Download EN-2-12-99

Endocrine
(2-12-99)
Hypopituitarism:
Causes: Ischemic necrosis
Ex - postpartum necrosis (Sheehan’s Syndrome)
Pituitary tumors (most common cause)
Aneurysms of intracranial carotid artery
Thrombosis
Infectious disease
Ex – pyrogenic abscess, TB, syphilis
Infiltrative disease
Ex – hymosiderin, amylloid
Immunologic (autoimmune)
Iatrogenic (head/neck surgery – poor prognosis)
Metabolic (especially renal failure, azotemia)
Most Common Cause = Pituitary tumor
A tumor may: Compress the gland within the sella
Invade the gland (destroy it)
Hemorrhage (pituitary apoplexy)
Causes of Secondary Hypopituitarism:
Destruction of the pituitary stalk
Hypothalamic disease
“Worst Case” Form = Panhypopituitarism = complete loss of pituitary function
The clinical features develop within a matter of hours or days
 DEATH
Often hard to recognize initially.
Often presents as a dysfunction of the target tissue (ex – adrenals)
Clinical Features:
ACTH Deficiency
TSH Deficiency
LH and FSH Deficiency
GH Deficiency
Prolactin Deficiency
ACTH Deficiency: Weakness
Postural hypotension
Malaise
Dehydration
Vomiting
Nausea
Hypothermia
Loss of axillary hair
Loss of pubic hair
TSH Deficiency:
Dry skin
Pallor
Mental slowing
Bradycardia
Hoarseness
Constipation
Reduced or absent menstruation
LH and FSH Deficiency:
Females: Amenorrhea, breast atrophy, dry skin
Age, duration, and magnitude dependent
Males: Reduced testicular size, loss of libido
GH Deficiency:
Kids: Total or partial impairment of growth
Adults: There is a normal, age-related decline
But – some adults do have the syndrome
 hyperlipidemia, osteoporosis
(appear to be correctable)
premature wrinkling and aging
increased body fat
Prolactin Deficiency: Results only in the absence of post-partum lactation
General Features:
Skin – decreased turgor and a waxy character (also a thinness)
Periorbital wrinkling (“premature aging”) (effects on the skin)
Mild anemia (normo/normo)
This is refractory to other forms of treatment
Mental slowing, apathy, delusions, paranoia, psychosis
(not always easy to appreciate this in the elderly)
Ex – Loss of the ability to do mental calculations and to concentrate
Short-term memory loss
Depression
Diagnosis: Do a direct assay of individual hormone levels.
This will show low to absent hormone concentrations.
If it’s a mild or partial hypopituitarism, it may be hard to tell if the clinical
features are due to a primary pituitary dysfunction or to a target organ
of the pituitary’s hormones.
Pituitary
Reduced T4
Reduced TSH
2o
Vs.
Thyroid
Reduced T4
Increased TSH
1o
 “Hypothyroid”
NOTE: Expect 4 of these on Quiz 2 (to differentiate 1o, 2o, 3o forms)
Hyperpituitarism:
Very distinct
Have subgroups of diseases
(with names for the disorders)
Except in cases of rare hormone-secreting tumors, hyperpituitarism usually involves
overproduction of only a single hormone  a single set of symptoms
The response is less dose-dependent
The clinical picture is usually distinct:
1o = a functional tumor
produces a biologically active substance
2o = most often caused by altered feedback
ex - hyperprolactinemia
due to increased estrogen secreted during pregnancy
OR an ovarian tumor
ACTH hypersecretion in response to hypofunction of the adrenals
Ex – Addison’s – bronze color due to 1o adrenal disease
TSH hypersecretion in response to hypofunction of the thyroid
1o GH Hypersecretion:
If it occurs prior to epiphyseal closure  gigantism
(due to the prolonged growth period due to the delayed epiphyseal closure)
If it occurs after epiphyseal closure  acromegaly
(disproportional tissue/bone/cell growth)
Acromegaly: Thickened skin
Increased pigmentation
Visceromegaly (large organs – spleen, etc)
Carpal Tunnel Syndrome
Thyroid enlargement
Arthropathy
Large hands/feet
Increased head size ( larger hat size)
Dx Criteria for GH Hypersecretion:
Clinical signs and symptoms
Elevated GH levels
But not absolute – can be suppressed by hyperglycemia
Normal: Increased glucose  decreased GH
Definitive: GH levels not suppressed by glucose
1o ACTH Hypersecretion:
Cushing’s Disease
90% of these result from a functional tumor
(ex – basophilic adenoma or bilateral hyperplasia)
Clinical:
Same as for adrenocortical adenoma
Most common in 30-60 year-old women
The disease causes a 2o hypercortisolism
Syndrome:
Hypercortisolism
due to exogenous cortisol administration or an overproduction
by the adrenals
Cushing’s:
Disease
Increased cortisol
Increased ACTH
Clinical:
Vs.
Syndrome
Increased cortisol
Decreased ACTH
Central obesity
Abdominal fat
Hypertension
Amenorrhea
Hirsutism
Muscular atrophy
Weight gain
Osteoporosis and compression fractures
Increased capillary fragility  increased skin lesions
Reduced wound healing
Hyperglycemia
Increased skin pigmentation
__??__
Dx: Typical clinical findings
Elevated plasma cortisol (in 50% of people)
Elevated urinary free-cortisol (in 85-95% of people)
(unbound cortisol)
Plasma ACTH elevated or inappropriate for the cortisol levels
Differential:
Adrenal tumor
Ectopic ACTH production
Prolactin Hypersecretion: Pharmacologic agents
CNS disorders
Inflammation/infections
Trauma
Neoplasms
Pituitary tumors
Idiopathic
Most common form of pituitary hyperfunction.
Most often due to a functional adenoma of the pituitary.
Present in at least 25% of infertile women.
Females: Oligomenorrhea or amenorrhea
Lactation
Mild hirsutism
Infertility
Males: Impotence
Decreased libido
Lactation (heroin is also a powerful stimulator of this)
Dx: Elevated prolactin levels
15 to 20 ng/ml to 10,000 ng/ml
if < 200 ng/ml:
if tumor:
TEST:
25 to 30 questions
Next Wednesday
1st hour, in the GYM
almost never due to a tumor
5000-10,000 ng/ml