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.
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.
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
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
Gestational diabetes mellitus (GDM) is a condition that develops during pregnancy when the body is not able to make enough insulin. GDM affects 2-10% of women during pregnancy.It is important to recognize and treat gestational diabetes as soon as possible to minimize the risk of complications to mother and baby.
Definition
Incidence
Types
Diabetogenic effect of pregnancy
Metabolic changes during pregnancy
Risk of uncontrolled DM on pregnancy
Diagnosis and evaluation
Medical management
Nursing management
Definition of Diabetes mellitus: It is inability to metabolize glucose properly. It is a chronic systemic disease, manifesting metabolic and vascular changes affecting every organ in the body.
a. Pregestational (preexisting) diabetes
Occurs when have type 1 or type 2 diabetes before becoming pregnant.
1-Type I Insulin-dependent (IDDM) (Insulin deficient).
2-Type II Non-Insulin dependent (NIDDM) (Insulin resistant).
b. Gestational diabetes mellitus (GDM).
Occurs diabetes when becoming pregnant.
a. Pregestational (preexisting) diabetes
Occurs when have type 1 or type 2 diabetes before becoming pregnant.
1-Type I Insulin-dependent (IDDM) (Insulin deficient).
2-Type II Non-Insulin dependent (NIDDM) (Insulin resistant).
b. Gestational diabetes mellitus (GDM).
Occurs diabetes when becoming pregnant.
Diabetes may appear only during pregnancy due to :-
1-Increased levels of antiinsulinas (estrogen, progesteron, human placental lactogen, and prolactine).
2-Decreased renal threshold for glucose (glucose loss in urine).
During early stage of pregnancy: Maternal hypoglycemia.
After the fourth month: increase glucose level in the blood due to placental hormones
During labor: liability to hypoglycaemia.
After delivery: glucose level return to prepregnant state.
Gestational Diabetes
Risk Factors
Maternal age >25
Family history
Glucosuria
Prior macrosomia
Previous unexplained stillbirth
Risk of uncontrolled diabetes on pregnancy
A- Maternal effect:
On pregnancy On labor On puerperium
-Abortion - premature -puerperal sepsis
-PET labor -PPH
-Polyhydramnios - Inertia - Abnormal
-Pressure symptom - Operative lactation
-Infection delivery
-Retinopathy
Risk of uncontrolled diabetes on fetus
1- Abortion
2- Congenital anomalies
Open neural defect, CHD, renal anomaly, sacral agenesis, small left colon syndrome(Approximately 40% to
50% of infants with this disorder have diabetic mothers, almost all of whom are insulin dependent , , imperforated anus.
3- Macrosomia
Fetal hyperglycaemia causes increase insulin secretion and lead to increase fetal fat deposition
Open neural defect
sacral agenesis
Macrosomia
Macrosomia
Macrosomia
Risk of uncontrolled diabetes on fetus
4- Intrauterine fetal death due to:
Congenital malformation, ketoacedosis, hypoglycaemia, superimposed PET.
5- Neonatal hypoglycemia
After delivery, glucose concentration fail, while neonatal insulin level remain high lead to neonatal hypoglycemia (Tremors, pallor, apnea, cyanosis)
Risk of uncontrolled diabetes on fetus
7- Hyperbilirubinaemia
Due to immature liver
8- Neonatal death due to:
Congenital anomalies
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
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
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
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mortality, and public health costs than all illicit drugs combined. The
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(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.
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5. CAUSES OF NEONATAL HYPOGLYCEMIA
An excess
of insulin in
the baby’s
blood
Limited
storage of
glycogen
Increased
glucose use
Decreased
glycogenoly
sis
Decreased
gluconeogene
sis
Decreased
gluconeogene
sis
6. PATHOGENESIS
Whole blood glucose is 15% less compared to the plasma value
The higher the hematocrit ,the lower the plasma and lower the glucose level .
Low blood glucose is normal in neonates if its transient .
Low level because continuous supply via placenta from the mother is cut-off
now having inconsistent supply
can’t judge the value in 1st 2-4 hour
start building up once feeding is commenced
Glycogenolysis is expected after the birth
Decrease insulin production
12. CONTINUITY
In resistant or persistent hypoglycemia the following drugs
should be considered: –
• Hydrocortisone: 10 mg/kg/day in two divided doses
intravenously
• Glucagon: 100 – 300 ug/kg/dose IM to a maximum of 3
doses in babies with adequate glycogen stores
• Diazoxide: 2 – 5 mg/kg/dose every 8 hrly orally
• Octreotide : Synthetic somatostatin in a dose of 2–10
ug/kg/day subcutaneously q 8 -12 hourly
• Babies with persistent or resistant hypoglycemia should
be REFERRED to a specialize center for farther
investigations
13. SIGNS AND SYMPTOMS OF NEONATAL HYPOGLYCEMIA
`• Bluish-coloured skin (cyanosis) or pale
skin
• Breathing problems, such as rapid
breathing (tachypnea), pauses in
breathing (apnea), or a grunting sound
• Irritability or listlessness
• Loose or floppy muscles (hypotonia)
• Vomiting or poor feeding
• Weak or high pitched cry
• Tremors, shakiness, sweating, or
seizures
18. GENERAL TREATMENTS FOR NEONATAL
HYPOGLYCEMIA
• If IV dextrose isn’t an option for a baby with NH, glucagon can be used as a treatment
and administered subcutaneously or intramuscularly.
• Glucagon can be used to treat babies who experience severe hypoglycemia and may not
have dextrose available to them.
• Babies who have experienced NH and are not being treated with dextrose or glucagon
should be fed within the first hour of life. These feedings should be done at two to three
hour intervals, and blood glucose concentrations should be monitored frequently within
20 to 30 minutes after being fed.
• Babies who are breastfed may need supplemental formula until the mother is able to
produce enough breast milk .
19. MANEGEMENT OF SEVERE HYPOGLYCEMIA
Start at
6mg/kg/min
Use central line
for infusion
greater than 12.5
Increase glucose
infusion by
2mg/kg/day till
BS>60mg/dl
Wait 8 to 12 hour
before tapering
Tapering should
slow and
gradually 6-8hour
Whenever possible
continue the
breastfeed to the
infant
21. Nursing care can assist in the prevention of neonatal hypolglycaemia, maintaining normoglycaemia, and when actively
treating a hypoglycaemic event
• Four major components of basic nursing care is keeping the baby:
• Warm,
• Pink,
• “Sweet”, referring to normoglycaemia
• Calm
• Refer to the Management of the neonate and/or Preterm infant management guideline for optimising basic care of the
neonate
• During the management phase of neonatal hypoglycaemia, careful consideration and action must be given to the cause of
the hypoglycaemia
• For example, if a baby is hypothermic and hypoglycaemic, it is equally important to manage the neonate’s temperature and
low BGL
• Management strategies within the flow chart below are subject to change dependent on individual patient factors
• Medical staff must order any new management strategies on EMR prior to initiation
• Timing of BGL testing/re-testing must be led by medical staff, and nursing staff must relay results back after each result
