Pituitary Disorders: Harsinen Sanusi / Husaini Umar

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Pituitary disorders

Harsinen Sanusi / Husaini Umar

Bagian Endokrin Metabolik


Fakultas Kedokteran
Universitas Hasanuddin

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ACTH
GH

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All hormones affect homeostasis

Thyroid
hormone
controls about 25% of basal metabolism in most tissues

exerts a permissive action for many hormones in addition to


Cortisol
its own direct effects

PTH regulates calcium and phosphorus levels

control vascular volume and serum electrolyte (Na, K) Mineralo


corticoid
concentration

Vasopres regulates serum osmolality by controlling renal free water


sin clearance

maintains euglycemia in the fed and fasted states Insulin


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Pituitary Tumors
> Pituitary tumors are the most
common diseases of the pituitary
gland

> Benign and monoclonal - arise from


single type of anterior pituitary cells

> Variable presentation

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Pituitary tumors
Microadenoma

Size
Macroadenoma

Hypersecretion

Function
Insufficiency

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Classification of pituitary tumors according to
size,invasiveness and expansion

Microadenomas Macroadenomas
(D < 10 mm) (D > 10 mm)

Intrasellar Extrasellar

Non invasive Invasive

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Excessive pituitary GH-Secretion Normal pituitary GH-Secretion
Pituitary Adenoma
• Commonest causes
• Majority are hypersecreting

Endocrinologic abnormality

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Pituitary hypersecretion due pituitary adenoma

PITUITARY ADENOMA
Somatothroph Adenoma :
ACROMEGALY – GIGANTISM (15%)
Lactothroph adenomas :
PROLACTINOMA (25%)

Thyrotroph adenomas : Secondary


Hyperthyroidism (< 1%)
Corticotroph adenomas :
Plurihormonal : CUSHING`S DISEASE (< 12%)
Gonadothrop adenomas : FSH/LH
GH+prolactin+hyperthr
raise (< 10%)
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Pituitary Hypersecretion

• PRL  most commonly


secreted by adenoma
Hyperprolactinemia

• G H  Acromegaly
• ACTH  Cushing’s disease

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ACROMEGALY
• Etiology : excessive pituitary GH
secretion
• GH-secreting pituitary adenoma  2nd
frequency
• Sex incidence : equal
• Mean age at diagnosis is + 40 years
• Adults : linear growth does not occur,
because of prior fusion of the epiphyses
of long bones
• Childhood & adoloscence  Gigantism
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ACROMEGALY

Clinical manifestations :

• Chronic GH hypersecretion  overgrowth of


bone is the classic feature particularly of the
skull and mandible
• Duration of symptoms usually 5-10 years
before the diagnosis established
• Increased late morbidity and mortality if
untreated  slowly progressive and
spontaneous remission
• Death : cardiac diss, diabetes, colon cancer
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ACROMEGALY

PITUITARY ADENOMA

GH
INCREASE

DERMATOLOGIC : EXCESSIVE SWEATING, OILY SKIN, ENLARGING SKIN TAG


MUSC.SKELETAL : ARTHRARLGIA,OSTEOARTHRITIS, LARGER HAT,RING, OR
SHOE SIZE, GAPS BETWEEN THE TEETH, KYPHOSCOLIOSIS
ENDOCRINE : HYPOTHYROIDISM, HYPOGONADISM, DM
NEUROLOGIC : HEADACHE, PERIPHERAL PARESTHESIA, VISUAL
DISTURBANCES
PULMONARY : OBSTRUCTIVE SLEEP APNEA
CARDIAC : INCREASED LEFT VENTRICULAR MASS, HYPERTENSION
GI : ORGANOMEGALY
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RENAL : HYPERCALCIURIA
Clinical manifestations

• Manifestation of GH excess
• Disturbance of other endocrine function
• Local manifestation

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Clinical manifestations
Clinical manifestations

1.Manifestation of GH Excess
Acral enlargement Parethesis
Soft tissue overgrowth Joint pain
Hyperhydrosis Hypertrichosis
Lethargy or fatigue Goiter
Weight gain Hypertension

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Gigantisme
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G
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T
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S
M

Adults : linear growth does not occur, because of prior fusion of the
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epiphyses of long bones. Childhood & adoloscence  Gigantism
Acromegaly

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Clinical manifestations
Clinical manifestations

2. Disturbance of other endocrine function


Hyperinsulinemia,
Glucose intolerance  other type of diabetes
Irregular or absent menses,
Decreased libido,
Hypothyroidism,
Galactorrhea,
Gynaecomastia,
Hyperadrenalism.

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Clinical manifestations

3. Local manifestations
Enlarged sella
Headache
Visual deficit

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Laboratory findings

GH hypersecretion > 10 ng /mL


Increase IGF-1 levels

postprandial hyperglycemia
serum insulin is increased
elevated serum phosphorus
hypercalciuria
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Initial steps diagnosis :

Neuro-radiologic studies w/ MRI


and
Neuro-ophthalmologic evaluation

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Imaging study
> Plain films/ x-ray :
Sellar enlargement (90% cases),
Enlargement of the frontal, maxillary
sinuses, and the jaw
Thickening of the calvarium
Increased thickness of the heel pad
> MRI

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Increase in heel pad thickness

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Visual Field Defects

• Bitemporal hemianopsia
• Visual loss
• Large tumor  diplopia, cranial
nerve dysfunction (N.III, IV, VI)

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Effects of pituitary
tumors on the
visual apparatyus

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ACTH Secreting Pituitary Adenoma
(Cushing Disease)

• Harvey Cushing  1932


• ACTH hypersecretion  billateral adrenal
hyperplasia
• Spontaneous hypercorticolism (Cushing
syndrome).
• DD: Adrenocorticosteroid excess-Ectopic
ACTH syndrome, and adrenal tumors
• Onset insidious, usual 20 -40 y, F:M =
8:1, Ectopic ACTH  M:F = 3:1
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Clinical Features of Cushing syndrome

Central obesity violaceous striae


hypertension hirsutism
glucose intolerance acne
gonadal disfunction poor wound healing
moon facies fungal infection
Plethora osteopenia

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Diagnosis & Treatment of Cushing disease

• Diagnosis :
Basal plasma ACTH

• Treatment :
Surgical treatment: microsurgery
Radiotherapy: Conventional radiotherapy
Medical therapy: no drugs supresses pituitary
ACTH secretion.
* Ketoconazole to inhibit adrenal steroid biosynthesis,
* Metyrapone, aminoglutethimide  reduce cortisol
hypersecretion
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Posterior pituitary Disorders

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Posterior Pituitary

Antidiuretic hormon ( ADH; Vasopressin )

Diabetes Insipidus : Deficient ADH


action

Synd Inappropriate ADH : High


plasma ADH concentration

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DIABETES INSIPIDUS

• Is disorder of water balance caused by


nonsmotic renal losses of water

• Etiology :
deficient arginine vasopressin (AVP=ADH)
secretion (central) or
end organ unresponsivenes to AVP
(nephrogenic)

• ADH is released from cells in the posterior


pituitary gland  increase water permeability
at the distal tubule and collecting duct of the
nephron
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DIABETES INSIPIDUS

Classification
Central DI  hypophysectomy, idiopathic,
familial, tumor/cyst, granuloma,
autoimmune
Nephrogenic DI  chronic renal disease,
hypokalemia,hypercalcemia, familial, etc

DD: Primary polydipsy (Psychogenic,


compulsive water drinking)

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DIABETES INSIPIDUS

Symptoms:
Thirst, polyurea, daily urine volume > 3 L
Hypernatremia  weakness,altered mental
status, coma, seizzures
Signs n physical examination is` usually
normal

Laboratory Evaluation:
Spesific gravity < 1.010
Urine osmolality < 300 m Osm/kg
Hypernatremia
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Diagnosis

• High plasma osmolality


• Urine osmolality reduced
• Water Deprivation test
Spesific - Gravity < 1.005 (200 mosm
/kg of water) and reduce 2% BW
• Plasma Vasopressin
☼ Low in Neurogenic DI
☼ N/high in nephrogenic DI
• ADH Radioimmunoassay
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Syndrome of inappropriate secretion of ADH
(SIADH)

Definition
Excess vasopressin becomes a clinical problem when there is
concurrent retention of water producing hypo-osmolality
Etiology
Malignant lung disease, TBC, lymphoma, CNS trauma, drugs
( clofibrat, chlorpropamide, HCT), HIV infection, endocrine
diseases ( adrenal insuff, myxedema)
Diagnosis
Hyponatremia
High ADH

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Syndrome of inappropriate secretion of ADH
SIADH
(SIADH)

Treatment
- Fluid therapy
- Diuretics

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Hyperprolactinemia

PRL hypersecretion is the most common endocrine


abnormality due to hypothalamic-pituitary disorders,
and PRL is the hormone most commonly secreted in
excess by pituitary adenomas (prolactinoma)

Indications for Prolactin Measurement


- Galactorrhoe
- Enlarged sella turcica
- Suspected pituitary tumor
- Hypogonadotropic, hypogonadism  
- Unexplained amenorrhea  
- Unexplained male hypogonadism or infertility
Etiology of Hyperprolactinemia

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Clinical features
  Galactorrhea
  ♀ : amenorrhea , oligomenorrhea with
anovulation, or infertility
  ♂ : decreased libido

Diagnosis : prolactin levels > 300 ng/L

Differential Diagnosis :
hyperprolactinemia : pregnancy, hypothalamic -
pituitary disorders, primary hypothyroidism, and
drug ingestion
Pituitay Insufficiency

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Pituitay Insufficiency

> Panhypopituitarism 
classic manifestation of
pituitary adenomas;
Hypogonadism c/ GnRH 
screened FSH/LH to
exclude primary gonadal
failure
> TSH or ACTH deficiency is
relatively unusual

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Replacement therapy for hypopituitarism

Axis Usual replacement therapy


Adrenal Hydrocortisone 15-40 mg/day
Thyroid Thyroxine 100 – 150 umg/day
Gonadal
Male Testosterone IM / patch
Female Cyclical oestrogen/progesterone orally/ patch
Fertility hCG + FSH
Growth Recombinant human GH
Thirst Desmopressin (DDAVP) 10-20ug-spray 1-3
x/day
Carbamazepine and thiazide use rarely in mild
DI nephrogenic
Breast
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(bromocriptine 2.5-15 mg/day)
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