ENDOCRINOLOGY

Diseases affecting anterior, posterior, thyroid, parathyroid and adrenal

Pituitary divided into 2. Anterior(adenohypophysis) and posterior(neurohypophysis).

Posterior site- ADH and oxytocin
Hypothalamus regulates the release of hormones from AP by hypothalamic releasing and
inhibiting hormones.

Diseases affecting anterior pituitary

Syndromes causing excess production of hormones arise from benign tumors of single cell
type
Microadenomas<1cm
Macroadenomas >1cm

Prolactin 50-60
GH 15-20
ACTH 10-20
Gonadotroph 10-20

HYPERPROLACTINEMIA
Common clinical problem among women
Galactorrhea-amenorrhea syndrome
Amenorhea- due to inhibition of GnRH which subsequently suppresses FSH and LH
Prolactin inhibits the LH surge causing ovulation
Men- common manifestations are ED and decreased libido

Etiology- pregnancy, early nursing, hypoglycemic, seizure, sleep, chronic renal failire
Autonomous production- pituitary adenoma aka prolactinoma. In men its macroadenoma
resulting in visual field deficit.
Macroadenomas can also obstruct pituitary stalk inhibiting dopamine transport from
hypothalamus therefore increasing prolactin. (DOPAMINE IS A PROLACTIN AGONIST)
Tumors- craniopharyngioma, meningioma, dysgerminoma, trauma
Decreased inhibitory action of dopamine due to drugs that block dopamine synthesis
(metoclopramide) and dopamine depleting agents (methyldopa and reserpine).
Primary hypothyroidism causing inc in TRH and increase in prolactin.
In short its either a local effect, tumor or reduced dopamine that causes
hyperprolactinemia.

CLINICAL MANIFESTATIONS
Galactorhea, menstrual abnormalities, amenorrhea, oligomenorrhea, osteopenia and
osteoporosis in chronic, infertility and gynecomastia in women
Men-hypogonadism, ed, decr libido,gynecomastia, infertility.

DX- always exclude local causes and hypothyroidism

TX- treat with cabergoline or bromocriptine(dopamine agonist)
Surgery only when not responsive to tx
Or if tumour has other neurologic deficits
Radiation if drug and surgery not useful

ACROMEGALY
Syndrome of excessive secretion of GH
Children- gigantism

Etiology
Pituitary adenomas- usually macro-75%

Clinical findings
Enlargement of hands and feet
Coarsening of facial features, thickening of skin
Shoe, hat, glove and ring sizes increase
Nose and mandible enlarge
Deeper voice
Increased sweating]
Internal organs are enlarged
Interstitial edema, OA, and entrapment neuropathy(carpal tunnel)
Menstrual prob- prolactin and GH co secreted
Cardiac prob (10-15%)

Impaired glucose tolerance and diabetes. Articular cartilage proliferates and causes severe
joint dx

DX- IGF 1 level is gold standard.

Confirmatory test- measure GH after 100g glucose orally
If GH remains high, its positive
Glucose load will normally suppress GH
GH is anti insulin
CT/MRI to locate tumor

TX- Transsphenoidal surgery

Somatostatin anaolgues- octreotide/ lanreotide
Dopamine agonists- bromocriptine/ cabergoline (10%)
DISEASES OF ADRENAL GLAND

Cushings syndrome/disease
Clinical syndrome due to prolonged exposure to cortisol

Etiology- exogenous, iatrogenic causes are the most common causes of Cushing due to
prolonged glucocorticoid use for therapeutic use.
Adrenal hyperplasia- due to increased ACTH which occurs in pituitary-hypothalamic
dysfunction or pituitary adenomas (60-80%)
Can also be secondary to non endocrine tumors such as bronchogenic carcinoma, thymus
carcinoma, pancreatic and bronchial ca)
Adrenal neoplasia- tumor or malignancy of adrenal gland (30%)

Clinical findings
Deposition of adipose tissues in sites such as face, moon face, interscapular buffalo hump,
and mesenteric bed (truncal obesity). Thin fragile skin (paper money skin)
Hypertension, muscle weakness, fatigability, diabetes mellitus
Osteoporosis caused by incr bone resorption, striae, easy bruisaibility
Women-acne, hirsutism, oligo/amen due to increased adrenal androgen
Emotional irritability and depression
Also causes hypokalemia (uncommon) and leukocytosis
Polyuria

DX- Dexamethasone suppression test

24H urine free cortisol
Midnight salivary cortisol(pt with cushing cortisol is elevated)

ACTH level is used to dx cushing. ACTH can be increased by pituitary adenoma or ectopic
source. The high dose dexamethasone test suppresses ACTH with pituitary cause.

ACTH low means the Cushings due to adrenal source

CT scan of adrenals done to check for tumor

ACTH high- MRI to look for adenoma pituitary or CT chest TRO ectopic causes

If both MRI and CT is negative, inferior petrosal sinus sampling done

HYPERALDOSTERONISM (Conns)

Hypersecretion of major adrenal mineralocorticoid, aldosterone, which reabsorbs water and

Na and excretes K and H+.

Primary hyper- due to adrenal problem (unilateral adrenal adenoma)

Secondary hyper- stimulus is from extra adrenal (low bp, low renal perfusion, renal artery
stenosis, decompensated liver cirrhosis)

CF- Primary hyperaldosteronism, have diastolic hypertension, hypernatremia,

hypokalemia(muscel weakness, fatigue, polyuria) and NO EDEMA
Secondary edema maybe present but no hypernatremia

DX- Plasma aldosterone conc and plasma renin activity (>20:1)

NaCl challenge. After inducing salt, the PAC should drop. If remain elevated, then
hyperaldosteronism

TX- Adrenal adenoma is treated surgically

Bilateral hyperplasia- spironolactone
Adrenal insufficiency

Divided into primary adrenocorticoid insufficiency (Addison) or secondary failure in the

elaboration of ACTH (failure of ACTH production or release)

Etiology- anatomic destruction to the gland (80%)

Autoimmune anatomic destruction
Infection, metabolic agents, surgical
TB is the leading cause

Clinical findings- weakness, paresthesia, cramping, intolerance to stress, irritability,

restlessness.
Hyperpigmentation of skin- tan,brown or dark
Arterial hypotension- lack of cortisol effect on vascular tone
GI- anorexia nervosa, cramping, diarhoea, vomiting
Acute Addisonian crisis- hypotension and fever
Low sodium, high potassium and mild acidosis are present
Salt craving

Secondary insufficiency- no hyperpigmentation and K+ not elevated

DX-
Rapid ACTH administration- check cortisol response after administrating COSYNTROPIN-
Cortisol levels should exceed- if abnormal, in primary ACTH will shoot up. In secondary ACTH
low or normal with normal increment of cortisol.
and cortisol measurement