Transient Neonatal Hypoglycemia, Revisited discusses glucose homeostasis in neonates and the types and management of neonatal hypoglycemia. After birth, neonates undergo a physiological transition as they adapt to intermittent feeding from transplacental glucose supply. This involves endocrine changes and the activation of pathways like glycogenolysis and gluconeogenesis to maintain blood glucose levels. Insulin secretion in neonates is not suppressed until very low glucose levels due to a lower threshold for insulin release that helps support growth in fetal life. Exposure to hypoxia after birth can prolong this fetal pattern of insulin secretion. Careful management is needed to avoid overtreatment of transitional hypoglycemia while preventing brain injury from severe hypoglycemia.
Approach to Hypoglycemia in Children.pptxJwan AlSofi
Introduction
DEFINITION
Symptoms and Signs of Hypoglycemia
Sequelae of Hypoglycemia
Hormonal Signal
Regulation of serum glucose
Disorders of Hypoglycemia
Classification of Hypoglycemia in Infants and Children
DIAGNOSIS
EMERGENCY MANAGEMENT
Approach to Hypoglycemia in Children.pptxJwan AlSofi
Introduction
DEFINITION
Symptoms and Signs of Hypoglycemia
Sequelae of Hypoglycemia
Hormonal Signal
Regulation of serum glucose
Disorders of Hypoglycemia
Classification of Hypoglycemia in Infants and Children
DIAGNOSIS
EMERGENCY MANAGEMENT
A progressive inflammatory hepatopathy
Several factors (eg, viral infection, drugs, environmental agents) may trigger an autoimmune response and autoimmune disease.
In a few patients with AIH, illness onset follows acute hepatitis A, hepatitis B, or Epstein-Barr virus infections.
Autoantibodies - in patients with chronic HCV infection, liver-kidney microsomal type 1 (LKM-1) antibody.
HLA status affects treatment outcome
A progressive inflammatory hepatopathy
Several factors (eg, viral infection, drugs, environmental agents) may trigger an autoimmune response and autoimmune disease.
In a few patients with AIH, illness onset follows acute hepatitis A, hepatitis B, or Epstein-Barr virus infections.
Autoantibodies - in patients with chronic HCV infection, liver-kidney microsomal type 1 (LKM-1) antibody.
HLA status affects treatment outcome
Neonatal hypoglycemia and hyperglycemia Dr vijitha ASVijitha A S
Neonatal hypoglycemia and hyperglycemia BY Dr VIJITHA A S
Hypoglycemia is most common metabolic problem seen in newborns
No universally accepted definition ; Hypoglycemia cut off variable
pediatrics emergency, hypoglycemia of infancy.
Glucose level can drop if:
There is too much insulin in the blood (hyperinsulinism). Insulin is a hormone that pulls glucose from the blood.
The baby is not producing enough glucose.
The baby's body is using more glucose than is being produced.
The baby is not able to feed enough to keep glucose level up.
Diabetes [2019]
There is little research into pae and diabetes. What there is indicates that further research should be done.
The attached research has been done from the perspective of prenatal alcohol consumption.
A search of diabetes research failed to find any mention of prenatal alcohol.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
3. Outline
1. Glucose homeostasis
2. Physiopathology of neonatal hypoglycemia
3. Types of Neonatal Hypoglycemia
4. Definition of Neonatal Hypoglycemia
5. Management
6. Take home message
4. Neonatal Hypoglycemia
Why is it a problem?
Neonatal hypoglycemia is a preventable cause of brain injury.
It is common, affecting 5–15% of all babies1 and approximately half of at-
risk babies2 and is associated with a range of adverse sequelae3,4
A lot of neonates with normal “Transitional Hypoglycemia” levels are
overtreated
The definition and the threshold at which treatment would prevent brain
injury, remains controversial
1. Hay WW, et al. Child Health and Human Development. J Pediatr. (2009) 155:612–7. doi: 10.1016/j.jpeds.2009.06.044
2. Harris D, et al. J Pediatr. (2012) 161:787–91. doi: 10.1016/j.jpeds.2012.05.022
3. Boluyt N, et al. Pediatrics. (2006) 117:2231–43. doi: 10.1542/peds. 2005-1919
4. Shah R, et al. Neonatology. (2019) 115:116–26. doi: 10.1159/000492859
6. Glycolysis
Glucose is broken
down to Pyruvate
Insulin receptor
Insulin
Nucleus
Mitochondria
Glucose
ATP
Glycogenogenesis
Storage form of glucose in the cell
Krebs cycle
2
1
Glycogen
7. Glycolysis
Glucose is broken
down to Pyruvate
If energy is needed
Insulin receptor
Nucleus
Mitochondria
ATP
Glycogenogenesis
Storage form of glucose in the cell
Krebs cycle
Glycogenolysis
If Hypoglycemia
3
2
1
Glycogen
LIVER
8. Glycolysis
Glucose is broken
down to Pyruvate
If energy is needed
Insulin receptor
Nucleus
Mitochondria
ATP Krebs cycle
Glycogenolysis
If Hypoglycemia
3
2
1
Gluconeogenesis
Formation of glucose from
non-glucidic substrates such
as amino-acids (5%), lactate
(70%) and glycerol (10%)
4
Glycogen
LIVER
2
9. 3 months Term
8 weeks
8 weeks Hepatic glycogen content Term
3.4 mg/g 50 mg/g
Capkova et al. Biol Neonate 1968;13:129-142
11. Glycemia
Continuous Glucose supply
Fetal glucose concentrations
are 80% of the maternal level
Fetal Liver
Fetal Pancreas
The fetal insulin level is independent of the mother’s level, as insulin does
not cross the placenta, but it is dependent on the fetal blood glucose level
Fetal Life
12. Glycemia
Fetal Liver
Fetal Pancreas
Insulin is an
Anabolic
Hormone
Insulin:
• Facilitates Glucose uptake by the cells
• Stimulates Glycogenogenesis
• Stimulates incorporation of amino acids into protein
• Stimulates lipogenesis
Continuous Glucose supply
Fetal Life
Fetal glucose concentrations
are 80% of the maternal level
15. Normal physiology
During fetal life glucose, lactate and amino acids are the principal sources of energy.
The fetus receives glucose from the mother achieving fetal plasma glucose
concentrations 70–80% of the maternal level.
The fetal insulin level is independent of the mother’s level, as insulin does not cross
the placenta, but it is dependent on the fetal blood glucose level.
During the last trimester of pregnancy when there is rapid growth, energy stores
(particularly glycogen and adipose tissue) are accumulated in preparation for birth.
It occurs due to the transition from continuous transplacental glucose supply from
the mother in-utero, to an intermittent supply from milk feeds.
Hawdon JM. Postnatal metabolic adaptation and neonatal hypoglycaemia. Paediatrics & Child Health. 2016;26(4):135-9.
16. Physiological transition beginning immediately after birth
Endocrine changes
Plasma insulin levels fall
Catecholamines and pancreatic glucagon are released
Essential enzymes for the production of glucose from stores of glycogen
and fat (glycogenolysis and gluconeogenesis), and the production of free
fatty acids (lipolysis) and ketones (ketogenesis) are switched on
Importantly, the production of these enzymes is inhibited by insulin, so
persistent high insulin levels prevent this normal adaptation
Hawdon JM. Postnatal metabolic adaptation and neonatal hypoglycaemia. Paediatrics & Child Health. 2016;26(4):135-9.
17. Physiological transition beginning immediately after birth
Endocrine changes
Glycogenolysis: production of glucose by the liver when stored glycogen is
broken down to form pyruvate in response to increased adrenaline and glucagon
concentrations and falling insulin levels
Gluconeogenesis: occurs during the first 8–12 hours of life when glycogen stores
are depleted
Stimulation of appetite and adaption to fast and feed cycle and promotion of
oxidative fat metabolism using lipid from fat stores and milk feeds
Delay in the first feed for 3–6 hours after birth results in approximately 10% of
babies not maintaining their plasma glucose levels above 32mg/dl
Hawdon JM. Postnatal metabolic adaptation and neonatal hypoglycaemia. Paediatrics & Child Health. 2016;26(4):135-9.
19. 150
140
130
120
110
100
90
80
70
60
50
40
Insulin secretion is
suppressed
Glucagon is secreted
Adrenaline, GH and
Cortisol secreted
Insulin:
• Facilitates Glucose uptake by the cells
• Stimulates Glycolysis & Glycogenogenesis
• Inhibits Gluconeogenesis & Glycogenolysis
• Prevents fatty acids β-oxidation
• Stimulates uptake and incorporation of
amino acids into protein
• Stimulates lipogenesis
Glucagon, Cortisol, Adrenaline and GH:
Stimulate Glycogenolysis & Gluconeogenesis
↑Glycemia
↓Glycemia
Insulin secretion is
stimulated
Healthy, >3-day-old neonates and children
20. 150
140
130
120
110
100
90
80
70
60
50
40
Insulin secretion is
suppressed
Glucagon is secreted
Adrenaline, GH and
Cortisol secreted
Insulin:
• Facilitates Glucose uptake by the cells
• Stimulates Glycolysis & Glycogenogenesis
• Inhibits Gluconeogenesis & Glycogenolysis
• Prevents fatty acids β-oxidation
• Stimulates uptake and incorporation of
amino acids into protein
• Stimulates lipogenesis
Glucagon, Cortisol, Adrenaline and GH:
Stimulate Glycogenolysis & Gluconeogenesis
↑Glycemia
↓Glycemia
Insulin secretion is
stimulated
Preterm, < 3-day-old neonates
21. Glucose Insulin release
Last day of gestation,
and pups on postnatal
day P1
Mature islets from
2-week-old and
adult rats
54mg/dl Nearly half of
the maximal response
to 450mg/dl glucose
90mg/dl Only >90mg/dl
450mg/dl 2-fold increase 4- to 5-fold greater
response at
450mg/dl glucose
Yang J, Hammoud B, Li C, et al. Decreased KATP channel activity contributes to the low glucose threshold for insulin secretion of rat neonatal islets.
Endocrinology 2021;162(9):bqab121
The glucose threshold for GSIS is lower in fetal and newborn rats
54
90
180
450
22. • An increase in the ATP to ADP ratio,
results in the closure of KATP
channels, membrane depolarization
and subsequent opening of voltage-
gated calcium channels (VGCC).
• The resulting increase in
intracellular calcium triggers insulin
granule exocytosis.
Jonathan E. Campbell et al. Nat Rev Mol Cell Biol. 2021 February ; 22(2): 142–158.
23. PHD: Prolyl hydroxylases
Hif1a: Hypoxia inducible factor
vHL: Von Hippel-Lindau
Yang J, Hammoud B, Li C, et al. Decreased KATP channel activity contributes to the low glucose threshold for insulin secretion of rat neonatal islets.
Endocrinology 2021;162(9):bqab121
• Hypoxia inducible factor HIF1a is
constitutively expressed but rapidly
degraded under normoxia via the von
Hippel-Lindau proteosomal pathway.
• Under hypoxic stress, HIF1a combines
with other transcription factors to
induce expression of various
mediators of the hypoxic response.
Hypoxia inducible pathway and sites of activation
24. The pathway of KATP channel trafficking from the Golgi to
the plasma membrane surface
• Increased trafficking of KATP channels on
the plasma membrane surface by leptin
or low glucose decreases insulin
secretion.
• In contrast, decreased trafficking in the
PHPT1 knockout mouse model cause
severe neonatal hyperinsulinemic
hypoglycemia
PHPT1: Phosphohistidine phosphatase 1
Park SH, et al. Leptin promotes K(ATP) channel trafficking by AMPK signaling in pancreatic beta-cells. Proc Natl Acad Sci U S A 2013; 110(31):12673–8.
Srivastava S, et al. Regulation of KATP channel trafficking in pancreatic beta-cells by protein histidine phosphorylation. Diabetes 2018;67(5): 849–60.
25. • Exposure to hypoxia
from E18 to P6 lowers
the glucose threshold
for GSIS in freshly
isolated islets from
newborn rat pups
Data from Yang J, Hammoud B, Ridler A, et al. Postnatal activation of hypoxia pathway disrupts b-cell functional maturation
Hypoxia in the perinatal period causes persistence of fetal
low glucose threshold for insulin release
26. Insulin in the fetal & neonatal period
Insulin is a growth hormone in fetal life
There is a hyper-insulinemic state in all newborns
There is a low glucose threshold for insulin release (insulin secretion is not
suppressed until very low levels of glucose)
Hypoxia in the perinatal period causes persistence of fetal low glucose
threshold for insulin release
27. Harris DL, Weston PJ, Harding JE. Alternative Cerebral Fuels in the First Five Days in Healthy Term Infants: The Glucose in Well Babies
(GLOW) Study. J Pediatr 2021;231:81-86
Plasma glucose and ketone levels in the first 5 days of life
in normal newborns
Shown are median glucose and BOHB levels in 67 mostly breastfed babies followed sequentially for 5 days
• The first phase is the period of hypo-
ketonemic hypoglycemia due to
Transitional Hyper-Insulinism during the
first 24–36 h after birth.
• In breast-fed newborns, this is followed
by a second phase of hyper-ketonemic
hypoglycemia between 48 and 72 h
after birth which then resolves as
plasma glucose rises into the normal
range for older infants and children
28. Harris DL, Weston PJ, Harding JE. Alternative Cerebral Fuels in the First Five Days in Healthy Term Infants: The Glucose in Well Babies
(GLOW) Study. J Pediatr 2021;231:81-86
• The first phase is the period of hypo-
ketonemic hypoglycemia due to
Transitional Hyper-Insulinism during the
first 24–36 h after birth.
• In breast-fed newborns, this is followed
by a second phase of hyper-ketonemic
hypoglycemia between 48 and 72 h
after birth which then resolves as
plasma glucose rises into the normal
range for older infants and children
Insulin inhibits Lipolysis
and Ketogenesis
Plasma glucose and ketone levels in the first 5 days of life
in normal newborns
Shown are median glucose and BOHB levels in 67 mostly breastfed babies followed sequentially for 5 days
32. Hypoglycemia-associated autonomic failure
Recurrent episodes of insulin-induced hypoglycemia have been shown to
blunt or completely prevent the secretion of counter-regulatory hormones
Cryer PE. Hypoglycemia-associated autonomic failure in diabetes. Am J Physiol Endocrinol Metab. 2001;281(6):E1115–E1121.
33. Plasma glucose values during the first
week of life in 344 healthy term
newborns
G, Pildes S, Cattamanchi G, Voora S, Lilien D. Plasma glucose values in normal neonates: A new look. The Journal of Pediatrics.
1986;109(1):114-117
Maternal Glucose Concentrations
Fetal Glucose Concentrations
The mean of fetal glucose levels persists
neonatally for the first 48 hours
34. Glucose Profiles in Healthy Term Infants in the First 5 Days:
The Glucose in Well Babies (GLOW) Study
Glucose Profiles in Healthy Term Infants in the First 5 Days: The Glucose in Well Babies (GLOW) Study. Deborah L. Harris et al. J Pediatr 2020;223:34-41
• A prospective masked observational
study 67 Healthy, term, AGA singletons
had continuous glucose monitoring and
repeated heel-prick plasma glucose
measurements (4 in the first 24 hours
then twice daily) from birth to 120
hours.
• Mean birth weight of 3584 ± 349 g, and
gestational age of 40.1 ± 1.2 weeks
35. Numbers of infants who experienced low and high plasma and
interstitial glucose concentrations over the first 120 hours after birth
Plasma Glucose concentration
Postnatal age
(in Hours)
Number of
infants
<27
mg/dl
<36
mg/dl
<47
mg/dl
>144
mg/dl
0-4 64 0 5% 19% 0
4-12 62 0 2% 18% 0
12-24 67 0 3% 12% 0
24-48 67 0 3% 13% 0
48-72 67 0 3% 10% 0
72-96 67 0 0% 1% 8%
96-120 67 0 0 0 0
Glucose Profiles in Healthy Term Infants in the First 5 Days: The Glucose in Well Babies (GLOW) Study. Deborah L. Harris et al. J Pediatr 2020;223:34-41
36. Glucose Profiles in Healthy Term Infants in the First 5 Days:
The Glucose in Well Babies (GLOW) Study
Glucose Profiles in Healthy Term Infants in the First 5 Days: The Glucose in Well Babies (GLOW) Study. Deborah L. Harris et al. J Pediatr 2020;223:34-41
Conclusions:
1. Healthy, term, AGA infants seem to complete their transition at 72 Hours.
2. Many have glucose concentrations below the accepted thresholds for
treatment of hypoglycemia
37. Early neonatal hypoglycemia in term and late preterm
small for gestational age newborns
690 SGA neonates
19.42% SGA neonates developed hypoglycemia (<40mg/dl)
3.7% neonates had to be transferred to the neonatal ward,
requiring IV glucose.
97% of hypoglycemic episodes occur during the first 2 h of
life.
2% neonates had symptomatic hypoglycemia
Risk Factors : C-section, small head circumference, low 1
minute Apgar score
Early Neonatal Hypoglycemia in Term and Late Preterm Small for Gestational Age Newborns
Lin-Yu Wang, Lin-Yen Wang, Yu-Lin Wang, Chung-Han Ho DOI: https://doi.org/10.1016/j.pedneo.2022.09.021
Hypoglycemia NICU admission Normal
38. Continuous glucose monitoring
in 102 newborn babies at risk of hypoglycemia
Results:
• Low glucose concentrations (<47mg/dl) were
detected in 32% with blood sampling and in 44%
with continuous monitoring.
• There were 265 episodes of low glucose
concentrations, 81% of which were not detected
with intermittent blood glucose measurement.
• 107 episodes in 34 babies lasted >30 minutes, 73%
of which were not detected with blood glucose
measurement.
Harris Et al.J Pediatr. 2010 Aug;157(2):198-202.e1.
39. Newborns “at risk” for “hypoglycemia”
Transient neonatal hypoglycemia
1. Preterm birth
2. Small or large for date
3. Infant of diabetic mother
4. Perinatal stress (birth asphyxia,
hypothermia, respiratory
distress, sepsis)
5. Poor feeding
6. Maternal use of beta blockers
Persistent neonatal hypoglycemia
1. Congenital hyperinsulinism
2. Hypopituitarism
3. Glycogen storage disease
4. Disorders of Fatty acid oxidation
defects
5. Other, rare genetic disease
Harris DL, et al. Incidence of neonatal hypoglycemia in babies identified as at risk. J Pediatr 2012;161:787-91.
40. Babies at risk
Generally, neonatal hypoglycemia is caused by one or more of:
Increased levels of insulin
Inadequate glucose supply
Inadequate body stores (glycogen, fat)
Decreased levels of counter-regulatory hormones (e.g. growth hormones,
cortisol, adrenergic hormones)
Disorders of glycogen metabolism (glycogenolysis)
Disorders of glucose production (gluconeogenesis)
Congenital anomalies, or mixed causes
Adamkin DH. Neonatal hypoglycemia. Seminars in Fetal and Neonatal Medicine 2017;22(1):36-41.
41. The incidence of neonatal hypoglycemia in babies
with different combinations of risk factors
J Pediatr 2012;161:787-91
IODM49%
LGA 39% SGA 56%
Preterm 59%
44% 50%
88% 44%
47%
52%
42. MEASUREMENT OF GLUCOSE
Whole blood glucose concentrations are up to 10% to 12% lower than
plasma values.
A higher hematocrit can lead to lower glucose concentrations, as does
marked hyperbilirubinemia.
Glucometers provide quick results at low cost, are readily available in
neonatal units, user-friendly and require small volumes of blood
Treatment in a markedly symptomatic infant should not be delayed until
laboratory confirmation of hypoglycemia.
Eustratia M. Hubbard et al. Clin Perinatol 48 (2021) 665–679
Beardsall K. Measurement of glucose levels in the newborn. Early Hum Dev. (2010) 86:263–7.
44. Definition of Hypoglycemia
0-4 Hours 4-24 Hours
American Academy of Pediatrics < 25 mg/dl < 35 mg/dl
The British Association of Perinatal
Medicine
< 36 mg/dl
World Health Organization < 47 mg/dl
Pediatric Endocrine Society (USA) < 50 mg/dl
(<48 Hours)
< 60 mg/dl
(>48 Hours)
Haute Autorité de Santé (France) <36 (if asymptomatic)
0-48 Hours
<45 (if symptomatic)
> 48 Hours
Adamkin DH. Pediatrics 2011;127:575-9.
British Association of Perinatal Medicine; 2017.
Williams AF. Bull World Health Organ 1997;75:261-90
Thornton PS, J Pediatr 2015;167:238-45.
Protocole National de Diagnostic et de Soins (PNDS)
45. G, Pildes S, Cattamanchi G, Voora S, Lilien D. Plasma glucose values in normal neonates: A new look. The Journal of Pediatrics.
1986;109(1):114-117
• The PES uses the mean values while
neonatologists use the 5th percentile
value to define Neonatal Hypoglycemia
• PES specialists care for small groups of
babies at very high risk of hypoglycemic
brain damage from rare congenital
disorders
• Neonatologists, are responsible for large
numbers of mostly low-risk newborn
babies.
• An additional concern is the potential
risk of medicolegal suits
Mean
5th %
46. Definition of Hypoglycemia
Should be correlated to:
• Intra Uterine Growth
• Gestational age
• Postnatal age (in hours)
• Concurrent metabolic demands
• Co-morbidities
• Availability of alternative fuels
47. Definition of Hypoglycemia
Hour specific nomogram (adapted from Bhutani et al.)
Analogous to
Should be correlated to:
• Intra Uterine Growth
• Gestational age
• Postnatal age (in hours)
• Concurrent metabolic demands
• Co-morbidities
• Availability of alternative fuels
48. Operational Threshold
1. A retrospective study of 661 preterm babies (birthweight < 1,850 g), which
reported that a glucose concentration of <47 mg/dl on three or more days was
associated with an increased risk of developmental delay at 18 months’
corrected age1
2. Another study recorded evoked potentials in 17 infants, of whom only five were
newborns2
None showed flattening of evoked potentials with a glucose concentration of >47
mg/dl, although some with a glucose concentration below this, still had normal
evoked potentials.
Both studies concluded that a glucose concentration of >47 mg/dl (2.6 mmol/l)
was likely to be safe.
1. Lucas A, et al. Br Med J. (1999) 318:195.
2. Koh TH, et al. Arch Dis Child. (1988) 63:1353–8.
49. Lower Treatment Threshold for Neonatal Hypoglycemia
Multicenter, Randomized, Noninferiority Trial
689 Newborns
≥ 35 weeks gestation and
at risk for hypoglycemia
Glucose <36mg/dl Glucose <47mg/dl
Mean cognitive score at
18 months
102.9± 0.7 102.2± 0.7
Mean motor score at 18
months
104.6± 0.7 104.9± 0.7
Lower Glucose threshold (36 mg/dl) are noninferior to
traditional threshold (47 mg/dl)
A.A.M.W van Kempen et al. N Engl J Med 2020;382:534-44.
50. • All infants born in 1998, at the University
hospital of Arkansas
• Had at least 1 recorded glucose concentration
in the first 3 hours of life
• Stratified to 3 glucose levels: < 35, < 40 and
<45mg/dL
• Data was matched with student achievement
test scores in 2008
• Conclusion: Approximately 50% reduction in
the odds of achieving proficiency in literacy
and numeracy at the age of 10 years
Association Between Transient Newborn Hypoglycemia
and Fourth-Grade Achievement Test Proficiency
Kaiser et al. JAMA Pediatr. doi:10.1001/jamapediatrics.2015.1631
51. Brain damage percentage in Hypoglycemic newborns
50
10
6 5
0
10
20
30
40
50
60
Symptomatic with seizures Symptomatic without
seizures
Asymptomatic Controls
Koivisto et al. Develop. Med. Child Neurol. 1972, 14,603-614
52. Brain damage percentage in Hypoglycemic newborns
50
10
6 5
0
10
20
30
40
50
60
Symptomatic with seizures Symptomatic without
seizures
Asymptomatic Controls
Koivisto et al. Develop. Med. Child Neurol. 1972, 14,603-614
All symptomatic babies with seizures
had ≥ 2 blood glucose <20mg/dl
None of the babies who had only one blood
glucose < 20mg/dl had brain damage
53. The three major forms of Neonatal Hypoglycemia, are all
due to Hyperinsulinism
Adapted from Stanley CA, Thornton PS and De Leon DD (2023) New approaches to screening and management of neonatal hypoglycemia based on
improved understanding of the molecular mechanism of hypoglycemia. Front. Pediatr. 11:1071206.
1. Transitional neonatal
hyperinsulinism
2. Perinatal stress-induced
hyperinsulinism in high-risk newborns
3. Genetic forms of
hyperinsulinism
Healthy Full-term Newborns High-risk infants: IODM, SGA, LGA, Preterm,
Perinatal asphyxia
Congenital Hyperinsulinism
Majority 10% 1/10,000-1/40,000
Transient, < 72 hours Prolonged, few days to few weeks Persistent, lifelong
Decreased trafficking of
KATP-channels to the beta-cell
plasma membrane
Exaggeration of the normal low fetal glucose
threshold for insulin release due to more severe
and prolonged exposure to perinatal hypoxemia
Permanent genetic defects in
various steps controlling beta-cell
insulin release
Feeding & Observation Screening/Management Dx before discharge
No brain damage Possible subtle cognitive deficiencies Severe brain damage
54. The three major forms of Neonatal Hypoglycemia, are all
due to Hyperinsulinism
Adapted from Stanley CA, Thornton PS and De Leon DD (2023) New approaches to screening and management of neonatal hypoglycemia based on
improved understanding of the molecular mechanism of hypoglycemia. Front. Pediatr. 11:1071206.
1. Transitional neonatal hyperinsulinism
Healthy Full-term Newborns
Incidence Majority
Duration Transient, < 72 hours
Mechanism Low glucose threshold for Insulin secretions because of
a decreased trafficking of KATP-channels to the beta-cell
plasma membrane
Management Feeding & Observation
Sequalae None
55. The three major forms of Neonatal Hypoglycemia, are all
due to Hyperinsulinism
Adapted from Stanley CA, Thornton PS and De Leon DD (2023) New approaches to screening and management of neonatal hypoglycemia based on
improved understanding of the molecular mechanism of hypoglycemia. Front. Pediatr. 11:1071206.
2. Perinatal stress-induced hyperinsulinism in high-risk
newborns
High-risk infants: IODM, SGA, LGA, Preterm, Perinatal
asphyxia
Incidence 10%
Duration Prolonged, few days to few weeks
Mechanism Exaggeration of the normal low fetal glucose threshold
for insulin release due to more severe and prolonged
exposure to perinatal hypoxemia
Management Screening/Management
Sequalae Possible subtle cognitive deficiencies
56. Adapted from Harris DL, Weston PJ, Harding JE. Alternative Cerebral Fuels in the First Five Days in Healthy Term Infants: The Glucose in
Well Babies (GLOW) Study. J Pediatr 2021;231:81-86
Term, healthy newborns
“At risk” newborns
Plasma glucose and ketone levels in the first 5 days of life
in normal newborns
Shown are median glucose and BOHB levels in 67 mostly breastfed babies followed sequentially for 5 days
57. The three major forms of Neonatal Hypoglycemia, are all
due to Hyperinsulinism
Adapted from Stanley CA, Thornton PS and De Leon DD (2023) New approaches to screening and management of neonatal hypoglycemia based on
improved understanding of the molecular mechanism of hypoglycemia. Front. Pediatr. 11:1071206.
3. Genetic forms of hyperinsulinism
Congenital Hyperinsulinism
Incidence 1/10,000-1/40,000
Duration Persistent, lifelong
Mechanism Permanent genetic defects in various steps controlling
beta-cell insulin release
Management Dx before discharge and lifelong treatment(± surgical)
Sequalae Severe brain damage
59. Hx & PE in Persistent Hypoglycemia
History should include the episode’s timing and its relationship to food,
birth weight, gestational age, and family history.
Physical examination should include looking for evidence of
hypopituitarism (micropenis or cleft lip or palate, short stature),
glycogenosis (hepatomegaly), adrenal insufficiency (recurrent abdominal
pain, hyperpigmentation, anorexia, weight loss), or Beckwith-Wiedemann
syndrome (omphalocele, hemihypertrophy, macroglossia). Congenital
adrenal hyperplasia (Ambiguous genitalia). Metabolic disorder (Perinatal
stress Shock, acidosis, seizures)
60. Screening for Hypoglycemia
The purpose of screening :
1. Identify infants with pathological forms of hypoglycemia
2. Prevent hypoglycemic brain injury.
61. David H. Adamkin, MD and COMMITTEE ON FETUS AND NEWBORN Pediatrics 2011;127:575–579
63. Oral dextrose gel
Oral dextrose gel 200 mg/kg (0.5 ml/kg of 40% dextrose), in combination
with feeding, is increasingly recommended as a first-line treatment for
asymptomatic neonatal hypoglycemia
A randomized trial of 237 late preterm and term babies at risk of neonatal
hypoglycemia (<47 mg/dl)
Compared with feeding alone, 40% oral dextrose gel plus feeding resulted in
fewer treatment failures (hypoglycemia after two treatment attempts),
reduced admission to NICU for hypoglycemia
Harris D, Weston PJ, Signal M, Chase JG, Harding JE. Dextrose gel for neonatal hypoglycaemia (the Sugar Babies Study): a randomised,
double-blind, placebo-controlled trial. Lancet. (2013) 382:2077–83.
64.
65. Thornton PS, Stanley CA, De Leon DD, et al. Recommendations from the Pediatric Endocrine Society for Evaluation and Management of Persistent
Hypoglycemia in Neonates, Infants, and Children
Hypoglycemia
HCO3, BOHB, Lactate, FFA
No Acidemia Acidemia
BOHB ↓
FFA ↓
BOHB ↓
FFA ↑
Transient neonatal Hypoglycemia
Perinatal stress Hyperinsulinism
Genetic Hyperinsulinism
Fatty acid oxidation defects
Lactate ↑ BOHB ↑
Gluconeogenesis defects Ketotic Hypoglycemia
Glycogenosis
GH deficiency
Cortisol deficiency
“Skip a feed test”
66. Recommendations from the Pediatric Endocrine Society for Evaluation and Management of Persistent Hypoglycemia in Neonates, Infants, and Children
Hypoglycemia
HCO3, BOHB, Lactate, FFA
No Acidemia Acidemia
BOHB ↓
FFA ↓
BOHB ↓
FFA ↑
Transient neonatal Hypoglycemia
Perinatal stress Hyperinsulinism
Genetic Hyperinsulinism
Fatty acid oxidation defects
Lactate ↑ BOHB ↑
Gluconeogenesis defects Ketotic Hypoglycemia
Glycogenosis
GH deficiency
Cortisol deficiency
Hypoketotic
Hypoglycemia
99.9%
67. Inborn errors of Metabolism
Glycogen storage diseases: These are a group of genetic disorders in which
the body is unable to store or release glycogen properly, leading to low
blood sugar levels. Examples include glycogen storage disease type I and III.
Disorders of fatty acid oxidation: These are a group of rare genetic disorders
in which the body is unable to break down fats for energy. Examples include
medium-chain acyl-CoA dehydrogenase deficiency and carnitine palmitoyltransferase deficiency.
Disorders of gluconeogenesis: Gluconeogenesis is the process by which the
body produces glucose from non-carbohydrate sources. Examples include fructose-
1,6-bisphosphatase deficiency and pyruvate carboxylase deficiency.
American Academy of Pediatrics Committee on Fetus and Newborn. (2011). Clinical report: Postnatal glucose homeostasis in
late-preterm and term infants. Pediatrics, 127(3), 575-579.
Saudubray, J.-M., Garcia-Cazorla, A., & de Lonlay, P. (2006). Inborn errors of metabolism overview. In P. Caballero, L. Allen, &
L. J. P. Dary (Eds.), Encyclopedia of Food Sciences and Nutrition (pp. 3489-3496)
68. Inborn errors of Metabolism
Congenital hyperinsulinism: This is a rare genetic disorder in which the
pancreas produces too much insulin.
Organic acidemias: Rare genetic disorders in which the body is unable to
break down certain amino acids and fatty acids. Some of these disorders
can also cause hypoglycemia. Examples include propionic acidemia and methylmalonic
acidemia
American Academy of Pediatrics Committee on Fetus and Newborn. (2011). Clinical report: Postnatal glucose homeostasis in
late-preterm and term infants. Pediatrics, 127(3), 575-579.
Saudubray, J.-M., Garcia-Cazorla, A., & de Lonlay, P. (2006). Inborn errors of metabolism overview. In P. Caballero, L. Allen, &
L. J. P. Dary (Eds.), Encyclopedia of Food Sciences and Nutrition (pp. 3489-3496)
69. Srinivasan G, Pildes RS, Cattamanchi G, Voora S, Lillen LD. Plasma glucose values in normal neonates: a new look. J Pediatr 1986;109:114e7.
What is the purpose of the transient neonatal Hypoglycemia?
Why all mammals have transient hypoglycemia in the first days of life?
Adaptation from continuous to intermittent glucose supply?
Stimulate appetite for feed-fast cycles?
Promote Gluconeogenesis?
A positive adaptation for the fetus that ensures secretion of adequate
insulin secretion to maintain growth?
70. Take home message
1. Anticipate Hypoglycemia in “at risk” newborns in the first hour of life
2. Screen “at risk” newborns 30 minutes after feeding them, in the first 2 hours
3. Symptomatic newborns <40mg/dl and asymptomatic ones with a glucose level
<25mg/dl (after first feed) should receive IV Dextrose
4. If after 4 hours of life Glucose is <35 mg/dl, give IV Dextrose
5. Asymptomatic infants with blood glucose levels of 36-45mg/dl should receive
enteral supplementation (D10%, Dextrose gel 40%)
6. Infants with hypoketotic hypoglycemia persisting beyond the first 72 hours,
should be investigated.