The document discusses aging and the endocrinology of aging. It notes that several hormone levels change with age: thyroid secretion decreases, the thymus gland involutes, cortisol levels decrease, and the pancreas decreases secretion of enzymes and hormones. Overall, some hormone levels like aldosterone, growth hormone, and estrogen decrease with age, while others like LH and FSH may increase, and still others like cortisol remain unchanged. These hormonal changes can lead to physical, sexual, and psychological symptoms in older individuals. The effects of declining testosterone and DHEA levels are also examined.
This document discusses precocious and delayed puberty. It defines precocious puberty as the development of sexual characteristics before age 8 or menstruation before age 10. Causes can be idiopathic, an intracranial lesion, or disorders like McCune-Albright syndrome. Treatment aims to slow bone maturation and reduce gonadotropin secretion, using medications like GnRH agonists. Delayed puberty is defined as lack of breast or pubic hair development by ages 13-14 or menarche after 16. Causes include hypogonadism, chronic illness, or eugonadism. Treatment depends on the underlying cause and may involve cyclic or combined estrogen therapies.
The document discusses various hormones including prolactin, TSH, FSH, LH, estrogen, progesterone, and androgens. It provides reference ranges, clinical significance, causes of abnormal levels, and diagnostic evaluations for each hormone. Key applications include using the hormones to evaluate fertility, ovarian function, thyroid function, adrenal function, and the causes of conditions like amenorrhea, hirsutism, and galactorrhea.
Biochemical changes in pregnancy, Physiological changes in pregnancy, maternal and fetal health assessment, assessment of complications in pregnancy, hormonal changes and physiological evaluations in pregnancy
This document discusses hypothyroidism and is presented by Maghan Das. It will state the functions of thyroid hormone, discuss the pathologic mechanisms of hypothyroidism including cretinism, myxedema, and Hashimoto's disease. Hypothyroidism can be congenital or acquired. Congenital hypothyroidism is caused by lack of TSH or abnormal thyroid hormone biosynthesis and can cause cretinism if untreated. Acquired hypothyroidism causes myxedema in adults and slows metabolism. Hashimoto's thyroiditis is an autoimmune cause of hypothyroidism that can destroy the thyroid gland.
This document provides guidelines for the diagnosis and management of premature ovarian insufficiency (POI). It defines POI as depletion of follicular activity before age 40, characterized by menstrual disturbances, raised gonadotropins, and low estrogen. The prevalence is approximately 1% in the general population. Causes include genetic factors, autoimmune disorders, infections, chemotherapy and radiation. Management focuses on hormone replacement therapy (HRT) to reduce long-term health risks, fertility options, and treatment of symptoms like reduced bone mineral density and increased cardiovascular risk.
This document discusses precocious and delayed puberty. It defines precocious puberty as the development of sexual characteristics before age 8 or menstruation before age 10. Causes can be idiopathic, an intracranial lesion, or disorders like McCune-Albright syndrome. Treatment aims to slow bone maturation and reduce gonadotropin secretion, using medications like GnRH agonists. Delayed puberty is defined as lack of breast or pubic hair development by ages 13-14 or menarche after 16. Causes include hypogonadism, chronic illness, or eugonadism. Treatment depends on the underlying cause and may involve cyclic or combined estrogen therapies.
The document discusses various hormones including prolactin, TSH, FSH, LH, estrogen, progesterone, and androgens. It provides reference ranges, clinical significance, causes of abnormal levels, and diagnostic evaluations for each hormone. Key applications include using the hormones to evaluate fertility, ovarian function, thyroid function, adrenal function, and the causes of conditions like amenorrhea, hirsutism, and galactorrhea.
Biochemical changes in pregnancy, Physiological changes in pregnancy, maternal and fetal health assessment, assessment of complications in pregnancy, hormonal changes and physiological evaluations in pregnancy
This document discusses hypothyroidism and is presented by Maghan Das. It will state the functions of thyroid hormone, discuss the pathologic mechanisms of hypothyroidism including cretinism, myxedema, and Hashimoto's disease. Hypothyroidism can be congenital or acquired. Congenital hypothyroidism is caused by lack of TSH or abnormal thyroid hormone biosynthesis and can cause cretinism if untreated. Acquired hypothyroidism causes myxedema in adults and slows metabolism. Hashimoto's thyroiditis is an autoimmune cause of hypothyroidism that can destroy the thyroid gland.
This document provides guidelines for the diagnosis and management of premature ovarian insufficiency (POI). It defines POI as depletion of follicular activity before age 40, characterized by menstrual disturbances, raised gonadotropins, and low estrogen. The prevalence is approximately 1% in the general population. Causes include genetic factors, autoimmune disorders, infections, chemotherapy and radiation. Management focuses on hormone replacement therapy (HRT) to reduce long-term health risks, fertility options, and treatment of symptoms like reduced bone mineral density and increased cardiovascular risk.
The document discusses the various stages of female development from embryonic development through menopause. It covers the neonatal period, childhood, puberty, adolescence, sexual maturity, climacterium, and senium. For each period, it describes the development of the reproductive system including the uterus, ovaries, and other genital organs. It provides details on hormonal influences, the onset of puberty and its stages, and physiological changes that occur during the various life stages of women.
This document defines and discusses andropause (also known as male menopause), including its definition, symptoms, epidemiology, pathophysiology, effects of testosterone deficiency, monitoring and risks/benefits of testosterone replacement therapy. Some key points are: andropause is characterized by declining testosterone levels and affects quality of life; symptoms include reduced energy, libido and erectile dysfunction; prevalence increases with age, with 20% of men over 60 and 50% of men over 75 having low testosterone; testosterone replacement can improve symptoms in men with very low levels if administered carefully under medical supervision due to risks like prostate issues.
Male gonadal function and dysfunction (male hypogonadism). Emphasis where made on the causes, types of male hypogonadism, diagnosis and treatment methods.
This presentation discusses the launch of Tibone® tablet by Masum Chowdhury. Some key points:
- Tibone® (tibolone) is a tissue-specific hormone replacement therapy for menopausal symptoms like hot flashes and osteoporosis.
- The presentation outlines Tibone®'s efficacy, safety profile, and effects on mood, sexuality, bones, cardiovascular system and more based on clinical experience.
- An action plan is proposed to position Tibone® as the first choice for menopausal symptom management and increase its prescription share over competitors like Livial and Uvilon.
Andropause, also known as male menopause, is the gradual decline in testosterone levels that occurs in men as they age. Unlike female menopause which is sudden, andropause is a slow process resulting in more subtle symptoms. Low testosterone can negatively impact many organ systems and quality of life. Treatment options include lifestyle changes as well as hormone replacement therapy administered through oral, injectable, or transdermal methods. However, testosterone therapy may increase risks for certain health conditions like sleep apnea and prostate issues.
This document discusses infertility and polycystic ovary syndrome (PCOS). It defines PCOS and outlines its diagnosis criteria. PCOS is diagnosed based on somatic or lab indicators of hyperandrogenism, oligo-anovulation, and polycystic ovarian morphology, while excluding other disorders. Treatment options for PCOS include weight loss, exercise, clomiphene, aromatase inhibitors, metformin, and gonadotropins. Long-term management may involve birth control pills, metformin therapy, and lifestyle changes to reduce risks of weight gain, hyperandrogenism, and cardiac or metabolic diseases.
This document summarizes a case of a 21-year-old female with primary amenorrhea and hot flashes. Her lab tests showed elevated FSH and LH levels consistent with premature ovarian insufficiency. The document defines premature ovarian insufficiency as cessation of menses before age 40 due to depletion or dysfunction of ovarian follicles. It discusses causes, risk factors, symptoms, diagnosis, and treatment options which include hormone replacement therapy and in vitro fertilization with donor eggs. Counseling is recommended to address psychological and family planning aspects.
This document discusses sperm DNA fragmentation testing in male infertility. It provides background on causes of male infertility and the significance of sperm DNA fragmentation. Normal values for semen analysis are outlined according to WHO guidelines. Methods for diagnosing DNA fragmentation including Comet, TUNEL, SCD, and SCSA assays are described. Factors that can cause DNA fragmentation including lifestyle, medical conditions, and environmental exposures are covered. The importance of selecting sperm with intact DNA for ART procedures like ICSI is emphasized. Lifestyle modifications and treatment of underlying conditions may help reduce DNA fragmentation before ART.
Thyroid Disorders & infertility Dr jyoti Agarwal , Dr Sharda Jain Lifecare Centre
Thyroid disorders can significantly impact fertility in both females and males. Hypothyroidism is associated with menstrual irregularities and anovulatory cycles in females which can lead to infertility. It may also cause delayed puberty. In males, untreated hypothyroidism from a young age can damage testicular development. The document discusses the prevalence of thyroid disorders like hypothyroidism and thyroid autoimmunity in infertile populations. It recommends evaluating thyroid levels through TSH tests for all women with infertility and treating any thyroid abnormalities. Treatment of hypothyroidism is important to improve fertility outcomes and IVF success rates.
Oxidative stress from reactive oxygen species can impair sperm function and contribute to male infertility. Antioxidants may help reduce oxidative stress and improve fertility outcomes. Oral antioxidant supplementation in men with oxidative stress issues has been shown to increase pregnancy and live birth rates when undergoing assisted reproductive technologies. However, more research is still needed to determine the best candidates, formulations, dosages and duration of treatment for oral antioxidant therapy in cases of male infertility related to oxidative stress.
Physiology of Male Infertility | Seeds of InnocenceSOI Delhi
Male Infertility is a inability that causes pregnancy in a female fertile. Male infertility is commonly due to Low sperm Count. Soi provides best male infertility treatment in delhi, ghaziabad - India. Call us : 9810350512
visit : www.seedsofinnocence.com
1. Puberty is defined as the transitional stage from childhood to adulthood that is characterized by physiological changes and development of secondary sex characteristics.
2. It typically occurs between ages 10-16 and is influenced by genetic and environmental factors such as nutrition, geography, and light exposure.
3. The stages of puberty include thelarche, adrenarche, growth spurt, menarche, and development of secondary sex characteristics over approximately 4.5 years.
Placental hormones lec by liza tarca, mdLiza Tarca
The document discusses the functions and hormones of the human placenta. It begins with an introduction to placental hormones and their production by the trophoblast. It then discusses the key placental hormones in detail, including human chorionic gonadotropin (hCG), human placental lactogen (hPL), estrogen, progesterone, and other protein hormones. For each hormone, it provides information on synthesis, levels during pregnancy, roles in sustaining pregnancy, and associated medical conditions. The document aims to educate on the endocrine functions and important hormones of the human placenta.
The document discusses pubertal disorders and their classification, causes, diagnosis, and management. It begins by defining key terminology related to puberty and describing the normal physiology and regulation of the hypothalamic-pituitary-gonadal axis during puberty. Pubertal disorders are classified as either precocious or delayed puberty. Causes of delayed puberty include hypergonadotropic hypogonadism due to genetic defects or acquired conditions, and hypogonadotropic hypogonadism caused by tumors or CNS disorders that disrupt the HPG axis. Assessment of pubertal development involves the Tanner staging system.
The document discusses the biochemical changes that occur in pregnancy, including increased secretion of hormones by the placenta such as estrogen, progesterone, human chorionic gonadotropin (HCG), and human somatomammotropin. These hormones play important roles like preventing menstruation and supporting fetal development. The placenta produces high quantities of hormones later in pregnancy. Additionally, the pituitary and other glands increase secretion of hormones like corticosteroids and thyroxine to support the mother and fetus.
Puberty is the stage of physical maturation triggered by increased secretion of hormones like Luteinizing Hormone and GnRH, resulting in sexual and somatic development. It involves breast development in females starting around age 10-14 and testicular growth in males around age 12-16. Puberty encompasses five stages of physical changes through Tanner stages including growth spurts that make individuals reproductively mature.
Recurrent pregnancy loss (RPL), also referred to as recurrent miscarriage or habitual abortion, is historically defined as 3 consecutive pregnancy losses prior to 20 weeks from the last menstrual period.
This document discusses menopause and hormone replacement therapy. It begins by defining menopause as the permanent stoppage of menstruation due to declining ovarian function. It then discusses the stages of menopause including perimenopause and the changes in hormones like FSH and estrogen that occur. The document notes that menopause is a natural process but can cause both short term symptoms and long term health issues if estrogen is not replaced. It evaluates the risks and benefits of different treatment options for menopause including lifestyle changes, alternative therapies, medical treatments, and hormone replacement therapy.
This document discusses menopause and andropause (the male equivalent). It defines menopause as when a woman's monthly menstrual cycle ends permanently, usually occurring around age 50. Andropause is a slow decline in testosterone production in men with age. Both result in lower sex hormone levels and can cause symptoms. The document reviews hormone production and roles, common symptoms, and natural treatment options focused on supporting the body's own hormone balance rather than external replacement.
The document discusses age-related changes to the endocrine system. It covers changes to the hypothalamic-pituitary-adrenal axis, growth hormone, thyroid, adrenal cortex and medulla, pancreas, and hypothalamic-pituitary-testicular axis. Key effects of aging include decreased hormone production and feedback inhibition as well as increased pituitary and adrenal involvement in stress response. Diagnosing endocrine disorders can also be challenging in elderly patients due to nonspecific symptoms and normal age-related endocrine changes.
Steroid hormones such as progestogens and androgens may play a role in epilepsy through various mechanisms. Progestogens have been shown to decrease seizure frequency in some women, especially during pregnancy. Their metabolite allopregnanolone has rapid anti-seizure effects independent of progesterone receptors. Androgens may also influence seizures and some rodent studies show metabolites like 3α-diol reduce chemically-induced seizures. Both progestogens and androgens may act through GABA receptors or by decreasing glutamate activity to influence neuronal excitability. Further research is needed to fully understand how steroid hormones and anti-epileptic drugs interact to impact seizures.
The document discusses the various stages of female development from embryonic development through menopause. It covers the neonatal period, childhood, puberty, adolescence, sexual maturity, climacterium, and senium. For each period, it describes the development of the reproductive system including the uterus, ovaries, and other genital organs. It provides details on hormonal influences, the onset of puberty and its stages, and physiological changes that occur during the various life stages of women.
This document defines and discusses andropause (also known as male menopause), including its definition, symptoms, epidemiology, pathophysiology, effects of testosterone deficiency, monitoring and risks/benefits of testosterone replacement therapy. Some key points are: andropause is characterized by declining testosterone levels and affects quality of life; symptoms include reduced energy, libido and erectile dysfunction; prevalence increases with age, with 20% of men over 60 and 50% of men over 75 having low testosterone; testosterone replacement can improve symptoms in men with very low levels if administered carefully under medical supervision due to risks like prostate issues.
Male gonadal function and dysfunction (male hypogonadism). Emphasis where made on the causes, types of male hypogonadism, diagnosis and treatment methods.
This presentation discusses the launch of Tibone® tablet by Masum Chowdhury. Some key points:
- Tibone® (tibolone) is a tissue-specific hormone replacement therapy for menopausal symptoms like hot flashes and osteoporosis.
- The presentation outlines Tibone®'s efficacy, safety profile, and effects on mood, sexuality, bones, cardiovascular system and more based on clinical experience.
- An action plan is proposed to position Tibone® as the first choice for menopausal symptom management and increase its prescription share over competitors like Livial and Uvilon.
Andropause, also known as male menopause, is the gradual decline in testosterone levels that occurs in men as they age. Unlike female menopause which is sudden, andropause is a slow process resulting in more subtle symptoms. Low testosterone can negatively impact many organ systems and quality of life. Treatment options include lifestyle changes as well as hormone replacement therapy administered through oral, injectable, or transdermal methods. However, testosterone therapy may increase risks for certain health conditions like sleep apnea and prostate issues.
This document discusses infertility and polycystic ovary syndrome (PCOS). It defines PCOS and outlines its diagnosis criteria. PCOS is diagnosed based on somatic or lab indicators of hyperandrogenism, oligo-anovulation, and polycystic ovarian morphology, while excluding other disorders. Treatment options for PCOS include weight loss, exercise, clomiphene, aromatase inhibitors, metformin, and gonadotropins. Long-term management may involve birth control pills, metformin therapy, and lifestyle changes to reduce risks of weight gain, hyperandrogenism, and cardiac or metabolic diseases.
This document summarizes a case of a 21-year-old female with primary amenorrhea and hot flashes. Her lab tests showed elevated FSH and LH levels consistent with premature ovarian insufficiency. The document defines premature ovarian insufficiency as cessation of menses before age 40 due to depletion or dysfunction of ovarian follicles. It discusses causes, risk factors, symptoms, diagnosis, and treatment options which include hormone replacement therapy and in vitro fertilization with donor eggs. Counseling is recommended to address psychological and family planning aspects.
This document discusses sperm DNA fragmentation testing in male infertility. It provides background on causes of male infertility and the significance of sperm DNA fragmentation. Normal values for semen analysis are outlined according to WHO guidelines. Methods for diagnosing DNA fragmentation including Comet, TUNEL, SCD, and SCSA assays are described. Factors that can cause DNA fragmentation including lifestyle, medical conditions, and environmental exposures are covered. The importance of selecting sperm with intact DNA for ART procedures like ICSI is emphasized. Lifestyle modifications and treatment of underlying conditions may help reduce DNA fragmentation before ART.
Thyroid Disorders & infertility Dr jyoti Agarwal , Dr Sharda Jain Lifecare Centre
Thyroid disorders can significantly impact fertility in both females and males. Hypothyroidism is associated with menstrual irregularities and anovulatory cycles in females which can lead to infertility. It may also cause delayed puberty. In males, untreated hypothyroidism from a young age can damage testicular development. The document discusses the prevalence of thyroid disorders like hypothyroidism and thyroid autoimmunity in infertile populations. It recommends evaluating thyroid levels through TSH tests for all women with infertility and treating any thyroid abnormalities. Treatment of hypothyroidism is important to improve fertility outcomes and IVF success rates.
Oxidative stress from reactive oxygen species can impair sperm function and contribute to male infertility. Antioxidants may help reduce oxidative stress and improve fertility outcomes. Oral antioxidant supplementation in men with oxidative stress issues has been shown to increase pregnancy and live birth rates when undergoing assisted reproductive technologies. However, more research is still needed to determine the best candidates, formulations, dosages and duration of treatment for oral antioxidant therapy in cases of male infertility related to oxidative stress.
Physiology of Male Infertility | Seeds of InnocenceSOI Delhi
Male Infertility is a inability that causes pregnancy in a female fertile. Male infertility is commonly due to Low sperm Count. Soi provides best male infertility treatment in delhi, ghaziabad - India. Call us : 9810350512
visit : www.seedsofinnocence.com
1. Puberty is defined as the transitional stage from childhood to adulthood that is characterized by physiological changes and development of secondary sex characteristics.
2. It typically occurs between ages 10-16 and is influenced by genetic and environmental factors such as nutrition, geography, and light exposure.
3. The stages of puberty include thelarche, adrenarche, growth spurt, menarche, and development of secondary sex characteristics over approximately 4.5 years.
Placental hormones lec by liza tarca, mdLiza Tarca
The document discusses the functions and hormones of the human placenta. It begins with an introduction to placental hormones and their production by the trophoblast. It then discusses the key placental hormones in detail, including human chorionic gonadotropin (hCG), human placental lactogen (hPL), estrogen, progesterone, and other protein hormones. For each hormone, it provides information on synthesis, levels during pregnancy, roles in sustaining pregnancy, and associated medical conditions. The document aims to educate on the endocrine functions and important hormones of the human placenta.
The document discusses pubertal disorders and their classification, causes, diagnosis, and management. It begins by defining key terminology related to puberty and describing the normal physiology and regulation of the hypothalamic-pituitary-gonadal axis during puberty. Pubertal disorders are classified as either precocious or delayed puberty. Causes of delayed puberty include hypergonadotropic hypogonadism due to genetic defects or acquired conditions, and hypogonadotropic hypogonadism caused by tumors or CNS disorders that disrupt the HPG axis. Assessment of pubertal development involves the Tanner staging system.
The document discusses the biochemical changes that occur in pregnancy, including increased secretion of hormones by the placenta such as estrogen, progesterone, human chorionic gonadotropin (HCG), and human somatomammotropin. These hormones play important roles like preventing menstruation and supporting fetal development. The placenta produces high quantities of hormones later in pregnancy. Additionally, the pituitary and other glands increase secretion of hormones like corticosteroids and thyroxine to support the mother and fetus.
Puberty is the stage of physical maturation triggered by increased secretion of hormones like Luteinizing Hormone and GnRH, resulting in sexual and somatic development. It involves breast development in females starting around age 10-14 and testicular growth in males around age 12-16. Puberty encompasses five stages of physical changes through Tanner stages including growth spurts that make individuals reproductively mature.
Recurrent pregnancy loss (RPL), also referred to as recurrent miscarriage or habitual abortion, is historically defined as 3 consecutive pregnancy losses prior to 20 weeks from the last menstrual period.
This document discusses menopause and hormone replacement therapy. It begins by defining menopause as the permanent stoppage of menstruation due to declining ovarian function. It then discusses the stages of menopause including perimenopause and the changes in hormones like FSH and estrogen that occur. The document notes that menopause is a natural process but can cause both short term symptoms and long term health issues if estrogen is not replaced. It evaluates the risks and benefits of different treatment options for menopause including lifestyle changes, alternative therapies, medical treatments, and hormone replacement therapy.
This document discusses menopause and andropause (the male equivalent). It defines menopause as when a woman's monthly menstrual cycle ends permanently, usually occurring around age 50. Andropause is a slow decline in testosterone production in men with age. Both result in lower sex hormone levels and can cause symptoms. The document reviews hormone production and roles, common symptoms, and natural treatment options focused on supporting the body's own hormone balance rather than external replacement.
The document discusses age-related changes to the endocrine system. It covers changes to the hypothalamic-pituitary-adrenal axis, growth hormone, thyroid, adrenal cortex and medulla, pancreas, and hypothalamic-pituitary-testicular axis. Key effects of aging include decreased hormone production and feedback inhibition as well as increased pituitary and adrenal involvement in stress response. Diagnosing endocrine disorders can also be challenging in elderly patients due to nonspecific symptoms and normal age-related endocrine changes.
Steroid hormones such as progestogens and androgens may play a role in epilepsy through various mechanisms. Progestogens have been shown to decrease seizure frequency in some women, especially during pregnancy. Their metabolite allopregnanolone has rapid anti-seizure effects independent of progesterone receptors. Androgens may also influence seizures and some rodent studies show metabolites like 3α-diol reduce chemically-induced seizures. Both progestogens and androgens may act through GABA receptors or by decreasing glutamate activity to influence neuronal excitability. Further research is needed to fully understand how steroid hormones and anti-epileptic drugs interact to impact seizures.
1) Male hypogonadism is caused by androgen deficiency and can affect multiple organ functions and quality of life. It has various forms that are caused by different factors and have implications for evaluation and treatment.
2) Diagnosis is based on clinical signs and symptoms of androgen deficiency along with low serum testosterone levels on two occasions. Treatment aims to restore testosterone levels to improve quality of life.
3) Testosterone replacement therapy options include oral, injectable, topical, and implant preparations. Risks include side effects and potential impacts on the prostate and cardiovascular and breast health that require monitoring.
OP MED Conf TESTOSTERONE with Anti estrogensMichael Lada
The document discusses the diagnosis and management of hypogonadism. It defines hypogonadism and outlines the key diagnostic steps including medical history, physical exam, and lab tests to distinguish between primary and secondary causes. The primary care management of hypogonadism is also reviewed, including treatment with testosterone and monitoring of side effects.
The document discusses the role of various endocrine glands and their hormones on the periodontium. It describes the central endocrine glands of hypothalamus and pituitary gland which regulate other endocrine glands. It then explains the peripheral endocrine glands like thyroid, parathyroid, adrenal and sex glands and the effects of their hormones like cortisol, thyroid hormones, parathyroid hormone and sex steroids on the periodontium and periodontal tissues. It proposes various mechanisms through which these hormones can influence the periodontium like their effects on immune cells, bacterial microbiota and gene expression of periodontal cells.
Source, synthesis and metabolism of androgensTHILAKAR MANI
Testosterone is the principal androgen produced by the testes and adrenal glands. It is synthesized from cholesterol through a series of enzymatic reactions regulated by LH and FSH. Most testosterone circulates bound to plasma proteins while a small fraction acts upon androgen receptors in target tissues like muscle and bone. There it is converted to the more potent dihydrotestosterone which influences male sexual development and secondary sex characteristics as well as spermatogenesis and behaviors. Androgens play an important role in protein synthesis, carbohydrate and mineral metabolism. Abnormalities in androgen levels or signaling can impact male reproductive function and health.
Male hypogonadism is caused by androgen deficiency which can negatively impact organ functions and quality of life. The goal of testosterone replacement therapy is to restore hormone levels to the normal range and alleviate symptoms. Common treatment options include injections, patches, gels, and implants which can restore sexual function, muscle strength, and bone density. Therapy requires monitoring for side effects like prostate issues or blood clots. Gonadotropins may also be used to stimulate testosterone production and spermatogenesis in hypogonadotropic hypogonadism.
This document discusses testosterone deficiency in males. It begins by introducing testosterone as the principal male sex hormone, playing a key role in male reproductive tissue development and secondary sexual characteristics. It then discusses levels of testosterone in adult males versus females, and the measurement and variations of testosterone levels. Common causes that can alter sex hormone-binding globulin and affect testosterone measurements are outlined. The document also covers primary and secondary testosterone deficiency, defining each and providing examples of causes. Androgen insensitivity syndrome is discussed as another cause of testosterone deficiency due to defects in androgen target organs. Age-related declines in testosterone are reviewed, along with studies on the prevalence of testosterone deficiency in aging males. Diagnosing
HYPOGONADISM 1Clinical evaluation and management of hypogoLizbethQuinonez813
HYPOGONADISM 1
Clinical evaluation and management of hypogonadism
United States University
FNP: 593 Acute illnesses across the lifespan
Brittany Chavez
12/10/2021
TITLE OF PAPER
Clinical evaluation and management of hypogonadism
The purpose of this paper is to discuss Hypogonadism in regard to clinical evaluation,
symptomatic presentation, management and evaluation of clinical guidelines. The paper will
explore differing viewpoints and key concepts in relation to hypogonadism. The effects of
cultural, spiritual and beliefs in treatment and evaluation, and the impact of research on this
endocrine imbalance. Also reviewed will be research studies addressing the clinical symptoms
and trials for new treatment options.
Review of topic and rationale for selection of topic
Hypogonadism is a common endocrine disorder originating from two causes. Primary
hypogonadism is caused from a direct androgen imbalance originating from the testes. This
clinical syndrome which the testes fail to produce physiologic levels of testosterone and a normal
number of spermatozoa due to defects in the hypothalamic-pituitary-gonadal axis at one or more
levels. (Ross & Bhasin, 2016). This topic was chosen due to the frequency of cases seen in the
family practice setting. Hypogonadism is a common disorder associated with low bone density,
poor muscle mass, anemia, and sexual dysfunction that affects men in a variety of ways. Among
secondary osteoporosis risk factors, male hypogonadism is one of the most important, accounting
for progressive bone loss in aging men, especially when late-onset hypogonadism is
diagnosed (LOH). (Rochira, 2020) This disorder can affect all aspects of life and greatly impact
the emotional state and feelings of self-worth. This paper will address primary hypogonadism in
terms of diagnostic, and treatment based on guidelines.
Evaluation of key concepts related to the topic
The key concepts evaluated for the paper includes disease process in formation of
androgen deficiency. Androgens are important for male reproductive and sexual functions, body
TITLE OF PAPER 3
composition, erythropoiesis, muscle and bone health, and cognitive functions. Symptoms
presentation commonly seen in the primary care setting. Diagnostic criteria in the evaluation to
determine the extent of deficiency in relation to the symptoms presented and the treatment
guidelines based on efficacy and positive outcomes.
Primary Hypogonadism (PHG) is often underdiagnosed in the clinical setting due to the
ambiguous symptoms presented often mimicking depression or often overlooked as normal
aging process. These symptoms may present with decreased libido, weight gain, fatigue, low
stamina, decrease in muscle mass, decreased energy, sleep disturbances, mood fluctuations and
irritability.
It is essential for the provider to consider hormonal deficiency into the differential
diagnosis to effectively diagnose and rule o ...
The document discusses the effects of various hormones from the endocrine system on the periodontium. It begins by describing the hypothalamus and pituitary gland which regulate hormone release from other endocrine glands. It then examines the effects of hormones from the thyroid, adrenal, pancreas, parathyroid, and gonads. Specific hormones like growth hormone, cortisol, insulin, and sex steroids are discussed in relation to periodontal health and disease. The document also proposes potential mechanisms of action for various hormones and reviews relevant literature on this topic.
The document discusses the effects of hormones from various endocrine glands on the periodontium. It describes how hormones from the hypothalamus and pituitary gland regulate other endocrine glands. It then examines the specific effects of hormones from the adrenal, thyroid, parathyroid, gonads and pancreas on periodontal tissues and the mechanisms by which they may influence periodontal health and disease. It also discusses how gender, age and hormone supplements can impact the effects of sex hormones on the periodontium.
Andropause, also known as male menopause, is defined as a syndrome of age-related low testosterone levels in older men. It is characterized by signs and symptoms that include reduced libido, erectile dysfunction, fatigue, depression and changes in body composition. The prevalence of low testosterone increases with age, affecting up to 49% of men over 80 years old. Testosterone replacement therapy can effectively treat the signs and symptoms of andropause and is generally safe for most men when monitored closely. However, risks include sleep apnea, prostate issues, cardiovascular effects and polycythemia.
This document discusses male gonadal function and dysfunction, including causes and treatment of hypogonadism. It covers primary hypogonadism conditions like Klinefelter syndrome and secondary causes such as tumors or drugs. Diagnosis involves measuring testosterone, LH and FSH levels. Treatment options for hypogonadism include testosterone replacement therapy via patches, gels or injections, with monitoring of side effects like prostate issues.
The document discusses male gonadal function and hypogonadism. It covers causes of primary and secondary hypogonadism, including Klinefelter's syndrome and Noonan's syndrome. Symptoms of hypogonadism before and after puberty are described. The challenges of diagnosing and treating hypogonadism in aging males are also covered, along with monitoring of testosterone replacement therapy and other treatment options.
Physiological reduction of the gonadal sex hormones in old ages results in declined neurogenesis especially in the hippocampus with the resultant age dependent memory and executive functions regressions.
Physiological reduction of the gonadal sex hormones in old ages results in declined neurogenesis especially in the hippocampus with the resultant age dependent cognitive impairment and risk of AD
This document discusses male reproductive endocrinology and related disorders. It covers the physiology of the hypothalamic-pituitary-gonadal axis and testosterone production. It then discusses specific conditions like gynecomastia and male hypogonadism. For gynecomastia, it describes the pathophysiology and treatments. For hypogonadism, it defines it and discusses the etiologies, symptoms, and diagnosis of both primary and secondary hypogonadism.
This presentation provides an overview of androgen deprivation therapy (ADT), also known as hormone therapy, for prostate cancer. It discusses the basic principles, including how prostate cancer cells rely on androgens like testosterone to grow. ADT aims to stop androgen production or block their effects. Methods include surgical removal of the testes, medications to reduce testosterone production, and anti-androgens to inhibit testosterone's action. Side effects from lowering testosterone levels can include hot flashes, fatigue, reduced libido and sexual dysfunction, as well as increased risks of osteoporosis, obesity, and cardiovascular issues over the long term.
Advanced nutrition for the brain series: stress, the HPA-axis and neuroinflammation. Targeted nutritional interventions for successful treatment of mental health conditions.
Inflammation is a major contributing factor to chronic modern illness and is driven, in part, by chronic stress and HPA-axis over stimulation. Mental health conditions, in particular clinical depression, are increasingly linked with neuroinflammation. As such, anti-inflammatory interventions are known to result in significant clinical benefits.
During this webinar Dr Bailey will discuss the biological mechanisms linking stress, chronic inflammation and mood disorders, together with a review of the current evidence for a targeted, anti-inflammatory nutrition approach to treatment. Nina will also clarify why some of the recent trials have failed to report benefits and how to optimise your anti-inflammatory interventions to treat clients with anxiety, depression, schizophrenia and PTSD.
Suvorexant, branded as Belsomra, is an insomnia medication that works by blocking orexin receptors in the brain. Orexin is a neuropeptide that promotes wakefulness, so blocking its receptors promotes sleep. Suvorexant is thought to exert its therapeutic effects for insomnia by inhibiting the wakefulness-promoting effects of orexin. A current study is investigating whether long-term use of suvorexant can slow the accumulation of amyloid plaques and tau tangles in the brain, which are hallmarks of Alzheimer's disease. The results so far suggest suvorexant may be able to temporarily reduce levels of these proteins.
The document discusses the relationship between hormones and behavior. It covers several topics:
- The endocrine system and its role in maintaining homeostasis, growth and development, and reproduction.
- Studies showing connections between sex hormones and cognitive functioning, aggression, mood, and sleep. Removing or adding hormones can impact behaviors.
- Early experiments by Berthold demonstrating changes in rooster behavior and appearance based on castration and testis transplantation.
- Conditions like Kallmann syndrome, Turner syndrome, and 5α-reductase deficiency that impact sexual development and behaviors due to hormone deficiencies or insensitivities.
- Evidence that testosterone levels relate to traits like aggression and can change based on
This document discusses hormones and their relationship to cancer development. It defines cancer and different types of tumors, and notes that over half of cancers in the US could be prevented through lifestyle changes. Tables show the most common cancers among men and women. The document discusses how hormones like estrogen can promote the growth of hormone-sensitive tumors through various mechanisms, including stimulating cell proliferation and producing genotoxic metabolites. It also discusses how hormones like insulin may increase cancer risk by influencing cell signaling pathways and metabolism.
Puberty is initiated by increases in hormones like leptin and kisspeptin which activate the hypothalamic-pituitary-gonadal axis, triggering the release of sex hormones and setting off physical changes. In females, puberty involves breast development, pubic hair growth, menarche, and ovarian and uterine maturation over 3-5 years starting around age 10. In males, it involves testicular growth, pubic hair growth, penis growth, voice deepening, and a growth spurt over 3-5 years starting around age 11. Throughout puberty, sex hormones influence brain development and increase emotional volatility and risk-taking behavior.
The document discusses population growth and food production since Thomas Malthus predicted that population growth would outpace food production, leading to catastrophe. It notes that while population has grown rapidly, food production has grown even faster. The summary also mentions that debates continue about the relationship between population growth, resource consumption, and environmental degradation.
The document discusses the placenta and its functions. It begins by defining the placenta and its origins from Latin. It then discusses:
1) Companies in Japan that produce extracts from human placenta to treat conditions like menopause and hepatitis.
2) The placenta's roles in transporting nutrients, gases, and waste between the mother and fetus. It has endocrine functions and produces hormones to maintain pregnancy and support fetal development.
3) The development of the placenta from the blastocyst stage through implantation and formation of the chorion and villi to facilitate exchanges between mother and fetus.
This document discusses gestational diabetes. It provides information on:
1. Gestational diabetes is a form of diabetes that develops during pregnancy in women who do not have diabetes otherwise. It is caused by pregnancy hormones and/or insulin deficiency.
2. While gestational diabetes usually resolves after delivery, it increases the mother's risk of developing type 2 diabetes later in life. It can also increase risks for the baby if not well controlled, such as being too large or jaundice.
3. Screening all pregnant women for gestational diabetes is recommended, as prior selective screening missed some cases. Screening and treatment can help reduce risks for both mother and baby.
This document discusses hormones involved in obesity and weight regulation. It describes how leptin signals fullness, while the set point is the weight maintained without effort to gain or lose. A higher set point occurs with more eating, lowering basal metabolism. Environmental factors, genetics, stress and chemicals can influence weight homeostasis by altering hormones. Obesity is associated with reduced testosterone in men and increased cancer risk. Ghrelin signals hunger opposite to leptin. The hypothalamus regulates food intake through a set point model to maintain a constant mass.
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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.
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).
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Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. What is Aging?
2
GENERAL-hormone production altered
THYROID- decreased secretion
THYMUS-involution of thymus gland
CORTISOL- decrease anti-inflammatory hormone
PANCREAS- decrease secretion of enzymes & hormones
The gradual and spontaneous changes that occur in maturation from infant to young adult. These changes create a normal physiologic decline seen
in middle and late adulthood.The process by which a cell looses its ability to divide, grow, and function. This loss of function ultimately ends in death.
Biological clocks act through hormones to control the pace of aging. Hormones effects growth, metabolism, temperature, inflammation and stress.
Aging is not a disease
4. Overall, some hormones are decreased, some unchanged, and some increased
with age.
Hormones that are usually decreased include:
Aldosterone
Calcitonin
growth hormone/insulin-like growth factor I axis (in somatopause)
Renin
Melatonine
In women, estrogen (in menopause )and prolactin levels usually decrease.
Testosterone (in andropause) levels usually decrease slightly as men age.
Dehydroepiandrosterone and its sulphate (in adrenopause)
Hormones that may increase include:
Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Norepinephrine
Hormones that remain unchanged or only slightly decreased include:
Cortisol
Epinephrine
Insulin
Parathyroid hormone
Thyroid hormones T3 and T4
25-hydroxyvitamin D
4
5. 5
Endocrine, Physical, sexual, psychological.
Endocrine Symptoms:
erectile dysfunction
Increased abdominal fat/increased waist
size
decreased vigor
fatigue
poor exercise tolerance
diminished strength and muscle mass
decrease in bone mineral density
decreased body hair
Sexual Symptoms:
decreased libido
decreased sexual activity
limited quality of orgasm
reduced ejaculate strength
reduced ejaculate volume
Psychological Symptoms:
Mood changes
Poor concentration
Loss of motivation
Reduced initiative
Memory impairment
Anxiety
Depression
Irritability
Insomnia
General reduction in intellectual activity
Poor work performance
7. The circulating levels of dehydroepiandrosterone (DHEA) and its
sulphate (DHEAS), which gradually decline with age, resulting
adrenopause.” The decline in DHEA(S) levels in both sexes contrasts
therefore with the maintenance of plasma cortisol levels and seems to be
caused by a selective decrease in the number of functional zona
reticularis cells in the adrenal cortex rather than regulated by a central
(hypothalamic) pacemaker of aging.
Steroidogenic acute regulatory protein (StAR) controls adrenal and
gonadal steroidogenesis. It was recently shown unequivocally that StAR
mRNA and protein are expressed within glia and neurons in discrete
regions of the mouse brain. Neurosteroids synthesized in the CNS appear
to attenuate age-relate memory and learning impairments.
The beneficial effects of PS and DHEA sulfate on age-related learning
and memory deficits appear to be mediated by NO-dependent pathway.
To determine whether the mechanism of attenuation was mediated
through the nitric oxide (NO) synthase (NOS) signal transduction
pathway, mice were pretreated with the NOS inhibitor, NG-nitrol-
arginine methyl ester (L-NAME). L-NAME inhibited the beneficial and
antiamnesic effects of PS and DHEA sulfate, and the effect of L-NAME
was blocked by the competitive substrate for NOS, L-arginine.
The adrenopause
7
8. During aging, GnRH levels declined. but the number of
neurons expressing ppGnRH mRNA remained constant.
Aging had no effect on pituitary responsiveness to GnRH.
Despite this similar LH response, the stimulatory effect of
LH on testosterone production declined, LH circadian
rhythmicity was blunted, and testosterone levels over 24 h
declined progressively with age.
Hence, deficits in testicular function during aging is
attributable, at least in part, to decreased GnRH rather than
decreased responsiveness of the anterior pituitary gland to
GnRH; this property and the attenuated circadian
rhythmicity of LH and testosterone secretion are
reminiscent of age dependent changes in the GH axis.
Aging also has impact on the opioid control of
gonadotropin secretion. Naloxone (opiate antagonist)
produced a significant dose-dependent increase in the
release of GnRH from the hypothalamic tissue fragments
that was age dependent. These results suggest that age-
related changes in endogenous opioid systems likely
contribute to differences in secretion of GnRH, which in
turn affects the dynamics of LH secretion and testosterone
production.
8
• Excitatory amino acids also regulate pulsatile secretion of
hypothalamic GnRH and LH.
To explore the significance of aging on this pathway, the
effects of GnRH and the glutamate receptor agonist NMDA
on gonadotropin and prolactin release were investigated in
prepubertal,young, middle-aged, and old rats. The release of
gonadotropins in response to GnRH was not age dependent,
and NMDA increased LH, FSH and prolactin secretion in all
age groups. However, the NMDA enhancement of LH, FSH,
and prolactin release was lowest in old rats. To investigate
whether the reduced LH response to NMDA in old rats
occurred at the hypothalamic level, the direct effects of
NMDA on GnRH release were evaluated in tissue fragments
from the preoptic medial basal hypothalamus.
The magnitude of GnRH release from these fragments was
inversely related to age, and determination of amino acid
content showed that aged animals had the lowest
concentrations of glutamate, taurine, and GABA. Hence, the
attenuated responsiveness of GnRH neurons to NMDA and
reductions in excitatory amino acids likely contribute to the
diminished pulsatile LH secretion typically observed in old
rats.
9. Pathophysiology of Andropause
Hypothalamus
Pituitary
Testes
Reduced Leydig cell number
Impaired Leydig cell function
Lower GnRH pulse amplitude
Attenuation of diurnal pulsatility
More sensitive to negative feedback
T
E
The decline in testosterone as men age results in part from a reduction in Leydig cell number to be 44% lower in men between the ages of
50 and 76 when compared to the men who were aged 20 to 48 years. decline in age related steroidogenesis results from a reduction in
steroidogenic enzyme activity and a decrease in cholesterol transfer to the mitochondria. It has been demonstrated that older men have a
subnormal testosterone response to beta HCG as well as recombinant LH administration. In older men with low T, LH levels may
increase, but usually remain within the normal range. Overall, studies suggest heightened sensitivity of the hypothalamus to negative
feedback as men age. Studies have also provided evidence of reduced GnRH amplitude as men age. Moreover, the normal circadian
pattern of GnRH secretion is attenuated with aging. FSH on the other hand is regulated neg by testis inhibin as well as GnRH. Inhibin
production decrease with aging and in all forms of testis failure. Thus FSH levels tend to be elevated to a greater extent than LH in
older men with low T.
9
11. Controlled trials of testosterone therapy in elderly males with low-normal testosterone levels
Age (years) Baseline T
(nmol/l)
T
administratio
n
Duration
(months)
Effects Side-effects
12.7 2.7 (SD)
[T <16.5]
Testosterone
(Testoderm,
scrotal patch)
6 mg/24 h
36 Lean body
mass -
,perception of
physical
functioning ,fat
mass. No
overall effect
on muscle
trength, BMD
(spine and hip),
lipids, and
bone markers
PSA (from 1.5
to 2.0
ng/ml) Hct
(>52% in
3 out of 54
subjects)
51 (22-78) 2.7 2.7 (SD)
[T <8.7]
Testosterone
(Testoderm,
scrotal patch),
6 mg/24 h
36 Libido, BMD
(L2-L4)
No effect on
muscle
strength, BMD
(hip), and
lipids
Hct (>52% in
1 out of
18 subjects) No
change
in PSA
76 ± 4 13.5[6.0]
[BT <4.4]
Testosterone
(transdermal
patch) 5.0
mg/day
12 Femoral BMD
, lean
body mass ,
body fat ¯
No effect on
muscle
strength
PSA (from 2.0
to 2.6
ng/ml) No
effect on Hct
11
Testosterone levels decline by about 100 ng/dL
per decade.
higher rate of ‘prostate events’ with
testosterone treatment.
GH levels decline by about 14% per decade, but
the risks of GH therapy outweigh the benefits
in non-GH-deficient people.
Although serum levels of many hormones
decline with age, additional research is needed
to prove that these declining levels are
pathologic and that hormone replacement
actually affects the aging process.
12. Testosterone Decrease in fat mass and increase in lean
mass and bone mineral density Mixed data
on the effect on cognition.
Dehydroepiandr
osterone
Inconsistent data on muscle mass, fat mass,
and strength. Insufficient evidence for
improvement in cognition.
Growth
hormone
Increase in lean body mass; decrease in fat
mass. Increase in bone mineral density.
Increase in mortality.
Vitamin D May improve muscle function
HORMONAL THERAPY Testosterone replacement also has the
potential to inhibit neurodegeneration by
maintaining expression of BDNF
in the aging brain.This is particularly important
because of the importance of BDNF in
maintaining noradrenergic
innervations during aging as well as its proposed
significance in Parkinson’s disease and AD.
12
13. Hormonal decline may be the most important
major contributor to aging. Physical changes during
aging have been considered physiologic, but there is
evidence that some of these changes are related to this
decline in hormonal activity.
For men - it is so gradual that men often reach their
mid-forties or fifties without noticing the negative
changes that have taken place in their body.
For women - hormonal changes can begin as early
as the mid to late thirties. The decline in hormones for
men is more gradual unlike in women’s menopause, which
is a more abrupt event.
In women, the amount of TSH produced does not decrease
with time, but it does in men.
With aging, the thyroid often becomes lumpy (nodular)
Metabolism gradually declines, beginning around age 20.
Less thyroid hormone may be produced, but there is also
less body mass (because of loss of muscle and bone tissue).
This means that thyroid function tests usually show results
within the normal range.
13
14. The somatopause
• Pituitary function, LH, FSH, and TSH decline
with age. therefore, that GH also has been
reported to decline with age beginning in the
third decade. This decrease is associated with
decreased insulin-like growth factor
concentrations. Pathologically decreased GH
is associated with decreased concentrations of
gonadal steroids in serum. Thus,
pathologically decreased GH is associated
with increasing fat, decreasing muscle mass,
and decreasing bone mass, all of which are
seen as age increases.
14
Body
fat
Lean body
mass
Strength Skeleton Cholesterol
Estrogen
deficiency in
healthy
women
no effect — —
Testosterone
deficiency in
healthy men
GH deficiency
in
healthy
individuals
15. 15
It is now well established that there is a physiological decline in food intake over the
life span. This has been termed the anorexia of aging hormones play a major. This
physiology of aging represents a major reason why older persons have a greater
propensity than younger ones to lose weight when they have a disease. Older persons
tend to have early satiation. This is due to two factors.
1. decrease in compliance of the fundus of the stomach with aging.
This occurs because food fails to cause appropriate release of nitric
oxide to relax the smooth muscles of the fundus.
2. CCK is a potent satiating agent. Older persons produce more CCK in
the duodenum both basally and in response to fat. The increase in
CCK is predominantly due to slower clearance in older persons than in
younger persons.
Leptin is anorectic and increases metabolic rate. Thus, it is a catabolic hormone.
Men develop a greater physiological anorexia of aging than do women. Beyond the
age of 70, fat mass declines in men. This would be expected to lead to a decline in
leptin levels, but a longitudinal study showed that leptin levels increase in older men.
This increase in leptin levels was related to the fall in testosterone levels that occurs
with aging.
Ghrelin Recently a peptide hormone called ghrelin was isolated from the fundus of
the stomach. Ghrelin causes the release of growth hormone and an increase in
feeding. Ghrelin or an analog appears to have potential as a therapy for the anorexia
of aging.
16. 16
thyroid function is imperative for normal
development in human aging.
cretinism, deficiencies in iodine and thyroid,
the link between thyroid hormones
and cognition.
At any age, low thyroid function is also
associated with cognitive decline, since
hypothyroidism is associated with brain hypo
metabolism.
In the aging population, low uptake of
glucose associated with Alzheimer’s disease
and may even present decades prior to any
clinical symptoms of neurodegeneration.
cognitive decline product of the aging
process and physiological effects in thyroid
function
17. With aging there is:
a decline in thyroxine production rate
small decline in triiodothyronine (T3) levels
Thyroid stimulating hormone (TSH) levels are
increased
antibodies to thyroid peroxidase increase with aging.
There is emerging evidence that, with aging, thyroid
hormone tends to be less capable of activating a number of
postreceptor biomarkers of thyroid function.
Excess and deficiency of thyroid hormone are two classical
examples of atypical presentation of disease in older
persons. Thus, early hypothyroidism is a biochemical
diagnosis in older persons.
Older persons often develop the low T3 syndrome or the
euthyroid sick syndrome. In these persons, T3 is markedly
decreased and thyroxine may be normal or decreased. TSH
levels may be decreased, unchanged, or increased. There is
no evidence that thyroid replacement improves outcomes in
this condition.
These abnormalities are mainly caused by autoimmunity and
are therefore an expression of age-associated disease rather
than a consequence of the aging process.
17
18. 18
With ageing as well as body weight, thyroid volume increases slightly.
Other factors, : cigarette smoking, chronic kidney disease, acute hepatic disease, and seasonal changes, increase thyroid volume.
no age-related changes of serum free and total T4 levels.
In aging, nocturnal pulses of TSH secretion in comparison to their younger counterparts
since aging TSH secretion, this effect is counter balanced, leading to unchanged T4 levels.
T3 levels also remain stable with aging.
Malnutrition and chronic illness important confounders in assessing thyroid function in the elderly.
Both cause serum T3 levels in absence of thyroid disease
other non-thyroidal illnesses with aging can decrease T4 conversion to T3
medications an important role in thyroid function in the elderly.
Lithium (hyperthyroidism), amiodarone (hyperthyroidism), estrogens and glucocorticoids (thyroid binding globulin status) can affect thyroid
function.
with age, increased prevalence of anti-thyroperoxidase and anti-thyroglobulin antibodies, especially in females above 60 years of age.
in centennials ، thyroid antibodies are rare in comparison to hospitalized patients
decrease in free T3/free T4 ratio with age in males, but not females, suggesting impaired T4 to T3 conversion in males.
increase T3 resistance index with age in males, but not females.
elevated TSH levels with age along with normal T4 levels a question about subclinical hypothyroidism
Ischemic heart disease and its association with thyroid function: any association
19. 19
prevalence of ischemic heart disease in individuals with subclinical hypothyroidism is
higher in younger compared to ages 65 and older
treatment of subclinical hypothyroidism has been shown to be associated with fewer
events of ischemic heart disease in the younger but not in older than age 70.
inverse correlation between subclinical hypothyroidism and ischemic heart disease.
These indicate TSH levels play a cardiovascular protective role.
high TSH levels and low T4 levels associated with a lower mortality survival
centenarians have significantly higher median serum TSH levels and lower T4 levels
compared with control group of thyroid disease-free individuals (median age of 68 years).
Hyperthyroidism, is not as common as hypothyroidism, but its prevalence does increase
in the elderly.
Depending on iodine intake in the given area, Grave’s disease and toxic multinodular
goiter are most common causes.
lower metabolic rate caloric restriction improve mortality rates in animals
20. 20
Thyroid hormone regulates metabolism via adrenergic stimulation
and glucose uptake. It plays a role in mitochondrial gene expression,
affecting mitochondrial oxidation in skeletal muscle. Effects of
hypothyroidism with aging can lead to lipid accumulation.
compromising metabolic activity. This can result in insulin resistance
and other features of metabolic syndrome. increased metabolic rate
has shown to cause early mortality by accelerating aging.
Basal metabolic rate usually declines with aging indicating a healthier
functional status and low energy requirements for maintaining
homeostasis. basal metabolic rates in the young and older individuals it
has been shown that the higher the metabolic rate in the younger
predictability the higher mortality. independent of other risk factors such
as body mass index, smoking status, daily physical activity, blood
pressure and diabetes In older individuals who fail to down regulate the
metabolic rate with age usually have poor health status and shown to
have higher risk of mortality.
atrial fibrillation due to hyperthyroidism is higher in the elderly but
other symptoms such as heat intolerance, tremors, and ocular
manifestations are less frequent .Non-thyroidal illness, fasting, and
drug-induced causes must be ruled out before making the diagnosis.
21. Pathophysiology of diabetes mellitus in older persons
The prevalence of type 2 diabetes is age-related. As age increases, on average, a small
increase in fasting hepatic glucose output is reported, with impairment of non-insulin-
dependent glucose disposal. In addition, insulin secretion is impaired with age, with less
insulin being released in the early and late phase after challenges. insulin resistance
increases with age. Other endocrine changes, particularly in adrenal function with age, may
also play a role in this process . In addition, dietary intake, activity, and body composition
alter with age and may play a role in increasing insulin resistance in older individuals.
21
The sex steroids, dopamine,
oxytocin, and 5-HT regulate
sexual behavior through
actions in the CNS. Because
the production of these
hormones and
neurotransmitters declines
during aging, it is hardly
surprising that aging is
commonly associated with a
decline in libido and sexual
performance.
Sexual Behavior and Aging
22. Adrenal Function
Adrenal medullary function and baseline serum
epinephrine and norepinephrine concentrations
apparently increase with advancing age. the
increasing incidence of type 2 diabetes and peripheral
insulin resistance undoubtedly is exacerbated by the
constant increased basal concentrations of epinephrine
and norepinephrine.
Adrenal cortical function also appears to increase
with age. Thus, mean glucocorticoid and
mineralocorticoid serum concentrations are higher
in older compared with younger individuals. The
target organ for mineralocorticoid activity (kidney),
however, becomes less responsive as age progresses,
and sodium losses become more fixed as age
progresses.
Increased basal adrenal medullary and cortical activity
reduces the functional reserve for either epinephrine/
norepinephrine or steroid hormones. This
circumstance provides less ability to respond to stress,
corresponding to an initial frailty syndrome. 22
Decreased skeletal mass associated with increasing age is
the result of a series of changes associated with aging:
Calcium absorption/transport in the intestinal mucosa
decreases with age
calcium intake also generally decreases with age
Renal function, including 1-α- hydroxylase activity,
decreases with age
1- α -Hydroxylase catalyzes the conversion of 25OHD to
1,25(OH)2D, the active metabolite of vitamin D.
Decreased 1,25(OH)2D leads to further diminution of
vitamin D sensitive calcium absorption.
decreasing calcium absorption from the gut:
(a) decreased calcium intake
(b) decreased calcium absorption
(c) decreased vitamin D-dependent calcium absorption
(d) The result of decreased calcium absorption is
increased dependence on skeletal calcium as a source
of needed calcium
Other changes related to age occur in mineral metabolism.
As renal function declines with age, PTH increases.
Increasing PTH is associated with increased osteoclastic
and osteoblastic activity. Such increased activity is
probably associated with more rapid loss of bone.
Skeletal/Mineral Metabolism
23. 23
Glucocorticoid Hormone
glucocorticoid secretion shows a strong 24-h rhythm with peak concentrations in the early morning and a trough in the late
afternoon. Glucocorticoids are known to play a role in the regulation of peripheral glucose mobilization and metabolism.
cortisol is essential for cognitive appraisal and affects numerous cognitive domains, including attention, perception, memory,
and emotional processing in humans. Glucocorticoids play an important role in many neural functions that are mediated by
classic genomic effects via intracellular glucocorticoid receptors or nongenomic mechanisms.
Cortisol also participates in energy metabolism and gene expression in the brain, and it coordinates behavioral adaptation to
the environmental and internal conditions through the regulation of many neurotransmitters and neural circuits. A progressive
increase in levels of circulating cortisol occurs with increasing age, as well as in brain degenerative processes, for instance in
Alzheimer’s disease. This has been interpreted as a malfunction of the hypothalamo-pituitary-adrenal axis, and, according to
the glucocorticoid-cascade hypothesis, is considered as a main agent of injury to the hippocampus and to lead to the
cognitive impairment of the elderly, and as an added pathogenic factor in brain degeneration.
Cortisol may affect the intracellular concentrations of Ca2+ by membrane receptors or ion channels, which is one of the
important accessory factors in axonal transport. It has been shown that increasing free intracellular calcium may induce the
phosphorylation of tau proteins, which belong to the family of MAP, and influence the axonal transport. Glucocorticoid
resistance exists in AD brain, and is related to the degree of neuropathological changes, suggesting that glucocorticoid
resistance in AD brain may contribute to neuroendocrinal changes, neuropathological mechanisms and dementia.
Glucocorticoid resistance in AD may disturb not only the neural functions but also the negative feedback regulation via
different brain areas such as hippocampus and result in an activation of the HPA-axis and contribute to the pathogenetic
process of AD and induce cascade changes, such as the loss of neuronal Ca2+ homeostasis, abnormal production and
degradation of amyloid β-peptide (Aβ), development of NFT and neuronal degeneration. A potential injury to the hippocampus
has been postulated by the “glucocorticoid cascade hypothesis” as deriving from the life-long exposure to the stress
glucocorticoid hormone.
24. Examples of neurodegenerative disease:
• Alzheimer’s disease
• Parkinson’s disease
• Frontotemporal dementia
• Amyotrophic lateral sclerosis
(Lou Gehrig’s disease)
• Spinocerebellar ataxia
• Huntington’s disease
24
Alzheimer’s disease is an irreversible, progressive brain disease that slowly
destroys memory and thinking skills. Once considered a rare disorder, is now seen
as a major public health problem that is seriously affecting millions of older
population . Although the risk of developing AD increases with age – in most
people with AD, symptoms first appear after age 60 – AD is not a part of normal
aging. It is caused by a fatal disease that affects the brain.
25. 25
estrogens have neuroprotective effects, including inhibition of
β-amyloid formation from its precursor protein. This may be
due partly to reduced accumulation of reactive oxygen and
nitrogen species.
Glucocorticoid-induced hippocampal neuronal damage also
seems to be reduced.
Neuroimaging studies in humans have implicated that estrogen
influences the pattern of brain activation during memory
processing, with regional increments in cerebral blood flow
and glucose metabolism and with modulation of activity in
specific brain regions affected during the early stages of AD.
This may be partly related to direct effects on cerebral blood
flow by estrogens.
Epidemiological studies have suggested that estrogen is
protective against the development and/ or progression of
neurodegenerative disorders. Thus, low circulating levels of
estrogen have been associated with an increased risk of AD.
The estrogen β-receptor ERb has a clear role in the
development of the cerebral cortex and also in survival of
hippocampal neurons after exposure to excitatory
neurotoxins.
In contrast, Era is the major receptor subtype expressed in
basal forebrain cholinergic neurons. Thus, estrogen probably
acts via ERa to enhance cognitive functions through the
production of acetylcholine. On the other hand, ERb is the
only estrogen receptor expressed in the dorsal raphe nucleus
suggesting important effects on the serotonin system,
indirectly affecting neuronal plasticity.
Altered CNS function appears to precede the metabolic,
reproductive, and cognitive deficiencies associated with
aging. neuroendocrine changes characterized by:
altered biological rhythms
reduced amplitude
altered frequency, and decreased orderliness of hormone,
neuropeptide, and neurotransmitter release.
Decline in activity of the brain during aging. The
amplitude of release of neurotransmitters and
neuropeptides declines and the rhythms of release
become more erratic. Experiments using tissue
transplants from fetal brain and administration of L-
dopa and GHS-R ligands show the feasibility of
reversing certain aspects of aging through
therapeutic intervention.
26. 26
Senile plaques
• Extracellular deposits
• Plaques described as “diffuse”,
“neuritic”, or “cored”
• These may represent different ages of
plaque
• Neuritic plaques are one of the
pathologic criteria for diagnosis of
Alzheimer’s disease
• Composed chiefly of beta amyloid
Beta amyloid is a 39-43 amino acid peptide
Derived from 700 amino acid amyloid precursor
protein (APP), may be processed to “amyloidogenic”
or “non-amyloidogenic” pathways
Beta amyloid
27. 27
In the menopausal transition, menstrual cycle regularity is progressively lost due to
insufficient numbers of FSH-sensitive follicles present at any time in the ovaries .
Cycles become persistently shorter first, due to advanced dominant follicle selection with
shorter duration of the follicular phase. Later, cycles may also become lengthened with
delayed initiation of dominant follicle growth or anovulatory bleeding after estrogen
withdrawal without evidence of corpus luteum function.
The complete loss of cyclic ovarian follicular activity is defined as the final menstrual period
followed by 12 consecutive months of amenorrhea (menopause).
1. Hot flushes are a sensation of warmth, often accompanied by skin flushing and
sweating. Hot flushes are thought to be related to the rate of oestrogen withdrawal and
the resulting vasomotor instability.Many women experience palpitations, or a sensation
of pressure within the head, frequently accompanied by weakness, fainting or vertigo
before the flush begins. Treatment (Hormone replacement therapy, Clonidine,
Progesterone)
2-Urinary incontinence
The lining of the urethra is responsive to oestrogen, and the postmenopausal fall in oestrogen
results in physical changes that can increase rates of urinary incontinenceTreatment (Pelvic
floor exercises and bladder training, Hormone replacement therapy)
3-Vaginal atrophy
4-Mood, depression and cognitive function
Frequent hot flushes and the resulting insomnia .declining oestrogen levels.Midlife is often a
time of social and emotional upheaval
5-wound inflammation :roles of estrogens
6-increased prevalence and severity of atherosclerosis :antiatherosclerotic properties of
estrogens
7-osteoporosis :decrease in Inh B level
28. 28
• The reproductive aging process is thought to be dominated by a gradual decrease in
both the quantity and the quality of the oocytes residing within the follicles present in
the ovarian cortex.Menopause is the final step in the process referred to as ovarian
ageing. The age related decrease in follicle numbers dictates the onset of cycle
irregularity and the final cessation of menses.
• At the fourth month of fetal development, the ovaries contain some 6–7 million
oocytes surrounded by a layer of flat granulosa cells to form the primordial follicle
pool .
• Due to a rapid loss of the great majority of the primordial follicles via apoptosis in the
second half of fetal life, at birth only 1–2 million primordial follicles remain.
• After birth, this high rate of follicle loss slows down somewhat, so that at menarche at
least 300,000 to 400,000 primordial follicles remain.
• below 1000 at the time of menopause
• Along with the decrease in follicle number, oocyte quality also diminishes (at least
after the age of 31 yr).
• The loss of oocyte quality is believed to be due to:
1- an increase in meiotic nondisjunction,
2-resulting in an increasing rate of aneuploidy in the early embryo at higher female ages.
3-accumulated damage of oocytes in the course of a woman’s life
4- age-related changes in the quality of the granulosa cells surrounding the oocyte.
Despite the profound changes in numbers and quality of follicles during the third
and fourth decade of life, the process of ovarian aging remains largely unnoticed.
From several sources, it has become clear that monthly fecundity gradually
decreases from the mean age of 30 yr onward.
29. Number of primordial follicles present in the ovaries
and the chromosomal quality of oocytes in relation to
female age and corresponding reproductive events.
A number of terms including ‘climacteric’,
‘perimenopause’, ‘menopausal transition’,
‘postmenopause’ and ‘menopause’ have been
used to refer to the stages of reproductive
aging surrounding the final menstrual period
(FMP).
The first standardized classification
guidelines for female reproductive aging were
proposed in 2001 at the Stages of
Reproductive Aging Workshop (STRAW).
The stages were nominated using the FMP as
a reference point, and were based on changes
in the pattern of menstrual cycles levels of
follicle-stimulating hormone (FSH).
The STRAW criteria
29
30. The Stages of Reproductive Aging (STRAW) criteria
The proposed STRAW criteria were deemed unsuitable
for application in women who: smoked, were obese or
underweight (body mass index <18 or >30), participated
in intense regular physical training, had chronic
menstrual irregularities ,had abnormal reproductive
anatomy
30
Fecundity per cycle according to female age. Mean rate for women aged 20–30 was
scaled as 1.00. For a woman aged 33 yr, the relative rate of 0.75 indicates that she has in
each cycle 75% of the chance of a woman aged 20–30 of getting pregnant.
31. 31
higher risk of cardiovascular disease
elevated serum triglycerides
prothrombotic effects
increased hepatic synthesis of
vascular inflammatory markers
risk of stroke increases,
venous thromboembolism increase
Estrogen treatment in women with severe
postmenopausal symptoms.
Estrogen :orally or topically, with transdermal
patch, or intravaginally.
Low-dose estrogen in relieving hot flashes.
first The lowest dose to decrease adverse effects
of HRT.
HDL does play a protective role in menopausal
women