endocrinesystem-121228084635-phpapp01

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Under the guidance of:Dr. Sandeep

Tandon

Professor and Head of Dept. of Pedodontics

Dr. Ambika SinghRathore

Dr. Rinku Mathur

Dr .Shantanu Jain

Dr. Tripti Sharma Ra

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CONTENT:

Introduction

Evolution of Endocrine system

Chemical characteristics of Hormones

Regulation of Hormone Release

Hypothalamus & its Hormone

Various glands and their importance

Disorders of Endocrine system common inChildren

References2


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INTRODUCTION:

Constant internal environment

(i.e., homeostasis) should be maintained.

Two systems help ensure communication:

Rapid transmission Long-lasting regulatoryaction

Both systems interact: Stimuli from the nervoussystem can influence the release of certain hormonesand vice versa.

NERVOUSSYSTEM

HORMONAL

Neuroendocrine

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EVOLUTIONOFENDOCRINESYSTEM The nervous systemcoordinates rapid and precise responses to

stimuli using action potentials.

The endocrine system maintains homeostasis and long-termcontrol using chemical signals.

The most primitive endocrine systems seem to be those of theneurosecretorytype, in which the nervous system either secretesneurohormones directly into the circulation or stores them inneurohemal organs (neurons whose endings directly contactblood vessels, allowing neurohormones to be secreted into the

circulation), from which they are released in large amounts asneeded.

True endocrine glands probably evolved later in the evolutionaryhistory of the animal kingdom as separate, hormone-secretingstructures.

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http://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossN.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossA.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossH.htmlhttp://www.britannica.com/EBchecked/topic/410737/neurosecretory-cellhttp://www.britannica.com/EBchecked/topic/410635/neurohormonehttp://www.britannica.com/EBchecked/topic/410631/neurohemal-organhttp://www.britannica.com/EBchecked/topic/69887/blood-vesselhttp://www.britannica.com/EBchecked/topic/69887/blood-vesselhttp://www.britannica.com/EBchecked/topic/69887/blood-vesselhttp://www.britannica.com/EBchecked/topic/69887/blood-vesselhttp://www.britannica.com/EBchecked/topic/410631/neurohemal-organhttp://www.britannica.com/EBchecked/topic/410631/neurohemal-organhttp://www.britannica.com/EBchecked/topic/410631/neurohemal-organhttp://www.britannica.com/EBchecked/topic/410635/neurohormonehttp://www.britannica.com/EBchecked/topic/410737/neurosecretory-cellhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossH.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossA.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossA.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossA.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossN.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossN.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossN.html


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CONVERGENT EVOLUTION:

Similarities among the endocrine systems ofcrustaceans, arthropods, and vertebrates.

The vertebrate endocrine system consists

of glands (pituitary, thyroid, adrenal), and

diffuse cell groups scattered in epithelial tissues.

Endocrine glands arise during development for all threeembryologic tissue layers (endoderm, mesoderm,ectoderm).

The type of endocrine product is determined by whichtissue layer a gland originated in.

Glands of ectodermal and endodermal origin: peptideand amine hormones;

Mesodermal origin glands:hormones based on lipids. 5
http://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossM.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossM.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossM.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.htmlhttp://www.emc.maricopa.edu/faculty/farabee/biobk/BioBookglossE.html


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WHAT ARE HORMONES?????

( TOSPURON)

Hormones are molecules thatare produced by endocrine

glands:i. The hypothalamus,

ii. Pituitary gland,

iii. Adrenal glands,

iv. Gonads, (i.e., testes andovaries),

v. Thyroid gland,

vi. Parathyroid glands, and

vii. Pancreas6


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The term endocrine implies that in response to

specific stimuli, the products of those glands are

released into the bloodstream.

The hormones then are carried via the

blood to their target cells.

The target cells for each hormone are characterized by

the presence of docking molecules(i.e., receptors) for

the hormone that are located either on the cell surface

or inside the cell. The interaction between the hormone and its receptor

triggers a cascade of biochemical reactions in the target

cell that eventually modify the cells function or activity.7


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CHEMICALCHARACTERISTICSOFHORMONES

Amines (from tyrosine)I. hydroxylation - catecholaminesII. iodination - thyroid hormones

Peptides/proteins Steroids (from cholesterol)

I. adrenocorticoidsII. sex hormones

III. active metabolites of vitamin D

Their mechanisms of action (e.g., whether they canenter their target cells and how they modulate theactivity of those cells) also differ.

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MECHANISMOFACTION:

STEROIDS: produced by gonads; structure similar to

cholesterol.

Enter their target cells and interact with the

cytoplasm or in the cell nucleus

Hormone-receptor complexes bind to certain regions

of the cells genetic material (i.e., the DNA)

Regulating the activity of specific hormone-responsive genes

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MECHANISMOFACTION:

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Amino acid derivatives:

are modified versions of building blocks of proteins.

thyroid gland & adrenal glands (i.e., the adrenal medulla)

Enter the cell, where they interact with receptor proteins that

are already associated with specific DNA regions. The

interaction modifies the activity of the affected genes.

Polypeptide and protein hormones:

found primarily in the hypothalamus, pituitary gland, and

pancreas

Because of their chemical structure, the polypeptide and

protein hormones cannot enter cells. Instead, they interactwith receptors on the cell surface.

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REGULATIONOFHORMONERELEASE

Constant feedback from the target glands to the

hypothalamus and pituitary gland ensures that the

activity of the hormone system involved remains

within appropriate boundaries.

To maintain the bodys homeostasis

Negative feedback mechanism

Short-loop feedback Positive-feedback mechanisms

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Negative Feedback Loop

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Positive Feedback Loop

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THEHYPOTHALAMUSANDITSHORMONES

Why is the Hypothalamus so Important?Eating and drinking,

Sexual functions and behaviors,

Blood pressure and heart rate,Body temperature maintenance,

The sleep-wake cycle, and

Emotional states (e.g., fear, pain, anger, andpleasure)

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Neurosecretory cells

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THEHYPOTHALAMIC-HYPOPHYSEAL

PORTALSYSTEM

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hypothalamic nuclei

superiorhypophysealartery superficial

capillary plexus

trabecular artery deepcapillary plexus

inferiorhypophysealartery

long portal veins

superficialcapillary plexus

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hypothalamic nuclei


capillary plexus

trabecular artery deepcapillary plexuslong portal veins

short portal veins


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hypothalamic nuclei


capillary plexus

trabecular artery deepcapillary plexuslong portal veins

short portal veinssecondary

capillaryplexus

adeno-

hypophysealcapillaryplexus inferior

hypophysealartery

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capillary plexus

deepcapillary plexuslong portal veins

short portal veins

hypothalamic nuclei

trabecular artery

adeno-

hypophysealcapillaryplexus

hypophyseal vein


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Corticotrophin (CRH) Somatostanin

ACTH

Gonadotropin (GnRH) Dopamine

LH & FSH

Thyrotropin (TRH) TSH

Growth-Hormone (GHRH)

GH

HYPOTHALAMIC

HORMONES

RELEASING INHIBITING

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THEPITUITARYANDITSMAJORHORMONES

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There is also an intermediate lobeinmany animals,but is rudimentary in humans.

For instance, in fish, it is believed to controlphysiological color change.

In adult humans, it is just a thin layer of cells

between the anterior and posterior pituitary.The intermediate lobe produces melanocyte-stimulating hormone(MSH), although thisfunction is often (imprecisely) attributed to theanterior pituitary.

INTERMEDIATE LOBE

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GROWTH HORMONE Most abundant of the pituitary hormones

Pivotal role in controlling the bodys growth

and development.

1. Stimulates the linear growth of the bones;

2. Promotes the growth of internal organs, fat (i.e.,adipose) tissue, connective tissue, endocrine glands,and muscle; and

3. Controls the development of the reproductive organs.

4. GH affects carbohydrate, protein, and fat (i.e., lipid)metabolism.

GH levels in the blood are highest during earlychildhood and puberty and decline thereafter. 26


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INDIRECTACTIONOFGROWTHHORMONE

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Two hypothalamic hormones control GH release:

(1) GHRH:stimulates GH release,

(2) Somatostatin:inhibits GH release.

Shor t -loop feedback com ponent :

GH acts on the hypothalamus to stimulate somatostatin

release.

In addition, GH release is enhanced by

Stress, such as low blood sugar levels (i.e.,

hypoglycemia) or severe exercise, and by the onset of

deep sleep.

Acute and chronic alcohol consumption have been

shown to reducethe levels of GH and IGF-1 in the

blood. 29


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PROLACTIN. Central role in the development of the female

breast and in the initiation and maintenance oflactation after childbirth.

Factors control Prolactin release:

1. Response to the rise in estrogen levels in theblood that occurs during pregnancy.

2. In nursing women, Prolactin is released inresponse to suckling by the infant.

3. Dopamine, which has an inhibitory effect.

4. Alcohol consumption by nursing women caninfluence lactation both through its effects on therelease of prolactin and oxytocin. 30


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POSTERIOR PITUITARY:

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VASOPRESSIN


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VASOPRESSIN Vasopressin (arginine vasopressin, AVP; anti-

diuretic hormone, ADH)is a peptide hormone

formed in the hypothalamus, then transported viaaxons to, and released from, the posterior pituitary.

Two principles site of action:

KIDNEY & BLOOD VESSEL

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MECHANISMSREGULATINGTHERELEASEOFAVP

Hypovolemia:decreased central venouspressure, the decreased firing of atrial stretchreceptors leads to an increase in AVP release.

Hypotension,whichdecreases arterial

baroreceptor firingand leads to enhancedsympathetic activity, increases AVP release.

Angiotensin II receptors located in a region ofthe hypothalamus regulate AVP release anincrease in angiotensin II simulates AVP release.

Increased sympathetic activation stimulatesAVP release

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OXYTOCIN HORMONE

I. Stimulates the contractions of the

uterus during childbirth.

I. In nursing women, the hormone activates milkejection in response to suckling by the infant

(i.e., the so-called let-down reflex).

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THEADRENALGLANDSANDTHEIRHORMONES

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Action of Cortisol:

1. Cortisol increases glucose levels in the blood bystimulating gluconeogenesis in the liver andpromotes the formation of glycogen in the liver.

2. Reduces glucose uptake into muscle and adipose

tissue,3. Promotes protein and lipid breakdown into products

(i.e., amino acids and glycerol, respectively) that canbe used for gluconeogenesis.

4. Protect the body against the deleterious effects ofvarious stress factors.

5. Suppress tissue inflammation in response to injuriesand to reduce the immune response to foreignmolecules. 36


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ACTION OF ALDOSTERONE:

Regulate the bodys water and electrolyte balance.

Conserve sodium and to excrete potassium from thebody.

Reducing water excretion and increasing blood

volume.

Decreases the ratio of sodium to potassiumconcentrations in sweat and saliva, therebypreventing sodium loss via those routes.

Controlled primarily by another hormone system, thereninangiotensin system, which also controls kidneyfunction. 37


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THETHYROIDANDITSHORMONES

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THYROID HORMONE PRODUCTION

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THYROID HORMONE PRODUCTION

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ACTIONOFTHYROIDHORMONE

Stimulates the production of certain proteins

involved in heat generation in the body, afunction that is essential for maintaining bodytemperature in cold climates.

Promotes other metabolic processes involvingcarbohydrates, proteins, and lipids that helpgenerate the energy required for the bodysfunctions.

Plays an essential role in the development of thecentral nervous system during late fetal and

early postnatal developmental stages. Required for the normal development of teeth,

skin, and hair follicles as well as for thefunctioning of the nervous, cardiovascular, andgastrointestinal systems

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Parafollicular C cells) in the thyroid gland produce

calcitonin,a hormone that helps maintain normal

calcium levels in the blood.

Specifically, calcitoninlowers calcium levels in the

blood by reducing the release of calcium from the

bones; inhibiting the constant erosion of bones

(i.e., bone resorption), which also releasescalcium; and inhibiting the reabsorption of calcium

in the kidneys.

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THEPARATHYROIDGLANDS

ANDTHEIRHORMONES

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ROLEOFPARATHYROIDHORMONE

Increases calcium levels in the blood, helping to

maintain bone quality and an adequate supply ofcalcium.

Causes re-absorption of calcium from and excretion

of phosphate in the urine.

Promotes the release of stored calcium from thebones as well as bone resorption.

PTH stimulates the absorption of calcium from the

food in the gastrointestinal tract.

Functions facilitated by a substance called1,25-dihydroxycholecalciferol, a derivative ofvitamin D. 44


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CALCIUMHOMEOSTASIS

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THEPANCREASANDITSHORMONES

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TWODISTINCTLYDIFFERENTFUNCTIONS

EXOCRINE ENDOCRINE

Digestive Enzymes

Islets of

Langerhans

PANCREAS

INSULIN GLUCAGON

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INSULIN & GLUCAGON

Beta cells of Islet Alpha cells of Islet

Blood sugar-lowering Increases blood glucose levels

hormone Actions opposite to insulin

Effect of Insulin:

1. Inhibits gluco-neogenesis

2. Insulin promotes the formation of storage formsof energy (e.g., glycogen, proteins, and lipids)and suppresses the breakdown of those storednutrients. 48


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REGULATION OF BLOOD GLUCOSE

LEVELS

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THEGONADSANDTHEIRHORMONES

OVARIES AND TESTES

They produce the germ cells.Synthesize steroid sex hormones that are

necessary for the development and function ofboth female and male reproductive organs and

secondary sex characteristics.Affect the metabolism of carbohydrates and

lipids, the cardiovascular system, and bonegrowth and development.

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DIABETES

''Type 1 diabetes is growing by 5% per year amongpre-school children in India.

It is estimated that 70,000 children, who are under15 years, developjuvenile type 1 diabeteseach year(almost 200 children a day!).

Symptoms of Diabetes in Children:

Stomach pains,

Headaches

Behaviour problems Weight loss, thirst, tiredness and frequent urination.

Detected through the presence of ketoacidosis52
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CAUSES:

Type I (Juvenile Diabetes): bodys inabilityto produce insulin

Genetic factors; environmental factors

Increased Type 2 Diabetes: linkedoverwhelmingly to lifestyle changes that havecontributed to increased weight problems andlack of activity in children. 53


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TREATMENT:

INSULIN: The advent of insulin pumps for

administration has allowed many children addedflexibility in their daily lives.

Monitoring blood sugar levels

Crucial factor

Diet:reduced consumption of fats and sugars,

intake fibers, vegetables and fruits.

Exercise: helps in lowering blood glucose levels

of the body54


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COMPLICATIONS

Sudden hypoglycemia & hyperglycemia

Immediately giving the child a glucose tablet orglucose beverage

LONG-TERM COMPLICATIONS

Problems of the kidney, heart, lungs, eyes, feetand nerves.

High blood sugar or high cholesterol levels55


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GIGANTISM Gigantism refers to abnormally

high linear growth due toexcessive action of insulin-like

growth factor-I (IGF-I) while the

epiphyseal growth plates are

open during childhood.

Acromegaly is the same disorderof IGF-I excess when it occurs

after the growth plate cartilage

fuses in adulthood.

Robert Wadlow, called the Alton

giant,who stood 8 feet 11 inches

tall at the time of his death in his

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CAUSES

Causes of excess IGF-I action may bedivided into 3 categories:

Those originating from primary GH excessreleased from the pituitary;

Those caused by increased GH-releasinghormone (GHRH) secretion or hypothalamicdysregulation; and

Hypothetically, those related to the excessiveproduction of IGF-binding protein, whichprolongs the half-life of circulating IGF-I. 57


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PITUITARYDWARFISM The achondroplastic

dwarf has anorthopedic reason forhaving short limbs anda short spinal

colum. The pituitarydwarflacks growthhormone (an endocrinereason).

SYMPTOMS: GH Deficiency

Low blood sugar59


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RISKFACTORS:

Disease of the hypothalamus of the brain

Disease of the front of the pituitary gland in the brain

Newborns who had some type of serious medical event (such

as a lack of oxygen) happen in the perinatal period, are at risk

for the type of growth hormone deficiency caused by damageto the hypothalamus.

TREATMENT:

Treatment with human growth hormone

theoretically corrects the deficiency, but ismost successful when the child is young. It mustbe given by injection.

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PRECOCIOUSPUBERTY Precocious puberty

describes pubertyoccurring at an unusuallyearly age.

CAUSES:

Central:

damage to the inhibitorysystem of the brain

hypothalamic hamartomaproduces pulsatile

gonadotropin-releasinghormone(GnRH)

Langerhans cellhistiocytosis 61
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PERIPHERALCAUSES

Secondary sexual development induced by sex

steroidsfrom other abnormal sources isreferred to asperipheral precocious puberty.

Causes can include: Endogenous sources

gonadaltumors (such as arrhenoblastoma)

adrenaltumors

germ cell tumor

congenital adrenal hyperplasia

McCuneAlbright syndrome Exogenous hormones

Environmental

As treatment for another condition62
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TREATMENT

GnRH agonists stimulate the pituitary to releaseFollicle Stimulating Hormone(FSH) andLuteinizing Hormone(LH).

One possible treatment is with anastrozole.Histrelinacetate.

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PEDIATRIC CUSHINGS SYNDROME
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PEDIATRIC CUSHINGS SYNDROME

(CS)

Rare in childhood and adolescence. Caused by prolonged exposure to excessive

glucocorticoids which can be secreted endogenouslyor administered exogenously.

Supra-physiological doses of exogenous gluco-corticoids in the form of topical, inhaled or oralcorticosteroids.

Eczema and asthma are common conditions in

childhood often requiring treatment withcorticosteroids.

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TREATMENT

Primary adrenal lesions

Surgical excision is the first-line therapy for acortical-secreting ACT.

Mitotane therapy appears to be the treatmentof choice

Cushings disease

Medical therapies such as MetyraponeandKetoconazoleto lower serum cortisol levels canbe used as a short-term measure, but cannot berecommended as long-term therapy. 67


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THYROID DISORDERS

Thyroid disease occurs lessfrequently in children than in adults, the signsand symptoms can be similar.

Congenital hypothyroidism

Affects infants at birth, and occurs in about 1 in4000 live-born babies.

Loss of thyroid function, due to the thyroidgland failing to develop normally.

Enzyme defect leading to deficient hormoneproduction, iodine deficiency and a brainpituitary gland abnormality.

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Within the first week of life, a heelprick blood sampleistaken to assess an infant's thyroid hormone level.

Infant is immediately given thyroid hormone replacement

therapy (T4 thyroxine). Normal growth and developmentshould then continue, with no adverse effects on the child'smental capacity.

Subtle symptoms: Severe:

1. Poor feeding Poor growth and development2. Constipation Dry skin & hair3. Low body temperature Slow tendon reflex4. Slow pulse Enlarged tongue5.

Prolonged jaundice, Umbilical hernia6. Increased sleepiness Puffiness & swelling7. Decreased crying.

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HYPERTHYROIDISMINNEWBORNS

Overactive thyroid gland: referred to as

NEONATAL HYPERTHYROIDISM.

If the mother has Graves' disease, the thyroid-

stimulating antibodies in her blood can cross theplacenta and stimulate the unborn child's thyroidgland,thus producing too much thyroid hormone.

Some newborns may hardly be affected if the levels

of antibodies are low. No treatment may be necessary as the mother's

antibodies will soon clear from the baby'sbloodstream, usually within 2 to 3 months.

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NEWBORNS WITH ADVANCED HYPERTHYROIDISM


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NEWBORNSWITHADVANCEDHYPERTHYROIDISM

TREATMENT

Anti-thyroid drugs is safe and effective, and will only beneeded for a short period of time, until the stimulating

antibodies pass from the baby's bloodstream.If the mother is on a high dose of anti-thyroid medication,

the diagnosis can be delayed by about a week until theinfant clears the anti-thyroid medication.

EXTREMELY FASTPULSE

IRRITABILITY

FLUSHED MOIST SKIN

INFANT TENDS TO BE THIN &LONG

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HASHIMOTO'STHYROIDITIS

The most common cause of

hypothyroidismin childrenand adolescents isHashimoto's thyroiditis, anautoimmune disease.

As the thyroid gland becomesincreasingly underactive,physical and mental changeswill become more obvious.

Symptoms of hypothyroidismdevelop very slowly

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SIGNSANDSYMPTOMS

The first sign is that the child's growth ratedecreases unexpectedly and skeletaldevelopment is delayed.

GOITRE

DecreasedEnergy

Lethargy

Dry Itchy Skin&

Constipation

WEIGHTGAIN

PoorConcentration 73


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TREATMENT

Thyroid hormone replacement istaken daily for life.

The dosage of thyroid hormone needs to be age-appropriate, as the body's demands for thyroid

hormone vary with age.

SIDE-EFFECTS:In children who have had long-standing

hypothyroidism, ultimate height potential may bepartly lost.As the child regains normal thyroid function,

behavioural problems may arise as their physicaland mental processes speed up

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GRAVES' DISEASE


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GRAVES DISEASE

The most common causeof hyperthyroidism inchildren and adolescentsis an autoimmunecondition called Graves'disease.

In Graves' disease thebody produces antibodiesthat stimulate the thyroidgland uncontrollably, tomake too much thyroidhormone.

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SIGNS AND SYMPTOMS

Increased Energy,

hyperactive, restless, Easilydistracted

Enlarged Thyroid Gland, fastpulse, nervousness, heat

intolerance, weight loss

Accelerated growth rate,Shaky hands

Muscle weakness, diarrhoea,and Sleep & behavioural

disturbances.76

TREATMENT


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TREATMENT Propylthiouracil (PTU) or Carbimazole.

Period of 'block and replace therapy' (anti-thyroiddrugs as well as thyroxine) is useful.

Throughout a child's treatment, thyroid hormone levels willneed to be monitored regularly, along with their clinicalsymptoms.

SIDE EFFECTSAnti-thyroid drugs can, however, occasionally stop the

production of white blood cells or platelets.

Sore throats, mouth ulcers, excessive bruising or skinrashes can indicate this.

The only safe action is to stop the medication until afterthe result of the blood test.

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REFERENCES


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REFERENCES: Susanne Hiller-Sturmhfel and Andrzej Bartke. The Endocrine

Syste An Overview.Alcohol Health & Research World; Vol.22(3):1998; 153-64

Ashley B. Grossman, Martin O. Savage.Pediatric CushingsSyndrome: Clinical Features, Diagnosis, and Treatment.ArqBras Endocrinol Metab 2007;51/8:1261-1271)

Kim E. Barrett, Susan M. Barman. GanongsReview of MedicalPhysiology;Vol.23:451-568

Arthur C. Guyton. Textbook of Medical Physiology 10thedi;993-

1019

K. Sembulingham. Essentials Of Medical Physiology;3rdedi;667-714 78


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Presented by:

Dr. Ruby Kharkwal1styear postgraduate studentDepartment of Pedodontics

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