1. PITUITARY DISEASES
Dr.Fakhir yousif

2. Hyperprolactinemia
Prolactinoma
Acromegaly
Craniopharyngioma
Diabetes insipidus

3. Causes of hyperprolactinemia
Common
Present with hypogonadism and/or galactorrhea
Drug induced
dopamine antagonist
antipsychotic, antidepressant, antiemitics
dopamine -depleting
reserpine, methyldopa
Estrogens(occp)
Causes of hyperprolactinemia
physiological
stress
pregnancy
lactation
nipple stimulation
sleep
coitus
exercise
baby crying

4. Pathological -prolactinoma -primary hypothyroidism -polycystic ovary
common
-prolactinoma
-primary hypothyroidism
-polycystic ovary
-macroprolactinemia
uncommon
-hypothalamic dis
-renal failure
-pit tumor secreting prolactin & GH
Rare
-chest wall reflex (herpes zoster)
- ectopic source

5. Clinical assessment In 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

6. Investigations -upper limit 500mU/L Exclude pregnancy
Measure serum prolactin
-upper limit 500mU/L
mU/L in non pregnant and lactating indicate stress and drugs, repeat test
mU/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

7. Management
Correct underlying cause(cessation of drug, thyroxin replacment for prim hypothyroidism)
Dopamine agonist (bromocriptin, cabergoline, quinagolide)
Treat prolactinoma

8. . Dopamine agonist therapy: drugs used to treat prolactinomas
Disadvantages
Advantages
Oral 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
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
μg/week 2 doses/week
Cabergoline
Untested in pregnancy
A non-ergot with few side-effects in patients intolerant of the above
μg/day Once daily
Quinagolide

9. 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.

10. 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

11. 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

12. 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

13. 2-ACROMEGALY Clinical features
GH SCREATION FROM PITUITARY TUMOR USUALLY MACROADENOMA
Clinical features
Before puberty –gigantism
In adults—acromegaly
In adolescent and persist ---combined
Headache and sweating are most common complaint.
Other features of hypopituitarism

15. 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 cancer f

16. 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

17. Somatostatines can be used as first line as alternative to surgery
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

18. 3-CRANIOPHARYNGIOMA
Benign tumors develop in cell rest of Rathke’s pouch
Located in sella tursica or commonly in suprasellar space
Cystic with solid component that may be calcified
More common than adenomas in young
Present as pressure symptoms, hypopituitarism or cranial DI. Also features of hypothalamic damage
Treated surgically by craniotomy
Radiotherapy usually needed
Often recur, causing morbidity of obesity, visual failure and water balance problems

19. Dr.Arwa M Fuzi Alsarrf

20. 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

21. 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.

22. Clinical features Investigations
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
Investigations
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

23. No coffee, tea or smoking on the test day
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 day
Free fluids until 0730 hrs on the morning of the test, but discourage patients from 'stocking up' with extra fluid in anticipation of fluid deprivation
No fluids from 0730 hrs
Attend at 0830 hrs for body weight, plasma and urine osmolality
Record body weight, urine volume, urine and plasma osmolality and thirst score on a visual analogue scale every 2 hrs for up to 8 hrs
Stop the test if the patient loses 3% of body weight
If plasma osmolality reaches > 300 mOsm/kg and urine osmolality < 600 mOsm/kg, then administer DDAVP 2 μg IM
100 Protocol Body_ID: TI

24. 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
Interpretation Body_ID: TI

25. 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