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
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
A power point presentation on thyroid hormones and thyroid inhibitors on subject of pharmacology suitable for reading by undergraduate medical students.
Introduction.
Biosynthesis
Types of Thyroid diseases
Thyroid Drugs
Antithyroid Drugs
Mechanism of action
Structure
Adverse Drug Reactions and Uses.
Reference
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.
Introduction.
Biosynthesis
Types of Thyroid diseases
Thyroid Drugs
Antithyroid Drugs
Mechanism of action
Structure
Adverse Drug Reactions and Uses.
Reference
Introduction to the endocrine system
Growth hormone: Mechanism of Action, secretion, regulation.
Prolactin
Sex hormones
Oral contraceptives
Corticosteroids
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
The content of presentation is as follows
- introduction to thyroid
- thyroid hormone synthesis
- type of thyroidism
- difference between hyperthyroidism and hypothyroidism
-treatment of hypothyroidism
- anti thyroid drug classification
- mechanism of anti thyroid drugs
-
Thyroid Gland and Disease of Thyroid GlandRanadhi Das
The thyroid gland is one of the largest endocrine glands.
The thyroid gland is located immediately below the larynx and anterior to the upper part of the trachea. It weighs about 15-20g.
It consists of 2 lateral lobes connected by a narrow band of thyroid tissue called the isthmus.
The isthmus usually overlies the region from the 2nd to 4th tracheal cartilage.
Thyroid and anti-thyroid drugs. Synthesis of thyroid hormoneAnkita
In this ppt we will get idea about thyroid and anti-thyroid drugs. how and where the thyroid hormone synthesis occur. regulation of thyroid hormone. get brief knowledge about anti-thyroid drugs, their action, MOA, adverse effect of anti-thyroid drugs and uses
It Gives Information about Thyroid disease(its type), Thyroid Gland & Thyroid System. The Presentation also Give information on Hyperthyroidism ( like its Etiology, Symptoms, Diagnostic Evaluation and Treatment.
A complete presentation on hypothroidism endocrine disorder based on latest editon of harrison and reference books. this presentation will help to learn about this second most common endocrine disorder.
- 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
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
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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.
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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.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
2. THYROID GLAND
It is an Endocrine Gland, found at
the front of Neck below Adam’s
Apple.
Produces three Hormones:-
Thyroxine T4
Triidothyronine T3
Calcitonin
T4 and T3 have same Biological
activity and termed as “Thyroid
Gland” secreted by Folliclular cell.
Calcitonin is produced by C Cells
which regulate Ca2+ metabolism.
3. CHEMISTRY AND SYNTHESIS
T4 and T3 are iodine containing thyronine derivatives:-
2tyrosineThyronine + 3I- 3,5,3’triiodothyronine (T3)
+ 4 I- 3,5,3’,5’tetraiodothyronine (T4)
Iodide Uptake
Oxidation and Iodination
Coupling
Storage and Release
Peripheral Conversion of T4 to T3
4. FOLLICLE CELL
NIS PDS
P
P
PLASMA FOLLICLE LUMEN
TSH
Stimulates gene
transcription for
this carrier
I-I-
IODIDE UPTAKE
Iodine obtain from food and water
Body Contains 30-50 mg out of which
1/5th in Thyroid
Actively transported by Na+: Iodide
Symporter (NIS) from blood to follicle
TSH stimulate uptake by 100 folds
6. FOLLICLE CELL
NIS PDS
P
P
PLASMA FOLLICLE LUMEN
I-I-
Thyroperoxidase
TG
T
DIT
MITMIT
T T
T
DIT
TG
T
T
T
T
T
Protein Synthesis
OXIDATION AND IODINATION
Follicle iodide carried across apical
membrane by Pendrin(PDS)
Iodide oxidized by Thyroid Peroxidase
which easily binds to tyrosil to form MIT
and DIT which are attached to
Thyroglobulin
8. FOLLICLE CELL
NIS PDS
P
P
PLASMA FOLLICLE LUMEN
I-I-
Thyroperoxidase
TG
T
DIT
MITMIT
T T
T
DIT
TG
T
T
T
T
T
Protein Synthesis
COLLOID
MIT+DIT =Triidothyronine T3
DIT+DIT =Thyroxine T4
COUPLING AND STORAGE
Tyrosil Residue Couple to Form T4 and
T3
TSH stimulate both Coupling and
Oxidation
Thyroglobulin transported to Colloid
present interior of follicle
9. FOLLICLE CELL
NIS PDS
P
P
PLASMA FOLLICLE LUMEN
I-I-
Thyroperoxidase
TG
T
DIT
MITMIT
T T
T
DIT
TG
T
T
T
T
T
Protein Synthesis
COLLOID
MIT+DIT =Triidothyronine T3
DIT+DIT =Thyroxine T4
10. FOLLICLE CELL
NIS PDS
P
P
PLASMA FOLLICLE LUMEN
I-I-
Thyroperoxidase
TG
T
DIT
MITMIT
T T
T
DIT
TG
T
T
T
T
T
Protein Synthesis
COLLOID
MIT+DIT =Triidothyronine T3
DIT+DIT =Thyroxine T4
T
G
TG
L
T4
T3
T4
T3
MIT
DIT
I-
deiodination
RELEASE AND CONVERSION
Thyroid Colloid is taken by endocytosis
Broken by Lysosymal Protease
T4 and T3 are released while MIT and DIT
are re-utilized
Normal Human Secretes 60-90μg of T4
and 10-30μg of T3
Peripheral tissue, Liver, Kidney convert
about 1/3rd T4 to T3 by Iodothyronine
deiodinase
Target tissue take up T3 for metabolic need
11. FOLLICLE CELL
NIS PDS
P
P
PLASMA FOLLICLE LUMEN
I-I-
Thyroperoxidase
TG
T
DIT
MITMIT
T T
T
DIT
TG
T
T
T
T
T
Protein Synthesis
COLLOID
MIT+DIT =Triidothyronine T3
DIT+DIT =Thyroxine T4
T
G
TG
L
T4
T3
T4
T3
MIT
DIT
I-
deiodination
13. ACTION
T4 and T3 have same quantitatively action
Growth and Development:-
Essential for normal growth
Control protein synthesis
Hypothyrodism suffer nervous system mostly
Cause impaired intelligence and slow movement
Intermediary Metabolism:-
Lipid:
Indirectly enhance lypolysis
Results in increase plasma free fatty acid
Hyperthyroidism cause hypocholesterolemia
Carbohydrates:
Metabolism Stimulated
Increase utilization of sugar
Absorption from intestine is faster causes
hyperglycaemia
14. Protein:
Regulate Protein Synthesis, mainly catabolise
Weight Loss in Hyperthyroidism
Calorigenesis:-
Increase BMR by stimulating cellular metabolism and resets energy state
CVS:-
Increase peripheral demand
Increase cardiac actions:- HR, FOC and output
Myocardial O2 consumption is decreased in hypothyroidism
Nervous System:-
Hypothyroidism: mental retardation (cretinism),
sluggishness (myxoedema)
Hyperthyroidism: anxiousness, nervousness, excitable,
Tremor and weakness
GIT:-
Propulsive activity of gut is increased-
Diarrhea: hyperthyroidism
Constipation: Hypothyroidism
15. MECHANISM OF ACTION
T4 and T3 penetrate cell by active transport and produces action
by combining with nuclear Thyroid Hormone Receptor (TR)
bound to TRE in enhancer region of target gene along with co-
repressor causes gene transcription suppression
When T3 bind to ligand binding domain of TR, TR heterodimerizes
and undergoes conformational change
This causes corepressor release and coactivator binding these
induces gene expression
Gene transcrtiption Production of mRNA Protein Synthesis
various metabolic and anabolic effect
Repression by T3: The unliganded TR allow gene transcription
while binding of T3 to TR halt process
Tachycardia, high BP, tremor, hyperglycemia are mediated by
sensitization of adrenergic receptors to catecholamines
16. Mechanism of action of thyroid hormone on nuclear thyroid hormone receptor (TR).
T3—Triiodothyronine; T4—Thyroxine; TRE—Thyroid hormone response element; RXR—
Retinoid Xreceptor; mRNA—Messenger ribonucleic acid; 5’DI—5’Deiodinase
17. DRUG IN HYPOTHYROIDISM
Clinically, 1-thyroxine is preferred because of more sustained and uniform
action as well as lower risk of cardiac arrthymias
Pharmacokinetic: ~ 75% oral bioavailability
Uses:
Cretinism: Failure or defect in thyroid development, usually in infants,
treatment should be fast (8-12 μg/kg daily)
Adult Hypothyroidism (Myxoedema): Disorder caused by autoimmmune
thyroiditis or thyroidectomy, Simple Goiter in iodine deficiency, Antibodies
against thyroid H2O2 / Thyroglobulin, Drugs such as 131I iodide, Li also
causes (start low dose 50μg daily& increased every 2-3 week to 100-200μg)
Myxoema Coma: Emergency caused by progressive mental deterioration,
Rapid thyroid replacement (200-500μg i.v. followed by
100μg OD till oral therapy instituted)
Nontoxic Goitre, Thyroid Nodule, Empirical Use:
Mental depression, Obstimate Constipation
Marketed Preparation: Eltroxin 25μg, 50μg, 100μg tab;
Thyronorm tab
18. THYROID INHIBITORS
These drugs lower the functional capacity of the hyperactive thyroid
gland (treat hyperthyroidism)
Thyrotoxicosis is due to excessive secreation of thyroid hormone two
main causes:-
Grave’s Disease: Autoimmune disease, IgG antibodies to TSH receptor
bind and show TSH like effect, feedback mechanism is inhibited because
TSH levels are low
Toxic Nodular Goiter: Produces thyroid hormone independent of TSH
CLASSIFICATION:-
Inhibit Hormone Synthesis (Anti thyroid Drugs):-
Propylthiouracil, Methimazole, Carbimazole
Inhibit Iodide Trapping (Ionic Inhibitors):-
Thiocynates (-SCN), Perchlorates (-ClO4), Nitrates(-NO3)
Inhibit Hormone Release:-
Iodine, Iodides of Na and K, Organic Iodide
Destroy Thyroid Tissue:-
Radioactive Iodine (131I, 125I, 123I)
19. ANTITHYROID DRUGS (THIOAMIDES)
Propylthiouracil
Methimazole
Carbimazole
Mode of Action:-
Bind to Thyroidperoxidase and prevent oxidation of iodide residue,
thereby:-
Inhibition of iodination of tyrosine residues in thyroglobulin
Inhibition of coupling of iodotyrosine residue
They do not interfere with trapping of iodide and do not modify T3 and T4
action
They do not affect release of T3 and T4 and show no effect till thyroid is
depleted
Propylthiouracil inhibit T4 to T3 conversion while Methimazole and
Carbimazole cannot while they antagonizes former
Pharmacokinetic: All drugs are quickly absorbed orally and widely
distributed in body
20. FOLLICLE CELL
NIS PDS
P
P
PLASMA FOLLICLE LUMEN
I-I-
Thyroperoxidase
TG
T
DIT
MITMIT
T T
T
DIT
TG
T
T
T
T
T
Protein Synthesis
COLLOID
MIT+DIT =Triidothyronine T3
DIT+DIT =Thyroxine T4
T
G
TG
L
T4
T3
T4
T3
MIT
DIT
I-
deiodination
Thioamides and Excess I-
Propylthiouracil Methimazole
Carbimazole
21. Adverse Effect:-
Hypothyroidism and goiter can occur due to overtreatment of drug but
reversible on stopping treatment
GI intolerance, Skin Rashes and Joint Pain
USES:-
Controls thyrotoxicosis in both Grave’s disease and toxic nodule goiter
Clinical improvements starts after 1-2 weeks or more
Advantage:- No surgical risk, reversible hypothyroidism, use for children
Disadvantage:- Prolonged treatment, Drug toxicity
Marketed Preparation:-
Propylthiouracil: 50-150 mg TDS followed by 25-50 mg BD-TDS
for maintenance PTU 50 mg
Methimazole: 5-10 mg TDS initially, maintenance dose
5-10 mg OD-BD
Carbimazole: 5-15 mg TDS initially, maintenance dose
2.5-10 mg OD-BD Neo Mercazole, Thy rozole, Antithyrox
22. IODINE AND IODIDES
Constituent of thyroid hormone and potentiate thyrotoxicosis but excess
causes inhibition of hormone release “Thyroid Constipation”
Endocytosis of colloid and proteolysis of thyroglobulin comes to a halt
USE:-
Preoperative preparation for thyoidectomy in Grave’s disease
Thyroid storm
Prophylaxis of endemic goiter
Antiseptic
Adverse effect:-
Acute: Swelling of lips, eyelids, fever joint pain
Chronic: Inflammation of mucous membrane, salivation, headache,rashes
Marketed Preparations:-
Lugol’ Solution (5% iodine in 10% KI solution)
Lugol’s Solution; Colloid Iodine 10% Collosol 5 mg
24. RADIOACTIVE IODINE
Stable isotope 131I is medicinal important (half life 8 days)
Both diagnostic and therapeutic use:-
Diagnostic: γ-rays are useful in tracer studies 25-100 μCurie is given,
counting or scanning is done at intervals, No damage to thyroid at this dose
Thrapeutic: β-particles are used for their destructive effectb on thyroid
cells 131I concentrated in thyroid colloid and emit radiation from within and
penetrates only 0.5-2 mm
Average 3-6 mCurie is used on the basis of thyroid size. The response is
slow and starts after 2 weeks
Advantage:-
Simple an inexpensive
No surgical Risk, Scar or Injury
Cure is permanent after control
Disadvantage:-
Hypothyroidism
Long latent response period
Not suitable for young patients