2. Anatomophysiology of Pituitary
gland
Master gland
Functionally secreted different hormones:
– Effect directly or
– Indirectly
Effect on secretion of other gland
– Growth & organ maturity
– Function of different part of body
3. Anatomophysiology of Pituitary
gland
It has tow parts:
1. Neurohypophase
Effect on Kidney & Uterus
– Oxytocin
– Vasopressin
Antidiuretic hormone (ADH)
8. Pathophysiology
Almost all acromegaly pts has invisible
adenoma
Tumors located along sella torsica
Growth hormone level is due to tumor size
If primary sign of acromegaly occur, either
the tumor is not too big we can Dx.
9. Etiology
Increase hypothalamus (GRH) gonadotrpin
releasing hormone & Decrease
somatostatine
Primary disease of pituitary gland or
hypophyse
10. Etiology
Carcinomas secreted GRH rarely
Pancreas tumor & CA of branches
– Secreted GRH
Gangliocytoma of hypothalamus
– GRH or Somatostatine
11. Clinical finding
Excess of GH causes:
– Chronic disease with progressive fatigue
– Over growth of soft tissue & bone
– Occur middle age
Excess of GH in age before closeness of
Epiphase membrane
15. Clinical finding
Over growth of:
– Bones
– Soft tissues
– Hands & legs
– Large cranium
– Big tongue
– Extended dental space
(Proganthism)
16. Clinical finding
Acromegaly pts are similar to each other
But not similar to their family
Harsh breathing sound (hollow sounding)
– Due to larynx & sinus hypertrophy
Warm and wet hands
Skin oily & hairy
17. Clinical finding
Change appear
Fatigue and tiredness
Hyper metabolism
– Excess sweat
Long sleep
Neurological & muscular skeletal signs:
– Headache, numbness of extremities
18. Clinical finding
Muscular weakness
Joint pain
Shoulder pain
Knee pain
Kyphosis
HTN 1/3
– Due to ↓ rennin & aldosteron and ↑
plasma volume and sodium
19. Clinical finding
Half of pts have LVH without HTN
Either No history of heart disease due
to acromegly, but CHF will occur
Amenorrhea
Impotence
Hirsutism
Temporary depression after treatment
20. Clinical finding
Kidney hypertrophy
Hepatomegly
– Without dysfunction
Goiter is common
2.7% Hyperthyroidism
Increase mortality:
– Death occur due to:
CVS, Neuro vascular disorder & Resp. disease
New treatment method decrease mortality
21. Lab exam
Abnormal GTT 20-40%
Diabetes mellitus 13-20%
Insulin resistance 80%
Due to ↑ Vit.D:
– ↑ Urine calcium
– 1/5 pts. Renal stone
22. Lab exam
Hypercalcimia is due to primary
Hyperparathyroidism, not acromegaly
Hyperprolactinemia in half of pts and causes:
– Glactorrhea
– Amenorrhea
– Decrease libido
23. Dx:
Acromegaly pts after 9 year shows signs
When pts is doubtful for acromegaly
Previous photo should compare to new
GH evaluation is not good method,
because maybe normally high specially in
female.
24. Dx:
Standard test:
– Evaluation of GH 60min after 100g glucose orally
– >2ng/ml in male and
– >5ng/ml in female is diagnostic for acromegaly
25. Dx:
If Lab exam is not supported
Radiologic exam required
90% pts cranium & sphenoidal
radiography is diagnostic.
Cranial radiography shows:
– Increased bone density
– Big sinus (proganthism)
CT and MRI size of tumor
27. Treatment
Goal of treatment:
– Return GH level to normal
– Extenuate tumor size or
– Avoid tumor growing
– Preservation normal function of pituitary gland
28. Treatment
Either with routine manner can’t recover all
those goals.
Surgery:
– Transsphenoidal pituitary microsurgery
– Treatment of choice
– Recover the disease
29. Treatment
GH level become normal in few hours
Soft tissue change to normal
Chance of relapse & tumor growth either
surgery is successful
31. Treatment
Medical treatment:
– Long acting Dopamin agonist
Bromochriptine not so effective if used alone, but
it is effective when used with other manners
90% pts has good response with 20-60mg
Rather than no effect on GH, but size of hands and
head become smaller.