VII.

THYROID AND PARATHYROID

OUTLINE
A. Thyroid Production
B. Thyroid disorders
I. PITUITARY GLAND: ANATOMY AND
1. Hypothyroidism
PHYSIOLOGY
2. Hashimoto’s Thyroiditis
A. Pituitary and Hypothalamus
3. Endemic Goiter
B. Feedback
4. Wolff-Chaikoff Effect
C. Anterior Pituitary Gland
5. Hyperthyroidism
(Adenohypophysis)
6. Graves’ Disease
1. Growth Hormone
C. Parathyroid disorders
2. Prolactin
1. Hypoparathyroidism
3. Thyroid Stimulating
2. Hyperparathyroidism
Hormone (TSH)
VIII. ADRENAL GLAND
4. Adrenocorticotropic
A. Adrenal cortex
Hormone (ACTH)
1. Zona glomerulosa
5. Gonadotropic Hormones
2. Zona fasciculata
(Luteinizing Hormone &
3. Zona reticularis
Follicle Stimulating
4. Triggers of Secretion
Hormone)
i. Glucocorticoids
D. Posterior Pituitary Gland
ii. Mineralocorticoids
(Neurohypophysis)
iii. Androgen
1. Antidiuretic Hormone
B. Adrenal Medulla
(ADH-Vasopressin)
C. Diseases Associated with Adrenal
2. Oxytocin
gland
II. GENERAL DISORDER OF THE ANTERIOR AND
1. Primary Adrenocortical
POSTERIOR PITUITARY
Insufficiency
A. Hypopituitarism
(adrenalcortex)
B. Multiple Pituitary Hormone
2. CAH
Deficiency (MPHD)
3. Cushing Syndrome vs
1. Congenital Disorders
Cushing Disease
i. Hall-Pallister Syndrome
4. Pheochromocytomas
ii. Septo-optic Dysplasia
IX. DIABETES MELLITUS
iii. Severe, Early Onset
A. Causes of Diabetes Mellitus
MPHD
B. Detection of Diabetes Mellitus
2. Acquired Disorders
C. Acanthosis Nigricans
C. Isolated Growth Hormone
D. Complication: Diabetic
Deficiency
Ketoacidosis
D. Growth Hormone Insensitivity
E. Mechanisms of Diabetes
III. CLINICAL FEATURES CONGENITAL
F. Classification of Diabetes
HYPOPITUITARISM
Ketoacidosis
A. Chronic GH Deficiency
B. Treatment
IV. HYPERPITUITARISM I. PITUITARY GLAND: ANATOMY AND
A. Growth Hormone Excess
B. Treatment
PHYSIOLOGY
V. DIABETES INSIPIDUS
A. Central Diabetes Insipidus A. PITUITARY AND HYPOTHALAMUS
B. Nephrogenic Diabetes Insipidus ● The pituitary gland is the major regulator of an
C. Diagnosis elaborate hormonal system. The pituitary gland
D. Treatment receives signals from the hypothalamus and responds
by sending pituitary hormones to target glands. The
VI. CENTRAL PRECOCIOUS PUBERTY target glands produce hormones that provide negative
A. Sexual Maturity Rating (SMR) feedback at the level of the hypothalamus and
B. Normal Sexual Development pituitary
C. Abnormality
HYPOTHALAMUS
D. Precocious Puberty ● Connection between the nervous system and the
endocrine system
 PEDIA (013) Pediatric Endocrine Disorders
● Releases hormone that stimulate or inhibit the
production of hormones in the ANTERIOR
PITUITARY
SIRMATA 2024
PITUITARY
● Master Gland ” ability to interpret and respond to
signals in the hormonal system
○ The pituitary's central role in this hormonal
system and its ability to interpret and
respond to a variety of signals have led to its
designation as the master gland .

● Regulate amount of hormone released into

bloodstream by target organs
● Located inside the sella turcica
○ The pituitary gland is located at the base of
the skull in a saddle-shaped cavity of the
sphenoid bone called the sella turcica. The
bony structure protects and surrounds the
pituitary bilaterally and inferiorly
● Divided into 2:
○ Anterior: ADENOHYPOPHYSIS (80%)
○ Posterior: NEUROHYPOPHYSIS (20%)

B. FEEDBACK
Figure 1. Anatomy and Physiology of the Hypothalamus
and Pituitary Gland

● What is the most significant hormone in the anterior

pituitary? - GROWTH HORMONE
● It increases the linear growth of a person. this means
that the soft tissue will grow and it enhances the
protein synthesis/ it also increase the cellular mass of
any person
● This causes glucose to increase also however it is a
negative feedback for your growth hormone
● Growth hormone and thyroid hormone comes together
and glucose is the enemy
● GH-releasing hormone stimulates the release of
growth hormone
● Ghrelin - hormone produced during hunger (“gutom”) -
high amount in the stomach and hypothalamus.
● Physiologic condition of sleep also increases growth
hormone
● Others: exercise, trauma, acute illness, fasting
● Somatostatin - inhibits growth hormone
● Somatomedin - another term for insulin growth factor Figure 3. Negative Feedback Mechanism of the HPA Axis
1 - increases cellular make up.
○ If you have problems with growth, you can
request this one and it will show a decrease ● Golden rule:
○ THYROID HORMONE COINCIDES WITH ○ any excess product will cause negative
GROWTH HORMONE feedback
● Connected to the pituitary by the pituitary stalk ○ any deficit product will cause positive
feedback

C. ANTERIOR PITUITARY
(ADENOHYPOPHYSIS)

1. GROWTH HORMONE

Increase Decrease

Hormones GH releasing Somatostatin

hormone Glucocorticoid
Ghrelin Negative
gutom ” high feedback of IGF
amounts in 1
stomach Free fatty acids
and also (FFA)
hypothalamus
Figure 2. Hypothalamus

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 PEDIA (013) Pediatric Endocrine Disorders
Physiologic Sleep, exercise, Hyperglycemia,
conditions physical stress, hypothyroidism
trauma,
acute illness,
puberty and
fasting(hypoglyce
mia)
Table 1. Growth Hormone
● Human GH is a 191-amino-acid single-chain
polypeptide that is synthesized, stored, and secreted
by somatotropes in the pituitary
● GH is secreted in a pulsatile fashion under the
regulation of hypothalamic hormones. The alternating
secretion of GH-releasing hormone, which stimulates
GH release, and somatostatin, which inhibits GH
release, accounts for the rhythmic secretion of GH.
● Ghrelin, a peptide produced in the arcuate nucleus of
the hypothalamus and in much greater quantities by
the stomach, also stimulates GH secretion
● GH increases linear growth , bone thickness, soft
tissue growth, protein synthesis, fatty acid release
from adipose, insulin resistance and glucose
● IGF 1 (Insulin like Growth Factor)
○ Mediates MITOGENIC EFFECT of growth
hormone to tissues
○ Previously known as somatomedin
○ Circulating IGF-1 is synthesized primarily in
the liver and formed locally in mesodermal
and ectodermal cells, particularly in the
growth plates of children, where its effect is
exerted by paracrine or autocrine
mechanisms
SIRMATA 2024
actively inhibited by dopamine, a peptide
produced by neurons in the hypothalamus.
Disruption of the hypothalamus or pituitary
stalk can result in elevated PRL levels
● Dopamine
○ Inhibits prolactin and is released by
hypothalamus
○ Dopamine antagonists, states of primary
hypothyroidism, administration of thyrotropin
releasing hormone (TRH), and pituitary
tumors result in increased serum levels of
PRL
○ Dopamine agonists and processes causing
destruction of the pituitary cause reduced
levels of PRL.
○ This is a catecholamine
○ This inhibits GH, thyroid hormone and
prolactin
○ During pregnancy, there is no prolactin yet.
on birth, the baby suckle (nipple stimuli) and
causes the production of prolactin
○ Galactorrhea but no suckling yet -
postpartum increase of prolactin
○ Tumors – increase prolactin levels. if the
involvement is partial, it just clings on the
organ, this causes increased hormone
production. if there is complete inv
○ movement of the affected program, this
decreases its function.
3. THYROID STIMULATING HORMONE
(TSH)

2. PROLACTIN Increase Decrease

Hormones Thyrotropin Dopamine

Increase Decrease releasing Somatostatin
hormone (TRH) Glucocorticoid
Hormones Thyrotropin Dopamine Negative
releasing Agonist feedback of T3,
hormone (TRH) TSH
Dopamine
Antagonist Physiologic - -
conditions
Physiologic Disruption of Destruction of
conditions hypothalamus pituitary Table 3. TSH
and pituitary stalk Pregnancy
Pituitary tumors (due to high ● TSH is stored in secretory granules and released into
Primary estrogen and circulation primarily in response to TRH, which is
hypothyroidism progesterone) produced by the hypothalamus.
(causes high ● Stimulates release of Thyroxine (T4) and Tri
TRH) iodothyronine (T3) from thyroid gland through the
Postpartum formation of cyclic adenosine monophosphate and the
Sucking and G protein second messenger system
nipple stimuli ● Increases thyrotropin-releasing hormone in the
hypothalamus
● Increases thyroid mass
Table 2. Prolactin ○ Low inactivity and atrophy of thyroid gland
○ High hypertrophy and hyperplasia of thyroid
● Prolactin constantly secreted: gland
○ Initiation and maintenance of lactation (milk ○ Deficiency of TSH results in inactivity and
production) atrophy of the thyroid gland, whereas excess
○ versus Oxytocin ––“milk letdown” release of TSH results in hypertrophy and hyperplasia
milk by contraction) of the thyroid gland.
○ There is production of milk and is different
with oxytocin since it only helps with milk
letdown process – it will help the muscles to
4. ADRENOCORTICOTROPIC
contract and release the milk HORMONE (ACTH)
○ The regulation of PRL is unique because ● CORTISOL - last product of ACTH; important in
PRL is consistently secreted unless it is glucose that is why in fasting or stress, it increases.

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
● Secretion of LH is inhibited by androgens and
Increase Decrease estrogens
REMEMBER!!
Hormones Corticotropin ANP (atrial PRIMARY - TARGET ORGAN
releasing Natriuretic SECONDARY - PITUITARY
hormone(CRH) peptide) TERTIARY - HYPOTHALAMUS
Arginine Opiods
Vasopressin ● ACTIVIN - increases FSH
Oxytocin ● INHIBIN - inhibits FSH (because it is produced by the
Angiotensin II Y chromosome)
Cholecystokinin ● If estrogen increases, progesterone is decreased.
● estrogen - increased during puberty and not during
Physiologic Stress pregnancy
conditions Fasting
(hypoglycemia)
D. POSTERIOR PITUITARY
Table 4. ACTH
(NEUROHYPOPHYSIS)
● Secreted in diurnal pattern ● Consists of neurons of the SUPRAOPTIC and
○ (HIGHEST IN MORNING, low at afternoon PARAVENTRICULAR nuclei of the hypothalamus
and LOWEST 1 2 hrs AFTER ● 2 hormones produced by neurosecretion in the
SLEEP/evening) hypothalamic nuclei and RELEASED from posterior
● From proteolytic cleavage of POMC pituitary
(Proopiomelanocortin) ○ Arginine Vasopressin antidiuretic hormone
● POMC - precursor peptide (ADH)
● remember! MELANIN - darkening of skin. if there is ○ Oxytocin
POMC, there is darkening
○ Hence has pigmentary effect in humans
(same substrate with melanocyte stimulating
hormone) Causes darkening of skin (ex.
Addison’s disease)

5. GONADOTROPIC HORMONES
(LUTEINIZING HORMONE &
FOLLICLE STIMULATING HORMONE)
● Seen in both sexes

Increase Decrease

Hormones Gonadotropin LH inhibited

releasing Androgen and
hormone (GnRH) estrogen Figure 4. Anatomy and Physiology of the
Activin FSH inhibited Hypothalamus and Pituitary Gland
Increase FSH Inhibin (Sertoli
Facilitates LH cells)
induced ● Functional unit
testosterone ○ Neurons of supraoptic and paraventricular
production nuclei
○ Neuronal axons (forms pituitary stalk)
Physiologic - - ○ Neuronal terminals (median eminence of the
conditions posterior lobe)
● 2 hormones ADH and oxytocin
Table 5. Gonadotropic Hormones

FSH (FOLLICLE STIMULATING HORMONE) 1. ANTIDIURETIC HORMONE (ADH -

● Female Ovarian Granulosa cells follicular VASOPRESSIN)
development of the ovary estrogen ● Inhibits urination
● Male Testicular Sertoli cells gametogenesis in the
testis Increase Decrease
● Main function of female is to reproduce -
PROGESTERONE Physiologic Increased
● Secretion of FS is suppressed by gonadal production conditions plasma
of inhibin, a 31-kDa glycoprotein produced by the osmolality
Sertoli cells (dehydration or
hypernatremia)
LH (LUTEINIZING HORMONE) Osmoreceptors in
● Female ovarian theca cells progesterone the hypothalamus
● Male Leydig cells produce testosterone
● hormone that best describes male - testosterone Decreased blood
● LH promotes luteinization of the ovary and Leydig cell volume
function of the testis Baroreceptors in
the carotid sinus

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024

(aortic A. HYPOPITUITARISM
arch)
Table 6. ADH
● ADH antidiuretic hormone
○ No diuresis (urination) decrease urine output
by concentrating urine
○ Recruits water channels (aquaporin 1 and 2)
in the renal collecting duct causing water to
be reabsorbed
○ ADH regulates water conservation at the
level of the kidney by increasing the
permeability of the renal collecting duct water
○ dehydration = ADH is activated because we
now want to retain the water in our body. the
osmoreceptors of the hypothalamus tells the
pituitary to release ADH Figure 6. Classification of Hypopituitarism

● Hypopituitarism denotes underproduction of 1 or

2. OXYTOCIN multiple pituitary hormones
● Affected children have postnatal growth impairment
and other endocrine deficiencies that are specifically
Increase Decrease
corrected by hormone replacement
● The pituitary produces 6 hormones and the most
Physiologic Nipple sucking or
important hormone is the growth hormone because of
conditions stimulation
the abundance of somatotrophs
Distention of the
reproductive tract
B. MULTIPLE PITUITARY HORMONE
Table 7. Oxytocin DEFICIENCY (MPHD)
● Stimulates uterine contraction labor and delivery ● Mutations of 7 candidate genes account for 20% of
● Breast smooth muscle contraction Milk let down reflex MPHD
● Others: for orgasm, social recognition, pair bonding, ● Congenital
anxiety, trust, love and maternal behavior. ○ PROP1 and POU1F1 expressed late in
● Most recently, through the interaction with its G Pituitary(especially the anterior)
protein–coupled receptor in pancreatic and adipose ○ HESX1, LHX3, LHX4, OTX2, SOX3 AND
tissue, oxytocin appears to play a significant role in PITX2 Expressed early and not restricted to
appetite regulation and obesity by inducing anorexia. pituitarY
○ At least 12 genes have been implicated in
II. GENERAL DISORDER OF THE ANTERIOR the complex genetic etiology of
holoprosencephaly
AND POSTERIOR PITUITARY
1. CONGENITAL DISORDERS

i. HALL-PALLISTER SYNDROME
● Absent Pituitary- main problem
● hypothalamic hamartoma- benign tumor
● polydactyly
● nail dysplasia
● bifid epiglottis- usually 1 curve
● imperforate anus
● anomalies of heart, lung and kidneys.
● Mnemonic: PALISTER HaL
○ P: Pituitary failure, polydactyly
○ A: Anus imperforate
○ L: Lung anomalies
○ S: Skull/ Craniofacial abnormalities
○ T: Throat/ Bifid epiglottis
○ E: Epileptic (Seizures)
○ R: Renal anomalies
○ H: Hypothalamic hamartoma
Figure 5. Pituitary Gland ○ L: Laryngeal cleft

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 PEDIA (013) Pediatric Endocrine Disorders
Figure 7. Imaging of Patient with Hall-Pallister
Syndrome
ii. SEPTO-OPTIC DYSPLASIA
● Sella turcica has a problem and optic chiasm
● Nystagmus visual
● impairment in infancy,
● Optic nerve and brain abnormalities
● Pituitary hormone deficiencies
● Triad:
○ SMALL anterior pituitary
○ REDUCED pituitary stalk
○ ECTOPIC posterior pituitary bright spot-
OPTIC NERVE INVOLVEMENT
● Primary etiology is hypothalamic dysfunction
● GH deficiency is the most observed abnormality
● Neuroimaging demonstrates optic nerve and brain
abnormalities and is associated with anterior and/or
posterior pituitary hormone deficiencies in up to 75%
of the cases
Figure 7. Septo-optic Dysplasia
iii. SEVERE, EARLY ONSET MPHD
● ACTH is also affected
● Includes deficiency of ACTH
● Triad:
○ Anterior pituitary DYSPLASIA
○ Absence or attenuated pituitary stalk
○ Ectopic posterior pituitary bright spot
● Male predominance
2. ACQUIRED DISORDERS
● Any lesion that damages the hypothalamus, pituitary
stalk, or anterior pituitary
can cause pituitary hormone deficiency
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SIRMATA 2024
● Tumors, infections, autoimmune, irradiation]
● Because such lesions are not selective, multiple
hormonal deficiencies are usually observed
● Diabetes insipidus is more frequent in acquired than in
congenital hypopituitarism
● Craniopharyngioma
○ Most common lesion causing pituitary
hormone deficiency
○ in the sella turcica, that is why it inhibits
production of pituitary hormone
C. ISOLATED GROWTH HORMONE
DEFICIENCY
GENETIC FORMS
● IGHD is caused by abnormalities of the GH-releasing
hormone receptor, GH genes, and genes located on
the X chromosome
● Abnormalities:
○ GH releasing hormone receptor: Recessive
loss of function mutations in the receptor for
GH releasing hormone interfere with
proliferation of somatotropes during pituitary
development and disrupt the most important
signals for release of GH
○ GH gene: Unequal crossing over meiosis
produced variety of gene deletion specifically
the GH1 gene causing fetal or postnatal
growth retardation
○ Genes located on X chromosome
○ 2 loci in X chromosome is associated with
hypopituitarism
○ Xq21.3 q22 Bruton thymidine kinase (BTK)
gene = hypogammaglobulinemia and IGHD
○ Xq24 27 SOX2 transcription factor gene =
IGHD and intellectual disability
ACQUIRED FORMS
● GH Axis is more susceptible to disruption by acquired
conditions.
● Conditions:
○ Radiotherapy seen after 5 years of therapy of
total dose >/= 35 Gy
■ Children who receive radiotherapy
for central nervous system tumors,
leukemia, or total body irradiation
prior to hematopoietic stem cell
transplant are at risk for developing
GH deficiency
■ More subtle defects are seen with
doses around 20 Gy
○ Meningitis
○ Histiocytosis
○ Trauma
● Subnormal stage of pubertal development compared
to chronological age.
D. GROWTH HORMONE INSENSITIVITY
● CAUSED by disruption of pathway distal to production
of GH.
● Laron syndrome: Involves mutation of GH receptor
○ Resembles severe IGHD severe short
stature of > 4 SD BELOW the mean present
by 1 year old
○ Resting and stimulated GH levels tend to be
high and insulin-like growth factor (IGF) 1
levels are low
● Labs
○ Resting and stimulated GH high
○ Insulin like growth factor (IGF1) low
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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
○ despite having high GH hormone, the
receptors are insensitive, then will cause low
function

III. CLINICAL FEATURES CONGENITAL

HYPOPITUITARISM

Figure 9. GH levels are measured at different times after

drug administration depending on the drug.

● Arginine infusion (500 mg/kg IV given over 30

minutes), clonidine (0.15 mg/m2 orally [maximum 0.25
mg]), levodopa (10 mg/kg orally for children; 500 mg
orally for adults), and glucagon (0.03 mg/kg IV
[maximum 1 mg]). GH levels are measured at different
times after drug administration depending on the drug.
Figure 8. Length-for-age, GIRLS ● Because no single test is 100% effective in eliciting
GH release (1), two GH provocation tests are done
PHYSICAL EXAMINATION (typically on the same day). GH levels generally peak
● Normal head circumference round, broad short face, 30 to 90 minutes after administration of insulin or the
depressed saddle nose and small, onset of arginine infusion, 30 to 120 minutes after
● Frontal bossing levodopa, 60 to 90 minutes after clonidine, and 120 to
● Sparse hair facial, axillary and pubic 180 minutes after glucagon.
● Delayed dentition
● High pitch voice B. TREATMENT
● Pudgy appearance excess of body fat with
ow muscle mass ● Treatment started as soon as possible
● Extremities are small but well proportioned ○ To decrease the gap of height of the patient
● Micropenis seen in childhood but becomes towards his/her classmates
● normal in adults ● GH and GnRH agonist
● Delayed maturation delayed puberty for ○ Interrupts PUBERTY
3-7 years ○ Delay epiphyseal fusion and prolong growth
● Specific features ○ The recommended initial dose of rhGH for
○ Nystagmus septo-optic dysplasia treatment of GH deficiency is 0.16-0.24
○ Micropenis beyond adults hypoadrenalism mg/kg/wk (22 to 35 μg/kg/day).
and hypothyroidism ○ RhGH is administered subcutaneously once
daily
A. CHRONIC GH DEFICIENCY CRITERIA FOR STOPPING TREATMENT
● Poor linear growth ● Patient decides that he/she is “TALL ENOUGH”
● Delayed skeletal Age ● Growth rate < 1 inch/year
● Peak level of GH (<10 ng/mL) in each two provocative ● Bone age >14 years girls
tests ● Bone age > 16 years boys
○ Insulin tolerance test
○ Arginine infusion
○ Clonidine
○ Levodopa
○ glucagon

● Remember that glucose increase GH, but if you are

insulin intolerant, then hypoglycemia and decrease
GH

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
CLASS AMERICAN CHILDREN OF BOTH SEXES
FROM 0-18 YEARS OLD
● WHY LEFT? BECAUSE RIGHT HAND IS ALWAYS
USED CAUSING WEAR AND TEAR ON BONES
INCREASING VARIABILITY
● There might be manipulations in the right handed
people, and may cause fracture. This cant be used for
left handed people because this is the atlas
● Compare with the same age

IV. HYPERPITUITARISM
● GIGANTISM
○ Young person
○ Open epiphyses
● ACROMEGALY
○ Closed epiphyses

● Hyperpituitarism causes increased growth hormone

levels.For gigantism, they are young who are exposed
to high GH while their epiphyseal plates are open,
causing longitudinal growth. For acromegaly, they
were exposed to the GH during the closure of the
epiphyseal plates.

Figure 10. GnRH Agonists Mechanism of Action.

A. GROWTH HORMONE EXCESS
● GIGANTISM
○ Longitudinal growth acceleration
○ Coarse facial features and long hand/feet
○ Pituitary gigantism is rare but usually seen
with pituitary adenoma
● ACROMEGALY
○ Enlarged distal parts
○ Large skull, nose broad, tongue enlarged
○ their bones are still normal.
● BOTH
○ Fatigue and lassitude (Lassitude – lazy
attitude, looks like they are always sleepy)
○ GH high – >100 ng/mL
■ No suppression afteR glucose
tolerance test (hyperglycemia)
■ Fails to lower GH <5ng/mL after
1.75g/kg oral glucose, GH is still
high
■ Glucose tolerance test – measures
ability of IGF-1 to suppress GH
secretion

B. TREATMENT
● Somatostatin analogs
○ Octreotide suppresses GH <2.5 ng/mL and
normalize IGF 1 levels
○ Tumor shrinkage also occurs with octreotide
but is generally modest.
○ Octreotide injection in the pediatric
population has been used at doses of 1-40
μg/kg/24 hr
● For pituitary adenoma
○ Trans sphenoidal surgery
● GH and Prolactin oversecretion
○ Bromocriptine binds to pituitary dopamine
type 2 (dopamine agonist)
○ Remember, dopamine inhibits GH, prolactin,
and even thyroid hormone release.
Figure 11. Bone Age with Greulich- Pyle Atlas ○ Marked hyperprolactinemia as a result of
plurihormonal adenomas that secrete both
GH and prolactin
BONE AGE WITH GREULICH-PYLE ATLAS
○ Mammosomatotroph – most common type of
● Used to detect bone age
GH secreting cells involved in gigantism
● GREULICH AND PYLE TOGETHER STUDIED 1,000
● Pegvisomant
LEFT HAND RADIOGRAPHS OF HEALTHY MIDDLE
○ GH receptor antagonist

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
○ If the GH cannot be reduced, we can use this
to inhibit its receptors. ● Posterior pituitary
○ It effectively suppresses GH and IGF-1 levels ● ADH or Vasopressin Deficiency
in patients with acromegaly caused by
pituitary tumors as well as ectopic GHRH
hypersecretion

V. DIABETES INSIPIDUS

Figure 13. Central DI

B. NEPHROGENIC DIABETES INSIPIDUS

● There is vasopressin insensitivity. Despite having
normal or high ADH, the problem there is that there
are defective aquaporins, which are water channels
that allow water reabsorption in the collecting duct.
Figure 12. Diabetes Insipidus
● Vasopressin effects on Kidney via V2 receptors-
Inserts aquaporin 2 water channel in the apical
● ”DAMI IHI”. meaning to say there is high urine output membrane.
because there is a problem with the ADH. ADH is an ● Patients with nephrogenic diabetes insipidus have an
anti-urination, however if there is no ADH, there will ability to respond to ADH and produce dilute urine
be an increased urine output. despite an increase in plasma osmolality.
●
● Manifests clinically with polyuria and polydipsia and
can result from either vasopressin deficiency (central ● Kidney
DI) or vasopressin insensitivity at the level of the ● Vasopressin Insensitivity
kidney (nephrogenic DI [NDI]). ● Defective Aquaporin-2
● 2 types
○ Central DI
■ There is low or absent ADH
○ Nephrogenic DI
■ There is vasopressin insensitivity.
● Both central DI and NDI can arise from inherited
defects of congenital or neonatal onset or can be
secondary to a variety of causes

A. CENTRAL DIABETES INSIPIDUS

● ADH (Vasopressin) is secreted in the posterior
pituitary and it is the principle regulator of plasma
tonicity Figure 14. Nephrogenic DI
● If Dehydrated: Plasma tonicity increases (Higher
solids than fluids) Hence ADH is released causing
anti-diuresis and vascular pressor activity (increase
BP)
● ADH is synthesized in the paraventricular and
supra-optic nuclei
● The normal response to increased plasma osmolality
is conservation of water by the kidney. In central
diabetes insipidus, this does not occur because of an
absence of ADH secretion.

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
● In central DI, when you remove the patient cannot still
concentrate the urine, if you give them DDAVP (an
ADH analog) then it will treat the central DI.
● However in nephrogenic DI, the problem there is the
aquaporin itself. Even if you are giving DDAVP, there
will be no improvement with that patient.
● Remember that in central DI there is inadequate ADH
hence if you give synthetic ADH like that of
desmopressin it will cause urine concentration.
However in nephrogenic DI – even with high ADH, the
kidney will be unable to concentrate the urine

D. TREATMENT
● Central DI – administer DDAVP
● Nephrogenic DI – thiazide diuretic
(hydrochlorothiazide and metolazone)
○ Thiazide – enhances sodium excretion which
causes proximal tubule to reabsorb both
sodium and water leading to overall
decrease in urine output. It usually acts in the
loop of Henle, by inhibiting it, it will now
cause the excretion of sodium. With this,
there will be a compensatory effect with that
Figure 15. Structure of Nephron; Collecting Tubules- Aquaporins
of the PCT which will increase the
reabsorption of sodium, once absorbed the
● This is your nephron, it has a glomerulus and ducts water will follow.
which will help to produce your urine. Just remember
that in the collecting ducts there are aquaporins,
which are water channels that can be activated by Clinical Syndrome of Cerebral Salt Central
ADH. The ADH binds to these areas to cause the Parameters Inappropriate Wasting DI
opening of these gates, which let the water pass from ADH (SIADH) Syndrome
urine to the blood (reabsorption).
● At the collecting duct, aquaporin 2 is found and as a Vasopressin High Low Low
water channel causes water to move into the level
hypertonic inner medullary interstitium and be
reabsorbed. Urine High High Low
Sodium
AQUAPORIN 2
● Allows water to be reabsorbed back Serum Low Low High
● Makes urine concentrated Sodium

Urine Output Low High High

C. DIAGNOSIS
● SERUM osmolarity - > 300 mosm/kg
● URINE osmolarity - < 300 mosm/kg (high urine output
yet NOT CONCENTRATED) -> dehydration
● However – may have <300 but >270 serum osmolarity
● Remember that the normal osmolarity of your blood is
between 275-295 mosm/kg but with clinical symptoms
of polyuria and polydipsia
○ Do water deprivation test
Primary should concentrate urine after water
polydipsia deprivation.
Central DI unable to concentrate urine but
increases urine osmolarity after DDAVP
(deamino-8-d-arginine vasopressin) –
desmopressin acetate injection
Nephrogenic unable to concentrate urine after water
DI deprivation and after DDAVP injection
Table 8. Diagnosis of Primary Polydipsia, Central DI,
& Nephrogenic DI
● Primary polydipsia is behavioral, when you drink a lot
of water because you’re anxious or you make this as
a relaxation technique, then you will have an
increased urine output because of increased water
intake. If you deprive this person with water, then the
patient can now concentrate the urine.
Intravascular High Low Low
volume
Treatment Oral fluid Give sodium DDAVP
restriction chloride and
water (PNSS)
Table 9. Clinical Parameters
● Differences of each might be asked not only in my
exams but also on your board exam. So please take
note!!
● Central DI - there is low ADH, there will be high urine
output , thus you cannot concentrate the urine which
explains the low urine sodium. High serum sodium
because there is low water. Because of low water the
BP will be low also.
● SIADH (opposite of Central DI) – due to high ADH
level – prevents the water secretion in the nephrons
thereby concentrating the urine (often urine osmol
>150) and decreasing urine output. There is
hypertension. Tx: restrict oral fluid because you are
already overloaded with fluid.
● However, Cerebral Salt Wasting Syndrome – due to
insult (probably from trauma, infection or tumors which
affects the cerebrum) in your brain causing release of
atrial natriuretic peptide (ANP) leading to increase
sodium excretion in the urine and thereby attracting
water to be excreted hence increase urine output.

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 PEDIA (013) Pediatric Endocrine Disorders
Main problem here is you lose sodium in the urine
causing diuresis, because where sodium goes water
will follow. You lose more salt than the water, which
explains the low sodium in serum despite losing fluid.
VI. CENTRAL PRECOCIOUS PUBERTY
A. SEXUAL MATURITY RATING (SMR)
SIRMATA 2024
● Menarche – happens 2.5 years after thelarche hence
females usually menstruate after 2 years of increasing
breast size “for some”. Do not be confused, that the
menarche is not the first sign of puberty. The first sign
of puberty will always be Thelarche.
● In girls, early menstrual cycles may be more irregular
than they are with normal puberty. The initial cycles
are usually anovulatory, but pregnancy has been
reported as early as 5.5 yr of age.
● In boys, testicular biopsies have shown stimulation of
all elements of the testes and spermatogenesis has
been observed as early as 5-6yr of age.
● In affected girls and boys, height, weight, and osseous
maturation are advance.

C. PRECOCIOUS PUBERTY

Males Females

Precocious Puberty < 9 years old < 8 years old

Delayed Puberty > 14 years old > 13 years old

Table 11. Precocious vs. Delayed Puberty

Central Peripheral

● Gonadotropin ● Gonadotropin
Dependent Independent
Figure 16. Sexual Maturity Rating (SMR) ● True ● Pseudopuberty
● ISOSEXUAL ● Some secondary sex
● Sexual development may begin at any age and ● Activated characteristics
generally follows the sequence observed in normal hypothalamic- appear but no
puberty. pituitary-gonadal activation of the
● So to better help you memorize this one: activation hypothalamic-pituitar
● Stage I is pre-adolescent – childhood, nothing ● Most common y-gonadal interplay
happened cause – ● Maybe from
● Stage 2 – ”S” - breast budding (only 2 - primary hypothalamic excessive estrogen/
mound), sparse hair, scrotum enlarged hamartomas testosterone
● Stage 4 – Secondary mound (2x2 = 4), Coarse is supplementation
fours, scrotum darkens, increase in breadth of penis
● Stage 3 – in between, Curling occurs, Penis grows in
Table 12. Central vs. Peripheral Precocious Puberty
length
● Stage V is mature/adult type (adult triangle – medial
surface of thigh hair) VII. THYROID AND PARATHYROID GLAND

B. NORMAL SEXUAL DEVELOPMENT

Male Female

Gonadarche (11-12 years Thelarche (10-11 years old)

old) → pubarche → → pubarche → growth spurt
adrenarche → growth spurt → menarche

Peak height velocity – Peak height velocity –

happens in SMR 3-4 happens in SMR 2-3
Figure 17. Thyroid Disorders

Table 10. Normal Sexual Development

● Gonadarche (enlargement of testes / scrotum)–
increase in testes >/= 4 ml volume or 2.5cm longest
diameter
● Thelarche – increase breast size “breast budding”
● Adrenarche in male- more on testosterone for sperm
production.
● Females have an earlier onset secondary sexual
characteristics and earlier growth spurt, that is why
during elementary school, the females usually are
taller than males at about grade 5-6 then at high
school, the male then becomes taller

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A. THYROID PRODUCTION B. THYROID DISORDERS

1. HYPOTHYROIDISM
● Decrease thyroid hormone
● Decrease metabolic processes

CONGENITAL HYPOTHYROIDISM
● Deficient Production Of Thyroid Hormone
● Primary – defect of the thyroid gland (primary means
there is a problem of your thyroid gland, secondary
problem in pituitary, tertiary there is a problem in
hypothalamus)
○ Primary: thyroid gland
○ Secondary: pituitary
○ Tertiary: hypothalamus
● Thyroid dysgenesis – 80-85% of cases
■ Dyshormonogenesis
■ Goiter is almost always present
● Secondary- defect of TSH stimulation (central or
Figure 18. Thyroid Hormone Production hypopituitary hypothyroidism)
○ Possible risk factor: fetal exposure to
THYROID HORMONE PRODUCTION excessive iodide.
● Iodide transportation
○ Iodine deficiency or endemic goiter – most
● Production of thyroglobulin
● Oxidation of iodine common cause of acquired congenital
● Organification hypothyroidism WORLDWIDE
● Esterification
● Endocytosis
● Lysosomal degradation
● Thyroid-binding-globulin

Figure 19. Thyroid Hormone Effects

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
● Irradiation of area of thyroid
○ Incidental to treatment of Hodgkin lymphoma
or Head and neck CA
● Ingestion of meds with iodides
● Why is it that if you ingest iodides it will cause
hypothyroidism? However, in high amounts of iodide it
will now cause negative feedback. Remember iodide
could now become iodine by means of your oxidation
process and it will now combine with thyroglobulin
because of that there would be a negative feedback in
your iodine because of the high amount of iodides.
○ Amiodarone – consist of 37% iodine
● Endemic Goiter (cretinism)
○ Low intake of iodine
○ low iodine means that there would be low T3,
T4
○ Seawater is rich in iodine hence goiter is rare
Figure 20. Clinical Manifestations of Congenital Hypothyroidism in people beside the sea. Those who are in
the uplands have low intake levels of iodine.
● Remember chronic lymphocytic thyroiditis or
● Remember that the thyroid enhances your metabolic
Anti-thyroid antibodies, also amiodarone
rate and if there is a problem like prolongation and the
processes of your entire body is also delayed. Hence,
remember the physiology of your liver, the bilirubin 2. HASHIMOTO’S THYROIDITIS
from your unconjugated rbc can cause jaundice.
● Lymphocytic infiltration with biopsy of the thyroid
● Prolonged physiologic jaundice – caused by delayed ● Goiter and growth retardation - most common
maturation of glucuronide conjugation – earliest sign manifestation
of congenital hypothyroidism ● Thyroid function test – normal except TSH which may
● Fontanels are widely observed at birth, maybe an be moderately elevated
early recognition of congenital hypothyroidism. If there ○ Subclinical hypothyroidism
is a problem in your thyroid there is also a problem in ● Anything for hypothyroidism there is high TSH
the maturation of your bone. Hence, the fontanels are ● For hyperthyroidism there is high T3 and T4
wide because the bones are immature. ● For Hashomoto’s Thyroiditis there is ANTIBODY to
TPO (thyroid peroxidase) and Thyroglobulin
DIAGNOSTIC AND THERAPEUTIC MANAGEMENT
● SERUM LEVELS OF T4 OR FT4 ARE LOW
○ T4 is very abundant and in high amount
○ T3 is smaller in amount however more potent
○ If you have a decrease in thyroid hormone
the first one to go down is your T4. However,
because the T3 is small in amount
sometimes it may be normal or low hence it
is insignificant.
● T3 IS INSIGNIFICANT
● TSH IS HIGH – ELEVATED >100mU/L (you can
usually see in congenital hypothyroidism)
● Thyroid scan (diagnostic tool)
○ Ectopic thyroid tissue – diagnostic of thyroid
Dysgenesis
● Levothyroxine – oral t4 supplement
○ Usually for life
○ Overtreatment – risk for craniosynostosis
and temperament problem

ACQUIRED HYPOTHYROIDISM
● Chronic lymphocytic thyroiditis (Hashimoto’s
thyroiditis)
Figure 21. Hashimoto’s Thyroiditis
○ The patient may have an infection before,
there is an inflammation so that there would
be production of antibodies
○ this is autoimmune 3. ENDEMIC GOITER
○ With anti-thyroid antibodies CRETINISM
○ Most common cause of acquired ● Deficient iodine stimulates – increased efficiency in
hypothyroidism thyroid (does not pertain to the number of thyroid)
● Thyroidectomy (if you remove the thyroid, now you hormone synthesis–iodine liberated in the tissues
won’t have thyroid hormones) returned rapidly to the gland – resynthesize t3 –

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
increase activity of thyroid – compensatory ○ ↑ Nail growth, onycholysis
hypertrophy and hyperplasia
● Serum t4 low
● Circulating t3 (fT3) high
6. GRAVES’ DISEASE
○ Very potent compared to t4 ● Excessive secretion of thyroid hormone
● Normal TSH ● Autoimmune disorder – producing thyroid stimulating
immunoglobulins (TSIs) - Suppresses plasma TSH
● Ophthalmopathy- Antibodies against antigens shared
by thyroid and eye muscle.
○ This is great evidence that your patient
probably has Graves’ disease.
● Pathophysiology of Graves’ Disease is because of
autoimmune disease it will now cause the
thyroid-stimulating immunoglobulin and some will now
attack the receptor of thyrotropin (remember:
Figure 22. Goiter thyrotropin receptors are the one inside your pituitary).
With these antibodies attached to the receptors the
TSH will now be problematic it will now cause
● Most serious consequence of iodine deficiency overproduction of thyroid hormones. Unlike the
includes 2 overlapping syndromes antibodies of TPO and Thyroglobulin it will decrease
● Administration of single intramuscular injection of the T3 and T4.
iodinated poppy seed oil to women - prevents iodine ● Thyrotropin receptor antibody (TRSAb)- Binds to
deficiency in future pregnancies up to 5 years. receptor of TSH and causes thyroid hyperplasia and
● When you are considering cretinism or low iodine you overproduction of Thyroid hormone (high t3, t4)
● Then lastly the emotional disturbances accompanied
request for T3 and T4 and you will see the disparity.
by motor hyperactivity-Earliest sign in children
There is normal TSH. (Increase metabolic rate, increased sympathetic
● What is the problem in endemic goiter when you have response)
low iodine? Their consequences are either neurologic ● Please differentiate properly the following
or myxedematous. Problems like mental retardation, antibodies:
problems in your neurological examination. In ○ ANTIBODY TO TPO AND
Myxedematous type these may cause generalized THYROGLOBULIN – causes hypothyroidism
○ THYROTROPIN-RECEPTOR ANTIBODY –
swelling and also growth and development problems. causes hyperthyroidism
But this may also. overlap. ○ So if you see a female who have retracted
eyelids with hand tremors, increase appetite,
irritability and insomnia à Graves and not
Neurologic type Myxedematous type your sleep-deprived classmate
● Thyroid Storm (With very high thyroid hormone
levels it will now cause a metabolic abnormality which
is known as Thyroid Storm)
Mental retardation, deaf Delayed growth and ○ Burch-Wartofsky point scaling (Sensitive to
mutism, standing and sexual development thyroid storm, if you have a score of more
gait abnormality, Myxedema than 45)
pyramidal signs (generalized swelling) ○ Life threatening acute onset of hyperthermia,
(clonus, Babinski and Absence of goiter severe tachycardia, heart failure and CNS
patellar hyper-reflexia) disturbance
TREATMENT
Table 13. Neurologic vs. Myxedematous Type ● 2 antithyroid drugs
○ Methimazole
■ 10 times more potent than PTU, longer
4. WOLFF-CHAIKOFF EFFECT half life (But for OB-GYNE, during 2nd
● Large administration of iodide – inhibits organification and 3rd trimester they used MTZ, but for
(iodine attaching to your thyroglobulin) of iodine and board exam, if there’s a question
decrease synthesis of thyroid hormone addresing what is the medication used
● Application: High iodine can be given to patients with for thyroid storm, you must choose PTU)
Graves’ disease (hyperthyroidism). ○ PTU (propylthiouracil)
■ MUST REMEMBER! The only meds
● Remember in hyperthyroidism, T3 and T4 are
used for pregnant patient who is
increased. diagnosed with thyroid storm (used only
5. HYPERTHYROIDISM on 1st trimester because it is less likely
to cross placenta)
● Increased levels of thyroid hormone in the blood
■ Heavily protein bound (meaning less
● Symptoms: ↑ thyroid hormone effects → “speeds
teratogenic that may affect
things up”
organogenesis of the embryo) hence
○ General: ↑ weight loss, ↑ appetite, ↑ body
less to cross the placenta and breastmilk
temperature, heat intolerance, sensitivity to
■ better for pregnant and nursing
heat
mothers
○ Cardiovascular: ↑ tachycardia, palpitations,
■ It is also a liver - toxic drug
arrhythmias, hypertension
○ Beta adrenergic blocker
○ GI: ↑ diarrhea
■ propranolol or atenolol
○ Nervous: ↑ anxiety, nervousness, irritability,
■ Adjunct (meaning added therapy) to
insomnia, tremors
antithyroid drugs in thyroid storm
○ Skin: ↑ Sweating, hair growth, fine, soft hair

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 PEDIA (013) Pediatric Endocrine Disorders
■ It will decrease your heart rate or
palpitations
● According to the book, PTU is used during pregnancy
● But according to the new guidelines followed by
Philippine Obstetric and Gynecology Society, PTU is
only used in 1st trimester then changed to
methimazole due to higher risk of hepatotoxicity with
PTU.
C. PARATHYROID DISORDERS
PARATHYROID HORMONE
Figure 23. Parathyroid Glands
FUNCTIONS OF THE PARATHYROID GLANDS
● Regulates calcium
● PTH - calcium to the blood
● vs. Calcitonin - (it tones the bone) calcium to the
bone
● Review of parathyroid hormone physiology:
○ PTH from the Parathyroid gland has a main
function to regulate calcium specifically
during HYPOCALCEMIA hence causing
many mechanisms to increase Calcium in
the blood
○ A counterpart of PTH is Calcitonin which is
seen in the Thyroid gland released during
HYPERCALCEMIA hence causing BONE
RESORPTION leading to lowering of calcium
in blood
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SIRMATA 2024
Figure 24. Function of Parathyroid Glands
● During hypocalcemia, the parathyroid gland has 2
cells, the oxyphil and the chief cells (the main cell
releases PTH). The most important one, the Chief
cells releases PTH in the bloodstream
● Leading to 3 effects on 3 organs namely the Bone, the
Kidneys and the Intestine
○ Calcium in the blood, there is bone
resorption (bone broken down)
● The PTH binds to the Osteoblast (Bone deposition -
“bone BUILDING”) to be inhibited and to Stimulate
Osteoclast (bone Resorption - “bone Cutting”)
which will yield the substrates of Calcium and
Phosphate from the bone to the bloodstream - high
calcium, high PO4. Hence, you need to inhibit
Osteoblast and stimulate osteoclast.
● In the kidneys, PTH interacts with the DISTAL
Convoluted tubule to REABSORB Calcium from the
ultrafiltrate but EXCRETES Phosphate in the process
- high calcium, lowers PO4
● Last, PTH has an indirect effect on the Intestine by
helping in with converting the inactive Vitamin D ( 7
–dehydrocholesterol) to the active form Vitamin D
(1,25 dihydroxycholecalciferol or better known as
Calcitriol) by stimulating 1 alpha hydroxylase in the
kidney - remember that 7 dehydrocholesterol will pass
first in the liver to be converted into 25 -
hydroxycholecalciferol then goes to the kidney to be
acted by 1alpha hydroxylase into 1,25
dihydroxycholecalciferol) - This vitamin D (calcitriol)
will now help increase calcium channels in the
intestine to absorb food sources of calcium - high
calcium. Remember, in order to activate Vitamin D,
you need to be exposed to sunlight. The UV light will
now cause the polymerization process and will now
activate the Vitamin D.
● With increase blood calcium that maybe too much -
hypercalcemia - stimulates the Thyroid gland to
produce CALCITONIN (it will tones the bones) which
has only 1 effect: binds to the osteoclast to be
inhibited causing higher OSTEOBLASTIC activity
(increases bone BUILDING, and decrease CUTTING
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 PEDIA (013) Pediatric Endocrine Disorders
of your bone) using the substrate Calcium and
phosphate (both are rich in your bones) from the
blood towards the bone
● Has little effect on the kidney and intestine but
reverses the effect of PTH that leads to calcium to
decrease.
SIRMATA 2024
● Long standing hypocalcemia - teeth erupt late and
irregularly - remember that calcium deposits are
important in the growth of our teeth
● Chvostek Sign - Cheek sign, tap the preauricular
area where your branches of facial nerve passes
through, it will elicit spasm in patients with
hypoparathyroidism.

1. HYPOPARATHYROIDISM
CAUSES OF LOW PTH SECRETION
● Aplasia or Hypoplasia of Parathyroid Hormone
○ DiGeorge syndrome - CATCH 21
(Remember: CARdiac abnormalities, Thyroid
dysplasia problem, Low Calcium and
CHromosome 21)
● Maternal Hyperparathyroidism
○ meaning the maternal side is high in PTH
thus it will suppresses the neonatal secretion
of PTH leading to transient TETANY within 3
weeks of life when you cut the umbilical cord
losing the source of PTH from the mother.
● Thyroidectomy causing Iatrogenic disruption of
PTH Figure 26. Chvostek sign
○ Parathyroid gland function should be
monitored for this patients
○ Remember if you cut the thyroid gland you ● Trousseau’s Sign - if there is low calcium, expect this
might as well cut the parathyroid glands sign to be elicited.
● Deposition of Iron or Copper Pigment at
Parathyroid gland
○ Suspected in patients with Thalassemia and
Wilson’s Dse respectively
● Autoimmune
○ Addison's Disease and Chronic
Mucocutaneous Candidiasis

CLINICAL FEATURES

Figure 27. Trousseau’s Sign

CLINICAL LABORATORIES
● Serum Ca: low at 5-7 mg/dL
● Serum PO4: high at 7-12 mg/dL
● Low PTH: at immunometric assay
● Radiographs
○ X-ray of bones: increased density limited to
metaphyses - deposits of heavy metal
poisoning
○ Cranial CT Scan - calcification in basal
ganglia

TREATMENT
● 10% Calcium Gluconate IV – 5-10 mL or 1-3mg/kg
● 1,25-D calcitriol supplementation
● Reduced high phosphorus diet
● Milk, eggs and cheese

2. HYPERPARATHYROIDISM
CAUSES
● Primary defect of Parathyroid Gland: Adenoma or
hyperplasia
Figure 25. Clinical Features of Hypoparathyroidism
● Compensatory: From low hypocalcemic states →
secondary hyperparathyroidism
● Part of MEN (Multiple Endocrine Neoplasia)
● Remember that calcium is important in controlling the Syndrome: Hyperparathyroidism, Jaw Tumor
neuron’s threshold action potential which is the critical Syndrome
point before neuron activates, hence when you lower ○ Parathyroid adenomas with fibro-osseous
the calcium, it also lowers the threshold potential jaw tumors
causing more NEUROMUSCULAR irritability

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LABORATORIES
● High calcium (usually ionized calcium elevated)
● Serum phosphorus low
● Magnesium low
● PTH elevated
● Calcitonin normal

RADIOGRAPHIC STUDIES
● RESORPTION OF SUBPERIOSTEAL BONE – seen
in the phalanges of the hand

Figure 28. AP View of the right hand in a patient with MEN 1

TREATMENT
● Surgical exploration for parathyroid adenoma Figure 31. Adrenal Gland
● Total parathyroidectomy
○ For persistent high serum calcium ● In the full-term infant, the combined weight of both
adrenal glands is 7-9 g.
● At birth, the inner fetal cortex makes up approximately
80% of the gland and the outer “true” cortex, 20%.
● Within a few days the fetal cortex begins to involute,
undergoing a 50% reduction by 1 mo of age.
Conversely, the adrenal medulla is relatively small at
birth and undergoes a proportionate increase in size
over the 1st 6 mo after birth.
● By 1 yr, the adrenal glands each weigh <1 g. Adrenal
growth thereafter results in adult adrenal glands
reaching a combined weight of 8 g. The zonae
fasciculata and glomerulosa are fully differentiated by
about 3 yr of age. The zona reticularis is not fully
developed until puberty.

Figure 30. Total Parathyroidectomy

VIII. ADRENAL GLAND

● The adrenal gland is part of the endocrine because it
has the processes the will increase your sodium,
glucose, or sex hormones
● The adrenal glands are on of the kidneys
● It has two parts: the adrenal cortex at the periphery or
at the border and the adrenal medulla will be the inner
layer.

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A. ADRENAL CORTEX

Figure 33. Hormone Production of the Adrenal Gland

● Before we go through the specific functions of each

hormone. Let us understand how each of these are
made by each of the layers
● Remember that cholesterol will be the substrate to
Figure 32. Adrenal Gland and its Layers make aldosterone, cortisol and sex hormone
testosterone.
● The adrenal cortex – outer layer of the adrenal gland
which is located on top of the kidney. 1. ZONA GLOMERULOSA
● The adrenal cortex – outer layer of the adrenal gland
which is located on top of the kidney.
● It is subdivided into 3,
○ the outermost, zona glomerulosa, which
produces mineralocorticoid – aldosterone
(most potent natural mineralocorticoid in
humans), which regulates the sodium and
potassium, and is crucial in maintaining
blood pressure
○ The middle, zona fasciculata, produces the
glucocorticoid – cortisol (the most potent
natural glucocorticoid in humans), which
helps maintain sugar level, by promoting
breakdown of glycogen and increased
glucose production, it also helps reduce
inflammation and suppresses immune
system. The zona fasciculata is the largest
zone.
○ The innermost, zona reticularis, produce
ANDROGENS, such as testosterone and
DHEAS (dehydro-epi-androsterone sulfate
which helps make both testosterone and
estrogen). Causes sexual development and
function with bone and muscle growth. Figure 34. Mineralocorticoids → Aldosterone
Sex hormones - reti
To better memorize: use the mnemonic GFR - ACS ● In the zona glomerulosa which is the outermost layer,
G – glomerulosa ---> Aldosterone the pregnenolone is converted to progesterone by the
● You might as well remember aldosterone 3b hydroxysteroid dehydrogenase type 2
(glomerulosa) acts in your kidneys; specifically your ● The are 7 steps that will produce your cholesterol to
glomerulus causing sodium retention your pregnenolone and to your progesterone
F – Fasciculata ---> cortisol ● The important thing is the 21- hydroxylase enzyme
● Cortisol - fasting (fasciculata) - glucose which will shunt the progesterone and pregnenolone
R – Reticularis ---> Sex hormones (Testicles - towards your aldosterone
Testosterone) ● This enzyme is also important to make glucocorticoids
● The progesterone then is converted to 11
deoxycorticosterone by 11 hydroxylase
● The deoxycorticosterone enters the mitochondria to
be converted to the final product, aldosterone by
aldosterone synthase

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 PEDIA (013) Pediatric Endocrine Disorders
2. ZONA FASCICULATA
Figure 35. Glucocorticoids → Cortisol
● In the zona fasciculata, pregnenolone and
progesterone are converted by 17alpha hydroxylase
to 17 hydroxypregnenolone and
hydroxyprogesterone. This enzyme is not expressed
in the zona glomerulosa, which consequently cannot
synthesize 17-hydroxylated steroids.
● The 17 progesterone will be converted to 11
deoxycortisol by 21 hydroxylase enzyme and finally
be converted to cortisol
● Thus, inherited disorders in these enzymes affect both
aldosterone and cortisol synthesis
3. ZONA RETICULARIS
Figure 36. Sex Hormones → Estradiol
● When you shunt again the 17- OH progesterone and
17-OH pregnenolone by means of the 17-20 lyase, it
will lyse the 17 and 20 part of the molecule creating
dehydro-epi-androsterone (dhea)
● The zona reticularis and to some extent in the zona
fasciculata, the 17 hydroxylase enzyme converts 17
hydroxypregnenolone to dehydro-epi-androsterone
(dhea)
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● The dhea is converted to androstenedione by 3b
hydroxysteroid and be further converted in other
tissues to testosterone and estrogen in th the blood
stream
● This may be further converted in other tissues
to testosterone and estrogens.
● The main function of the zona reticularis are the
testicles (testosterone)
4. TRIGGERS OF SECRETION
GLUCOCORTICOID (CORTISOL
● Pro-opiomelanocortin (pomc) precursor peptide -->
released by acth --> pulse secretion of acth and
cortisol every 30-120 mins --> highest during waking,
low at afternoon and evening, lowest 1-2 hrs after
sleep
● ACTH have diurnal pattern of secretion, high in the
morning, low in the evening
ALDOSTERONE
● Renin-angiotensin system and potassium levels
● Aldosterone is important because it needs sodium
reabsorption, retain the sodium
● Remember the Renin-Angiotensin pathway when you
have increase renal blood flow secondary to the
blood pressure, it will now cause the renin to
secreted, that is why it will cause your glomerulus
17 sodium reabsorption
● That sodium reabsorption will now enhance the
pathway of hypertension, because sodium is
reabsorbed water will be absorbed increasing your
vascular resistance, that is what we call hypertension
● That is why we inhibit this to lower the blood pressure
● Aldosterone has another function; decrease
potassium by means of excretion in the urine
ADRENAL ANDROGENS
● Increasing secretion beginning 6-7 yrs old (female)
and 7-8 yrs old (male)
● Rise until late puberty
● Makes the secondary sexual characteristics, which
will indicate puberty
Table 13. Triggers of secretion
● Just remember in glucocorticoid release due to stress
(you are stress waking up and you are relax during
i. GLUCOCORTICOIDS (CORTISOL)
● Glucocorticoids are essential for survival.
● The term glucocorticoid refers to the
glucose-regulating properties of these hormones.
● sleep)
● Functions of glucocorticoids are increase glucose and
suppression of immune system
● That is why it is important for anti-inflammatory
medication we use glucocorticoids, corticosteroids to
cause suppression of immunity
● Increase serum glucose
○ Gluconeogenesis in the liver glucose
production
○ Cellular resistance to insulin dec. glucose
uptake
○ That is why when we have hypoglycemia due
to fasting cortisol increases glucose
● Inc. free fatty acids
○ Enhance lipolysis but decrease glycerol
production
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 PEDIA (013) Pediatric Endocrine Disorders
● Positive inotropic effect
○ Incr. left ventricular work index
● Suppress immune system
○ inhibit glycolipids and prostaglandin
precursors thereby decreasing cytokine
production
○ Anti-inflammatory
● Suppress linear growth and skeletal maturation
○ Thereby prolonged use of steroids in children
should be limited
● Long term effect calcium and bone metabolism
○ Osteoporosis
● Glucocorticoids primarily increase glucose and
suppress immune system
● Treatment for allergy – skin asthma and bronchial
asthma
● Treatment for low glucose patients in ICU care
● However, glucocorticoids have multiple effects on
carbohydrate, lipid, and protein metabolism. They also
regulate immune, circulatory, and renal function. They
influence growth, development, bone metabolism, and
central nervous system activity.
● In stress situations, glucocorticoid secretion can
increase up to 10-fold. This increase is believed to
enhance survival through increased cardiac
contractility, cardiac output, sensitivity to the pressor
effects of catecholamines and other pressor
hormones, work capacity of the skeletal muscles, and
capacity to mobilize energy stores.
ii. MINERALOCORTICOID
(ALDOSTERONE)
Figure 37. Function of Mineralocorticoid
● Conserve Serum Sodium and excrete
○ potassium and hydrogen ion
○ Important in maintaining intravascular
volume (BP increases)
○ Sodium retention (reabsorption)
○ Acidifies the urine
● Mineralocorticoid means the mineral Sodium is
retained while the mineral potassium is excreted out
● Mineralocorticoids have more limited actions than
glucocorticoids. Their major function is to maintain
intravascular volume by conserving sodium and
eliminating potassium and hydrogen ions.
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● They exert these actions in the kidney, gut, and
salivary and sweat glands.
● Mineralocorticoid receptors are found in the heart and
vascular endothelium, and aldosterone increases
myocardial fibrosis in heart failure
● Mineralocorticoids have their most important actions
in the distal convoluted tubules and cortical collecting
ducts of the kidney, where they induce reabsorption of
sodium and secretion of potassium.
● In the medullary collecting duct, they act in a
permissive fashion to allow vasopressin to increase
osmotic water flux
iii. ANDROGEN
● Important in the preservation of secondary sexual
characteristics (especially for men)
● Testosterone
○ Lowers the voice pitch
○ Increase mature hair
○ increase sperm production
○ If there is an excess there will be
repercussions
● The adrenal contribution to circulating estrogen levels
is mainly important in pathologic conditions such as
feminizing adrenal tumors.
● Adrenal androgens contribute to the physiologic
development of pubic and axillary hair during normal
puberty.
● They also play an important role in the
pathophysiology of congenital adrenal hyperplasia,
premature adrenarche, adrenal tumors, and Cushing
syndrome.
B. ADRENAL MEDULLA
Figure 38. Blood Pressure Calculator
● The principal hormones of the adrenal medulla are the
physiologically active catecholamines: dopamine,
norepinephrine, and epinephrine
● Physiologic Active catecholamines are produced
● Norepinephrine, Epinephrine and Dopamine
○ Important in raising mean arterial blood
pressure
● Epinephrine and Dopamine
○ Inc. both blood pressure and Cardiac output
● Norepinephrine
○ Only increases peripheral vascular
resistance
● Overall increase sympathetic tone
● Just remember these things regarding the adrenal
medulla.
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 PEDIA (013) Pediatric Endocrine Disorders
○ Catecholamines (Epinephrine,
Norepinephrine and Dopamine)
○ Hypertension - because it increases your
sympathetic tone thus there are now
repercussions
C. DISEASES ASSOCIATED WITH
ADRENAL GLAND
● Primary adrenocortical insufficiency meaning there is
a problem with your adrenal gland; that is why there
will be low adrenal hormones but there is high ACTH
● Secondary adrenocortical insufficiency there is a
problem with your pituitary gland.
● Primary Adrenocortical Insufficiency (adrenal cortex)
○ Addison’s Disease
○ Low adrenal hormones with compensatory
high ACTH
● Secondary Adrenocortical Insufficiency (anterior
pituitary gland)
○ Low ACTH → hypofunction of adrenal cortex
(low cortisol and low catecholamines)
● Congenital Adrenal Hyperplasia
● Cushing Syndrome vs Cushing Disease
● Pheochromocytoma
1. PRIMARY ADRENOCORTICAL
INSUFFICIENCY (ADRENAL CORTEX)
Figure 39. Clinical Manifestation of Addison’s Disease
● The most common cause of Addison’s disease is
AUTOIMMUNE destruction of Adrenal Glands
○ Antibodies attack the adrenal gland which
will cause Addison’s disease
● The most common infectious cause of Addison’s
disease is Meningococcemia
● (Waterhouse – Friderichsen Syndrome) - affect the male, but may affect affect the female
meningococcemia decreases the blood pressure
going to the adrenal glands
● There is destruction on your adrenal glands which
leads to decrease adrenocortical hormone production
● If there is no ACS (no aldosterone. no cortisol, sex
hormones):
○ there will be hypoglycemia because there is
no cortisol,
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○ there is no suppression (fighting off) immune
system it will shoot up causing now fever
○ There is hyponatremia because there is no
aldosterone
○ No sex hormones which will cause
derangement, however it will just be minimal
in effect
● With low adrenal hormones, it will send a positive
feedback to the anterior pituitary increasing ACTH
● Remember the POMC (pro-opiomelanocortin) which is
similar to ACTH.
● When the anterior pituitary gland produces ACTH
production, the POMC will also increase and is
shunted towards the melanin production dark skin
(hyperpigmentation) in the face but hypopigmentation
in the periphery (vitiligo)
● Primary adrenal insufficiency in children is most
frequently caused by genetic conditions that are often
but not always manifested in infancy and less often by
acquired problems such as autoimmune conditions
● Susceptibility to autoimmune conditions often has a
genetic basis, and so these distinctions are not
absolute.
With abnormal adrenal cortex and adrenal medulla leading to:
● Low cortisol problems in immunity, sugar
● Low aldosterone hyponatremia, convulsions
● low catecholamines low blood pressure, syncope, GI
symptoms (low sympathetic, High parasympathetic
reaction)
2. CONGENITAL ADRENAL
HYPERPLASIA
Figure 39. CAH
● More than 90% of CAH cases are caused by
21-hydroxylase deficiency.
● When 21-hydroxylase is lacking there is high
substrate of 17-OH (when there is no enzyme the
substrate will increase and the product will be low)
● That is why the lack of th 21-hydroxylase enzyme can
be detected in newborn screening
● Male – early secondary sex characteristics (hairy) less
affected than females
● There is now what we call female hermaphroditism,
because there is increase substrate, the will go to
make the sex hormone testosterone, because of that
there will be increase testosterone and will really
causing clitorismemgaly
● Low sodium and chloride, low cortisol, low glucose
● High potassium, high renin, high aldosterone
● This P450 enzyme (CYP21, P450c21) hydroxylates
progesterone and 17-hydroxyprogesterone to yield
11-deoxycorticosterone and 11-deoxycortisol,
respectively.
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 PEDIA (013) Pediatric Endocrine Disorders
● These conversions are required for synthesis of
aldosterone and cortisol, respectively. Both hormones
are deficient in the most-severe, “salt-wasting” form of
the disease.
● Slightly less-severely affected patients are able to
synthesize adequate amounts of aldosterone but have
elevated levels of androgens of adrenal origin; this is
termed “simple virilizing disease”.
● These 2 forms are collectively termed classic
21-hydroxylase deficiency.
Mnemonic
● CAH: C + A is like 2
● Adrenal – androgen → for MALES females are more
affected because they have excess male hormone
causing them to become male like
3. CUSHING SYNDROME VS.
CUSHING DISEASE
Figure 40. Clinical Manifestation of Cushing Syndrome
CUSHING SYNDROME
● Result from abnormal high level of cortisol
● This can be iatrogenic or the result of endogenous
cortisol secretion, a result of either an adrenal tumor
or of hypersecretion of corticotropin
(adrenocorticotropic hormone [ACTH]) by the pituitary
(Cushing disease) or by a tumor
Caused by:
● Prolonged exogenous administration of glucocorticoid
hormones especially at the high doses used to treat
lymphoproliferative disorders.
● Most common cause
● Cushing’s disease – due to pituitary adenoma
increased ACTH production leads to Increase cortisol.
Excessive ACTH secreted by a pituitary adenoma
causes bilateral adrenal hyperplasia
● With high cortisol it will now cause lipolysis
dysfunction, the lipids will go to areas where they do
not normally go,which will increase fat pads, causing:
FEATURES
● Buffalo hump
● Moon facies
● Hirsutism
● Abdominal striae (centralization of lipids in the
abdomen, similar to pregnant patients)
● Humpy dumpy features
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● Just remember that cushing syndrome is due to
prolonged use of steroids patients who have allergies
or patients in lymphoproliferative disorders that need
suppression.
● Because of high cortisol it suppresses your immune
system causing infection, bruises etc.
Cushing syndrome is generalized program with high
cortisol
● The cushing disease is due to pituitary adenoma
causing release of high amount of ACTH
○ This is a subtype of cushing syndrome
● Signs of Cushing syndrome have been recognized in
infants younger than 1 yr of age. The disorder
appears to be more severe and the clinical findings
more flagrant in infants than in older children.
4. PHEOCHROMOCYTOMAS
Figure 41. Pheochromocytomas
● There is a problem with your adrenal medulla, there is
a tumor
● Catecholamines secreting tumors from chromaffin
cells
○ Catecholamines increases sympathetic tone,
which increases hypertension
● Most common site of origin – 90% in Adrenal medulla;
however, tumors may develop anywhere along the
abdominal sympathetic chain and are likely to be
located near the aorta at the level of the inferior
mesenteric artery or at its bifurcation.
● High Epinephrine and Norepinephrine levels
● Sustained Hypertension in children
● High Urine Vanillylmandelic acid (VMA)
○ Metabolite of catecholamines
○ High catecholamine degration leads to high
VMA
● It’s the metabolite of the catecholamines
● The RULES of 10 in pheochromocytomas
● 10% malignant
● 10% bilateral
○ Board exam question pheochromocytomas
are usually unilateral because they are 10%
bilateral and usually involves one adrenal
gland
● 10% extra-adrenal
● 10% familial
● 10% children (between 6 and 14 years old)
● Just remember that pheochromocytomas have
hypertension and that you can diagnose by high urine
VMA
POINTS TO REMEMBER
Adrenal cortex
● Addison disease – low adrenal hormones
● Cushing syndrome – High adrenal hormone
(especially cortisol)
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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
Adrenal Medulla
● Pheochromocytomas – high catecholamines
A. CAUSES OF DIABETES MELLITUS
(epinephrine and norepinephrine)
TYPE 1 TYPE 2
IX. DIABETES MELLITUS
● VIRAL INFECTION ● POLYGENIC
Type 1 Type 2 ● Especially Congenital DISEASE
Rubella Syndrome ● Aggravated by high
● Formerly known as ● Formerly known as ● Rubella virus will caloric intake and
Insulin Insulin RESISTANT attack the pancreas low physical activity
DEPENDENT DM DM or Adult onset specifically the beta ● Central Obesity
or JUVENILE DM DM or cells causing lack of ● Lifestyle problem
○ Younger age ● NON-INSULIN insulin ● Most important
group DEPENDENT DM ● Lack of exposure to lifestyle factor
● Low or absent ○ Resistance to childhood infections associated with DM
production of insulin happens ● hygiene hypothesis ● Because High
INSULIN by beta later on ● Lack of breastfeeding glucose make up of
cells of the ● Breastfeeding is the patient and
Pancreas protectant from type 1 high fat intake
○ Problem with diabetes there would be
beta cells ● early initiation of resistance to
○ This is the cow’s milk protein insulin
reason why there ● Genetically ● Even if you are
is dependence in susceptible releasing m,uch
insulin ● with familial history insulin if there is a
● Most common problem with the
endocrine-metaboli receptor there
c disorder of would be Type 2
childhood DM
● preclinical B-cell Table 15. Causes of Diabetes Mellitus
autoimmunity with
progressive defect
of insulin secretion B. DETECTION OF DM
● transient remission
“honeymoon
period” Impaired Glucose Diabetes Mellitus
Tolerance
Table 14. Types of Diabetes Mellitus
FASTING GLUCOSE: Symptoms of (Polyuria,
100-125 mg/dL Polydipsia, Polyphagia,
glucosuria and ketonuria
PLUS RANDOM BLOOD
GLUCOSE >200 mg/dL

And Or

2 hour plasma glucose FASTING GLUCOSE >/=

during Oral glucose 126 mg/dL Or
Figure 42. Pancreas
tolerance test >/= 140 bur 2 hour plasma glucose
<200 (OGTT) >/= 200 mg/dL
● Diabetes mellitus (DM) is a common, chronic,
Table 16. Detection of DM
metabolic disease characterized by hyperglycemia as
a cardinal biochemical feature.
● HbA1c is more for the adult type, for DM in the young
● The Pancreas has both endocrine and exocrine
age we just request random blood sugar and fasting
function.
blood sugar
Endocrine function has 3 types of cell
● However, if you are already treating the patient on a
● Alpha cells – secretes glucagon (increase glucose
longer basis and you need to know if your patient is
towards the bloodstream)
taking in or poorly taking in the medication you might
● Beta cells – secretes Insulin (decrease glucose in the
as well check the Hba1C
bloodstream and increase uptake of glucose towards
● Impaired glucose tolerance is a pre-diabetic condition
the cell
or a risk to go to DM later on
● Delta cells – secretes somatostatin – inhibitory
function towards growth hormone.

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
epinephrine, glucagon, cortisol, GH → Accelerated
C. ACANOTHIS NIGRICANS lipolysis and impaired lipid synthesis → Increase total
lipids, cholesterol, triglycerides, and free fatty acids →
Ketone body formation → Metabolic acidosis and
rapid deep breathing

F. CLASSIFICATION OF DKA

Normal Mild Moderate Severe

CO2 20-28 16-20 10-15 <10

HCO3 <15 <10 <5

pH 7.35-7.45 <7.3 <7.2 <7.1

Clinical No change Oriented, Kussmaul Kussmaul or

Figure 43. Acanthosis Nigricans alert but respirations, depressed
fatigued oriented but respirations,
sleepy;
● Dark pigmentation of skin creases/flexural areas depressed
arousable
○ Because of high ACTH which is related to sensorium
melano corticotropin to coma
● Sign of INSULIN RESISTANCE
● More associated with type 2 DM Table 17. Classification of DKA

D. COMPLICATION: ● Remember that with metabolic acidosis it triggers a

DIABETIC KETOACIDOSIS
● Metabolic acidosis, with high ketones
● Glucose >200 mg/dL
Mechanism Behind DKA
● Because of insulin resistance there would be high
glucose production but there is impaired utilization
● meaning that glucose will not go inside the cell thus
remaining in the bloodstream
● Leading hyperglycemia, causing glucose in the urine,
causing osmotic diuresis, where glucose goes water
will follow, causing polyuria and urinary loss of
electrolytes
● When there is polyuria there will be polydipsia, this the
compensatory mechanism of the osmotic receptor in
the hypothalamus, however there is still dehydration
● Dehydration causes the compensatory mechanism of
the catecholamines and all other counter regulatory
hormones (epinephrine,glucagon, cortisol and growth
hormones), which can cause accelerated lipolysis, fat
metabolism to meet your gluconeogenesis
● The byproduct of gluconeogenesis are the ketones,
which will cause acidosis in the blood
● Acidosis in the blood causes the rapid deep breathing
or Kussmaul
ARTERIAL BLOOD GAS
● Venous pH <7.3
● Bicarbonate of <15 mmol/L
● Metabolic acidosis
KETONEMIA AND KETONURIA
● Importance of urinalysis with ketone studies
PRECIPITATING FACTORS
● Trauma, infection, vomiting, psychological
disturbances
E. MECHANISMS OF DM
● Insulin deficiency → Excessive glucose production →
Impaired glucose utilization → Hyperglycemia with
glucosuria → Osmotic diuresis (glucose attracts
water) → Polyuria, urinary losses of electrolytes →
Dehydration and polydipsia → Hypersecretion of
compensatory increase in the respiratory rate in order
to reduce dissolved carbon dioxide (CO2) and thus
maintain serum pH. An initial phase of tachypnea
progresses through hyperpnea (increased tidal
volume) and culminates into the pre-terminal
respiratory pattern of Kussmaul Respiration.
● If there is metabolic acidosis there would be
respiratory alkalosis as a compensation, to lose the
CO2
● That is why if the patient is near comatose there is
Kussmaul respiration
● The CO2 in ABG will now be decreased,however it
will not compensate enough hence pH is lower until it
causes fatigue on respiratory muscles leading to
further metabolic acidosis secondary
● You need to address the patient and the medication
for that is to give insulin to decrease the glucose and
the destroy the cascades of events
● We also hydrate the patient because there is
dehydration
● DKA is the end result of the metabolic abnormalities
resulting from a severe deficiency of insulin or insulin
effectiveness.
● The latter occurs during stress as counterregulatory
hormones block insulin action. DKA occurs in 20-40%
of children with new-onset diabetes and in children
with known diabetes who omit insulin doses or who do
not successfully manage an intercurrent illness.
X. TEST YOUR KNOWLEDGE
1. This endocrine gland regulates the amount of
hormone released into the bloodstream by the target
organs and is located inside the sella turcica. This
organ is called the “Master Gland.”
a. Hypothalamus
b. Pituitary
c. Thyroid Gland
d. Adrenal Gland
2. The following hormones are secreted by the anterior
pituitary, except:
a. Growth hormone
b. Prolactin
c. Oxytocin
d. ACTH

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024
3. Which of the following decreases the release of growth
hormone?
a. Ghrelin
b. Sleep
c. Fasting
d. Somatostatin
4. Which of the following will decrease the release of prolactin?
a. Dopamine and its agonist
b. Sucking and nipple stimuli
c. TRH
d. Pituitary tumors
5. This hormone directly influences the thyroid gland to secrete
T3 and T4.
a. TRH
b. TSH
c. ACTH
d. CRH
6. With high ACTH, the patient will eventually have darkening
of skin which can be noted in Addison’s Disease. Which
component can explain the hyperpigmentation in these
patients?
a. ANP
b. POMC
c. Oxytocin
d. Cholecystokinin
7. Which of the following gonadotropic hormones will increase
testosterone hormone?
a. FSH
b. LH
c. Inhibin
d. Estrogen
8. Which of the following is the function of anti-diuretic (ADH)?
a. Inhibits defecation
b. Increases dehydration
c. Decreased blood pressure
d. Inhibits urination
9. Which of the following is NOT a function of oxytocin?
a. Stimulates uterine contraction
b. Breast smooth muscle contraction
c. Orgasm
d. Milk production
10. Which organ causes the release of 2 hormones that were
initially produced by the neurosecretion of the supraoptic and
paraventricular nuclei of the hypothalamus?
a. Adrenal gland
b. Thyroid gland
c. Anterior pituitary
d. Posterior pituitary

Answers: B, C, D, A, B, B, B, D, D, D

XI. REFERENCES
1. Dr. Cadiente’s PPT Presentation
2. Nelson’s Textbook of Pediatrics. 21st Edition.

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 PEDIA (013) Pediatric Endocrine Disorders SIRMATA 2024

APPENDIX

Figure 1. Anatomy and Physiology of the Hypothalamus and Pituitary Gland

Figure 2. GnRH Agonists Mechanism of Action.

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Figure 3. Structure of Nephron; Collecting Tubules- Aquaporins

Figure 4. Thyroid Hormone Production

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Figure 5. Function of Parathyroid Glands

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Figure 7. Hormone Production of the Adrenal Gland

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