PITUITAR

Y
GLAND

ANTERIOR PITUITARY GLAND

AKA (master gland; adenohypophysis)
HORMO
NE

TARGET(S)

FUNCTION

PRL

BREASTS

Stimulates breasts to produce milk ( pregnancy;

breast feeding)

GH

ALL CELLS IN Stimulates growth & repair

THE BODY

ACTH

ADRENALS

Stimulates adrenal gland to produce hormone called

cortisol.

LH &
FSH

OVARIES (F)
TESTES
(M)

Stimulates ovaries to produce estrogen &

progesterone & the testes to produce
testosterone & sperm.

TSH

THYROID

Stimulates the thyroid gland to produce its own

hormone called thyroxine.

DISORDERS OF
ANTERIOR
PITUITARY
GLAND

HYPOPITUITARISM

-impaired production/ failure o secrete hormone hormones that

affect many of bodys functions.
ETIOLOGY:
congenital
Acquired TBI, Pituitary tumor, (tuberculosis) in which it
infiltrate the gland that can result in a reduction in function
3 MC causes:
Adenoma of Ant. Pituitary
Sheehans syndrome (postpartum pituitary necrosis)
Empty sella syndrome (pituitary gland shrinks or become
flattened)

EPIDEMIOLOGY:
rare disorder
Affect both F & M
can occur at any time in life
PATHOPHYSIOLOGY:
-low target hormone levels that stimulates
trophic hormone production
-as adenoma increase in size it will compress
over hypothalamic pituitary stalk leading to
decreased supply of the secretor hormones

Clinical Manifestations:
GH deficiency
ACTH deficiency
TSH deficiency
GONADOTROPIN deficiency
TREATMENT:
-Hormone Replacement Therapy (depends on the specific
hormone deficiency)
Glucocorticoids
Thyroid hormone
Growth hormone
Vasopressin
Sex steroids

SPECIFIC CONDITIONS OF HORMONAL

DEFICIENCY:

A. PITUITARY APOPLEXY
-hemorrhagic infarction of pituitary tumor
-considered a neurosurgical emergency
Presents: Severe headache;Nausea & vomiting ;vertigo
TREATMENT: transsphenoidal decompression
corticosteroids if symptoms are mild
B. EMPTY SELLA SYNDROME

pituitary gland shrinks or become flattened

C.LYMPHOCYTIC HYPOPHYSITIS
-presumed to be autoimmune
-ACTH deficiency is most common
D. CRANIOPHARYNGIOMA
-arise near pituitary stalk
-these tumors are often large ,cystic & locally
invasive
*usally with signs of inc intracranial pressure
including headache, vomiting, hydrocephalus
TREATMENT:
TRANSSPHENOIDAL SURGICAL RESECTION

HYPERPITUITARISM
-hypersecretion of pituitary hormones
Etiology:
-Pituitary microadenoma
-PROLACTINOMA (MC adenoma in children F>M)
-CORTICOTROPINOMA
-SOMATOTROPINOMA
-THYROTROPINOMA
EPIDEMIOLOGY:
-rare in children than adults

ORDER OF FREQUENCY WITH WHICH HORMONE

SECRETION OCCURS IN PITUITARY TUMOR:
PRLGHACTHGONADOTROPINTSH

PRL excess

Hyperprolactinemia

GH excess

Acromegaly/
Gigantism
Cushings Disease

ACTH excess
GONADOTROPIN
excess
TSH excess (rare)

Menstrual disorders
Secondary
hyperthyroidism

Clinical manifestation:
-amenorrhea; galactorrhea-due to hyperprolactinemia(F)
-gynecomastia
(M)
DIAGNOSIS:
MRI of Head for detecting & measuring prolactinomas
-to look for mass lesion
TREATMENT:
Dopamine agonist drug
(BROMOCRIPTINE)(CABERGOLINE)
-Decreases PRL secretion &reduce size of lactotroph adenomas in
90% of patients

(BROMOCRIPTINE)- given twice a day

(CABERGOLINE)- administered once/twice a week

- more effective than bromocriptine

- but causes nausea;postural hypotension

TRANSSPHENOIDAL SURGERY
1.

Pts. Who do not respond to medical treatment

2.

Women who have microadenoma, desire

pregnancy & cannot tolerate medical
treatment.

RADIATION THERAPY
Used to prevent regrowth of residual tumor in pt.
with a very large macroadenoma after
transsphenoidal debulking

GROWTH HORMONE DEFICIENCY

-inadequate secretion of GH

ETIOLOGY:
-brain tumor; infection; radiation exposure
EPIDEMIOLOGY:
6,000 adults/yr in US; 15-20%of cases childhoodadulthood
CLINICAL PRESENTATION:
(ADULT)
dec muscle strength; low physical & mental energy; poor memory;
emotional instability & impaired sleep
(CHILDREN)- short stature; increased fat; micropenis; high pitched voice

PATHOPHYSIOLOGY:
-results in alteration in the physiology of different
systems of the body
TREATMENT:
-GH replacement
given by injection (back of arms, thighs,
buttocks)
(natural GH deep sleep)

ACROMEGALY & GIGANTISM

Acromegaly- abnormal growth of the hands, feet
& face
Gigantism- excessive growth & height
significantly above average.
ETIOLOGY:
-GH excess from pituitary
-pituitary adenoma
EPIDEMIOLOGY:
-acromegaly (MC)- start n the 3rd decade of life
-gigantism (rare)- may begin at any age of life

ACROMEGALY

GIGANTISM

CLINICAL PRESENTATION:
ACROMEGALY
GIGANTISM
Hypertrichosis

Hyperhidrosis

Thick & hard nails

Tall stature

Noticeably large pores

mild to moderate obesity

Enlargement of lower lip &

nose

Exaggerated growth of hands,

feet with thick fingers & toes

Oily skin (acne not common) Coarse facial features

Deepening of creases on
forehead & nasolabial folds

Protruding forehead

Wide spacing of teeth & jaw

protrusion

Jaw protrusion

TREATMENT:
-somatostatin analogues
-GH receptor antagonist
-surgical resection of GH secreting adenoma

ADRENOCORTICOTROPIC
HORMONE DEFICIENCY

-Dec or absent production of ACTH

ETIOLOGY:
-congenital/ acquired.
-ACTH deficiency leads to adrenal insufficiency
CLINICAL MANIFESTATION:
-fatigue, weakness, anorexia, vomiting, nausea
TREATMENT:
-Glucocorticoid replacement therapy

CUSHING SYNDROME
(ACTH-PRODUCING
-a disease due to chronic exposure of tissues to
ADENOMA)
excess glucocorticoid hormones from endogenous
or exogenous sources.
EXOGENOUS- due to therapeutic use of
glucocorticoids/ACTH
ENDOGENOUS

- 70% CUSHINGS DISEASE

- 15% ectopic ACTH secretion
- 15% primary adrenal tumor

Either pituitary origin or

adrenal origin

CUSHINGS DISEASE
SYNDROME
EPIDEMIOLOGY:
F>M | 5:1
Peak incidence: 25-40 y.o

CUSHINGS

Signs & Symptoms:

Obesity & thin skin (80%)

Moon faces & Hypertension (75%)

Purple skin striae & Hirsutism (65%)

Menstrual d/o & Plethora (60%)

Abnormal glucose tolerance & impotence (55%)

Proximal muscle weakness &truncal obesity (50%)

Acne , bruising &mental changes (45%)

Osteoporosis (40%)

edema of LE (30%)

Hyperpigmentation (20%)

Hypokalemic alkalosis& DM (15%)

TREATMENT:
SURGERY
MEDICATION(bromocriptine)
RADIOTHERAPY
*when surgery cannot be done or not successful, control
of hypercorticolism may be attempted with medication
*Pituitary radiation may be useful if surgery fails for
cushings disease.

-gradual withdrawal of glucocorticoid(exogenous

cushing)
-surgical resection of causative tumor (endogenous
cushing)

POSTERIOR PITUITARY GLAND

AKA neurohypophysis
HORMONE
OXYTOCIN

AVP (arginine
vasopressin)

TARGET(s)
Uterus &
mammary
glands
Kidneys or
arterioles

FUNCTION
Uterine
contractions;
lactation
Stimulates
water
retention;
raised blood
pressure by
contracting

DIABETES INSIPIDUS
imbalance of water secondary to antidiuretic
hormone insufficiency AKA arginine vasopressin
(AVP)
2 MAJOR FORMS:

Central DI- dec. secretion of AVP

Nephrogenic- dec. ability to concentrate urine

because of resistance to ADH action in the kidney.

Triad:

Polydipsia- excessive quantity of urine

Anorexia- loss of appetite

Polyuria- excessive thirst

ETIOLOGY:
CENTRAL DI:
Idiopathic- 30%
Malignant or benign tumors of pituitary 25%
Cranial surgery- 20%
Head trauma- 16%
Nephrogenic DI:
Hypokalemia
Renal disease
hyperglycemia
EPIDEMIOLOGY:
-3

cases/ 100 000 in US

CLINICAL PRESENTATION:

Bladder enlargement
Hydronephrosis- literally water inside the kidney
tenderness
Pain radiating to testicle or genital area

TREATMENT:
CENTRAL DI:
DESMOPRESSIN(intranasal/orally)-inc urine conc
&dec urine flow
NEPHROGENIC DI:
Give diuretics for urine losses & salt reduction

ADIPSIC HYPERNATREMIA
-A defect in thirst mechanism even with salt excess
ETIOLOGY:
-Hypothalmic lesion
-impaired osmoreceptors that regulate AVP secretion
CLINICAL MANIFESTATION:
Tachycardia
Postural hypotension
muscle weakness
Acute renal failure

PATHOPHYSIOLOGY:
-a deficiency of thirst results in failure to drink
enough water to replenish obligatory renal and
extrarenal losses, causing hypertonic
dehydration.
TREATMENT:
-administer water orally by using hypotonic
fluids(alert)
-via IV

Syndrome of Inappropriate Antidiuretic Hormone(SIAD)

ETIOLOGY:
-loss of sodium through urine due to ADH hypersecretion
hyponatremia is a result of an excess water rather than
a deficiency of sodium
RISK FACTORS:
Increasing age >30
Low body weight

CLINICAL PRESENTATION:
Early symptoms:
Anorexia
Nausea
Malaise
Headaches
muscle cramps
irritability
drowsiness
seizures
coma

TREATMENT:
ACUTE setting
Fluid restriction
Hypertonic saline
CHRONIC setting
Demeclocycline
EMERGENCY setting
Inducing central pontine myelinolysis(CMP)