ACROMEGALY AND GIGANTISM
Head to foot examination
Face
Prominent brow,thick wrinkles in the forehead
Wide spaced teeth, macroglossia
Prominent nasolabial fold
Seborrhea,acne,hirsutism
Fundus:
Optic atrophy
Papilledema
Retinopathy-diabetic/hypertensive
Eye:
Angioid streaks,bitemporal hemianopia ,ophthalmoplegia
Neck:
goiter,
Parathyroid,pituitary and pancreatic tumor called wermer syndrome-
(Multiple endocrine neoplasia)
Voice:
deep or highpitched if hypogonodal
Chest:
gynecomatia, galactorrhea
Cardiomegaly,with S3 S4
Back:Kyphosis
Joints
Wide spread osteoarthritis
Abdomen:
Hepatosplenomegaly
Palpable kidney
Testicular atrophy
Lower
limbs:Proximal muscle weakness,osteoarthritis of hip and
knee,palpable peroneal nerve and foot
drop
Ankle:Hung
up reflex
Large feet,thick
heel,heel pad thickness increased
Hands;Spade
like hands,spatulate fingers,positive tinel,s sign
Thenar wasting and weak opponens,
Sweaty palms
Arm;Hypertension,
Palpable
Ulnar nerve,supraclavicular nerve,
proximal muscle weakness and atrophy of shoulder
girdle
Axilla:acanthosis
nigricans,fibroma molluscum
CNS;Emotional lability
In gigantism
In addition to all the above findings tall tature(7-8feet height) s seen
In acromegaly Growth hormone excess occurs after the closure of epiphysis.
So bone cannot grow long but grows wide.
In gigantism growth hormone excess occurs before the
closure of epiphysis.
ACROMEGALY –Indications of disease activity:
1.Severity of seborrhea,sweating.
2.number of fibromatous molluscae.
3.Degree of hypertension
4.serial measurement of visual field and visual
acuity.
5.degree of glycosuria, ,hyperglycemia.
6.plasma level of somatomedin.
Mechanism
of polydipsia in Acromegaly:
1.dehydration due to hyperhydrosis
2.osmotic diuresis (in 10%( secondary to glucose
intolerance(in 50%)
3.diabetes insipidus.
Mechanism
of galactorrhea in acromegaly:
1. concomittant adenomatous secretion of prolactin(in30%)2.Compression
of posterior pituitary stalk by
adenoma causing reduced ingress oh prolactin inhibiting
factor(PIF)
2. Reduced pituitary TSH leading to compensatory elevation
of hypothalamic elevation of TRH and resultant stimulation of prolactin release.
Diagnosis:
1. Typical
body configuration, visual field defect and skeletal changes seen on
radiological examination.
2. Serial
levels of basal plasma growth hormone is important in follow up.
Treatment
Surgery or irradiation of the tumor
Substitution therapy
of adrenal ,thyroid and gonodal hormones for resultant hypopituitorism
After surgery.
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