This document provides information on evaluating and treating delayed puberty. It defines delayed puberty and discusses the main causes, which include constitutional delay of puberty, hypogonadotropic hypogonadism, and hypergonadotropic hypogonadism. Evaluation involves assessing medical history, physical exam including Tanner staging, lab tests of hormone levels, bone age, and imaging if needed. Treatment depends on the underlying cause, and may include observation, sex hormone therapy, or treating any underlying medical conditions.
Congenital Adr Hyperplasia (CAH) can appear at any age from birth to puberty where it can lead to ambiguous genitalia. It is due to absolute or relative deficiency of 17 Hydroxylase or 21 Hydroxylase enzyme.
Congenital Adr Hyperplasia (CAH) can appear at any age from birth to puberty where it can lead to ambiguous genitalia. It is due to absolute or relative deficiency of 17 Hydroxylase or 21 Hydroxylase enzyme.
precocious puberty is one of the grey areas for pediatricians and gyenecologists. this is an attempt to answer some of the questions the content is references taken from authorative textbooks
There is general inconsistency in the nomenclature used to describe abnormal uterine bleeding (AUB) classification system for AUB, which has been approved by the International Federation of Gynecology and Obstetrics (FIGO) Executive Board as a FIGO PALM-COEIN classification system.
AIS is a genetic condition where affected people have male chromosomes and male gonads with complete or partial feminization of the external genitals
An inherited X-linked recessive disease with a mutation in the Androgen Receptor (AR) gene resulting in:Functioning Y sex chromosome and abnormality on X chromosome
precocious puberty is one of the grey areas for pediatricians and gyenecologists. this is an attempt to answer some of the questions the content is references taken from authorative textbooks
There is general inconsistency in the nomenclature used to describe abnormal uterine bleeding (AUB) classification system for AUB, which has been approved by the International Federation of Gynecology and Obstetrics (FIGO) Executive Board as a FIGO PALM-COEIN classification system.
AIS is a genetic condition where affected people have male chromosomes and male gonads with complete or partial feminization of the external genitals
An inherited X-linked recessive disease with a mutation in the Androgen Receptor (AR) gene resulting in:Functioning Y sex chromosome and abnormality on X chromosome
L6-8.Disorders of the reproductive system.pptxDr Bilal Natiq
In the male, the testis serves two principal functions: synthesis of testosterone by the interstitial Leydig cells under the control of luteinising hormone (LH), and spermatogenesis by Sertoli cells under the control of follicle-stimulating hormone (FSH) (but also requiring adequate testosterone).
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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
3. INTRODUCTION
• Definitions:
• Delayed puberty is defined as the lack of pubertal
development by 2 SD above the mean age for the
general population.
• An absence of an increase in testicular volume (less
than 4 mL) at 14 yr in a boy or
• absence of any breast development at 13 yr in a
girl.
• delay in the onset, progression or completion of
puberty sufficient to cause concern to the
adolescent, parents or physician.
4. • In boys, a period of 3.2 +/– 1.8 (mean +/–
SD) years is necessary to achieve adult
testicular volume after the onset of
puberty.
• In girls, the period from breast budding to
menarche is 2.4 +/–1.1 (mean +/– SD)
years.
• Therefore, evaluation is warranted if more
than 4–5 yr has elapsed from the onset of
puberty to adult testicular size in boys or
menarche in girls.
Pubertal arrest
5. • in girls:
• lack of breast
development by 13
• more than five years
between breast
growth and menstrual
period
• lack of pubic hair by
age 14
• failure to menstruate
by age 15-16
• in boys:
• lack of testicular
enlargement by age
14
• lack of pubic hair by
age 15
• more than five
years to complete
genital enlargement
INTRODUCTION
6. • occurs in approximately 3% of children.
• In boys, delayed puberty is often constitutional
and functional. (63 %)
• In girls, delayed puberty is less common and
often organic.
• Delay of puberty leads to delay in the
acquisition of secondary sex characteristics,
psychological problems, defect in reproduction
function and the reduction of bone mass.
INTRODUCTION
7. • Normal puberty is initiated
by the onset of pulsatile
secretion of gonadotropin-
releasing hormone (GnRH)
from the hypothalamus.
• These pulses cause
release of luteinizing
hormone (LH) and follicular
stimulating hormone (FSH)
from the pituitary gland.
• These pituitary
gonadotropins then
circulate to the gonads and
stimulate production of sex
steroids.
9. • The first group represents temporary
delays of puberty that are functional
disorders, most commonly,
constitutional delay of growth and
puberty.
10. • The second is hypogonadotropic
hypogonadism, in which hypothalamic or
pituitary failure results in deficiency of
circulating gonadotropins.
11. • Finally, hypergonadotropic hypogonadism
results from primary gonadal failure,
resulting in elevated serum gonadotropin
levels.
12.
13.
14. CONSTITUTIONAL DELAY
OF PUBERTY AND GROWTH
• The the single most common cause in both genders.
• more often in boys than in girls.
• It represent the extreme of the normal physiologic
variations .
• CDGP is a diagnosis of exclusion.
• Children with constitutional delay are more likely to
be short for age. with a history of relatively normal
growth rate.
• delays in bone maturation . Delay in adrenarche
15. • Frequently, there is a family history of late
menarche in the mother or sisters or a
delayed growth spurt in the father.
• sporadic cases are also seen.
• Puberty is not delayed beyond the
chronological age of 16 yr in females and 18
yr in males,
• the onset of puberty corresponds better with
bone age (BA) than chronological age
CONSTITUTIONAL DELAY
OF PUBERTY AND GROWTH
26. Evaluation of Pubertal Delay
• HISTORY:
• totally absent or had started but then arrested.
• family history of constitutional delay of puberty.
• Family history of infertility .
• The review of symptoms.
• Perinatal history
• prior medical illness.
• Medication.
• psychosocial deprivation
27. • Nutritional habits, exercise intensity.
• Neurologic symptoms such as headache,
visual disturbances,seizures, and intellectual
disability .
• sense of smell.
• Hypoglycemia.
• Cancer history :Radiation, Chemotherapy
• history compatible with testicular injury
(bilateral cryptorchidism, surgery, irradiation,
bilateral torsion)
Evaluation of Pubertal Delay
28. • growth parameter Ht,Wt,BMI .weight for
height.
• The growth velocity ,Arm span.
• pubertal staging.
• Systemic exam. dysmorphisim
• visual field exam. Fundoscopy.
• Evaluation of the sense of smell.
• associated congenital abnormalities (eg,
midline defects, cleft lip/palate,
cryptorchidism, and microphallus ) .
PHYSICAL EXAMINATION
29.
30. • BOYS
• Increase in testicular size is usually the
first sign of puberty in boys
• testicular size greater than 4 mL in
volume or a longitudinal measurement
greater than 2.5 cm is consistent with the
onset of pubertal development.
• Scrotal skin also changes in texture and
reddens in early puberty.
PHYSICAL EXAMINATION
33. • GIRLS
• Breast development in girls begins with
formation of breast buds.
• This development is frequently unilateral
for several months.
• Development of axillary and pubic hair
may or may not accompany the onset of
puberty.
• the vaginal mucosa changes from a
reddish to pink.
PHYSICAL EXAMINATION
36. • Testosterone
• an 8AM total serum testosterone
concentration level greater than 45
ng/dL (1.6 nmol/L ) indicates the
inception of puberty
LAB
37. • estradiol
• a plasma estradiol of more than 9
pg/mL (32 pmol/l) is indicative of
puberty.
• Elevations are reassuring for onset of
early puberty.
• but levels below the limit may be
seen in early puberty.
LAB
38. • serum gonadotropin levels (LH and
FSH).
• baseline serum gonadotropin values are
typically low in both constitutional delay
of puberty and congenital GnRH
deficiency.
• If elevated, the etiology for gonadal
failure should be further investigated
based on the differential diagnoses.
LAB
39. • Sleep-associated gonadotropin
secretion
• Normal puberty begins at night with
the onset of episodic LH secretion
coincident with the onset of sleep.
• In compare to those with CDGP
,Hypogonadotropic children typically
do not experience an increase in
serum LH during sleep
LAB
40. • Karyotyping :
• if physical examination suggest the
presence of a genetic syndrome .
• Also in any short girl.
• GnRH stimulation testing:
• limited benifit
LAB
41. • Bone age :
• may be obtained at the initial visit to
assess skeletal maturation and
repeated over time if needed.
• Skeletal age more closely correlates
with sexual development than does
chronological age.
• Bone age more than 13 for girls and
14 for boys less likely to constitutonal.
imaging
42. • Pelvic /scrotal ultrasound:
• Indicated when an dysgenesis is
suspected to determine the presence or
absence of internal organs.
imaging
43. • MRI:
• should be obtained in patients with
hypogonadotropic hypogonadism.
imaging
45. • The aim of treatment:
• Development of age-appropriate secondary
sex characteristics .
• Induction of a growth spurt without inducing
premature epiphyseal closure.
• achievement of normal muscle mass and
bone mineral density for age.
• improvement in psychosocial wellbeing.
• in some patient reversal of GnRH defceincy.
TREATMENT
46. • constitutional delay:
• conservative management with observation
over 6 mo to 1 yr may be warranted.
• Constitutional delay of growth and puberty
can cause significant psychosocial stress,
particularly in males.
• Cases must be evaluated on an individual
basis for psychosocial distress, and
subsequent need for intervention.
TREATMENT
47. • in cases of clearly permanent
hypogonadism, therapy should be initiated
at a normal pubertal age to avoid the
delay of growth and psychological effect
of pubertal delay.
TREATMENT
48. CDGP VS HH
• Determining the etiology of delayed
puberty during initial evaluation can be
challenging.
• clinicians often cannot distinguish
constitutional delay of growth and puberty
(CDGP) from isolated hypogonadotropic
hypogonadism (IHH).
49. • A family history of delayed puberty is
strongly suggestive of CDGP (seen in
50–75%).
• Adolescents with CDGP may have
delayed adrenarche and pubarche along
with delayed gonadal development.
• The presence of progressive pubertal
development by age 18 yr in boys or 16
yr in girls is the “gold standard” for
differentiating CDGP from HH.
CDGP VS HH
51. • most physicians advocate a period of “watchful
waiting”.
• including periodic evaluation, reassurance, and
psychological counseling .
• short course of testosterone therapy may be
initiated .
• A low dose of testosterone enanthate (50–100 mg
given intramuscularly every 4 wk) for 4–6 mo will
stimulate linear growth and secondary sexual
characteristics without inappropriately accelerating
bone age.
TREATMENT of constitutional delay of
growth and puberty in boys
52. • Testosterone enanthate, administered by intramuscular
injection, is the most common method of pubertal induction
and maintenance .
• Various schemes have been proposed, but most authors
advocate a starting dose of 50 mg every 4 wk.
• When the pubertal growth spurt is well established, the dose
should be gradually increased to a full adult dose of 200 mg
every 2 wk.
• When hypogonadism is diagnosed at a prepubertal age,
testosterone therapy may be started as early as a bone age of
11–12 yr .
TREATMENT of permanent
hypogonadal state in boys
53. • Testosterone:
• Testosterone therapy is utilized for induction
of puberty in boys with constitutional delay of
puberty, hypogonadotropic hypogonadism,
and hypergonadotropic hypogonadism.
• testosterone esters Intramuscularly are the
most commonly used.
• Testosterone enanthate and cypionate are
preferred over testosterone propionate
TREATMENT (MALE)
54. • testosterone esters, such as enanthate 50
mg monthly given IM for 4–12 months.
• Thereafter, the doses are gradually
increased with 50 mg every 6 to 12 months.
• After reaching 100-150 mg monthly
,decrease interval to every 2 weeks.
• Then adult dose 200 mg every 2 weeks.
TREATMENT (MALE)
55. • The following schedule also may be
proposed :
• first year: 25 mg every 2 weeks;
• second year: 50 mg every 2 weeks;
• third year: 100 mg every 2 weeks;
• fourth year onward: 200 mg every 2
weeks .
TREATMENT (MALE)
56. • Transdermal Testosterone:
• a scrotal patch and a nongenital patch.
• When applied daily, result in similar
testosterone concentrations to those
seen in normal young men in
magnitude and diurnal variation.
TREATMENT (MALE)
57. • Transdermal Testosterone:
• substantially more expensive than
testosterone esters .
• can produce skin reaction .
• not yet approved in males younger than
age 18 years
• their effectiveness in induction of puberty
remains unclear
TREATMENT (MALE)
58. • Side effect:
• acne, and gynecomastia.
• fast skeletal maturation leading to impaired
adult height.
• excessive aggressiveness.
• excessive stimulation of libido, priapism,
polycythemia,
• obstructive sleep apnea mainly in obese
subjects
TREATMENT (MALE)
59. • Beneficial effects:
• decline in total plasma cholesterol and
LDL concentrations,
• increased lean body mass.
• decreased risk of osteoporosis .
TREATMENT (MALE)
60. Testosterone
Not for use in boys with
bone age <10 years.
Erythrocytosis, weight
gain, prostate
hyperplasia.
Premature epiphyseal
closure .
Local side effects (pain,
erythema)
Initiate after age 12 years of
age at 50 mg every 4
weeks. Increase with 50 mg
every 6 to 12 months. After
reaching 100-150 mg
monthly ,decrease interval
to every 2 weeks. adult dose
200 mg every 2 weeks
Testoserone
enathate, cypionate
and propionate. IM
Can cause POMEAdult dose 1000 mg every
10-14 weeks.
Testosterone
undecanoate.IM
Local irritation. Avoid
contact with other
Can be started when 50%
adult dose with
intramuscular testosterone
achieved.
Testosterone gel
TREATMENT (MALE)
61. Testosterone
the levels of testosterone
seem to be slightly more
erratic.
hepatotoxic
at the starting dose of 40
mg/daily in the morning.
Oral testosterone
undecanoate
Gum irritation30 mg per buccal system.
30 mg twice a day
trans-buccal
testosterone
TREATMENT (MALE)
66. TREATMENT (male)
• Oxandrolone:
• Can be used for Induction of a pubertal
growth spurt in CDGP .
• the mechanism of action is unclear.
• it is anabolic steroid that increases
growth velocity without promoting
excessive skeletal maturation
• Doses of (0.1 mg/kg/day, 1.25 or 2.5
mg/d for 3–12 months).
67. • Human chorionic gonadotropin
• hCG can be used to induce puberty in
CDGP.
• hCG 1500 U twice weekly, either SC
or IM, for 6 months.
• The use of hCG appears to be more
physiologic and potentially safer than
Testesterone
• However, HCG is more expensive
and requires multiple injections.
TREATMENT (male)
68. • aromatase inhibitor
• An aromatase inhibitor, e.g., letrozole
(2.5 mg/PO) in addition to Testosterone.
• appears to increase the final Ht to
approach mid-parental.
TREATMENT (male)
69. • Dihydrotestosterone (DHT)
• 50 mg IM every 2 weeks, for 4 months.
• is associated with appearance of
secondary sex characteristics increased
lean body mass and decreased body fat
with no change in IGF-I.
• may increase the potential for final Ht.
TREATMENT (male)
70. • Estrogen :
• either long-term low doses, or gradual
increases in dose providing adequate
time for pubertal growth, and gradual
breast development.
• For constitutional : conjugated estrogen
0.3 mg po daily for 3-6 months
TREATMENT (GIRLS)
71. • For other indications:
• Premarin (conjugated estrogen) may be
used at a dose of:
• 0.3 mg every other day for 6 months
followed by an increase to every day for 6
months
• then 0.625 mg daily for 6 months,
• followed by 1.2 mg.
TREATMENT (GIRLS)
72.
73. • A progesterone should be added after
two years of estrogen , after full breast
development or if spotting occurs.
• This is usually administered as:
• Provera (medroxyprogesterone) at a
dose of 5–10 mg or
• micronized progesteroneat 200 mg/day
(eg, Prometrium) for 10–14 d
TREATMENT (GIRLS)
74. • After adult doses of estradiol and
medroxyprogesterone are reached, oral
contraceptive pill may be substituted for
separate preparations of these
compounds.
TREATMENT (GIRLS)
75. • In girls without a uterus, such as in
androgen insensitivity or XY gonadal
dysgenesis, the same guidelines for
estrogen replacement can be used,
but there is no need for the addition of
progesterone.
TREATMENT (GIRLS)
76. GNRH THERAPY
• In some cases of hypogonadotropic
hypogonadism, pulsatile administration of
gonadotropin releasing hormone has
resulted in induction of puberty .
• frequently used for stimulation of
spermatogenesis or induction of ovulation
in infertile adult patients.
77. • Patients of either sex with hypogonadotropic
hypogonadism are potentially fertile
• to initiate gametogenesis, the typical
approach to fertility induction is pump-
administered GnRH therapy (assuming an
intact pituitary gland)
• or parenteral combination gonadotropin
treatment (synthetic LH/hCG and
recombinant FSH) .
further TREATMENT
78. follow-up and monitoring
• regular clinical follow-up assessing
growth and pubertal progression
every 3-6 months
• bone age assessment.
79. • Testesterone:
• 1. therapy should restore serum testosterone levels into the mid-
normal range for pubertal stage.
• 2. measurement of testosterone should be:
• - testosterone enanthate or cypionate: midway between
injections.
• - i.m. long-acting testosterone undecanoate: before the new
injection.
• - transdermal testosterone patch: 3-12 hours after application.
• - transdermal testosterone gel application: after 1-2 weeks
independently from application.
• - buccal testosterone tablet: immediately before the application
of new tablet.
follow-up and monitoring
80. • Haematocritus.
• the discontinuation of therapy is
required if hematocrit is greater than
54% until it decreases to a safer
level).
follow-up and monitoring
81. • LH and FSH :
• the assessment of LH and FSH has
poor clinical value
follow-up and monitoring
82. references
• 1- Ines L.sedlmeyeri. Delayed Puberty:
Analysis of a Large Case Series from an
Academic Center. J Clin Endocrinol Metab
87: 1613–1620, 2002
• 2- Jennifer Harrington.Distinguishing
Constitutional Delay of Growth and Puberty
from Isolated Hypogonadotropic
Hypogonadism: Critical Appraisal of
Available Diagnostic Tests. J Clin
Endocrinol Metab 97: 3056–3067, 2012
83. • 3-Ines L.sedlmeyeri. Pedigree Analysis
of Constitutional Delay of Growth and
Maturation: Determination of Familial
Aggregation and Inheritance Patterns.
(J Clin Endocrinol Metabolism
87(12):5581–5586, 2002
• 4-Taneli Raivio, Reversal of Idiopathic
Hypogonadotropic Hypogonadism. N
Engl J Med 2007;357:863-73.
references
84. • 5-Jürgen Brämswig, Disorders of Pubertal
Development Dtsch Arztebl Int 2009; 106(17): 295–
304
• 6-Vidhya viswanathan .Etiology and Treatment of
Hypogonadism in Adolescents. Pediatric Clin North
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• 7-Shalender Bhasin .Testosterone Therapy in Men
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Endocrinol Metab 95: 2536 –2559, 2010
references
85. • 8- Ashraf T. Soliman, An approach to
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