The document discusses the anterior pituitary gland and disorders of the hypothalamus and pituitary. It provides details on: - The six hormones produced by the anterior pituitary (TSH, ACTH, LH, FSH, GH, and prolactin) and their functions. - Disorders that can cause hypopituitarism like tumors, trauma, genetic mutations that impact hormone production. - Specific hormone deficiencies like growth hormone deficiency in children and adults, and ACTH deficiency which can cause secondary adrenal insufficiency. - Diagnosis of ACTH deficiency involves low cortisol and ACTH levels along with stimulation tests to check adrenal response.

1. ENDOCRINOLOGY
ANTERIOR PITUITARY
Mukesh Sah, MD

2. OUTLINE
what is endocrinology
•
outline of endocrinology
•
the anterior pituitary
•
disorders of the hypothalamus
•
hypopituitarism
•
pituitary tumors
•

3. David and Goliath

4. !The study of glands and the hormones they
produce
!Endocrine vs Exocrine

5. ENDOCRINE
Hormones – “to set in motion”, aptly describes the dynamic actions of
hormones as they elicit cellular responses and regulate physiologic
processes through regulated feedback mechanisms

7. FUNCTIONS OF HORMONES
• growth and development
• maintenance of homeostasis
• reproduction

8. ENDOCRINE DISORDERS
• hormone excess
hormone deficiency
•
• hormone resistance
• gland tumors/cancers

9. HORMONAL FEEDBACK AND
REGULATORY CONTROL
• feedbackcontrol
autocrineand paracrine
regulation
•
• hormonalrhythms

10. ANTERIOR PITUITAR
Y

11. ANTERIOR PITUITAR
Y
• also called the “master gland”
• orchestrates the complex, regulatory function of other hormones
• produces six (6) hormones
• LH
• FSH
• ACTH
GH
•
TSH
•
Prolactin
•

12. ANTERIOR PITUITAR
Y
HORMONES
secreted in a pulsatile manner
•
affected by an array of hypothalamic factors
•
elicits specific responses in peripheral target
tissues
•

13. y
ANATOMY AND DEVELOPMENT
• ~600mg
located within the sella
turcica ventral to the
diaphragma sella;
•
it consists of anatomicall
and functionallydistinct
anteriorand posterior
lobes.
•
•

14. DEVELOPMENT

15. 1. PROLACTIN
• 198 amino acids
• weakly homologous to GH and HPL
• synthesizedin lactotrophs which constitutes 20% of the anterior
pituitary
lactotropes and somatotropes are derived from a common
precursor cell that may give rise to a tumor that secretesboth
PRL and GH.
•
• Marked lactotrope cell hyperplasia develops during pregnancy
and the first few months of lactation.

16. 1. PROLACTIN
• secretion: pulsatile
• Normal levels: 10-25 ug/L (women) 10-20 ug/L (men)
Peak: during REM
•
• Half life: 50 min
• Stimulated by: after exercise, meals, sexual intercourse, minor surgical
anesthesia, chest wall injury, acute myocardial forms
of acute stress. PRL levels increase
procedures, general
infarction, and other
markedly (about tenfold) during pregnancy and decline rapidly within
2 weeks of parturition
• Inhibited by: Glucocorticcoids, TSh

18. 1. PROLACTIN
Action: member of the type 1 cytokine receptor family
•
PRL acts to induce and maintain lactation,decrease
reproductive function, and suppress sexual drive.
•
These functionsare geared toward ensuring that
maternal lactation is sustained and not interrupted
pregnancy.
•
by
suppresses hypo- thalamicgonadotropin-releasing
hormone (GnRH) and pituitary gonadotropin secretion and
by impairinggonadal steroidogenesis in both womenand
men.
•

19. PROLACTIN
In the ovary, PRL blocks folliculogenesisand inhibits
granulosa cell aromatase activity, leadingto
hypoestrogen- ism and anovulation.
•
• PRL also has a luteolyticeffect, generating a shortened,
or inadequate, lutealphase of the menstrual cycle.
• In men,attenuated LH secretion leads to low
testosterone levels and decreased spermatogenesis. These
hormonal changes decrease libido and reduce fertility in
patients with hyperprolactinemia.

20. 2. GROWTH HORMONE
most abundant anterior pituitary hormone
•
constitutes 50% of anterior piutitary cells
•
development and secretion is mediated by a
specific Pit-1 nuclear transcription factor
•

21. 2. GROWTH HORMONE
Secretion: pulsatile
•
Normal levels:
•
Peak: night time at sleep onset
•
Half life: <0.5 ug/L
•
Stimulated by: GHRH, estrogen,
•
• others: sepsis, stress, exercise and physical trauma, prolonged
fasting and malnutrition, L-arginine, dopamine and apomorphine
Inhibited by: Somatostatin, chronic GC use, obesity, glucose load
•

22. 2. GROWTH HORMONE
action: pattern of secretion determines action, the higher
correlates with lineargrowth and liver enzyme secretion
pulsatililty in men
•
induces protein synthesis and nitrogen retention
•
impairs glucose tolerance by antagonizing insulin action.
•
stimulates lipolysis, leading to increased circulating fatty acid levels, reduced
omental fat mass,and enhanced lean body mass.
•
promotes sodium, potassium, and water retention and elevates serum levels of
inorganic phosphate.
•
Linear bone growth occurs as a result of complex hormonal and growth factor
actions,includingthose of IGF-I.
•
stimulates epiphyseal prechondrocyte differentiation. These precursor cells
produce IGF-I locally, and their proliferation is also responsive to the growth factor.
•

23. 2. GROWTH HORMONE
Insulin like growth factor
•
a potent growth and differentiation
mediates the effects of GH
factor that
•
major source is the liver
•
peaks at 16 years old then declines with age
•
levels decrease with cachexia and malnutrition
•

24. 3. ADRENOCORTICOTROPHIC
HORMONE (ACTH)
constitutes 20% of pituitary cells population
•
derived from POMC precursor
•
stimulated by CRH from the hypothalamus
•

25. 3. ADRENOCORTICOTROPHIC
HORMONE (ACTH)
Secretion: pulsatile and follows a circadian rhythm
•
Peak: 6am and nadirs at 12 mn
•
Normal values: 4-22 pg/ml
•
half life:
•
• stimulatedby: increased by physicaland psychological stress,
exercise, acute illness,and insulin-induced hypoglycemia.
Inhibited by: elevated cortisol levels
•

26. 3. ACTH
Action: The major function of the HPA axis is to maintain
•
metabolichomeostasis and mediate the neuroendocrine
stress response.
• ACTH induces adrenocortical steroidogenesis by
sustaining adrenal cell proliferationand function.
• The receptor
receptor, is a
stimulating a
for ACTH, designated melanocortin-2
GPCR that induces steroidogenesis by
cascade of steroidogenic enzymes

27. 4. GONADOTROPHINS: FSH
AND LH
Gonadotrophs constitute 10% of pituitary cells
•
and produce 2 hormones: FSH and LH
β
B-hCg

28. 4-5. LH AND FSH
normal values: 5-20 IU/L
•
Stimulated by: GnRH, estrogen
•
inhibited by: sex steroids, inhibin
•

29. 4-5. LH AND FSH
• Action: The gonadotropin hormones interact with their respective
GPCRs expressed in the ovary and testis, evoking germ cell
develop- ment and maturation and steroid hormone biosynthesis.
In women, FSH regulates ovarian follicle development and
stimulates ovarianestrogen production.
•
• LH mediates ovulation and maintenance of the corpus luteum.
• In men, LH induces Leydig cell testosterone synthesis and
secretion,and FSH stimulates seminiferous tubule development and
regulates spermatogenesis.

30. 6. THYROID STIMULATING
HORMONE (TSH)
constitutes 5% of pituitary cell population
•
normal value: 0.1-5 mu/L
•
stimulated by: TRH, thyroid damage, prolonged
•
goitrogen exposure
inhibited by: dopamine, somatostatin,
glucocorticoids, increased FT4 and FT3
•

31. 6. TSH
Action: stimulates thyroid hormone and release
•

32. HYPOPITUITARISM

33. HYPOPITUITARISM
Inadequate production of anterior
of hypopituitarism.
pituitary hormones leads to features
•
• can be secondary to:
• inherited disorders
• acquired (more common)
compressive effects of tutors
•
• local pituitary or hypothalamic
damage
trauma, inflammation or vascular
• hypothalamic failure with resultant pituitary failure

34. Prop 1 defect-combined GH, PRL, TSH and gonadotrophin def
possibility of ACTH deficiency with resultant hypocortisolism
Clinical features: growth and mental retardation, patients do not enter puberty
spontaneously
Transcription Factor defect
Pit 1 mutation - Combined GH, TSH and PRL def.
clinical features: growth failureand hypothyroidism
Birth trauma,
haemorrhage,
asphyxia, breech

35. Septo-optic dysplasia -
mutation
of HESX1 gene.
features: midbrain defects, dysgenesis of
corpus collusumand septum pellicidum
Clinical features: hypertelorism,syndactyly,
cleft palate, micropenis,anosmia
Endo features: Diabetes insipidus,short stature,
hypothyroidism
Prader-Willi Syndrome
deletion of SNRPN and NECDIN gene on chromosome 15q.
Endocrine features: hypogonadotropic hypogonadism,
hyperphagia-obesity, adult onset diabetes mellitus
Clinical features: chronic muscle hypotonia, mental retardation
Multiplesomatic defects

36. Leptin and leptin receptor mutation - broad spectrum hypothalamic disorders.
Clinical features: hyperphagia, obesity,and central hypogonadism.
Endocrinefeatures: Decreased GnRH production in these patients results in
decreased pituitary FSH and LH synthesisand release =hypogonadism.
Bardet-Biedtl - very rare geneticallyheterogeneous disorder.
Clinical features: mental retardation, renal abnormalities,obesity,and hexadactyly,
brachydactyly, or syndactyly. Retinal degeneration begins in early childhood (blind by age 30)
Endocrine features: Central diabetes insipidusand GnRH deficiency occurs in 75% of males and
half of affected females

37. Kallman Syndrome-mutation of the X-linked KAL gene responsible for
migration of GnRH neurons in the hypothalamus
-associated with other genetic mutations
clinical features: anosmia, color blindness, cleft palate, renal abnormalities,
cryptoorchidism, neurologic and renal abnormalities
Endocrine features: GnRH deficiency,delayed puberty, features of hypogonadism,
amenorrhea and infertility (females), micropenis (males)

38. • frequen
pituitar
• Diabete
• Growth
• Hypogo
hyperpr
Acquired Hypopituitarism
• may mimic an adenoma
• damageto hypothalamus and pituitary
• resultsin trophic hormone deficiencies
tly involve both hypothalamic and
y neuronal and neuorochemical tracts.
s insipidus occurs in half of patients.
retardation occurs before puberty.
nadotropic hypogonad- ism and
olactinemia are also common.
• occurs mostly in post partum women
• presents with progressive headache/sx of mass effect
• MRI resembles pituitary adenoma
• Elevated ESR, mildly increased PRL
• resolves spontaneously (usually)

39. ACQ UIRED
:
CRANIAL IRRADIATION
• resultsin long term hypothalamicand pituitary
dysfunction
• childrenand adolescents are more susceptible to
long term damage after whole brain or head or neck
irradiation
• hormonal abnormalitiescorrelate stronglywith
irradiationdose and time interval

40. ACQ UIRED
:
CRANIAL IRRADIATION
up to 2/3 of patients develop hormonal
insufficiency after 50 gy (5000 rads) directed
skull
•
at
usually develop after 5-15 years
•
reflects hypothalamic damage rather than pituitary
cell dysfunction
•
usual pattern: GH>LH/FSH>ACTH
•

41. PITUITAR
Y
APOPLEXY
Acute intrapituitary hemorrhagic vascular events can cause substantial damage to the
pituitary and surrounding sellar structures.
Apoplexy is an endocrine emergency that may result in severe hypoglycemia, hypotension
and shock, central nervous system (CNS) hemorrhage, and death.
Risk factors: Pituitary adenoma; postpartum (Sheehan’s syndrome); or in association with
diabetes, hypertension, sickle cell anemia, or acute shock.
The hyperplasticenlargement of the pituitary, which occurs
increases the risk for hemorrhage and infarction.
normally during pregnancy,
Acute symptoms
severe headache with signs of meningeal irritation,
bilateral visual changes, ophthalmoplegia,
cardiovascular collapse and loss of consciousness.

42. PITUITAR
Y
APOPLEXY
Pituitary computed tomography (CT) or MRI may
reveal signs of intratumoral or sellar hemorrhage, with
pituitary stalk deviation and compression of pituitary
tissue.
•

43. PITUITAR
Y
APOPLEXY
Management:
•
Glucocorticoids - no evident visual
impaired consciousness
loss or
•
Surgery - progressive visual loss, cranial nerve
palsy, loss of consciousness, visual deficits, severe
ophthalmoplegia
•
•

44. EMPTY SELLA
• often an incidental MRI finding, and may be associated with
intracranial hypertension.
• usually have normal pituitary function, implying that the
surrounding rim of pituitary tissue is fully functional.
• Hypopituitarism, may develop insidiously.
• Pituitary masses also may undergo clinically silent infarction
and involution

45. DISORDERS
1.DEFICIENCY

46. GROWTH HORMONE
DEFICIENCY

47. DISORDERS OF GROWTH AND
DEVELOPMENT
The growth plate is dependent on a variety of
hormonal stimuli, including GH, insulin-like growth
factor (IGF) I, sex steroids, thyroid hormones,
paracrine growth factors,and cytokines.
This growth-promoting process also requires caloric
energy, amino acids, vitamins, and trace metals and
consumesabout 10% of normal energy production.

48. Linear growth is pituitary dependent.
Bone age is delayed in GHD
Short child + delayedbone age = hormonal/systemic disorder Short
child + normalbone age = genetic cartilage disorder or growth plate
disorder

50. GH DEFICIENCY IN CHILDREN
• GH deficiency - Prop 1 or Pit 1 defect
GHRH mutation
•
GH insensitivity - defect of GH receptor (Laron dwarf)
•
Nutritionalshort stature - caloric deprivation and
malnutrition,uncontrolled diabetes
•
Psychosocialshort stature - emotional and social
deprivation
•

51. ADULT GH DEFICIENCY
Acquired hypothalamic or
pituitary somatotroph damage
Follows a sequential order of
hormone loss:
GH - FSH/LH - TSH - ACTH

52. Treatment:

53. ACT
H
DEFICIENC
Y
• Secondaryadrenal insufficiency
pituitary ACTH deficiency.
occurs as a result of
It is characterized by fatigue, weakness, anorexia,
nausea, vomiting, and, occasionally, hypoglycemia.
•
In contrast to primaryadrenal failure, hypocortisolism
associated with pituitary failure usually is not
accompanied by hyperpigmentation or
mineralocorticoid deficiency.
•
•

54. ACT
H
DEFICIENC
Y:
ETIO LO
GY
glucocorticoid withdrawal
•
resection of ACTH secreting adenoma (pituitary
surgery)
•
mass effects from a sellar/suprasellar mass
•
mutation of POMC gene
•

55. ACT
H
DEFICIENC
Y:
DIAGNO SI
S
• low cortisol and low
ACTH
• ACTH stimulation test
• insulin tolerancetest
metyrapone testing
•

56. Optimal Diagnostic Test
Sensitivity)of)250)µg)cortictotropi
n
stimulation)test)
92%
IVCorticotropin
Stimulation Test/ACTH
stimulation test
Administration of cosyntropin
Cortisol determination at 0,30, 60 min
Peak cortisol response of
>18 ug/dl or >500nmol/L at
30 or 60 min indicates adrenal
sufficiency

59. ACT
H
DEFICIENC
Y:
TREATMEN
T
Glucocorticoid hormone therapy for the
improvement of features of ACTH deficiency
•
Hydrocortisone
•
Prednisone
•

60. GONADOTROPIN DEFICIENCY
hypogonadism is the most common feature of
pituitary deficiency/ adult hypopituitarism
•
often a harbinger of hypothalamic or pituitary
lesions that impair GnRH production or delivery
through the pituitary stalk.
•
hypogonadotropic hypogonadism is a common
presenting feature of hyperprolactinemia.
•
•

61. HYPOGONADOTROPIC
HYPOGONADISM
• Genetic Idiopathic
•
Kallman syndrome
• starvation
•
• mutationsin DAX1,
kisspeptin, GPR 54 gene
stress
•
anorexia nervosa
•
mutations in LHB and
FSHB subunit
•
extreme exercise
•

62. HYPOGONADOTROPIC
HYPOGONADISM: PRESENTATION
• Women Men
•
decreased ovarian function secondary testicular failure
• •
decreased libido and potency
oligomenorrhea •
•
decreased muscle mass and
weakness
• amenorrhea •
• infertility
reduced facial and body hair
growth
•
decreased libido
•
• decreased vaginal secretions facial fine lines
•
soft testes
• reduced breast size •
osteoporosis
• osteoporosis •

63. HYPOGONADOTROPIC
HYPOGONADISM: DIAGNOSIS
MEN
•
• Women
Low LH/FSH
•
Low LH/FSH
•
Low testosterone
•
• Low estradiol
low sperm counts
•
• GnRH testing
GnRH testing
•
MRI
•
MRI
•

64. HYPOGONADOTROPIC
HYPOGONADISM: TREATMENT
• Women
MEN
•
• cyclic replacement
oestrogen and
progesterone
of Testosterone injections
•
or gel or skin patches for
hCG and GnRH for
fertility
•
• Gonadotropintreatment
for induction of ovulation
•

65. ANTERIOR PITUITAR
Y
TUMOR
SYNDRO ME
S

67. OPHTHALMOLOGIC
EVALUATION
Cranial Nerve III, IV
ophthalmoplegias)
or IV palsies (diplopia, ptosis
•
occasionally CN V palsy
•
bitemporal hemianopsia
•
homonymous hemianopsia
•

68. LABORATORY INVESTIGATION
serum prolactin
•
serum IGF-1 levels
•
24 hour urine cortisol and 1 mg DST
•
FSH/LH
•
TSH and FT4 and FT3
•
8 am cortisol and testosterone
•

69. TREATMENT OVERVIEW
Goals of Management
n o rm a liza t io n
secretion,
o f exc es s
•
Successful management
requires accurate diagnosis amelioration of symptoms
shrinkage or ablation of large
tumors
•
•
Clinical features arise from
local mass effects and
hormone hypo or hyper
relief of adjacent structure
•
compression.
pres erva t io n
anterior
secretion caused by either o f res idu a l
•
adenoma OR by the
treatment
resultant
pituitary function
prevention of recurrence
•
•

70. MANAGEMENT
hypothalamic damage
insufficiency.
amenable to medical tx
type benefits side effects
transspenoidal surgery
preferred procedure
better visualisation
avoids invasion of brain
tissue
mortality rate 1%
permanent DI 20%
CSF leak 4%
CN nerve damage or
septal perforation 10%
radiation
usually as adjuvant
or for residual tumor post
surgery to prevent re
growth
transient: nausea/
vomiting, or alopecia
leading to hormonal
Rare : optic neuritis, CV
risk
medical
highly specific to tumor
type
ACTH tumors are not

73. SELLAR MASSES

74. SELLAR MASSES
other than pituitary adenomas may arise from the
•
brain, hypothalamic area or from pituitary tissues
lesions exhibit features specific to its location
•

75. Hypothalamic lesions
hyperthermia
sweating, vomiting and
hypertension and gastric
location features
anterior and pre optic
area
paradoxical vasoconstriction
tachycardia
posterior
periodic hypothermia syndrome
- episodes of hypothermia,
bradycardia
ventro-medial hyperphagia and obesity
central
elevated catecholamine and
cortisol = arrhythmias,
erosions

76. HYPOTHALAMIC LESIONS
Craniopharyngiomas - benign , cystic, suprasellar masses
•
• Features: headaches, visual field defects and hypopituitarism
• ageof onset: <20 yrs old, symptoms of increased ICP
,
behaviour/personalitychanges, growth retardation,
insipidus
diabetes
• management: surgery and radiotherapy
• Rathke’s cysts - small cysts usually found incidentally
Features: hydrocephalus, diabetes insipidus and
•
hyperprolactinemia

77. HYPOTHALAMIC LESIONS
sella chordomas and meningiomas- may have
•
signs of compression
histiocytosis X - eosinophilic infiltration of
•
hypothalamus
features: Diabetes insipidus, exopthalmos
•
and lytic lesions of bone

78. HYPOTHALAMIC LESION
Pituitary metastases - occurs in 3% of cancer
•
patients (half from breast cancer)
usually presents with diabetes insipidus,
rarely with pituitary insufficiency
•
Hypothalamic gliomas/optic gliomas - may
•
present with visual loss

79. HYPOTHALAMIC LESIONS
Brain Germ cell tumors - may secrete bHCG
•
Features: diabetes insipidus,precocious puberty,
•
visual field defects, GH deficient (short stature)
• Hypothalamic hamartomas or gangliocytomas
• may produce GnRH - (psychomotor delay, laughing
seizures and precocious puberty),GHRH and CRH

80. PITUITAR
Y
ADENOMAS AND
HYPERSECRETION SYNDROMES

81. PITUITAR
Y
ADENOMAS
Most common cause of pituitary hormone
hypersecretion and hyposecretion syndromes adults.
•
in
They account for ~15% of all intracranial
neoplasms and have been identifiedwith a
population prevalence of ~80/100,000.
•
Seen incidentally at autopsy in 25% of patients
and 10% in all brain imaging
•

82. PITUITAR
Y
ADENOMAS
• benignneoplasm
• featuresdepend on
hormones
the tutor cells hyper secreting the
• hormonallyactive tumors are characterised by hyper
secretion,autonomous controla and lack of feedback
responsiveness physiologic inhibitorypathways

85. 1. HYPERPROLACTINEMIA
most common cause of pituitary hyper secretion
both men and women
in
•
prolactin secreting adenomas are the most
common cause of PRL > 200 ug/L
•
other causes of increased PRL :
microprolactinoma, stalk phenomenon, drugs, renal
failure, hypothyroidism
•

86. HYPERPROLACTINEMIA

87. HYPERPROLACTINEMIA

88. PRESENTATION AND DIAGNOSIS
MALES
FEMALES
diminished libido
infertility
visual loss
low testosterone
hypogonadism
galactorrhea
impotence
amenorrhea
galactorrhea
infertility decreased
libido weight gain
hirsutism (women)

89. GALACTORRHEA
the inappropriate discharge of
milk-containing fluid from the
breast
•
considered abnormal if it persists
longer than 6 months after
•
childbirth or discontinuation
breast-feeding
of
may vary in color
•
maybe unilateral or bilateral
•
associated with
hyperprolactinemia
•
•
Management:
• Treatment of underlying
disorder
• Goal is to normalize PRL
• Withdraw offending meds

90. PROLACTINOMA
• Tumors arising from lactotrope cells
functioning pituitarytumors,
account for about half of all
• prevalence of ~10/100,000 in men and ~30/100,000 in women.
• Mixed tumors that secrete combinations of GH and PRL, ACTH
and PRL, and rarely TSH and PRL are also seen.
microadenoas <1cm - usually with no invasion (female to male
ratio 20:1)
•
• macroadenomas >1 cm, may impinge optic nerves (F:M ration
1:1)

91. PRESENTATION
MALES
FEMALES
diminished libido
infertility
visual loss and headaches
low testosterone
hypogonadism galactorrhea
impotence
amenorrhea
galactorrhea
infertility decreased
libido weight gain
hirsutism (women)

92. MANAGEMENT
• Medical
bromocriptine
•
• cabergoline
• Surgical
Radiation
•

93. 2. ACROMEGALY
• GH hypersecretion
is usually the result
of a somatotrope
adenoma but may
rarely be caused by
extrapituitary
lesions
•

94. ACRO MEGA
LY:
PRESENTATIO
N
presentation maybe
indolentand not clinically
diagnosed for 10 yrs
•
children and adolescents:
pituitary gigantism
•
(GH hypersecretion prior
to longbone closure)
•

95. size
ment
s
ACRO MEGA
LY:
PRESENTATIO
N
increased foot/hand
•
frontal bossing
•
mandibular enlarge
•
coarse facial feature
•
hyperhidrosis
•
deepening of voice
•
arthropathy
•
proximal muscle weaknes
•
acanthosis
•
visceromegaly
•

96. ACRO MEGA
LY
• Coronary heart disease,
cardiomyopathy with
arrhythmias, Most significant impact
of GH excess is on the CV
system
•
• left ventricular hypertrophy,
decreased diastolicfunction
overall mortality
increased 3x
•
hypertension
•
• Obstructivesleep apnea
10 year less survival than
age match control
•
• Diabetes mellitus
• higher rates of malignancy
•

98. LABORATORY INVESTIGATION
GH levels not reliable (due to pulsatile nature
GH)
of
•
IGF 1 - useful laboratory screening test
•
The diagnosis of acromegaly is confirmed by
demonstrating the failure of GH suppression to
<0.4 μg/L within 1–2 h of an oral glucose load (75 g)
•

99. MANAGEMENT
• surgery(Transsphenoidal
surgery)
somatostatin analogues
•
• GH receptor antagonist
dopamine agonists
•
• radiation

100. CUSHING’S SYNDROME: ACTH
PRODUCING ADENOMA
10-15% of all pituitary adenomas
•
most common cause of endogenous
hypercortisolism
•
usually small micro adenomas
•
more common in women
•

101. DIAGNOSIS AND PRESENTATION
#1 Is this really Cushing’s?
#2 Where is it coming from?

103. NON FUNCTIONING OR
GONADOTROPHIN SECRETING TUMORS
Includethose that secrete little or no pituitary hormones as
well as tumors that produce too little hormone to result in
recognizable clinical features
•
most common type of pituitaryadenoma and are usually
macroadenomas at the time of diagnosis because clinical
features are not apparent until tumor mass effects occur.
•
usually originate from gonadotrope cells. These tumors
typically produce small amounts of intact gonadotropins
(usually FSH) as well as uncombined α, LH β, and FSH β
subunits.
•

104. NON FUNCTIONING OR
GONADOTROPHIN SECRETING TUMORS
Features:
•
• oftenpresent with optic chiasm pressure and other
symptoms of local expansion
• may be incidentallydiscovered on an MRI performed
for another indication (incidentaloma).Rarely, menstruwal
disturbances or ovarian hyperstimulation o
• possiblehypogonadism
• slightly elevated prolactin (stalk compression)

106. FINALLY

107. TSH SECRETING ADENOMAS
TSH-producing macroadenomas are very rare
•
oftenlargeand locally invasivewhen they occur.
•
Patients usually present with thyroid goiterand
•
hyperthyroidism, reflecting overproduction of TSH.
Diagnosis
•
• elevated serumfreeT4
levels, inappropriately normal
high TSH secretion,
or
MRI evidence of a pituitary adenoma.
•

108. TSH SECRETING ADENOMAS
Management:
•
TSS
•
somatostatin
•
anti thyroids
•
thyroid ablation
•

109. Thank you