-Introduction
-Synthesis
-Pharmacological Action
-Mechanism of action
-Drugs in Hypothyroidism
-Thyroid Inhibitors
-Drugs in Hyperthyroidism
Introduction to the endocrine system
Growth hormone: Mechanism of Action, secretion, regulation.
Prolactin
Sex hormones
Oral contraceptives
Corticosteroids
A power point presentation on thyroid hormones and thyroid inhibitors on subject of pharmacology suitable for reading by undergraduate medical students.
Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex of vertebrates, as well as the synthetic analogues of these hormones
In this PPTs you will get in depth information about insulin and the first class of oral hypoglycemic agents , Sulfonylurea.
useful for GPAT and Third Year B.Pharm students.
Introduction:
@ Thyroid releases T3 & T4
@ The ratio of T4 to T3 is 5:1, so most of the hormone released is
thyroxine
@ Most of the T3 in the blood is derived from thyroxine
@ T3 is three to four times more potent than T4
@ The affinity of the receptor site for T3 is about ten times higher than that for T4
Introduction to the endocrine system
Growth hormone: Mechanism of Action, secretion, regulation.
Prolactin
Sex hormones
Oral contraceptives
Corticosteroids
A power point presentation on thyroid hormones and thyroid inhibitors on subject of pharmacology suitable for reading by undergraduate medical students.
Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex of vertebrates, as well as the synthetic analogues of these hormones
In this PPTs you will get in depth information about insulin and the first class of oral hypoglycemic agents , Sulfonylurea.
useful for GPAT and Third Year B.Pharm students.
Introduction:
@ Thyroid releases T3 & T4
@ The ratio of T4 to T3 is 5:1, so most of the hormone released is
thyroxine
@ Most of the T3 in the blood is derived from thyroxine
@ T3 is three to four times more potent than T4
@ The affinity of the receptor site for T3 is about ten times higher than that for T4
This lecture includes classification of antithyroid drugs, mechanism of action, adverse effect, therapeutic uses and advantage and disadvantages of them
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
3. • Metabolic function –
– CHO metabolism:
• glycogenolysis
• Increase gluconeogensis
• glucose absorption from GIT
• Enhance glycolysis – rapid uptake of glucose by the cell.
– Net result - blood glucose level
– On protein metabolism: protein catabolism
– On fat metabolism:
• mobilization of fat,
• oxidation of FA FFA
– On BMR: BMR
Pharmacological actions of thyroid hormone
4. • Growth : growth
• On GIT:
– appetite & food intake.
– rate of secretion of digestive juice.
– motility of GIT diarrhea often result in hyperthyroidism
• On CVS:
• Enhance tissue sensitivity to catecholamines
• cardiac output
• On nervous system:
• excitable effect.
• Has role on development of brain in fetal & 1st few weeks of
postnatal life
• Muscle weakness due to protein catabolism
6. 6
●Synthesis Of Thyroid hormone
Steps
1. Transport of iodide into the thyroid gland by sodium-iodide
symporter
2. Iodide is oxidized by thyroidal peroxidase to iodine
3. Tyrosine in thyroglobulin is iodinated and forms MIT & DIT- iodide
organification ( MIT- monoiodotyrosine, DIT- Diiodotyrosine)
4. Iodotyrosines condensation within thyroglobulin molecule
MIT+DIT→T3; DIT+DIT→T4
7. 5. T4, T3, MIT & DIT - released from thyroglobulin by
exocytosis & proteolysis of thyroglobulin .
6. The MIT and DIT are deiodinated within the gland,
and the iodine is reutilized.
- T4 & T3 ratio within thyroglobulin - 5:1
- Most of the T3 circulating in the blood is derived
from peripheral metabolism of thyroxine.
-T3 is three to four times more potent than T4
- receptor affinity of T3 about ten times higher than
T4
Cont’d
8. • Transport of Thyroid Hormones
• T4 and T3 in plasma - bound to protein - thyroxine-
binding globulin (TBG) – Reversibly
• Only about 0.04% of total T4 & 0.4% of T3 exist in the
free form.
9. Variable T4 T3
Vd 10L 40L
Extrathyroidal pool 800 mcg 54 mcg
Daily production 75 mcg 25 mcg
Half-life 7 days 1 day
Total Serum level
Free Serum level
5-12 mcg/dl
0.7-1.86 ng/dl
70-132 ng/dl
0.23-0.42 ng/dl
Amount bound 99.96% 99.6%
Biologic potency 1 4
Oral absorption 80% 95%
Metabolic
clearance/d
1.1L 24L
Daily secretion 93% (80 μg/d) 7% (4 μg/d)
11. 11
Thyroid drugs
● Pharmacokinetics
Orally easily absorbed; the bioavalibility of T4 is 80%, and T3 is 95%.
Drugs that induce hepatic microsomal enzymes (e.g., rifampin,
phenbarbital, phenytoin, and etc) improve their metabolism.
● DRUGS
levothyroxine (L-T4)
liothyronine (T3)
liotrix (T4 plus T3)
12. 12
●Mechanism of actions of
thyroid hormones
T3, via its nuclear receptor,
induces new proteins
generation which produce
effects
13. • Synthetic levothyroxine --thyroid replacement and
suppression therapy.
• Adv:
-high stability
-uniform
-low cost
-lack of allergenic foreign protein
-easy laboratory measurement of serum levels
-long half-life -7 days (once-daily administration)
-In addition, T4 is converted to T3 intracellularly; thus,
administration of T4 produces both hormones.
-Generic levothyroxine preparations provide comparable
efficacy and are more cost-effective than branded
preparations.
14. • liothyronine (T3)is 3 to 4 times more potent than
levothyroxine.
• Use:
short-term suppression of TSH.
• Disadv:
- Shorter half-life -24 hours (not recommended for
routine replacement therapy which requires multiple
daily doses)
- Higher cost
- Difficulty of monitoring.
- Its greater hormone activity and consequent greater
risk of cardiotoxicity- avoided in patients with cardiac
disease. It is best.
15. • Liotrix - Mixture of thyroxine and liothyronine
.
-Expensive
- Oral administration of T3 is unnecessary ,so
combination is not required ( levothyroxine
preferable)
17. 17
Class Representative
Thioamides
propylthiouracil Inhibitors of
thyroxine synthesismethylthiouracil
methimazole
carbimazole
Anion inhibitors perchlorate
Thiocyanate
inhibitors of iodide
trapping
Iodinated contrast
media
diatrizoate, iohexol
Iodides KI, NaI inhibition of
hormone release
Radioactive iodine
β-R blockers
131I
propranolol
Miscellaneous sulphonamides,
phenylbutazone, thiopental
sodium, lithium,
amiodarone, domarcaprol
Antithyroid drugs
18. Thioamides
• Prevent hormone synthesis by inhibiting the thyroid
peroxidase-catalyzed reactions and blocking iodine
organification.
• Block coupling of the iodotyrosines.
• Propylthiouracil and methimazole inhibit the
peripheral deiodination of T4 and T3 .
• Since the synthesis of hormones is affected, their
effect requires 4 weeks.
19. Cont’d
• Carbimazole cross the placental barrier & are
concentrated by the fetal thyroid - caution in pregnancy
• Methimazole associated with congenital malformations
• Secreted in low concentrations in breast milk- safe for the
nursing infant.
• Propylthiouracil is preferable in pregnancy:
– It crosses the placenta less readily
– Is not secreted in breast milk
20. Adverse reactions
• Nausea & GI distress
• An altered sense of taste or smell may occur with
methimazole
• Maculopapular pruritic rash – most common
• Hepatitis & cholestatic jaundice can be fatal
• The most dangerous – agranulocytosis (granulocyte count <
500 cells/mm2).
Cont’d
21. Cont’d
Use:
◦ Thyrotoxicosis: life long
◦ Pre operatively to make euthyroid
Advantage –
◦ Less surgical complication
◦ If hypothyroidism develops then therapy can be
stopped normal function
Disadvantage –
◦ Long term therapy
◦ Not practicable in unconscious patient
◦ Toxicity specially in pregnancy
22. Propylthiouracil Carbimazole
Thiourea derivative Imidazole derivative
Less potent More potent
Highly plasma protein bound Not so
Less transported across
placental barrier & milk
Can cross placental barrier
t½ 1-2 hours 6-10 hours
Multiple dose needed Single dose needed
No active metabolite Methimazole is the active
metabolite
T4 T3 is inhibited Not inhibited
23. • Perchlorate, Thiocyanate - block uptake of iodine
by the gland through competitive inhibition of
the iodide transport mechanism.
• Potassium iodide- block thyroidal reuptake of I- in
patients with iodide-induced hyperthyroidism.
• Potassium perchlorate is rarely used, associated
with aplastic anemia
Anion inhibitors
24. • M/A:
They inhibit organification
Hormone release
Decrease the size & vascularity of the
hyperplastic gland.
Iodides – inhibitors of hormone release
25. Cont’d
• Use:
–Thyrotoxic crisis
– Preparation for thyroidectomy(decrease the size & vascularity of
the hyperplastic gland)
–Prophylaxis in endemic goiter
• Adverse effect:
– Acute : swelling of lip, eye lid, face, angineurotic
edema of larynx, fever, joint pain, lymphadenopathy,
thrombocytopenia
– Chronic : ulceration of mucous membrane of mouth,
salivation, lacrimation, burning sensation in the mouth,
rhinorrhoea, GI intolerance
26. • These drugs rapidly inhibit the conversion of T4 to T3 in
the liver, kidney, pituitary gland, & brain.
• relatively nontoxic.
• Adjunctive therapy in the treatment of thyroid storm
• use as alternatives when iodides or thioamides are
contraindicated.
• Their toxicity is similar to that of iodides.
• safety in pregnancy is undocumented
Iodinated contrast media
27. • 131I is - used for treatment of thyrotoxisis
• Administered orally in solution as sodium 131I, it is
rapidly absorbed, concentrated by the thyroid, &
incorporated into storage follicles emits β particles &
X rays β particles damage the thyroid cells thyroid
tissue destroyed by piknosis replaced by fibrosis
• Use
– Diagnostic purpose 25-100μ curies in thyroid
function test
– Therapeutic use 3-6 milli curies in toxic nodular
goiter, graves disease, thyroid Ca.
Radioactive iodine
28. Cont’d
• Advantage :
– Easy administration
– Effectiveness
– Low expense
– Absence of pain
– In patient who have indication of operation but want
to avoid operation
– Once treated no chance of recurrence
• Disadvantage :
– Hypothyroidism
– Latent period of getting response (8-12 weeks)
29. Cont’d
• C/I : Pregnancy
Young patients
Hyperdynamic circulation
• Adverse effect :
– Hypothyroidism
– crosses the placenta to destroy the fetal thyroid
gland & is excreted in breast milk (baby become
hypothyroid)
30. Adjuncts to Antithyroid Therapy
• Hyperthyroidism resembles sympathetic overactivity
• Propranolol, will control tachycardia, hypertension,
and atrial fibrillation
• Diltiazem, can control tachycardia in patients in
whom beta-blockers are contraindicated
• Barbiturates accelerate T4 breakdown (by enzyme
induction) and are also sedative
31. Thyroid malfunction and Pregnancy
• In a pregnant hypothyroid patient- dose of
thyroxine should be adequate.
• This is because early development of the fetal
brain depends on maternal thyroxine.
• If thyrotoxicosis occurs, propylthiouracil is used
and an elective subtotal thyroidectomy performed.
32. Class Mechanism of Action and Effects Indications Pharmacokinetics, Toxicities,
Interactions
Antithyroid Agents
Thioamides
Propylthiouracil (PTU) Inhibit thyroid peroxidase reactions
block iodine organification inhibit
peripheral deiodination of T4 and T3
Hyperthyroidism Oral duration of action: 6–8 h
delayed onset of action Toxicity:
Nausea, gastrointestinal distress,
rash, agranulocytosis,
hepatitis,hypothyroidism
Iodides
Lugol solution Inhibit organification and hormone
release reduce the size and
vascularity of the gland
Preparation for surgical
thyroidectomy
Oral acute onset within 2–7 days
Toxicity: Rare (see text)Potassium iodide
Beta blockers
Propranolol Inhibition of adrenoreceptors inhibit
T4 to T3 conversion (only
propranolol)
Hyperthyroidism, especially
thyroid storm adjunct to
control tachycardia,
hypertension, and atrial
fibrillation
Onset within hours duration of
4–6 h (oral propranolol) Toxicity:
Asthma, AV blockade,
hypotension, bradycardia
Radioactive iodine 131I (RAI)
Radiation destruction of thyroid
parenchyma
Hyperthyroidism patients
should be euthyroid or on
blockers before RAI avoid in
pregnancy or in nursing
mothers
Oral half-life 5 days onset of 6–
12 weeks maximum effect in 3–
6 months Toxicity: Sore throat,
sialitis, hypothyroidism
33. Class Mechanism of Action Indications Pharmacokinetics,
Toxicities,
Interactions
Thyroid Preparations
Levothyroxine (T4 ) Activation of nuclear
receptors results in gene
expression with RNA
formation and protein
synthesis
Hypothyroidism maximum effect
seen after 6–8
weeks of therapy
Liothyronine (T3)