This document summarizes several endocrine system disorders including hyperthyroidism, hypothyroidism, hyperparathyroidism, hypoparathyroidism, Cushing's syndrome, Conn's syndrome, Addison's disease, and pituitary adenomas. It provides epidemiological data on certain disorders and describes associated symptoms, diagnostic evaluations, and medical management approaches. Multiple endocrine neoplasia syndromes are also briefly discussed.
Hyperthyroidism (overactive thyroid) occurs when your thyroid gland produces too much of the hormone thyroxine. Hyperthyroidism can accelerate your body's metabolism, causing unintentional weight loss and a rapid or irregular heartbeat
Hypothyroidism (underactive thyroid) is a condition in which your thyroid gland doesn't produce enough of certain crucial hormones.
Hyperthyroidism (overactive thyroid) occurs when your thyroid gland produces too much of the hormone thyroxine. Hyperthyroidism can accelerate your body's metabolism, causing unintentional weight loss and a rapid or irregular heartbeat
Hypothyroidism (underactive thyroid) is a condition in which your thyroid gland doesn't produce enough of certain crucial hormones.
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.
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.
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.
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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
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
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.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
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3. Epidemiology
• In a population-based study the overall prevalence of
multinodular goiter was 0.84%, with a higher prevalence
in females (1.6%) compared with males (0.1%)
• In NHANES-III individuals (≥12 yr of age), the overall
prevalence of hyperthyroidism was 1.3%, with the lowest
prevalence among Hispanics and other ethnicities (0.7%
each) and highest among Whites (1.4%)
• In the Nurses’ Health Study, the overall incidence of
hyperthyroid Graves’ disease was 4.6 per 1000 females
during 12 yr.
4. Assessment
• Health history—energy level, hand and foot size changes,
headaches, urinary changes, heat and cold intolerance,
changes in sexual characteristics, personality changes,
others
• Physical assessment—appearance including hair
distribution, fat distribution, quality of skin, appearance
of eyes, size of feet and hands, peripheral edema, facial
puffiness, vital signs
5. Palpating the thyroid gland from behind the client. (Source: Lester V. Bergman/Corbis)
5
6. Diagnostic Evaluation
Serum levels of hormones
Detection of antibodies against certain hormones
Urinary tests to measure by-products (norepinephrine,
metanephrines, dopamine)
Stimulation tests—determine how an endocrine gland
responds to stimulating hormone. If the hormone responds,
then the problem lies w/hypothalmus or pituitary
Suppression tests—tests negative feedback systems that
control secretion of hormones from the hypothalamus or
pituitary.
7. Overview of Endocrine system pathology
• symptoms of endocrine gland disorders are usually
due to increased hormone production, decreased
hormone production or mass lesions
• hypo-functioning of endocrine cells results in
decreased hormone levels
• hyperfunctioning of endocrine cells results in
increased hormone levels
• mass lesions are usually due to neoplasia or
hyperplasia
• Multiple endocrine neoplasia syndromes (MEN)
8. Certain syndromes are characterized by multiple
endocrine neoplasms
• MEN I (pituitary, parathyroid, pancreatic islet cell
neoplasia)
• MEN IIa (medullary thyroid carcinoma,
pheochromocytoma, parathyroid)
• MEN IIb (IIa + skin and mucosal nerve tumors)
9. Pituitary gland pathology
• Pituitary adenoma
• benign neoplasm of endocrine cells in the anterior pituitary
• symptoms due to release of excess hormones or pressure effects of
mass (compression of pitutary stalk and/or optic chiasm)
• endocrine effects depend on what hormone produced by the
adenoma
• 80% of pituitary adenomas produce hormones Prolactinoma (LH)
• most common pituitary adenoma produces prolactin
• identified earlier in young reproductive female because present
with amenorrhea, galactorrhea, infertility (microadenoma)
• surgery or medical therapy (bromocryptine) to remove
10. Pituitary adenoma
• Somatotropic adenomas
• neoplastic cells produce growth hormone
– gigantism results from excess growth hormone before
growth plates close
• generalized increase in body size with disproportionately
long legs, arms
– acromegaly results from excess growth hormone after
puberty
• enlargement of hands, feet, jaw, tongue, and soft tissue)
• Corticotropic adenoma
– neoplastic cells produce adreno-corticotropin hormone
– Cushing’s disease refers to the syndrome resulting from
excess glucocorticoid release by the adrenal cortex due to
excess ACTH
11. Pituitary hypofunction
• causes of pituitary hypofunction include
– congenital defect of pituitary gland (primary dwarfism)
– destructive tumor (pituitary adenoma)
– ischemia of the pituitary gland (Sheehan’s syndrome)
• symptoms
– weakness,
– Poor appetite,
– Weight loss,
– hypotension,
– amenorrhea
– secondary hypofunction of target organs
12. Diabetes insipidus
• lack of ADH
• usually due to destructive lesion in
hypothalamus, pituitary
• unable to resorb water, large amounts of
hypotonic urine
13. Pathology of the thyroid gland
• Thyroid hyperfunction (hyperthyroidism)
• major causes are Grave’s disease, some multinodular
goiters, tumors
– autoimmune disease due to antibodies targeting the TSH
receptor on thyroid follicular cells
– AB binds to TSH receptor causing release of thyroid hormones
– more common in females
– associated with other autoimmune disease
• symptoms of hyperthyroidism
– restless,
– nervous,
– emotional lability,
– sweating,
– tachycardia,
– diarrhea,
– weight loss with increased appetite
14. symptoms of hyperthyroidism
• restless,
• nervous,
• emotional lability,
• sweating,
• tachycardia,
• diarrhea,
• weight loss with increased appetite
• Exopthalmos occurs in Grave’s disease
17. Thyroid Tumors
Tumors of the thyroid gland are classified on the basis of being
benign or malignant.
If the enlargement is sufficient to cause a visible swelling in the
neck, the tumor is referred to as goiter.
All grades of goiter are encountered, from those, that are barely
visible to those producing disfigurement.
Goiter either symmetrical and diffuse or nodular.
It might accompanied by hyperthyroidism (toxin); others are non
toxic goiters
19. Management
Many goiters of this type decreased after correction of
iodine insufficiency.
When surgery is recommended, post operative
complications can be minimized by pre operative
iodide administration to reduce the size & vascularity
of goiter.
Prevention
Providing children in iodine-poor region with iodine
compounds.
Use of iodized salt.
20. Thyroid hypofunction (hypothyroidism)
• major causes are:
– agenesis,
– surgery,
– thyroiditis,
– iodine deficiency
• Symptoms of hypothyroidism
– cretinism and dwarfism if occurs in perinatal period or
infant
– myxedema if occurs in older child or adult
– sleepy, tire easily, cold intolerance, constipation, weak
• Treat with thyroid hormone replacement
21. Pathology of the parathyroid glands
Hyperparathyroidism
• major causes are parathyroid adenoma and
parathyroid hyperplasia
• symptoms of hyperparathyroidism
(hypercalcemia)
– bones, stones, moans, abdominal groans
Hypoparathyroidism
• causes of include surgery, congenital hypoplasia
• symptoms of hypoparathyroidism (hypocalcemia)
– muscle spasms, irregular heart beat, cardiac arrest (if
severe)
22. Pathology of the adrenal gland
• Adrenocortical hyperfunction-Hypercortisolism (Cushing’s syndrome)
• syndrome due to excess glucocorticoid hormones (cortisol)
• most common cause is exogenous steroids, other causes include
– adrenal hyperplasia or neoplasia
– hypersecretion of ACTH by pituitary gland (Cushing’s disease)
– ectopic ACTH (paraneoplastic syndrome)
• Dramatic appearance: central obesity, buffalo hump, moon
face, striae
• Hyperaldosteronism (Conn’s syndrome)
– syndrome due to excess mineralocorticoid hormone (aldosterone)
– causes include adrenocortical adenoma and adrenal hyperplasia
– present with hypertension and hypokalemia
23. Cushing’s Support & Research Foundation
Abdominal weight gain
Red, round ‘moon’ face
Thinning extremities
‘Buffalo hump’
High blood pressure
High blood sugar
Muscle weakness
Osteoporosis/Fractures
Infections
Blood clots
Visual field defects
Easy bruising
Thinning skin
Poor wound healing
Acne
Purple striae
Hirsutism
Female balding
Menstrual irregularity
Sleep disorders
Excessive hunger
Excessive thirst
Frequent urination
Sweating
Anxiety
Confusion
Concentration loss
Memory loss
Depression
Suicidal thoughts
Panic attacks
Illustration from Mayo Clinic Family Health Book, 2d. ed, 1996
Symptoms Vary
And may include
any number of these:
Courtesy of www.CSRF.com
24. Pathology of the adrenal gland…
• Adrenocortical hypofunction
–usually autoimmune destruction of
adrenals, also due to Tb, malignancy
• Addison’s disease
– autoimmune destruction of adrenal gland
–fatigue, weight loss, nausea, increased
infections, low Na, high K
25. Diseases of Adrenal Medulla
• Neuroblastoma
– malignant neoplasm of neuroblasts (primitive cells) in
neonates, infant
– treatment with chemotherapy, surgery, radiation (90
% cure)
• Pheochromocytoma
– a neoplasm (usually benign) derived from adrenal
medulla cells
– diagnosed on basis of dramatic clinical picture,
metabolites in urine
– treated by surgery