Hello there!
This is Jayhind Bharti from M-Pharmacy 1st year pharmacology,
the above uploaded ppt is on the topic anti-thyroid drug from "advance pharmacology - 2" of m pharm 2nd semister
initially i have discussed about the basics of thyroid gland, its synthesis procedure, what are its pharmacological action and all
further our main topic starts in which i have listed the class of drug which are used to treat hyper- thyroidism with their examples and have explained the moa of each class wit their possible adverse effect, side effect, advantages and disadvantages
lastly i have added some recent advancements in the field of anti- thyroid drug
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.
Presentation for Medical undergraduates for teaching pharmacology. It deals with Physiology of steroid hormones and their action along with agents which are used therapeutically with their action, adverse effects and therapeutic uses.
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.
Presentation for Medical undergraduates for teaching pharmacology. It deals with Physiology of steroid hormones and their action along with agents which are used therapeutically with their action, adverse effects and therapeutic uses.
Adrenoceptors are membrane bound receptors located throughout the body on neuronal and non-neuronal tissues where they mediate a diverse range of responses to the endogenous catecholamines- noradrenaline and adrenaline.
They are G protein coupled receptors.
Binding of catecholamine to the receptor is responsible for fight or flight response.
Adrenoceptors are membrane bound receptors located throughout the body on neuronal and non-neuronal tissues where they mediate a diverse range of responses to the endogenous catecholamines- noradrenaline and adrenaline.
They are G protein coupled receptors.
Binding of catecholamine to the receptor is responsible for fight or flight response.
the above presentation contain the history of the thyroid disorder, including the definition of thyrotoxicosis, and its two main cause that are graves' disease and another toxic nodular goiter and the classification of drugs that are used in hyperthyroidism i.e. hormone sythesis inhibitor, hormone release inhibitors, destroy thyroid tissue, and inhibit ionic trapping with it's example including the adverse effect and side effect and marketted preparation of the same and the agents which cause hypothyroidism and the agents which are used to prescribe in the pregnancy
Summary of thyroid and antithyroid drugs
-Introduction
-Synthesis
-Pharmacological Action
-Mechanism of action
-Drugs in Hypothyroidism
-Thyroid Inhibitors
-Drugs in Hyperthyroidism
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
-
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
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- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
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- GENE THERAPY
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- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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2 Case Reports of Gastric Ultrasound
4. THYROID GLAND
1. The thyroid gland is an endocrine gland.
2. The thyroid gland's location is in the front or anterior part of the neck, below
Adam's apple.
6. SYNTHESIS OF THYROID HORMONE
STEP 1. Transport of iodide into the thyroid gland by sodium-iodide
symporter
STEP 2. Iodide is oxidized by thyroidal peroxidase to iodine
STEP 3. Tyrosine in thyroglobulin is iodinated and forms MIT & DIT-
iodide organification ( MIT- monoiodotyrosine, DIT- Diiodotyrosine)
STEP 4. Iodotyrosines condensation within thyroglobulin molecule
MIT+DIT→T3; DIT+DIT→T4
STEP 5. T4, T3, MIT & DIT - released from thyroglobulin by exocytosis
& proteolysis of thyroglobulin .
7.
8. RELATION BETWEEN T3 AND T4
T4 &T3 ratio within thyroglobulin - 5:1
Most of theT3 circulating in the blood is derived from peripheral metabolism of
thyroxine.
T3 is three to four times more potent thanT4
Receptor affinity ofT3 about ten times higher thanT4
9. PHARMACOLOGICAL ACTION OF
THYROID HORMONE
1) Growth & Development
2) Intermediary metabolism
carbohydrate metabolism
protein metabolism
3) Cardiovascular system
4) Nervous system
5) Skeletal muscle
6) Haemopoiesis
7) On GIT
10. DISEASE OF THYROID GLAND
A) Hyperthyroidism/Thyrotoxicosis
Grave’s disease
Thyroid Nodules
12. Anti-thyroid drugs/ Thyroid inhibitors
Definition:
1. “These are the pharmacological agents which are used to lower the functional
capacity of hyperactive thyroid gland”
2. These are the agents used in treatment of thyrotoxicosis ( It is excess secretion
of thyroid hormone due to disorders; like
Graves disease( auto immune disease)
Toxic nodular goiter.
13. CLASSIFICATION
A) Thioamide derivatives
Ex:- Carbimazole , Methimazole , Propylthiouracil
B) Ionic inhibitors
Ex:- Thiocyanate (-SCN) , Perchlorates (-ClO4) , Nitrates (NO3)
C) Iodinated contrast media
Ex:- Oral ipodate , Ipanoic acid , Diatrizoate (I.V)
D) Inhibitor of hormone release
Ex:- Iodine , Iodides of Na, k Organic iodides
E) Radioactive iodine
Ex:- 131I (Radioactive iodine)
14. A) Thioamide derivatives
Ex:- Methimazole (carbimazole)
Propyl thiouracil (PTU)
These 2 are the major drugs used in the treatment of thyrotoxicosis
(Carbimazoles converted to methimazole in vivo).
15. MOA Thioamide derivatives
These drug inhibit thyroid hormone production by
a) inhibiting thyroid peroxidase which is required in intrathyroidal
oxidation of Iodide.
b) by inhibiting the iodination of tyrosine
c) by inhibiting coupling of MIT and DIT to form thyroid hormones
d) propylthiouracil also inhibits peripheral conversion of T4 to T3 by
inhibiting DID -1 enzyme
16. Adverse drug reaction
The most common adverse effect
Hypothyroidism and goiter
maculopapular pruritic rash
Other side effects:
GI intolerance, Skin rashes, joint pain.
Graying or loss of hair, loss of taste, fever & liver damage.
Agranulocytosis & Jaundice may occurs.
18. Advantages of Antithyroid drug
over surgery / I131 treatment
side effect like hypothyroidism can be reversed by stopping the
Can be used for children as well as young adults
Disadvantage:
Prolonged (often life long) treatment is needed
Not practicable in uncooperative/unintelligent patient.
20. B) Ionic inhibitors
Ex:- Perchlorate, Thiocyanate
MOA:-
block uptake of iodide by the gland through competitive inhibition
of the iodide transport mechanism.
They inhibit organification Hormone release Decrease the size &
vascularity of the hyperplastic gland decreases
21. Other drug
Potassium iodide-
Block thyroidal reuptake of I- in patients with iodide-induced
hyperthyroidism.
22. Use:
Thyrotoxic crisis –
Preparation for thyroidectomy
(decrease the size & vascularity of the hyperplastic gland)
Prophylaxis in endemic goiter
23. Adverse effect:
Acute :
swelling of lip, eye lid, face,
fever, joint pain,
lymphadenopathy, thrombocytopenia
Chronic :
ulceration of mucous membrane of mouth,
salivation,
lacrimation, burning sensation in the mouth, rhinorrhoea, GI
intolerance
24. C) Iodinated contrast media
Ex:- Oral ipodate , Ipanoic acid , Diatrizoate (I.V)
MOA:-
These drugs rapidly inhibit the conversion of T4 to T3 in the liver,
kidney, pituitary gland, & brain.
25. Uses
Ipodate has proved very useful in rapidly reducing T3 concentration
thyrotoxicosis (in thyroid storm)
as alternatives when iodides or thioamides are contraindicated.
Their toxicity is similar to that of iodides.
safety in pregnancy is undocumented.
26. D) Inhibitor of hormone release
Ex:- Iodine , Iodides of Na, k Organic iodides
Even if the iodine is one of the constitute of thyroid hormone but
still it acts as faster acting thyroid inhibitor
due to negative feedback mechanism iodide inhibit release of
thyroid hormone.
27. Preparation
1. Lugols solution: 5% iodine in 10% KI solution : 5- 10drops/day
2. Iodide salts (sod/pot) 100-300 mg/day
Within 1-2 days of starting of treatment causes inhibition of
secretion of thyroid hormone
while 10-14 days causes marked reduction in vascularity of gland &
which decreases the size of gland.
28. MOA
Actual mechanism is unknown;
It inhibits own transport in to thyroid cell ( Step 1 in thyroid
synthesis) by acting on NIS (Sodium Iodide symporter)
It attenuates TSH & cAMP & causes thyroid inhibition.
Also excess iodide rapidly interferes with tyrosine ( Iodination
step2)
29. Uses:
1) Preoperative preparation: For thyroidectomy in graves disease;
iodine for 10 days before surgery will given which makes gland less
vascular & easier to remove by operation.
2) Thyroid storm
3) Prophylaxis of endemic goiter: It is used as "iodized salt“.
Other use
Antiseptic: The tincture of iodine, povidone iodine is used as
antiseptic.
30. Adverse drug reaction:
1) Acute (It occurs in sensitive people). Shows symptoms like
swelling of lips, eyelids,
angio- edema of larynx (may be dangerous),
fever, joint pain, petechial haemorrhages.
2) Chronic overdose (iodism):
Inflammation of mucous membranes, salivation, rhinorrhoea,
sneezing, lacrimation, burning sensation in mouth, headache, rashes.
3) Long-term use of high doses can cause hypothyroidism & goiter.
4) If high dose given to pregnant women chance to hypothyroidism &
goiter in foetus.
31. E) Radioactive iodine
Ex- I131, I123 I125.
The stable form of isotope of iodine is I127 but medically useful
isotope is I 131
But one of the advantage of radioactive iodine is it produce necrosis
of cell (affected thyroid follicular cell) without damaging
neighboring tissue.
32. MOA
1. Administered orally in solution as sodium 131I,
2. it is rapidly absorbed, concentrated by the thyroid, & incorporated
into storage follicles
3. emits β particles & X rays
4. β particles damage the thyroid cells
5. thyroid tissue destroyed
6. replaced by fibrosis
33. Advantages:
Treatment with I 131 is inexpensive.
No surgical risk, scar
after treatment with I 131 Once hyperthyroidism is controlled, cure
permanent.
Disadvantages:
Hypothyroidism: About 5-10% patients of Graves' disease treated
become hypothyroid.
Very slow response was observed for treatment with I131.
during pregnancy drug is Contraindicated because it causes foetal
destruction.
I131 not suitable for young patients more likely to develop
genetic damage/cancer
34. 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