* Dr.Fakhir yousif
*Causes of hyperprolactinemia
HYPERPROLACTINEMIACommon Present with hypogonadism and/or galactorrhea
Pathological
Clinical assessmentIn women *galactorrhea (lactation in the absence of breast feeding) * hypogonadism : secondary hypogonadism, anovulation, infertility In men * decrease libido * reduce shaving *lethargy *rarly galactorrhea if associated with gyenicomastia Other features of hypopituit, local complication and hormone excess
*
Investigations
Exclude pregnancy Measure serum prolactin -upper limit 500mU/L -500-1000mU/L in non pregnant and lactating indicate stress and drugs, repeat test -1000-5000mU/L either due to drugs, microprolactinoma or dissconnection ->5000mU/L highly suggestive of macroprolactinoma Test for gonadal functions (testosterone, LH, FSH) TSH & T4 (to exclud primary hypothyroidism) MRI or CT scan if prolactin >1000mU/L Test for hypopituitarism*
Management
Correct underlying cause(cessation of drug, thyroxin replacment for prim hypothyroidism) Dopamine agonist (bromocriptin, cabergoline, quinagolide) Treat prolactinoma
*
Disadvantages
AdvantagesOral dose*
Ergotamine-like side-effects (nausea, headache, postural hypotension, constipation) Frequent dosing so poor compliance
Available for parenteral use Short half-life; useful in treating infertility
2.5-15 mg/day 8-12-hourly
Bromocriptine
Rare reports of fibrotic reactions in various tissues
Proven long-term efficacy
Limited data on safety in pregnancy Associated with cardiac valvular fibrosis in Parkinson's disease
Long-acting, so missed doses less important Reported to have fewer ergotamine-like side-effects
250-1000 μg/week2 doses/week Cabergoline
Untested in pregnancy
A non-ergot with few side-effects in patients intolerant of the above
50-150 μg/dayOnce daily Quinagolide
*
1-PROLACTINOMA
In premaenopausal women - mostly microadenoma, and present as hyperprolactinemia.In men and postmenopausal women – almost macroadenomas and present insidiously with mass effect.Occasionally can secrete excess GH and cause acromegaly.There is relation between prolactin conc and tumor size.Investigated like other pit tumors. *
Management
Medical Dopamin agonist drugs (reduce s prolactine and cause tumor shrinkage), can be withdrawn after few years in some patients with microadenoma. In macroadenomas only withdraw drugs after curative surgery or radiotherapy and under supervision. Bromocriptin and cabergoline (ergot derived) associated with fibrosis reaction in heart causing tricusped regurgitation*
Surgery and radiotherapy - only for macroadenomas that fail to shrunk with dopamine agonists - if patients intolerant for dopamine agonists - trans-sphenoidal surgery for microadenomas with 80% cure rate ( lower rate for macroadenoma) - radiotherapy for some macroadenoma to stop dopamine agonists
*
To achieve pregnancy - dopamine agonist may be followed by pregnancy - if microadenoma withdraw dopamine agonist if get pregnant - if macroadenoma continue dopamine agonist during pregnancy with follow up for visual field and prolactin
*
Clinical features
Before puberty –gigantismIn adults—acromegalyIn adolescent and persist ---combined Headache and sweating are most common complaint.Other features of hypopituitarism * 2-ACROMEGALYGH SCREATION FROM PITUITARY TUMOR USUALLY MACROADENOMA
*
Investigations
Measure GH during oral GTT---in acromegaly failure to suppress GH with paradoxical rise in 50% Prolactine elevated in 30% Other pit function tests In diabetics difficult to diagnose by GTT -measure IGF-1 *if only DM, IGF-1 is low *if DM with acromegaly, IGF-1 is high Colonoscopy to screen for colonic cancerf
*
Management
1.Surgical Trans-sphinoidal surgery as first line and to debulk the tumor Second line therapy with radiotherapy or medical according to post operative imaging and GTT results 2.Radiotherapy Second line if acromegaly persist after surgery Risk of hypopituitarism
*
3. Medical therapy -second line treatment following surgery may be stopped years following radiotherapy -somatostatines analogues octeriotides and lanreotide as slow release injections every few wks Somatostatines can be used as first line as alternative to surgery Dopamine agonists are less potent GH receptor antagonist pegvisomant as daily self injection for some patientsnot responding to somatostatin
*
3-CRANIOPHARYNGIOMA
Benign tumors develop in cell rest of Rathke’s pouchLocated in sella tursica or commonly in suprasellar spaceCystic with solid component that may be calcifiedMore common than adenomas in youngPresent as pressure symptoms, hypopituitarism or cranial DI. Also features of hypothalamic damageTreated surgically by craniotomyRadiotherapy usually neededOften recur, causing morbidity of obesity, visual failure and water balance problems *13- 3- 2012
Dr.Arwa M Fuzi Alsarrf*
4-DIABETES INSIPIDUS
Uncommon. Persistent excretion of excessive quantities of dilute urine and thirst. Types 1. cranial DI (deficient ADH secretion by hypothalamus 2. nephrogenic DI (renal tubules are not responding to ADH)Dr.Arwa M Fuzi Alsarrf
*
Causes of diabetes insipidus
Cranial Structural hypothalamic or high stalk lesion Idiopathic Genetic (dominant and recessive). Nephrogenic Genetic Metabolic (hypokalemia, hypocalcaemia) Drugs (lithium, demeclocycline) Poisoning (heavy metals) Chronic kidney disease (polycystic kidney ,sickle cell, infiltrative dis.*
Clinical features
Polyuria and polydipsia (5-20 L /day urine of low specific gravity and osmolality Potentially lethal condition if unconscious pt or hypothalamic damage Differntial d is primary polydipsia
* low serum ADH Urine <600 mOsm /kg + increase plasma osmolality >300mOsm/kg Water depreviation test 5% hypertonic saline infusion to inc plasma osmolality then measure ADH Pituitary function test and imaging
Investigations
water deprivation test ( To establish a diagnosis of diabetes insipidus, and differentiate cranial from nephrogenic causes) protocol
*
No coffee, tea or smoking on the test dayFree fluids until 0730 hrs on the morning of the test, but discourage patients from 'stocking up' with extra fluid in anticipation of fluid deprivationNo fluids from 0730 hrsAttend at 0830 hrs for body weight, plasma and urine osmolalityRecord body weight, urine volume, urine and plasma osmolality and thirst score on a visual analogue scale every 2 hrs for up to 8 hrsStop the test if the patient loses 3% of body weightIf plasma osmolality reaches > 300 mOsm/kg and urine osmolality < 600 mOsm/kg, then administer DDAVP 2 μg IM
Interpretation of water deprivation test
*Diabetes insipidus is confirmed by a plasma osmolality > 300 mOsm/kg with a urine osmolality < 600 mOsm/kg Cranial diabetes insipidus is confirmed if urine osmolality rises by at least 50% after DDAVP Nephrogenic diabetes insipidus is confirmed if DDAVP does not concentrate the urine Primary polydipsia is suggested by low plasma osmolality at the start of the test
Management
For cranial DI DDAVP (des-amino-des- aspartate-arginine vasopressin/ desmopressin. Long half life analogue of ADH Administered intranasally ,(5 ug morning and 10 ug evening). given IM in sick pts Adjust the dose according to s. level of Na&/or osmolality Excessive treatment cause water intoxication & hyponatremia For nephrogenic DI treated by thiazide diuretics and NSAID*