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CLINICAL ENDOCRINOLOGY :
ANTERIOR PITUITARY
M C VASIF MAYAN
Pituitary disorders
• 1. MASS – SECRETORY/ FUNCTIONING and COMPRESSIVE
• 2. GRANULOMAS
• 3. INFLAMMATORY ( HYPOPHYSITIS)
• 4. VASCULAR
• MASS Adenoma
• Tumours MEN-1, Mc Cune Albright, Carney syndrome
• Other Parasellar Rathke cyst,granular cell tumour, chordoma,
craniopharyngioma, meningioma, glioma, hematological
malignancy
• Granuloma Sarcoidosis
Hand Schullen Christian disease
Mets
• Hypophysitis Lymphocytic/ Granulomatous/ Xanthomatous
• Vascular Apoplexy/ Postpartum ( hemorrhage/ infarction)
Endocrinedisease
Hormone excess
Hormone
deficiency
Hormone
resistance
Pituitary Gland
• Located within the sella tursica
• Weight 600mg
• Contiguous to vascular and neurologic structures
• Cavernous sinuses
• Cranial nerves
• Optic chiasma
• Hypothalamic neural cells synthesize specific releasing and inhibiting hormones
• Secreted directly into the portal vessels of the pituitary stalk
• Blood supply derived from the superior and inferior hypophyseal arteries
Hypothalamic–Pituitary Axis
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
Pituitary Gland
• Anterior pituitary gland
• Secrete various trophic hormones
• Disease in this region may result in syndromes of hormone excess or deficiency
• Posterior pituitary gland
• More of a terminus of axons of neurons in the supraoptic and paraventricular
nuclei of the hypothalamus
• Storehouse for the hormones
• The main consequence of disease in this area is disordered water homeostasis
Anterior Pituitary Gland
• Anterior Pituitary “Master gland”
• Major blood source: hypothalamic-pituitary portal plexus
• Allows transmission of hypothalamic peptide pulses without significant systemic dilution
• Consequently, pituitary cells are exposed to sharp spikes of releasing factors and in turn release
their hormones as discrete pulses.
• Production of six major hormones:
• Prolactin (PRL)
• Growth hormone (GH)
• Adrenocorticotropin hormone (ACTH)
• Luteinizing hormone (LH)
• Follicle-stimulating hormone (FSH)
• Thyroid-stimulating hormone (TSH)
Anterior Pituitary Gland
• Anterior Pituitary “Master gland”
• Secreted in a pulsatile manner
• Elicits specific responses in peripheral target tissues
• Feedback control at the level of the hypothalamus and pituitary
to modulate pituitary function exerted by the hormonal
products of the peripheral target glands
• Tumors cause characteristic hormone excess syndromes
• Hormone deficiency
• may be inherited or acquired
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
HORMONE DEFICIENCY
• GONADOTROPIN DEFICIENCY
• ACTH DEIFICIENCY
• TSH DEFICIENCY
• PROLACTIN DEFICIENCY
• GROWTH HORMONE DEFICIENCY
• HYPOPITUITARISM
Adult Growth Hormone Deficiency
• First hormone to be affected
• Non functioning adenoma/ irradiation
• GH  FSH/LH  TSH  ACTH
•
• Adults
• Often asymptomatic
• Fatigue
• Decreased exercise tolerance
• Abdominal obesity
• Loss of muscle mass
• Abnormal lipid profile
• Reduced BMD
• Atherosclerosis , LV dysfunction, increased fibrinogen
Treatment : GH replacement 0.1 – 0.3 mg/day
Maximum upto 1.25 mg/day
Women need higher doses than men
Gonadotropin Deficiency
Women
• Oligomenorrhea or amenorrhea
• Loss of libido
• Vaginal dryness or dyspareunia
• Loss of secondary sex characteristics
(estrogen deficiency)
Men
• Loss of libido
• Erectile dysfunction
• Infertility
• Loss of secondary sex characteristics
(testosterone deficiency)
• Atrophy of the testes
• Gynecomastia (testosterone
deficiency)
Most common presenting feature of adult hypopituitarism
TSH Deficiency
• Hypothyroidism
• Atrophic thyroid gland
ACTH Deficiency
• Most commonly due to glucocorticoid withdrawal
• Results in hypocortisolism
• Malaise
• Anorexia
• Weight-loss
• Gastrointestinal disturbances
• Hyponatremia, hypoglycemia
• Pale complexion
• No features of mineralocorticoid deficiency
• Aldosterone secretion unaffected
Prolactin Deficiency
• Inability to lactate postpartum
• Often 1st manifestation of Sheehan syndrome
HYPOPITUITARISM
Etiology
• Anterior pituitary diseases
• Deficiency one or more or all anterior pituitary hormones
hypopituitarism
Developmenta /
structural
traumatic
Neoplastic
Infiltrative /
inflammatory
Vascular
infections
developmental
Transcription
factor defect
Aplasia / dysplasia
Congenital mass /
encephalocele
Primary empty
sella
Congenital
disorders
Hypopituitarism: Developmental and Genetic causes
•Septo-Optic dysplasia
•Prader Willi syndrome
•Kallman Syndrome
•Laurence-Moon-Biedl Syndrome
•Frohlich Syndrome (Adiposo Genital Dystrophy)
• Septo-Optic dysplasia
• Hypothalamic dysfunction and hypopituitarism
• may result from dysgenesis of the septum pellucidum or corpus callosum
• Affected children have mutations in the HESX1 gene
• involved in early development of the ventral prosencephalon
• These children exhibit variable combinations of:
• cleft palate
• syndactyly
• ear deformities
• hypertelorism
• optic atrophy
• micropenis
• anosmia
• Pituitary dysfunction
• Diabetes insipidus
• GH deficiency and short stature
• Occasionally TSH deficiency
•Kallman Syndrome
• Defective hypothalamic gonadotropin-releasing hormone (GnRH) synthesis
• Associated with anosmia or hyposmia due to olfactory bulb agenesis or
hypoplasia
• May also be associated with: color blindness, optic atrophy, nerve
deafness, cleft palate, renal abnormalities, cryptorchidism, and neurologic
abnormalities such as mirror movements
• GnRH deficiency prevents progression through puberty
• characterized by
• low LH and FSH levels
• low concentrations of sex steroids
•Laurence-Moon-Biedl Syndrome
• Rare autosomal recessive disorder
•Characterized by mental retardation; obesity; and
hexadactyly, brachydactyly, or syndactyly
• Central diabetes insipidus may or may not be associated
•GnRH deficiency occurs in 75% of males and half of
affected females
• Retinal degeneration begins in early childhood
• most patients are blind by age 30
•Renal abnormalities
Traumatic
Surgical resection
Radiation damage
Head injuries
Neoplastic
Adenoma
Parasellar mass
Rathke’s cyst
Craniopharyngioma
Hamartoma
Mets
Leukemia /
lymphoma
Meningioma
Infiltrative/Inflammatory
Lymphocytic
hypophysitis
Hemochromatosis
Sarcoidosis
Histiocytosis X
Granulomatous
hypophysitis
•LYMPHOCYTIC HYPOPHYSITIS
• Etiology
• Presumed to be autoimmune
• Clinical Presentation
• Women, during postpartum period with hyperprolactinemia
• Mass effect (sellar mass)
• Deficiency of one or more anterior pituitary hormones
• ACTH deficiency is the most common
• Diagnosis
• MRI - may be indistinguishable from pituitary adenoma
• Elevated ESR +
• Treatment
• Corticosteroids
• Hormone replacement
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
Vascular
Apoplexy
Pregnancy related
(infarction with DM ,
Sheehans)
Sickle cell disease
Arteritis
Quick Quiz!!!
• When should you suspect pituitary apoplexy?
•PITUITARY APOPLEXY
• Hemorrhagic infarction of a pituitary adenoma/tumor
• Considered a neurosurgical emergency
• Presentation:
• Variable onset of severe headache
• Nausea and vomiting
• Meningism
• Vertigo
• +/ - Visual defects
• +/ - Altered consciousness
• Symptoms may occur immediately or may develop over 1-2 days
Meningism is the triad of
nuchal rigidity (neck stiffness)
photophobia (intolerance of bright light)
headache
• Pituitary Apoplexy
• Diabetes
• Bleed into a pre existing adenoma
• Patients on warfarin
• Post partum ( sheehans)
• Hypertension
• Sickle cell anemia
• Shock
apoplexy
• Severe hypoglycemia
• Hypotension
• Shock
• CNS hemorrhage
Apoplexy
•Usually resolve completely if treated correctly and early
•Diagnose with CT/MRI
•Differentiate from leaking aneurysm
•Treatment:
•Medical therapy – if symptoms are mild
• Corticosteroids – high dose glucocorticoids
• Surgical – Trans sphenoid decompression
• Visual defects and altered consciousness
Infections
Fungal
(Histoplasmosis)
Parasitic
(Toxoplasmosis)
Tuberculosis*
Pneumocystis
carinii
Hypopituitarism
Diagnosis
• Biochemical diagnosis of pituitary insufficiency
• Demonstrating low levels of trophic hormones in the setting of low target
hormone levels
• Provocative tests may be required to assess pituitary reserve
Hypopituitarism
Treatment
• Hormone replacement therapy
• usually free of complications
Hormone Replacement
Trophic Hormone Deficit Hormone Replacement
ACTH Hydrocortisone (10-20 mg A.M.; 10 mg P.M.)
Cortisone acetate (25 mg A.M.; 12.5 mg P.M.)
Prednisone (5 mg A.M.; 2.5 mg P.M.)
TSH L-Thyroxine (0.075-0.15 mg daily)
FSH/LH Males
Testosterone enanthate (200 mg IM every 2 wks)
Testosterone skin patch (5 mg/d)
Females
Conjugated estrogen (0.65-1.25 mg qd for 25days)
Progesterone (5-10 mg qd) on days 16-25
For fertility: Menopausal gonadotropins, human chorionic gonadotropins
GH Adults: Somatotropin (0.3-1.0 mg SC qd)
Children: Somatotropin [0.02-0.05 (mg/kg per day)]
Vasopressin Intranasal desmopressin (5-20 ug twice daily)
Oral 300-600 ug qd
Take home points:
• Remember that the cause may be functional
• Treatment should be aimed at the underlying cause
• Not all KKK are hypopituitarism
• Hypopituitarism may present
• Acutely with cortisol deficiency
• After withdrawal of prolonged glucocorticoid therapy that has caused suppression of the HPA
axis
• Post surgical procedure
• TUBERCULOSIS
• DIABETES
• SYSTEMIC HYPERTENSION
• Post trauma
• Hemorrhage
Pituitary Tumors
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
Pituitary Tumors
•Microadenoma < 1 cm
•Macroadenoma > 1 cm
•Is the tumor causing local mass effect?
•Is hypopituitarism present?
•Is there evidence of hormone excess?
• Clinical presentation:
• Mass effect
• Superior extension
• May compromise optic pathways – leading to impaired visual acuity and visual
field defects
• May produce hypothalamic syndrome – disturbed thirst, satiety, sleep, and
temperature regulation
• Lateral extension
• May compress cranial nerves III, IV, V, and VI – leaning to diplopia
• Inferior extension
• May lead to cerebrospinal fluid rhinorrhea
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
Pituitary Tumors
• Diagnosis
• Check levels of all hormones produced
• Check levels of target organ products
• Treatment
• Surgical excision, radiation, or medical therapy
• Generally, first-line treatment surgical excision
• Drug therapy available for some functional tumors
• Simple observation
• Option if the tumor is small, does not have local mass effect, and is nonfunctional
• Not associated with clinical features that affect quality of life
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
Craniopharyngioma
• Derived from Rathke's pouch.
• Arise near the pituitary stalk
• extension into the suprasellar cistern common
• These tumors are often large, cystic, and locally invasive
• Many are partially calcified
• characteristic appearance on skull x-ray and CT images
• Majority of patients present before 20yr
• usually with signs of increased intracranial pressure, including
headache, vomiting, papilledema, and hydrocephalus
Craniopharyngioma
• Associated symptoms include:
• visual field abnormalities, personality changes and cognitive deterioration,
cranial nerve damage, sleep difficulties, and weight gain.
• Children
• growth failure associated with either hypothyroidism or growth hormone
deficiency is the most common presentation
• Adults
• sexual dysfunction is the most common problem
• erectile dysfunction
• amenorrhea
Craniopharyngioma
• Anterior pituitary dysfunction and diabetes insipidus are common
• Treatment
• Transcranial or transsphenoidal surgical resection
• followed by postoperative radiation of residual tumor
• This approach can result in long-term survival and ultimate cure
• most patients require lifelong pituitary hormone replacement.
• If the pituitary stalk is uninvolved and can be preserved at the time of
surgery
• Incidence of subsequent anterior pituitary dysfunction is significantly
diminished.
Prolactinoma
• Most common functional pituitary tumor
• Usually a microadenoma
• Can be a space occupying macroadenoma – often with visual field defects
• Although many women with hyperprolactinemia will have galactorrhea
and/ or amenorrhea
• The absence these the two signs do not excluded the diagnosis
• GnRH release is decreased in direct response to elevated prolactin, leading
to decreased production of LH and FSH
Prolactinoma
• Women
• Amenorrhea – this symptom causes women to present earlier
• Infertility
• Galactorrhea
• Men
• Impotence – often ignored
• Tend to present later
• Signs of mass effect
Hyperprolactinemia
• Essential to rule out secondary causes!!
• Drugs – basically all anti dopaminergic drugs
• Atypical antipsychotic – risperidone
• METOCLOPRAMIDE
• AMITRYPTILINE
• Alpha METHYL DOPA
• CCB – Verapamil
• Estrogen
• H2 antagonists - RANITIDINE
• Hypothyroidism
• CKD
• Cirrhosis
• Epileptic Seizures
•If prolactin level > 200mcg/L, almost always a
prolactinoma (even in a nursing mother)
•Prolactin levels correlate with tumor size in
the macroadenomas
•Suspect another tumor if prolactin low with a
large tumor
Prolactinoma
•Diagnosis
•Assess hypersecretion
• Basal, fasting morning PRL levels (normally <20 ug/L)
•Multiple measurements may be necessary
• Pulsatile hormone secretion
• levels vary widely in some individuals with
hyperprolactinemia
•Hypothyroidism should be excluded by measuring
TSH and T4 levels
Prolactinoma
•Treatment
•Medical
• Cabergoline – dopamine receptor agonist
• Bromocriptine - dopamine agonist
• Safe in pregnancy
• Will restore menstruation
• Decreases both prolactin and tumor size (80%)
•Surgical
• Transsphenoidal surgery
• Irradiation
Quick Quiz!!!
• What type of tumors are most prolactinomas?
• Prolactin levels >200 almost always indicate what?
• Do prolactin levels correlate with tumor size?
Answer
• What type of tumors are most prolactinomas? Microadenomas
• Prolactin levels >200 almost always indicate what? Almost always
indicates prolactinoma
• Do prolactin levels correlate with tumor size? Yes, in macroadenomas
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..
Growth Hormone Tumors
• Gigantism
• GH excess before closure of epipheseal growth plates of long bones
• Acromegaly
• GH excess after closure of epipheseal growth plates of long bones
• Insidious onset
• Usually diagnosed late
Growth Hormone Tumors
• May have DM or glucose intolerance
• Hypogonadism
• Large hands and feet
• Large head with a lowering brow and coarsening features
• Hypertensive – 25%
• Colon polyps
• 3-6 more likely than general population
• Multiple skin tags
Growth Hormone Tumors
• Diagnosis
• Screen:
• Check for high IGF-I levels (>3 U/ml)
• Remember, levels very high during puberty
• Confirm:
• 100gm glucose load
• Positive: GH levels do not increase to <5ng/ml
• Treatment
• Surgical
• Radiation
• Bromocriptine - temporary measure
• May decrease GH by 50%
• Octreotide
• For suboptimal response to other treatment
Quick Quiz!!!
• How do you screen for acromegaly?
Answer
• Check for high IGF-I levels (>3 U/ml)
Case 1
• 80-year-old man with history of hypertension (requiring three
antihypertensive agents) and type 2 diabetes mellitus (managed
with two oral hypoglycaemic drugs) was admitted with a fractured
neck of femur following a low-trauma fall.
• He was admitted to the orthopaedic ward to await fixation.
• However, he became hypotensive and required ionotropic support
and fluid resuscitation.
• His haemoglobin decreased (12.5 to 9.3 g/dl) and acute renal
dysfunction developed. The blood glucose was well controlled.
• Four days after admission the patient was considered fit for
hemiarthroplasty. Immediately postoperatively he became
hypoglycaemic and progressively drowsy, with no FND including visual
fields. Hyponatraemia and hypotension occurred.
• Full thyroid function testing showed hypothyroidism
• free T3 1.9 [3.4–5.6 pmol/L]
• free T4 6.4 [9–20 pmol/L]
• TSH 1.0 mU/L [0.3–5.5]
• Whats the diagnosis?
Case 2
• A previously healthy 64-year-old woman presented to the emergency room with a
three-day history of feeling generally unwell, drowsiness and acute onset, severe
headache.
• She had a decreased level of consciousness and a temperature of 39°C. No
ophthalmoplegia, visual field defect or other focal neurological signs were present.
She had a leucocytosis and raised C-reactive protein (CRP) with normal serum
sodium. The chest radiograph was unremarkable and computed tomography (CT) of
the brain was reported as showing involutional changes.
• Cerebrospinal fluid demonstrated
• 220 red cells per µL
• 408 white cells per µL (83% polymorphs, 17% lymphocytes)
• Proteins 1.7 g/L (NR 0.1–0.4)
• glucose 40 mg/dl
• The patient was presumed to have pneumococcal meningitis
• intravenous ceftriaxone was administered.
• No response
• Culture of CSF negative
• Hormone tests revealed panhypopituitarism
MRI brain showing a haemorrhagic lesion of the pituitary gland
extending to the optic chiasm causing displacement of the optic nerve,
consistent with pituitary macroadenoma
Diagnosis:
pituitary apoplexy related to haemorrhage with resultant
hypopituitarism
Hydrocortisone and thyroxine were commenced.
Mass reduced at 3 years of follow up
Anterior pituitary: endocinology, hypopituitarism apoplexy etc..

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Anterior pituitary: endocinology, hypopituitarism apoplexy etc..

  • 1. CLINICAL ENDOCRINOLOGY : ANTERIOR PITUITARY M C VASIF MAYAN
  • 2. Pituitary disorders • 1. MASS – SECRETORY/ FUNCTIONING and COMPRESSIVE • 2. GRANULOMAS • 3. INFLAMMATORY ( HYPOPHYSITIS) • 4. VASCULAR
  • 3. • MASS Adenoma • Tumours MEN-1, Mc Cune Albright, Carney syndrome • Other Parasellar Rathke cyst,granular cell tumour, chordoma, craniopharyngioma, meningioma, glioma, hematological malignancy • Granuloma Sarcoidosis Hand Schullen Christian disease Mets • Hypophysitis Lymphocytic/ Granulomatous/ Xanthomatous • Vascular Apoplexy/ Postpartum ( hemorrhage/ infarction)
  • 5. Pituitary Gland • Located within the sella tursica • Weight 600mg • Contiguous to vascular and neurologic structures • Cavernous sinuses • Cranial nerves • Optic chiasma • Hypothalamic neural cells synthesize specific releasing and inhibiting hormones • Secreted directly into the portal vessels of the pituitary stalk • Blood supply derived from the superior and inferior hypophyseal arteries
  • 8. Pituitary Gland • Anterior pituitary gland • Secrete various trophic hormones • Disease in this region may result in syndromes of hormone excess or deficiency • Posterior pituitary gland • More of a terminus of axons of neurons in the supraoptic and paraventricular nuclei of the hypothalamus • Storehouse for the hormones • The main consequence of disease in this area is disordered water homeostasis
  • 9. Anterior Pituitary Gland • Anterior Pituitary “Master gland” • Major blood source: hypothalamic-pituitary portal plexus • Allows transmission of hypothalamic peptide pulses without significant systemic dilution • Consequently, pituitary cells are exposed to sharp spikes of releasing factors and in turn release their hormones as discrete pulses. • Production of six major hormones: • Prolactin (PRL) • Growth hormone (GH) • Adrenocorticotropin hormone (ACTH) • Luteinizing hormone (LH) • Follicle-stimulating hormone (FSH) • Thyroid-stimulating hormone (TSH)
  • 10. Anterior Pituitary Gland • Anterior Pituitary “Master gland” • Secreted in a pulsatile manner • Elicits specific responses in peripheral target tissues • Feedback control at the level of the hypothalamus and pituitary to modulate pituitary function exerted by the hormonal products of the peripheral target glands • Tumors cause characteristic hormone excess syndromes • Hormone deficiency • may be inherited or acquired
  • 12. HORMONE DEFICIENCY • GONADOTROPIN DEFICIENCY • ACTH DEIFICIENCY • TSH DEFICIENCY • PROLACTIN DEFICIENCY • GROWTH HORMONE DEFICIENCY • HYPOPITUITARISM
  • 13. Adult Growth Hormone Deficiency • First hormone to be affected • Non functioning adenoma/ irradiation • GH  FSH/LH  TSH  ACTH • • Adults • Often asymptomatic • Fatigue • Decreased exercise tolerance • Abdominal obesity • Loss of muscle mass • Abnormal lipid profile • Reduced BMD • Atherosclerosis , LV dysfunction, increased fibrinogen
  • 14. Treatment : GH replacement 0.1 – 0.3 mg/day Maximum upto 1.25 mg/day Women need higher doses than men
  • 15. Gonadotropin Deficiency Women • Oligomenorrhea or amenorrhea • Loss of libido • Vaginal dryness or dyspareunia • Loss of secondary sex characteristics (estrogen deficiency) Men • Loss of libido • Erectile dysfunction • Infertility • Loss of secondary sex characteristics (testosterone deficiency) • Atrophy of the testes • Gynecomastia (testosterone deficiency) Most common presenting feature of adult hypopituitarism
  • 16. TSH Deficiency • Hypothyroidism • Atrophic thyroid gland
  • 17. ACTH Deficiency • Most commonly due to glucocorticoid withdrawal • Results in hypocortisolism • Malaise • Anorexia • Weight-loss • Gastrointestinal disturbances • Hyponatremia, hypoglycemia • Pale complexion • No features of mineralocorticoid deficiency • Aldosterone secretion unaffected
  • 18. Prolactin Deficiency • Inability to lactate postpartum • Often 1st manifestation of Sheehan syndrome
  • 19. HYPOPITUITARISM Etiology • Anterior pituitary diseases • Deficiency one or more or all anterior pituitary hormones
  • 21. developmental Transcription factor defect Aplasia / dysplasia Congenital mass / encephalocele Primary empty sella Congenital disorders
  • 22. Hypopituitarism: Developmental and Genetic causes •Septo-Optic dysplasia •Prader Willi syndrome •Kallman Syndrome •Laurence-Moon-Biedl Syndrome •Frohlich Syndrome (Adiposo Genital Dystrophy)
  • 23. • Septo-Optic dysplasia • Hypothalamic dysfunction and hypopituitarism • may result from dysgenesis of the septum pellucidum or corpus callosum • Affected children have mutations in the HESX1 gene • involved in early development of the ventral prosencephalon • These children exhibit variable combinations of: • cleft palate • syndactyly • ear deformities • hypertelorism • optic atrophy • micropenis • anosmia • Pituitary dysfunction • Diabetes insipidus • GH deficiency and short stature • Occasionally TSH deficiency
  • 24. •Kallman Syndrome • Defective hypothalamic gonadotropin-releasing hormone (GnRH) synthesis • Associated with anosmia or hyposmia due to olfactory bulb agenesis or hypoplasia • May also be associated with: color blindness, optic atrophy, nerve deafness, cleft palate, renal abnormalities, cryptorchidism, and neurologic abnormalities such as mirror movements • GnRH deficiency prevents progression through puberty • characterized by • low LH and FSH levels • low concentrations of sex steroids
  • 25. •Laurence-Moon-Biedl Syndrome • Rare autosomal recessive disorder •Characterized by mental retardation; obesity; and hexadactyly, brachydactyly, or syndactyly • Central diabetes insipidus may or may not be associated •GnRH deficiency occurs in 75% of males and half of affected females • Retinal degeneration begins in early childhood • most patients are blind by age 30 •Renal abnormalities
  • 29. •LYMPHOCYTIC HYPOPHYSITIS • Etiology • Presumed to be autoimmune • Clinical Presentation • Women, during postpartum period with hyperprolactinemia • Mass effect (sellar mass) • Deficiency of one or more anterior pituitary hormones • ACTH deficiency is the most common • Diagnosis • MRI - may be indistinguishable from pituitary adenoma • Elevated ESR + • Treatment • Corticosteroids • Hormone replacement
  • 31. Vascular Apoplexy Pregnancy related (infarction with DM , Sheehans) Sickle cell disease Arteritis
  • 32. Quick Quiz!!! • When should you suspect pituitary apoplexy?
  • 33. •PITUITARY APOPLEXY • Hemorrhagic infarction of a pituitary adenoma/tumor • Considered a neurosurgical emergency • Presentation: • Variable onset of severe headache • Nausea and vomiting • Meningism • Vertigo • +/ - Visual defects • +/ - Altered consciousness • Symptoms may occur immediately or may develop over 1-2 days Meningism is the triad of nuchal rigidity (neck stiffness) photophobia (intolerance of bright light) headache
  • 34. • Pituitary Apoplexy • Diabetes • Bleed into a pre existing adenoma • Patients on warfarin • Post partum ( sheehans) • Hypertension • Sickle cell anemia • Shock
  • 35. apoplexy • Severe hypoglycemia • Hypotension • Shock • CNS hemorrhage
  • 36. Apoplexy •Usually resolve completely if treated correctly and early •Diagnose with CT/MRI •Differentiate from leaking aneurysm •Treatment: •Medical therapy – if symptoms are mild • Corticosteroids – high dose glucocorticoids • Surgical – Trans sphenoid decompression • Visual defects and altered consciousness
  • 38. Hypopituitarism Diagnosis • Biochemical diagnosis of pituitary insufficiency • Demonstrating low levels of trophic hormones in the setting of low target hormone levels • Provocative tests may be required to assess pituitary reserve
  • 39. Hypopituitarism Treatment • Hormone replacement therapy • usually free of complications
  • 40. Hormone Replacement Trophic Hormone Deficit Hormone Replacement ACTH Hydrocortisone (10-20 mg A.M.; 10 mg P.M.) Cortisone acetate (25 mg A.M.; 12.5 mg P.M.) Prednisone (5 mg A.M.; 2.5 mg P.M.) TSH L-Thyroxine (0.075-0.15 mg daily) FSH/LH Males Testosterone enanthate (200 mg IM every 2 wks) Testosterone skin patch (5 mg/d) Females Conjugated estrogen (0.65-1.25 mg qd for 25days) Progesterone (5-10 mg qd) on days 16-25 For fertility: Menopausal gonadotropins, human chorionic gonadotropins GH Adults: Somatotropin (0.3-1.0 mg SC qd) Children: Somatotropin [0.02-0.05 (mg/kg per day)] Vasopressin Intranasal desmopressin (5-20 ug twice daily) Oral 300-600 ug qd
  • 41. Take home points: • Remember that the cause may be functional • Treatment should be aimed at the underlying cause • Not all KKK are hypopituitarism • Hypopituitarism may present • Acutely with cortisol deficiency • After withdrawal of prolonged glucocorticoid therapy that has caused suppression of the HPA axis • Post surgical procedure • TUBERCULOSIS • DIABETES • SYSTEMIC HYPERTENSION • Post trauma • Hemorrhage
  • 44. Pituitary Tumors •Microadenoma < 1 cm •Macroadenoma > 1 cm •Is the tumor causing local mass effect? •Is hypopituitarism present? •Is there evidence of hormone excess?
  • 45. • Clinical presentation: • Mass effect • Superior extension • May compromise optic pathways – leading to impaired visual acuity and visual field defects • May produce hypothalamic syndrome – disturbed thirst, satiety, sleep, and temperature regulation • Lateral extension • May compress cranial nerves III, IV, V, and VI – leaning to diplopia • Inferior extension • May lead to cerebrospinal fluid rhinorrhea
  • 47. Pituitary Tumors • Diagnosis • Check levels of all hormones produced • Check levels of target organ products • Treatment • Surgical excision, radiation, or medical therapy • Generally, first-line treatment surgical excision • Drug therapy available for some functional tumors • Simple observation • Option if the tumor is small, does not have local mass effect, and is nonfunctional • Not associated with clinical features that affect quality of life
  • 51. Craniopharyngioma • Derived from Rathke's pouch. • Arise near the pituitary stalk • extension into the suprasellar cistern common • These tumors are often large, cystic, and locally invasive • Many are partially calcified • characteristic appearance on skull x-ray and CT images • Majority of patients present before 20yr • usually with signs of increased intracranial pressure, including headache, vomiting, papilledema, and hydrocephalus
  • 52. Craniopharyngioma • Associated symptoms include: • visual field abnormalities, personality changes and cognitive deterioration, cranial nerve damage, sleep difficulties, and weight gain. • Children • growth failure associated with either hypothyroidism or growth hormone deficiency is the most common presentation • Adults • sexual dysfunction is the most common problem • erectile dysfunction • amenorrhea
  • 53. Craniopharyngioma • Anterior pituitary dysfunction and diabetes insipidus are common • Treatment • Transcranial or transsphenoidal surgical resection • followed by postoperative radiation of residual tumor • This approach can result in long-term survival and ultimate cure • most patients require lifelong pituitary hormone replacement. • If the pituitary stalk is uninvolved and can be preserved at the time of surgery • Incidence of subsequent anterior pituitary dysfunction is significantly diminished.
  • 54. Prolactinoma • Most common functional pituitary tumor • Usually a microadenoma • Can be a space occupying macroadenoma – often with visual field defects • Although many women with hyperprolactinemia will have galactorrhea and/ or amenorrhea • The absence these the two signs do not excluded the diagnosis • GnRH release is decreased in direct response to elevated prolactin, leading to decreased production of LH and FSH
  • 55. Prolactinoma • Women • Amenorrhea – this symptom causes women to present earlier • Infertility • Galactorrhea • Men • Impotence – often ignored • Tend to present later • Signs of mass effect
  • 56. Hyperprolactinemia • Essential to rule out secondary causes!! • Drugs – basically all anti dopaminergic drugs • Atypical antipsychotic – risperidone • METOCLOPRAMIDE • AMITRYPTILINE • Alpha METHYL DOPA • CCB – Verapamil • Estrogen • H2 antagonists - RANITIDINE • Hypothyroidism • CKD • Cirrhosis • Epileptic Seizures
  • 57. •If prolactin level > 200mcg/L, almost always a prolactinoma (even in a nursing mother) •Prolactin levels correlate with tumor size in the macroadenomas •Suspect another tumor if prolactin low with a large tumor
  • 58. Prolactinoma •Diagnosis •Assess hypersecretion • Basal, fasting morning PRL levels (normally <20 ug/L) •Multiple measurements may be necessary • Pulsatile hormone secretion • levels vary widely in some individuals with hyperprolactinemia •Hypothyroidism should be excluded by measuring TSH and T4 levels
  • 59. Prolactinoma •Treatment •Medical • Cabergoline – dopamine receptor agonist • Bromocriptine - dopamine agonist • Safe in pregnancy • Will restore menstruation • Decreases both prolactin and tumor size (80%) •Surgical • Transsphenoidal surgery • Irradiation
  • 60. Quick Quiz!!! • What type of tumors are most prolactinomas? • Prolactin levels >200 almost always indicate what? • Do prolactin levels correlate with tumor size?
  • 61. Answer • What type of tumors are most prolactinomas? Microadenomas • Prolactin levels >200 almost always indicate what? Almost always indicates prolactinoma • Do prolactin levels correlate with tumor size? Yes, in macroadenomas
  • 63. Growth Hormone Tumors • Gigantism • GH excess before closure of epipheseal growth plates of long bones • Acromegaly • GH excess after closure of epipheseal growth plates of long bones • Insidious onset • Usually diagnosed late
  • 64. Growth Hormone Tumors • May have DM or glucose intolerance • Hypogonadism • Large hands and feet • Large head with a lowering brow and coarsening features • Hypertensive – 25% • Colon polyps • 3-6 more likely than general population • Multiple skin tags
  • 65. Growth Hormone Tumors • Diagnosis • Screen: • Check for high IGF-I levels (>3 U/ml) • Remember, levels very high during puberty • Confirm: • 100gm glucose load • Positive: GH levels do not increase to <5ng/ml • Treatment • Surgical • Radiation • Bromocriptine - temporary measure • May decrease GH by 50% • Octreotide • For suboptimal response to other treatment
  • 66. Quick Quiz!!! • How do you screen for acromegaly?
  • 67. Answer • Check for high IGF-I levels (>3 U/ml)
  • 68. Case 1 • 80-year-old man with history of hypertension (requiring three antihypertensive agents) and type 2 diabetes mellitus (managed with two oral hypoglycaemic drugs) was admitted with a fractured neck of femur following a low-trauma fall. • He was admitted to the orthopaedic ward to await fixation. • However, he became hypotensive and required ionotropic support and fluid resuscitation. • His haemoglobin decreased (12.5 to 9.3 g/dl) and acute renal dysfunction developed. The blood glucose was well controlled.
  • 69. • Four days after admission the patient was considered fit for hemiarthroplasty. Immediately postoperatively he became hypoglycaemic and progressively drowsy, with no FND including visual fields. Hyponatraemia and hypotension occurred. • Full thyroid function testing showed hypothyroidism • free T3 1.9 [3.4–5.6 pmol/L] • free T4 6.4 [9–20 pmol/L] • TSH 1.0 mU/L [0.3–5.5] • Whats the diagnosis?
  • 70. Case 2 • A previously healthy 64-year-old woman presented to the emergency room with a three-day history of feeling generally unwell, drowsiness and acute onset, severe headache. • She had a decreased level of consciousness and a temperature of 39°C. No ophthalmoplegia, visual field defect or other focal neurological signs were present. She had a leucocytosis and raised C-reactive protein (CRP) with normal serum sodium. The chest radiograph was unremarkable and computed tomography (CT) of the brain was reported as showing involutional changes. • Cerebrospinal fluid demonstrated • 220 red cells per µL • 408 white cells per µL (83% polymorphs, 17% lymphocytes) • Proteins 1.7 g/L (NR 0.1–0.4) • glucose 40 mg/dl
  • 71. • The patient was presumed to have pneumococcal meningitis • intravenous ceftriaxone was administered. • No response • Culture of CSF negative • Hormone tests revealed panhypopituitarism
  • 72. MRI brain showing a haemorrhagic lesion of the pituitary gland extending to the optic chiasm causing displacement of the optic nerve, consistent with pituitary macroadenoma
  • 73. Diagnosis: pituitary apoplexy related to haemorrhage with resultant hypopituitarism Hydrocortisone and thyroxine were commenced. Mass reduced at 3 years of follow up