PITUITARY GLAND

ANTERIOR PITUITARY GLAND AKA (master gland; adenohypophysis)

HORMONE TARGET(S) FUNCTION

PRL BREASTS Stimulates breasts to produce milk ( pregnancy; breast feeding)

GH ALL CELLS IN THE BODY

Stimulates growth & repair

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 body’s 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• Sheehan’s 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 emergencyPresents: Severe headache;Nausea & vomiting ;vertigoTREATMENT: 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, hydrocephalusTREATMENT:TRANSSPHENOIDAL SURGICAL RESECTION

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

ORDER OF FREQUENCY WITH WHICH HORMONE SECRETION OCCURS IN PITUITARY TUMOR:PRL→GH→ACTH→GONADOTROPIN→TSHPRL excess Hyperprolactinemia

GH excess Acromegaly/ Gigantism

ACTH excess Cushing’s Disease

GONADOTROPIN excess Menstrual disorders

TSH excess (rare) 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 SURGERY1. Pts. Who do not respond to medical treatment2. Women who have microadenoma, desire

pregnancy & cannot tolerate medical treatment.

RADIATION THERAPYUsed 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 childhood→adulthood

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 & GIGANTISMAcromegaly- abnormal growth of the hands, feet & faceGigantism- 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 GIGANTISMHypertrichosis 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 ACTHETIOLOGY: -congenital/ acquired.-ACTH deficiency leads to adrenal insufficiency

CLINICAL MANIFESTATION:-fatigue, weakness, anorexia, vomiting, nausea

TREATMENT:-Glucocorticoid replacement therapy

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

EXOGENOUS- due to therapeutic use of glucocorticoids/ACTHENDOGENOUS - 70% CUSHING’S DISEASE - 15% ectopic ACTH secretion - 15% primary adrenal tumor

Either pituitary origin or adrenal origin ↓ ↓ CUSHING’S DISEASE CUSHING’S SYNDROME

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

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:SURGERYMEDICATION(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 cushing’s disease.

-gradual withdrawal of glucocorticoid(exogenous cushing)-surgical resection of causative tumor (endogenous cushing)

POSTERIOR PITUITARY GLANDAKA neurohypophysisHORMONE TARGET(s) FUNCTION

OXYTOCIN Uterus & mammary glands

Uterine contractions; lactation

AVP (arginine vasopressin)

Kidneys or arterioles

Stimulates water retention; raised blood pressure by contracting arterioles.

DIABETES INSIPIDUSimbalance 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 flowNEPHROGENIC 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 hypersecretionhyponatremia 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 MalaiseHeadachesmuscle cramps irritability drowsiness seizures coma

TREATMENT:ACUTE setting• Fluid restriction• Hypertonic saline

CHRONIC settingDemeclocycline

EMERGENCY settingInducing central pontine myelinolysis(CMP)