Pituitary gland - Two type of cells:
1. Chromophobes
 Lies in the sphenoid bone, the sella turcica
 Developed from:
 Oral cavity
 Brain
 two parts:
1. adenohypophysis (anterior)
- the oral component
- outpocketing of ectoderm from the roof of
primitive mouth
- grows cranially, forming a Rathke’s pouch
that eventually constricts and separates
from the pharynx
- consists of: pars distalis, pars tuberalis,
pars intermedia
2. nuerohypophysis (posterior)
- the neural component (endoderm?);
- neurohypophyseal bud grows from the floor
of future diencephalon as a stalk
(infundibulum)
- remain attached to the brain
- consists of pars nervosa & infundibulum
 Hypothalamic-hypophyseal tract
- Bundle of axons from the hypothalamus to
neurohypophysis
- extends from the supraoptic nuclei and
paraventricular nuclei into the pars nervosa
- Supraoptic = ADH
Paraventricular= oxytocin
 Hypothalamic-hypophyseal portal system
- 2 group of vessels:
a. Internal carotid
 Superior hypophyseal
arteries- supply the median
eminence & infundibulum
 Inferior hypophyseal
arteries- supply the
neurohypophysis
b. Hypophyseal vein
- Primary plexus formed at the superior
arteries that irrigate the median eminence
and infundibulum > rejoins to form
secondary plexus at the adenohypophysis
and drains into hypophyseal vein
ANTERIOR PIT GLAND
 Pars distalis
- Composed of cords of well-stained
endocrine cells with fenestrated capillaries
and reticular CT
2. Chromophils
2.1 Acidophils: somototrophs (GH)
& lactotrophs (prolactin)
2.2 Basophils:
Corticotrophs (ACTH),
Gonadotrophs (LH and FSH) &
Thyrotrophs (thyrotropin)
 Pars tuberalis
- Most are gonadotrophs
 Pars intermedia
- Zone of basophilic cells
- Contains colloid-filled cyst
POSTERIOR PIT GLAND
 Does not contain cells that synthesize its two hormone
 Composed of neural tissue, unmyelinated axons,
branched glial cells called pituicytes
 Hormones accumulate in the axonal dilation
(swellings) called Herring bodies (neurosecretory
bodies)
- Contain either oxytocin and ADH that are
bound to neurophysin I and II, respectively.
Thyroid Gland
 Developed from foregut endoderm near the base of
the tongue
 Thyrocytes can be low columnar if active; squamous if
hypoactive
 Basal: rough ER; Apical (facing the lumen): golgi
complex, secretory granules, phagosomes, lysosomes,
microvilli
Parafollicular cells (C cells)
- Appears on the periphery of follicular
epithelium as single or cluster
- Derived from neural crest
- Larger than follicular cells, stains less
intensely
- Secretes calcitonin
 Secretion of TSH in the pituitary is also increased by
exposure to cold and decreased by heat and stressful
stimuli
 GROWTH & DEVELOPMENT
Prenatal Development
MUSCLES
 Cross-striated- developed from myotome or
mesoderm of pharyngeal arches
 Smooth muscle- splanchnic mesoderm
 Skeletal muscle- mesoderm of somites and limb buds
CUTANEOUS
 Newborn covered with vernix caseosa
 Lanugo more abundant in premature
 Scalp hair may be lost and replaced
permanently by 2 years
 Sweat glands have NO function for temperature
regulation until 1 mos
NERVOUS SYSTEM
 Differentiation continues on postnatal period
 Myelinization completed by 6 to 12 mos;
some nerves up to 2 years
 Gradual slowing of growth of the brain at
midchildhood to 10 years
 Cerebrospinal fluid 200 ml by 10 yrs
 Pandy’s reaction (level of protein in the CS
fluid) positive in 50% of newborn and
premature but NOT LATER THAN 6 mos
 20-40 mg/dL is the normal
 CS cells range from 20-30 mm3 in neonate
to 10/mm3 later
 Pineal body normally calcifies at 10 years
SENSORY
 Pain sensation is not developed in a newborn; this
hyposthesia last for a week
 Movements and crying are the response to
pain
 Less at 1-2 mos
 At 7-9 mos can localize the site of pain and
withdraw from it
 12-16 mos shoves the painful stimulus away
and brings the hand to the irritated area
 Visual sensation is achieved only at 16 weeks of age
 Macula and fovea does not differentiate
completely until 6 yrs.
 At 7 yrs 20/20 vision is achieved
 Hyperopia in small infants
 Auditory system is FUNCTIONAL from BIRTH as long as
external ear is cleaned
 At 6 mos localization of sound and
recognition of familiar voices.
 Middle ear similar to adult but tympanic
membrane is more horizontal
 Able to taste BUT cant distinguished flavours
 At 3 mos taste discrimination is achieved;
changes in formula milk may be refused
CIRCULATORY SYSTEM
 At BIRTH, foramen ovale and the ductus venosus
become functionally closed
 Morphological/anatomical closure of
foramen ovale requires 8 mos or more
 Ductus arteriosus functionally closed after 8 to 12
weeks
 Anatomical closure at 1-3 mos
 140-160/min normal fetal heart rate
 HR slightly higher in females
 100-110/min at 1-7 years
 Below 100 from then on
 BP in child changes day to day; systolic and diastolic
increases with age
 Lower in premature than in term
LYMPHATIC SYSTEM
 Increase in neonate > peaks at 6-7 yrs old > reduction
during adult life
 Spleen is the largest organ in proportion to the body at
birth and increases in weight to 12 times at adult life
and does not atropy unlike the nodules
BLOOD
 Lymphocytes is the only blood cells found outside the
marrow
 At term, 80% cord fetal haemoglobin
 5% remains at 5 mos of age
 Fetal haemoglobin is lower babies who have
been clamped early
 At birth, neutrophil is predominant
 1 week, lymphocytes predominate
 4 yrs of age lymphocytes = neutrophil
 8 yrs leuckocyte count similar to adult
IMMUNITY
 Newborn has passive immunity up to 6-9 mos of age
 Antitoxin and antiviral IGG is transferred better than
antibacterial antibodies
 Antiviral diminish, antibacterial rises by 2
mos of age
 Colostrum has higher titer of enteric antitoxin
 Immunity of breastfeeding babies is SIMILAR to
bottlefed
 Premature considerably low
DIGESTIVE SYSTEM
 Small intestine measures 300-350 cm at birth. At 1 yr
undergoes 1.5 times increase in length and 700 cm at
puberty
 Ascending colon is short in newborn
 Sigmoid filled with meconium
 Rectum relatively longer in newborn
 Amylase and lipase are low in newborn, lipase stay low
throughout childhood
 Bacterial flora establish during the first few hours after
birth
 L. bifidus in breastfed
 L. acidophilus artificially-fed
 Stool has its own development
 Meconium in first day of life
 Transitional stool last for 3 days (liquid to
mushy, greenish with blood streaks) AFTER
meconium
 Positive for occult blood during the 72 hrs
 In breastfed it is homogenous, pasty,
yellow, sour odor
 In artificial, firm, less homo, pale yellow,
sticky, foul-smelling
RESPIRATORY SYSTEM
 Larynx is 1/8 the adult size at birth
 After 3 yrs, it is longer and wider in boys
 Trachea is 4 cm long in adult
 Bifurcation is at the T3 or T4 thoracic
vertebra AT BIRTH
 At 4 years, level of T5
 At 12 years, between T5 and T6
 Newborn is resistant to anoxia
 Can stand anoxia for 14 min
 30-60/min normal RR of infants (first 2 yrs)
 20-30/min from 2-14 yrs
URINARY SYSTEM
 Extracellular fluid in newborn is twice that of adult
which decreases during infancy and adolescence
 50% of extracellular volume is exchange
 Infant is susceptible to dehydration during
illness
 Daily excretion of 1000 ml in the GI tract,
50% are reabsorbed
 Electrolyte concentration is high in neonate than in
adults
 Blood Ph is slightly lower
 Normally the baby may not void 12 to 24 hrs after birth
 Mature function achieved at 5-6 yrs of age
SKELETAL SYSTEM
 Ossification has taken place in all long bones at birth;
radiologically visible
 Secondary ossification appears AFTER birth
EXCEPT in the distal epiphyses of the femur
w/c occurred during the last two fetal mos;
Its absence indicates prematurity
 0-5 yrs- presence of ossification center
5-14 yrs- calcification of cartilaginous areas
14-25- epiphyseal fusion
 At birth, anteroposterior and lateral dimaters of chest
are equal
 Shoulders elevated
 Neck hardly seen
 From 3-10 yrs, chest becomes broader and flatter; ribs
slope down
 Manubrium sterni goes down and the neck
appears longer
 Two concavities at birth:
 Cervical convex appears at 3 mos
 Lumbar curvature shows when the child
starts to walk and develops fully by 3 yrs
GENITAL ORGANS
 Seminiferous tubues are solid at birth and develops
lumen at childhood
 Testes enlargement and spermatogenesis at puberty
 At birth, ovarian cortex is filled with primordial follicles
DENTITION
 As early as 4 mos, hard tissue formation begins
No of teeth = age in months – 6
 Teething when delayed beyond 12 mos should
necessitate investigation of thyroid, parathyroid etc.
Postnatal Development
HUMAN GROWTH CURVE
 3 basic components:
 First phase: rapid and rapidly decelerating
growth of first 3 yrs of life; fetal growth
factors
 Second phase: steady and slowly
decelerating growth in middle childhood;
GH mediated
 Third phase: pubertal growth spurt; sex
hormones
 The first 3 yrs of postnatal life is crucial
 Catching up growth may NOT BE ABLE to FULLY
compensate what has been missing
 Lower-cut point is 5th percentile
 Upper-cut point is 95th percentile
 Values between the 5th and 95th are considered normal
 Consider the use of “age as of nearest birthday”
MNEMONICS

LENGTH: 50cm

WEIGHT: 3000kg

Growth Velocity (cm) = H2-H1/T (yr)

 Must be on the 50th centile

 If growth is less than 50, it will lead to loss of
height compared to the mean

Wasting:

actual weight
x 100
ideal weight for actual length/height
Sexual Maturity Rating*
Classification:
Normal ≥ 90% DEVELOPMENTAL MILESTONE
Mild 80-90%
Moderate 70-80%  Motor
Severe <70% i. Gross
Stunting: ii. Fine
 4 mos- hold breast/bottle
actual length/height 
x 100 7 mos- picks up food and put it into his
ideal length for age mouth
 End of 1 yr- use spoon w/spillage
Classification:  2 yrs- use fork
Normal ≥95  5 yr- use knife
Mild 90-95
Moderate 80-90 WRITING MOVEMENTS
Severe <80
From 1-6 yrs:  7 mos- hold crayon
 18 mos- vertical stroke
 Below 6 mos
 2.5 yr- circle
Weight in grams= age in mos x 600 + BW
 4 yr- cross
 From 6 to 12 mos
 6 yrs- objects (house, man etc); write w/
Weight in grams= age in mos x 500 + BW
regularity
 From 2 to 6 years
 12 yrs- style of writing is set
Weight in kg= age in yr x 2 + 8
 Adaptive- ability to utilize and manipulate objects,
motor and sensory
From 6-12 yrs:
coordination in problem solving, resourcefulness in
utilizing past experience in adjusting to new situation
 Weight in lbs= age in yrs x 7 + 5
 Language
*1 kg= 2.2 lbs
 Reflex sound- crying & feeble gestures
Height:  Babbling- 3rd to 8 mos; meaningless
repetition of sounds like Mama, Dada
 Height in cm= age in yrs x 5 + 80  Gestures- 4th mos; express needs
*1 in= 2.54 cm  Word usage- comprehend what is said to
him; end of 1st yr one word sentences
 Personal-social- habits affecting feeding, sleeping,
bowel and bladder control and ability to get along
  Holds bottle
 Imitate sound
 Waves bye

1 mos: 10 mos:

 Raises head less than 45 deg  Pulls self to stand

 Hands fisted  Thumb finger grasp
 Follows object to midline
 Smile 11 mos:

2 mos:  Walk w/ support

 Head control at 45 deg 12 mos:

 Hands no longer fisted
 Follows object past midline  Stand alone
 Laugh  Walk alone
 Attempts to use spoon
3 mos:
15 mos:
 Head control 90 deg
 Hands together  Walks backward
 Squeals  Drinks from a cup

4 mos: 18 mos:

 Rolls over  Seat on chair

 Grasp object placed in hand
 Move head towards the sound 2 years:

5 mos:  Runs well

 Good head control 2 ½ years:

 Reaches for object
 Turns to sound  Jump

6 mos:
 Gessel Developmental Test:
 No head lag DQ= maturity/chronological age x 100
 Chews  Intellectual Development:
IQ= mental/chronological age x 100
7 mos:
Pediatric Examination
 Sits with support
 Rakes small object  Newborn
 Ma when crying  Perform APGAR 1 min. after birth, and 5
 Recognize familiar faces min. , 10 min.
 Feed self with crackers  If 5 min is less than 7, advanced CPR
 Appearance, Pulse, Grimace, Activity,
8 mos: Respiration
 Gastric contents aspirated in premature
 Sit w/o support
 Transfer object from hand to hand
 Dada, Mama
 Peek a boo

9 mos:

 Stands holding on
 Creeps
  Acrocyanosis
o Blue cast to the hands and feet when
exposed to cold
o If does not disappear w/in 8 hrs or with
warming, cyanotic CHD should be
considered
 Harlequin dyschromia
o Cyanosis of of one half of the body
 Mongolian spot in the buttocks and back
 Responsiveness is best noted about 2-3 hrs  Milia- small whitish papules made up of distended
sebaceous gland that covers the nose
 Erythema toxicum- erythematous macules with central
pinpoint vesicles appearing like a flea bites; systemic
defect is generalize, if localized mainly due to pressure
effects
after feeding  Physiologic jaundice
 Symmterical position, limbs semiflexed, hips o Appears on 2nd and 3rd day peaks on 5th day
abducted o Disappear w/in a week
 Breech babies, legs and head o If jaundice appears at 24 hrs likely to be
extended pathologic
 Franck breech, abducted and o Persist beyond 2-3 weeks suspicions of
externally rotated biliary atresia or liver disease
 Tremors of the arms and legs during the  Salmon patch or nervus simplex
first 48 hrs are seen o Flat, irregular, light pink patches seen on
 After 4 days, may signify CNS nape, upper eyelids, forehead, upper lip
disease o Disappear by 1 yr
 Port wine stains- darker, purplish lesions on the face or
Temperature extremities (ila)

 Rectal temp; axillary temp for premature Head

 Average of 37.5- 37.8 C
 Anterior fontanels measure 4-6 cm
Pulse o Closes 12-18 mos
 Posterior fontanels measure 1-2 cm
 140-160 beats/min fetal
o Closes by2 mos
 100-110/min at 1-7 years
o Enlarged may be present in hypothyroidism
 Below 100 from then on
 Capput succedaneum
Respiratory rate o Swollen scalp from subcu edema
o cross sutures
 30-60 newborn  Cephalohematoma
 20-40 early childhood o Swelling of the scalp due to subperiosteal
 15-25 late childhood hemorrhage
o Does not cross sutures
Skin
 Craniosynostosis
o Premature closure of the sutures
 Covered w/ vernix
o Craniotabes- softening of cranial bones
 Pinkish, elastic in FT; transparent in PT; dry aNd
desquamated in PoT (pingpong ball)
 Cutis marmorata  Transillumination
o mottled appearance o Hydranencephaly- thinned cerebral cortes;
entire head lights up
o Vasomotor changes in the dermis and subcu
o Porencephaly- partially absent
due to cooling or radiant exposure to heat;
may last for month o Subdural hygroma- extracortical fluid
o Prominent in PT & congenital accumulation
hypothyroidism and Down syndrome
  Palpebral fissure
o Upslanting- Down syndrome
o Downslanting- Noonan syndrome
o Short- fetal alcohol syndrome
 Epstein pearls
 Doll’s test
 Brushfield spots

Neck

 Look for lymphadenopathy

JAUNDICE

ETIOLOGY

Hyperbilirubinemia arises from:

1. Overproduction of bilirubin that liver cells can’t cope

up with the increased load of indirect bilirubin
2. Undersecretion of bilirubin such that liver fails to
adequately secrete bilirubin from the blood into the
bile

Overproduction

1. Rhesus haemolytic dsease

2. ABO incompatibility
 Unlike Rhesus infants are not as severely
affected
3. Maternal-fetal and feto-fetal transfusion
 Maternal rbc will enter the fetal circulation
 In monozygotic twin, one twin will
exsanguinate leaving one twin anemic and
one plethoric
4. Non-immune haemolytic anemias
 Enzyme deficient red cells which hemolyze
upon exposure to drugs such as excess in
vit. K
5. Abnormal RBC
6. Hemoglobinopathies
7. Extravascular hemolysis
1. Heme catabolism form choleglobin and
verdohemoglobin as indirect by-products that will Undersecretion
result to formation of unconjugated bilirubin
(indirect) 1. Decrease glucoronyl transferase activity
2. Indirect bilirubin bound to albumin for transport to  First few days of life
the liver cells  Peak at 5 days
3. Dissociated from the carrier albumin at the liver cell  Termed as “physiologic jaundice”
and then transferred to the hepatic cell in unbound  NOT CONSIDERED PHYSIOLOGIC IF longer
form than 2 weeks & bilirubin levels greater
4. Glucorinidation by glucuronyltransferase in the than 12 mg/dl for full term and 15 mg/dl in
hepatic cell to form conjugated bilirubin preterm
5. Transport to the bile canaliculus for excretion by X 2. Pregnane-3-alpha. 20 beta-diol in breastmilk
and Y transport proteins  Breastfeeding stopped temporarily for 48
6. Conjugated bilirubin is transported to the large hrs to drop the bilirubin levels
bowel, acted by the intestinal flora converted into 3. Thyroid hormone
urobilinogen  Increase the activity of
7. Some will undergo enterohepatic circulation where glucoronyltransferase
conjugated bilirubin will deconjugate and is readily 4. Competitive conjugation of bilirubin by drugs
absorb by the intestine 5. Galactosemia
 Absence of galactose-1-phosphate uridyl
Unconjugated- lipid soluble transferase
 This transferase willreduce activity of the
Conjugated- water-soluble enzyme phosphoglucomutase essential in
the metabolism of glucose from glycogen
 In full-term, above 7mg/dl is associated with visible
to glucuronic acid
jaundice
6. Infectious agents
 Accumulates outside the vascular space
7. Hypoglycemic state- role of glucose
8. Circulatory insufficiency and obstruction of bile ducts
 KERNICTERUS
 High levels of unconjugated bilirubin deposits in the
brain
 Likely to occur on infants whose albumin levels are
usually low; existing hypoxia and acidosis w/c
interferes with albumin-binding capacity of bilirubin
 Rare in healthy term infants; serum level below 25
mg/dl in the absence of hemolysis
 Less mature infant, the greater the susceptibility
 Toxicity starts as low as 8-12 mg/dl
 Lethargy, hypotonia, poor feeding followed by
opisthotonus (backward arching of the head, neck
and spine)
MANAGEMENT
 Regardless of the cause of jaundice if bilirubun levels
reach 20 mg/dl do a double volume exchange
transfusion (160-180 Ml/kg)
 If the indirect bilirubin is not rising:
 Administration of Phenobartital
 30-60 mg/kg per day for 2-3
weeks prior to delivery
 5 mg/kg per day to infants
 Increase development of
glucuronyltransferase
 Phototherapy
 Photoisomerization to soluble
breakdown products that are
excreted rapidly in the bile and
urine
 Infant is unclothed
 Epposure to ten 2 watt daylight
or blue fluorescent lamp at 30
inches above
 Dehydration, diarrhea, bronze
baby syndrome,
thrombocytopenia, ECG
abnormalities is seen
 Babies eyes shielded to avoid
retinal degeneration
 Continued until the 5th day
 Use of double phototherapy
lights and bili-blankets increases
the effect
PITUITARY HORMONES
GROWTH HORMONE
 Somatotropic hormone or somatotropin
 Exerts its effect directly on all or almost tissues in the
body
 Once epiphysis close in the long bone further
lengthening cannot occur; tissues of the body can
continue to grow
Metabolic effects
 Promotes protein synthesis
 Enhances transport of amino acids through
the plasma membrane to the interior of
the cells
 Increase RNA translation causing protein
to synthesized in greater amount
 Increase transcription of DNA to form RNA
to promote more protein synthesis
 Reduce the breakdown of protein; act as
“protein sparer”
 Enhances fat utilization for energy
 Cause release of fatty acids from adipose
tissue thereby increasing the fatty acd
concentration in the blood
 Enhances conversion of FA to acetyl CoA
 Fat is used more than carbohydrates and
protein
 Cause an increase of lean body mass
(protein anabolic effect)
 Utilization of fat by GH requires several hr
to occur
 Excessive amount have a ketogenic effect
 Liver will released acetoacetic
acid into the body fluids from
fat mobilization
 Excessive fat mobilization
frequently causes fatty liver;
w/o carbohydrate it has the
potential to reduce synthesis of
fat by the liver.
 Decrease carbohydrate utilization
 Decrease glucose uptake in tissues
 Increase glucose production by the liver
 Increase insulin secretion
 “insulin resistance”
 Diabetogenic
 Carbohydrate and insulin is necessary for
GH to be effective
 Growth hormone stimulates cartilage and bone growth
 The effect of growth hormone is affected by
somatomedins
 Liver stimulated by GH will produce
somatomedin C or IGF-I
 Pygmies in Africa have normal GH but
unable to synthesize significant amount of
 IGF-I; Levi-lorain dwarf also have this
problem
 Regulation of GH (stimulate secretion):
 Starvation
 Hypoglycaemia or low concentration of
fatty acid
 Excercise
 Excitement
 Trauma
 Ghrelin
 GH is secreted in pulsatile pattern, increasing and
decreasing
 Increases during the first 2 hrs of sleep
(noon and midnight)
 GH secretion is more correlated with protein
deficiency than glucose insufficiency.
 GH is controlled by GHRH and somatostanin
 TSH is also known to stimulate prolactin secretion
DISORDERS OF PITUITARY GLAND
Panhypopituitarism
 Means decreased secretion of ALL anterior pituitary
hormones
 Results from craniopharyngioma or thrombosis of
pituitary blood vessels
 General effects are:
 Hypothyroidism
 Depressed production of gluccorticoids by
adrenal glands
 Suppressed secretion of GNRH
 A hormone deficiency is:
 Primary- if is due to target organ failure
 Secondary- due to lack stimulation from
the pituitary which may result from either
deficiency of releasing hormone or intrinsic
pituitary disease
ETIOLOGY
Developmental defects
 Aplasia or absence of pituitary gland (rare)
 Midline defects of skull and brain
 Cleft lip and cleft palate are found to have deficiency
of GH
Idiopathic hypopituitarism
 Sporadic or familial
 Classified as:
 Type I- autosomal recessive; inherited
multiple hormone deficiency
Type IA- growth hormone deletion;
develop antibodies against GH nd become
resistant to GH therapy
Type IB- no GH deletion; carry small
amount of GH in serum
 Type II- autosomal dominant; multiple
hormone deficiency when transmission is
X-linked
 Type III- when X-linked transmission; no
abnormality in GH and no development of
GH antibodies
Tumors and Infiltrative lesion
 Craniopharyngioma is the most common that involves
the hypothalamus and pituitary gland
 GH deficiency is common
 Gonadotropin deficiency leading to
absence/delay in pubertal development
 TSH and ACTH is not as common
 Endocrine testing showed deficiency of GH, FSH & LH,
cortisol and increase prolactin
 Radiologic diagnostic of the skull may show
calcification
 MRI confirms the presence of tumor
Psychosocial dwarfism
 Reversible disorder in response to a noxious
environment
 Licking toilet bowls, antisocial characteristics,
voracious appetite and speech defect
Unresponsiveness to GH
 Laron type dwarfism
 GH is biologically active but ineffective
because of lack IGF-I
 Autosomal recessive
 Empty sella syndrome
 Enlarged pituitary fossa resulting from
arachnoid hernition through an incomplete
sella diaphragm
CLINICAL MANIFESTATION
 Children with classic GH deficiency are identified by
their short stature that fall below the 25th percentile
in the growth chart
 Growth velocity CONSISTENTLY subnormal over a
period of time
 Body is PROPORTIONATE
 Overweight with increased subcutaneous fat in the
trunk
 Head circumference is normal BUT growth of facial
bone is delayed w/ some frontal bossing and
underdeveloped nasal bridge
 Cherubic appearance
 External genitalia underdeveloped
 Delay in skeletal and dental development
 High pitched voice
  Hypoglycemia may occur because of the absence of
the gluconeogenic effects of GH and lack of insulin
antagonism
 If ACTH is also absent more profound
hypoglycaemia is possible (cortisol
stimulates also stimulates gluconeogenesis
and opposes insulin action)
 Hypoglycemic seizures
 Symptoms of hypothyroidism may be present if there
is TSH deficiency but are not as marked as in
congenital hyperthyroidism
 ACTH deficiency is subtle until provocative tesing with
insulin or metyrapone is done
DIFFERENTIAL DIAGNOSIS
 Hypopituitarism w/ GH deficiency is PROPORTIONAL
dwarfism
 Gonadal dysgenesis or Tuner syndrome is
most common in females shortness
 Low hairline
 Short neck with webbing
 Cubitus valgus
 Horshoe kidney
 Bicuspid aortic valve &
coarctation of aorta (common
CHD)
 Lab test shows high level of
gonadotropins
 Ultasound of pelvic organ reveal
small uterus and ovaries may
not be evident
 Constitutional short stature may be
considered as secondary to hypothalamic
dysfunction
 Short stature
 Delay sexual maturation
 Bone age approx height age
 Familial history of delay
 Normal height at later age
 Genetic short stature
 Positive family history for
 Investigation of other target organs
shortness
 Osseous development
equivalent to chronological age
 Sexual maturation at
appropriate age
DIAGNOSIS
 Not dependent on clinical manifestation but
confirmed by abnormal growth hormone and other
pituitary function test
 Early diagnoses for infants with hypoglycaemia,
micropenis, midfacial malformation, neonatal injuries
 Roentgenographic and Imaging studies
from traumatic delivery, breech presentationa &
growth retardation before 2 y/o
 Provocative test that stimulate secretion and release
of GH:
 Sleep
 Exercise
 Exercise tolerance test
 Patient fasted for 4 hrs and
blood is drawn
 Exercise for 20 min then second
blood sample taken
 After 20 min of rest third blood
sample is taken
 Significant value is 7ng/ml in
any of the specimens
 Hypoglycaemia
 Induced by giving insuln at dose
of 0.05 to 0.1 unit/kg IV
 Blood is taken 0, 15, 30, 45, 60
 True blood glucose should fall
below 50%
 Normal GH concentration of 7
ng/ml
 Stress
 Estrogen
 L-dopa
 Replaced arginine
 Children weight<10 kg: 125 mg
 10-30 kg: 250 mg
 >30 kg: 500 mg
 Blood specimens taken at 0, 30,
60 and 90 min
 Clonidine
 Dose of 100-150 ug/m2 after an
overnight fast
 Blood collected at
0,30,60,90,120 and 150 min
 7 ng/ml GH is normal
 Propanolol
 Arginine
 Definitive test for GH deficiency
 Usually not available
 Thyroid function by TSH and T4
determination
 Adrenal glands assessed with levels of
plasma cortisol in the morning and once in
late afternoon
 Gonadal dysfunction
 Hyperprolactenemia should be
determine with hypogonadism
*estrogen and progesterone
inhibit prolactin
 GnRH administered to
determine anterior pit response
 craniopharyngioma - intracranial
calcification of the skull
  idiopathic pituitarism- sella may appear
small
 tumors of the adenohypophysis- sella is
eroded
 MRI and CT scan
TREATMENT
 Surgery of the pituitary fossa s subject to severe
complication
 GH therapy when GH is deficient
 Coexisting deficiency should be treated
 In Thyroid hormone deficiency GH cannot
exert its maximal effort w/o thyroxine
 Dose of 0.07-0.1 IU/kg body weight or 2 to
3 IU/m2 body surface SUBCU 6 to 7 time
per week
 growth increments of greater than
9cm/per for those who receive continuosly
for 6 mos
 other shown annual growth of 11.3 cm in
children below 5 y/o
 smaller growth increments in age 15 or
older
PHYSIOLOGICAL FUNCTION OF THYROID HORMONE
 Thyroid hormone increases transcription of large
number of gene
 Increases cellular metabolic activity
 exception such as brain, retina, spleen,
testis and lungs
 increase as much as 60-100 percent above
normal
 rate of utilization of food for energy is
accelerated
 increase protein synthesis while at the
same time catabolism is increased
 growth rate accelerated
 mental processes excited
 activity of other endocrine glands is often
increase
 Thyroxine increased quantities of certain intracellular
enzyme
 Increase the overall metabolism of the cell
 Increase utilization of 02, glucose, fats and
proteins
 Mitochondria increases in the cell
 Rapid utilization of carbohydrates because
of increase of the enzyme, alpha-
glycerophosphate dehydrogenase, which
degrades carbohydrates
 There is a long latent period before thyroxine activity
begins
 Once it begins it activity increases
progressively and eaches to maximum of
about 12 days
 Decreases with a halftime of about 15 days
 Some activity persist as long as 6 weeks to
2 mos later
 T3 has short latent period of 6 to 12 hours
 More rapid rate of absorption
EFFECTS OF THYROXINE ON METABOLISM OF DIETARY
SUBSTANCES
Effect on carbohydrate
 Increase rate of glucose absorption in the GI tract and
increase glucose utilization by cells
Effect on fat
 Accelerates fat metabolism more than any other
foodstuff
 Ministering thyroxine shortens the time of
carbohydrate, consequently fats must then be utilized
for a longer portion of the day than normally
 Fats deposited rapidly than normally if simultaneous
intake of carbohydrate
 Increased thyroid hormone DECREASE the quantity of
circulating fats in the blood and liver
Effect on protein and growth
 Increase both protein anabolism and catabolism
 Increase the rate of gluconeogenesis because of
increase mobilization of proteins and release of
amino acid available for energy
Effect on vitamin
 Thyroxine increases the NEED for vitamins
 B12, thiamine, vit B compounds, vit C
 Small amt of thyroxine is needed for the conversion
of carotene into vit A by the liver
Effect on bone and calcium
 Increase osteoclastic activity more than osteoblastic
activity
 Bone becomes porous and greater quantities of
calcium and phosphorus
 It also increases the rate of parathyroid hormone
secretion for bone absorption
EFFECTS OF THYROXINE TO BODILY MECHANISM
Basal metabolic rate
 Increase to as much as 100 percent
 No thyroid, BMR falls to aprox half normal
Body weight
 Increase thyroxine decrease body weight
  Effects o not always occur because thyroxine  One of the stimuli for thyroxine release is exposure to
enhances appetite cold
 Emotional reaction can also increase output
Growth  High concentration of iodide in the blood seems to
decrease all activities of the thyroid gland
 Anabolism of protein cannot occur w/o thyroxie thus  Thyroxine affect gonads
GH is not significant w/o presence of thyroxine  In males, lack of thyroxine cause loss of
libido
Cardiovascular system  In female, lack causes menorrhagia and
polymenorrhea; conversely,
 Increase blood flow n cardiac output
oligomenorrhea in hyperthyroid
 Increase O2 consumption cause greater
metabolic products that cause vasodilation CONGENITAL HYPOTHYROIDISM
 Heart rate increases; thyroxine has direct excitability
of the heart  Most common cause of preventable mental
 Blood volume increase slightly retardation
 Increased arterial pressure  Thyroid hormone has an essential role in
 Increased strength of heatbeat the proper development of brain
 May be transient: associated w/ prematurity and
Respiration neonatal illness
Permanent: primary, secondary, tertiary
 Increase the rate and depth because of inc. O2 and
Primary: majority of cases , T4 is low and TSH is high
formation of CO2
ETIOLOGY
GI tract
1. Thyroid dysgenesis
 Increased the rate of secretion of digestive juices
2. Thyroid dyshormogenesis
 Increased motility; often diarrhea is associated with
3. Hypothalamic or pituitary dysfunction
increased thyroxine; lac of thyroid causes
4. Maternal antithyroid
constipation
5. Maternal autoimmunity
6. Immaturity
CNS

*goitrous: thyroid dyshormogenesis & maternal

 Increase the cerebration.
antithyroid
 Hyperthyroid is likely to develop extreme
nervousness, anxiety complexes, extreme worry or
*congenital nonendemic hypothyroidism: inborn defect in
paranoia
thyroid metabolism
 Increase synaptic activity BUT DOES NOT influence
peripheral nerve activity CLINICAL MANIFESTATION

Muscles  Not suspected at birth; signs and symptoms may

manifest by the 4th mos of life
 Makes muscle react with vigor but extreme thyoxine
 Common Signs and Symptoms:
muscles become weakened because of excess protein
 Prolonged jaundice
catabolism
 Constipation
 Lack of thyroid causes muscles to be sluggish,
 Lethargy
contract readily but relax slowly
 Poor feeding
 Hypothermia
Sleep
 Suggestive clinical features:
 Prolonged gestation w/ large birth size
 Hyperthyroid often has a feeling of tiredness bec of
 Large anterior fontanel
the effect in the muscles BUT because of increase
 Posterior fontanel greater than 1cm
activity in CNS the person has difficulty in sleeping
 Respiratory distress
 Hypothyroid suffer from extreme somnolence
 Peripheral cyanosis
 Delayed onset of stooling
 Abdominal distension
 Vomiting and edema
 Hypertelorism
  Swollen eyelids
 Narrow palpebrl fissures
 Broad nose with depressed bride
 Open mouth with large tongue
 Narrowed chest w/ curved back
 Disproportionally short
DIFFERENTIAL DIAGNOSIS
 Disproportionate dwarfism
 Neuromascular disorders (Werdnig-Hoffman and
Prader-Willi)
 Muscular hypertrophy
 Down syndrome
 Muculopolysacchridosis (Hurler’s and Hunters)
 Panhypopituitarism and storage disease
LABORATORY
 Low to almost nil serum T4 levels
 TSH reaching 100 MiU/ml
 Newborn screening is recommended
 Thyroid scanning
 Establish etiology; define the location, size
and fxn
 Thyroid ultrasound to detect presence of
gland
 Radioactive iodine uptake helpful in
thyroid dysgenesis and inborn errors of
thyroid synthesis
 Other ancillary lab:
 CBC with peripheral smear- relevant in
those who present pallor
 Bilirubin levels- those who developed
prolonged jaundice and in CH,
unconjugated hyperbilirubenemia is
expected
 EKG- in long standing hypothyroidism,
decreased voltage may be secondary to
myedematous myocardium
 Bone age- marked delay in bone age as
seen in x-ray for infants less than 3 mos
and the left hand including the wrist for
older infants will support CH
TREATMENT
 Sodium levothyroxine
 First year: 5-10
 1-5 yrs: 4-6
 5-10 yrs: 3-5
 >10 yrs: 2-3
 Overtreatment is avoided during first two years
because it will led to premature closure of cranial
sutures
 TSH should be at normal level of below 10 Miu/L
 Bone age should be kept w/in chronological age
PROGNOSIS
 Early treatment is correlated with
neurodevelopmental outcome
GOITERS IN CHILDREN
 Goiter- any enlargement of the lobe or lobes of
the thyroid gland to at least the patient’s
terminal phalanx of the thumb
 Grade 0: No goiter
 Grade 1a: enlarge thyroid on
PALPATION
 Grade 1b: TG visible w/neck
extended
 Grade 2: TG visible w/ neck in normal
position
 Grade 3: TG visible at a distance of 10
m
 Endemc goiters- those areas w/ lack of iodine
like Zamboanga del Sur and Basilan
HASHIMOTO’S THYROIDITIS
 Chronic lymphocytic thyroiditis
 Disorder common in girls t 9:1 female to male
ratio
 Occurs frequently n children w/ chromosomal
abnormalities such as Down, Turner, Klinefelter
and Noonan, congenital rubella etc.
 3 stages of disease:
 Thyroid hyperplasia- increased
output of thyroid
 Euthyroidism- normal thyroid
 Hypothyroidism- all the excreted
thyroid are already used up
 High titers of thyroid antibodies
SIMPLE COLLOID GOITER (Adolescent goiter, nontoxic goiter)
 Autoimmune of thyroid growth-stimulating
immunoglobulin
 Gland is normal and are not risk to develop
hypothyroidism
 Autosomal recessive inheritance with female
preponderance
CONGENITAL GOITERS
 Occur in areas of iodine deficiency
 Result from antithyroid substance; defect in thyroid
hormone synthesis
 Charac. in Pendred’s syndrome
 “dumping phenomenon”- administration
of thiocyanate result in discharge of
previously adminstred radioactive iodine
form
THYROID NEOPLASIA
  Multinodular- goiter suggest benign condition
Solitary nodule- malignant
 Important etiology is irradiation

ACQUIRED HYPOTHYROIDISM

 Develop after the first 2 years of life

 In endemic, lack of iodine
 In nonendemic, Hashimoto’s thyroiditis
 Less severe than CH
 Growth retardation, muscle pseuhypertrophy and
sexual disorder

HYPERTHYROIDISM

 Thyrotoxicosis
 Grave’s disease is the predominant cause of adult
 Autoimmune disorder w/ production of
immunoglobulins against antigens in the
thyroid
 Rare in childhood
 Girls are predominantly affected
 Eye signs present:
 Moebius’ sign: inability of convergence
 Von Graefe’s: lid la
 Stellwag’s sign: retraction of upper lid and
infrequent blinking
 Joofroy’s sign; inability to wrinkle forehead
on upward gaze
 In children, frequent winking and blinking
instead of Stellwag’s sign

NEONATAL HYPERTHYROIDISM

 2 forms:
 Acquired congenitally by transplacental
passage of thyroid stimulating substance
and is usually transitory w/ spontaneous
remission in 3 mos
 Infant’s own disorder immunological
mechanism and tend to last longer