ANTERIOR

PITUITARY LOBE
HORMONES
Growth Hormone Agonist
Somatotropin
■ a protein that stimulates linear body growth in
children and regulates cellular metabolism in both
adults and children
■ lipolysis
■ production of free fatty acids
■ blood glucose
■ Promotes positive nitrogen balance
somatropin (Humatrope)
somatrem (Protropin)
Growth Hormone Agonist
Indications
■ Children with GH deficiency before
ephiphyseal closure
■ Growth stimulation during Turner’s Syndrome
■ Treatment of cachexia
■ AIDS wasting
■ Positive nitrogen balance in patients with
severe burns
■ Prader-Willi Syndrome in children
Short bowel syndrome
Growth Hormone Agonist
C/I
■Obese patients
■Patient’s with closed epiphysis who do not
have GH deficiency
■Patients with cancer
Growth Hormone antagonist
Somatostatin
■Synthetic: Octreotide & Lanreotide
Pegvisomant
Growth Hormone Excess
Acromegaly
■ Long bones will not grow in adults because the
epiphyses are closed, but bones of the extremities
(hands, feet, jaw, and nose) will enlarge
Thickened skin and soft tissues
Management:
■ Surgery
■ Dopamine agonists (cabergoline & bromocriptine)
■ Octreotide
Gonadotropin-releasing hormone

release of the gonadotropins

folliclestimulating hormone (FSH) and
luteinizing hormone (LH) from the
anterior pituitary
Gonadotropin
 treatment of infertility
 Menotropins: (human menopausal gonadotropins or hMG)
urine of postmenopausal women and contain both FSH and
LH
 Urofollitropin: FSH obtained from postmenopausal women and
is devoid of LH.
 Follitropin alfa and follitropin beta: human FSH from
recombinant DNA technology
 Human chorionic gonadotropin (hCG): placental hormone that
is excreted in the urine of pregnant women.
 Adverse effects:
■ Ovarian enlargement
■ ovarian hyperstimulation syndrome
■ Multiple births
Prolactin
Prolactin serum levels increase:
■ during pregnancy and breast-feeding
■During & after sleep starts (episodic
during thee day)
■during stress
normal range of serum prolactin
■1 to 20 ng/mL
Prolactin Inhibiting Hormones
Dopamine: increase growth hormones
among individuals; inhibits growth
hormone among acromegalics
Cabergoline
Bromocriptine
■dopamine agonist
■inhibits prolactin release
■treatment of hyperprolactinemia
POSTERIOR PITUITARY LOBE
HORMONES
Oxytocin
■ uterine contraction (induces labor, prevents
post- partum hemorrhage)
■ milk ejection
 Vasopressin / Anti-Diuretic Hormone
(ADH), Desmopressin
■ acts on the collecting tubule  ↑ H2O
resorption
■ treatment of diabetes insipidus (DI)
Rowel P. Catchillar, MS
Anatomy of the Adrenal Cortex
adrenal cortex concentric zones
■zona glomerulosa (aldosterone
production)
■zona fasciculata (glucocorticoids)
■zona reticularis (adrenal androgens)
ACTIONS OF THE CORTICOSTEROIDS

Adrenal corticosteroids exert effects on

almost every organ in the body
essential for homeostasis, for coping
with stress, and for the very
maintenance of life
ACTIONS OF THE CORTICOSTEROIDS

Carbohydrate, Protein, and Fat

Metabolism
■ blood glucose
■ protein catabolism (negative nitrogen
balance)
■ lipid catabolism (ketosis)
ACTIONS OF THE CORTICOSTEROIDS

Electrolyte and Water Metabolism

■Na retention = K Depletion
■ Ca excretion
ACTIONS OF THE CORTICOSTEROIDS

Cardiovascular Function
■cardiac output
■potentiate the responses of vascular
smooth muscle to the pressor effects of
catecholamines
ACTIONS OF THE CORTICOSTEROIDS

Immune and Defense Mechanisms

■inflammatory and immunological
responses constitute the basis for their
therapeutic efficacy
■promote apoptosis and reduce survival,
differentiation, and proliferation of a
variety of inflammatory cells, including T
lymphocytes and macrophages
ACTIONS OF THE CORTICOSTEROIDS

Other Endocrine Organs

■suppressive actions on certain endocrine
systems
■inhibit thyroid-stimulating hormone
■anticalcemic (amplification of the actions
of parathyroid hormone)
■attenuation of luteinizing hormone
secretion
ADVERSE EFFECTS
Osteoporosis (most damaging effect of
long term corticosteroids).
Glucocorticoid administration is the
most common cause of drug-induced
osteoporosis
■Bisphosphonates
■Calcitonin: inhibits bone resorption
ADVERSE EFFECTS
The Infectious Process
■ heightened susceptibility to serious bacterial,
viral, and fungal infections
■ Local infections may reactivate and spread,
and infections acquired during the course of
therapy may become more severe and even
more difficult to recognize
■ increase risk of wound infection, and delay
healing of open wounds
ADVERSE EFFECTS
Effects on Gastric Mucosa
■ formation of peptic ulcers, with hemorrhage
or perforation or reactivation of a healed
ulcer
Hyperglycemic Action
Ophthalmic Effects
■ Cataract formation (especially if patient has
RA)
■ increase in intraocular pressure
ADVERSE EFFECTS
Central Nervous System Effects
■Psychiatric side effects induced by
glucocorticoids may include mania,
depression, or mood disturbances
Fluid and Electrolyte Disturbances
■retain sodium and water during steroid
therapy
Pseudorheumatism
Additional Effects
acne, striae, truncal obesity, deposition
of fat in the cheeks (moon face) and
upper part of the back (buffalo hump),
and dysmenorrhea
AIDS + glucocorticoids: Kaposi’s
sarcoma becomes activated or
progresses more rapidly
Withdrawal
Glucocorticoids are not withdrawn abruptly
but are tapered. The doses are altered so
that the condition being treated will not
flare up and recovery of the hypothalamic–
pituitary axis will be facilitated. Tapering
the dose may reduce the potential for the
development of Addison-like symptoms
associated with steroid withdrawal.
THERAPEUTIC USES OF STEROID
HORMONES
Replacement Therapy
Inflammatory States
Leukemia
Shock
Congenital Adrenal Hyperplasia
Replacement Therapy
Addison’s disease
■adrenal insufficiency , Hyperpigmentation
& postural hypotension
Cortisol (20 to 30 mg/day) + 9--
fluorocortisol (0.1 mg/day)
Inflammatory States
wide range of effects on virtually every
phase and component of the inflammatory
and immune responses
Rheumatoid arthritis is the original
condition for which anti-inflammatory
steroids were used, and they remain a
mainstay of therapy
Asthma & COPD
Guillain-Barré syndrome
Shock
Prompt intensive treatment with
corticosteroids may be lifesaving when
an excessive inflammatory reaction has
resulted in septic shock
Congenital Adrenal Hyperplasiaa

due to 21-hydroxylase deficiency

corticotrophin secretion  adrenal
hyperplasia occurs, adrenal
androgens
androgens causes virilization,
accelerated growth, and early
epiphysial fusion
DRUGS USED IN THE DIAGNOSIS OR
TREATMENT OF ADRENOCORTICAL
ABNORMALITIES
Corticotropin
■provides enhanced amounts of all
endogenously secreted adrenocortical
hormones, including androgens
Cosyntropin
■screening test to assess adrenocortical
insufficiency
DRUGS USED IN THE DIAGNOSIS OR
TREATMENT OF ADRENOCORTICAL
ABNORMALITIES
Metyrapone
■ differential diagnosis of both adrenocortical
insufficiency and Cushing’s syndrome
(hypercortisolism)
■ treatment of Cushing’s syndrome
Aminoglutethimide
■ competitive inhibitor of desmolase, the enzyme
that catalyzes the conversion of cholesterol to
pregnenolone
■ Cushing’s syndrome that results from adrenal
carcinoma and in congenital adrenal hyperplasia
DRUGS USED IN THE DIAGNOSIS OR
TREATMENT OF ADRENOCORTICAL
ABNORMALITIES
Mitotane
■ drug of choice for the treatment of primary adrenal
carcinoma when surgery or radiation therapy is not
feasible
Ketoconazole
■ treatment for Cushing’s syndrome in patients
undergoing surgery or receiving pituitary radiation
Mifepristone (RU 486)
■ treatment of hypercortisolism
Dexamethasone
■ Large dose: diagnosis of Cushing syndrome
(Hypercoltisolism)