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D’YOUVILLE COLLEGE
PMD 604 - ANATOMY, PHYSIOLOGY, PATHOLOGY II
Lecture 9: Endocrine Pathology
G & H chapters 75 - 78 & Robbins chapter 20
1.
Origin of Endocrine Disorders:
• hypofunction: deficient hormonal responses may result from:
- hyposecretion from agenesis or faulty gland development or a genetically
based
disorder of hormone synthesis
- malignant (highly anaplastic) tumors of glands
- glandular damage from infection, injury (infarction), autoimmune attack,
atrophy from lack of tropic hormone stimulation, excessive surgical removal
of a neoplasm
• insensitivity of target tissue (hormone resistance):
- due to genetically based failure of target tissue metabolism
- autoimmune attack on hormone receptors
• hyperfunction: excessive hormonal effects may result from:
- hypersecretion from a tumor (benign or minimally anaplastic)
- breakdown of negative feedback control
- ectopic secretion (by tumors in nonendocrine tissues, e.g., lung neoplasm)
- deficiency of normal clearance of hormone from bloodstream, e.g., sequel
to liver disease
2.
Disorders of Anterior Pituitary:
• hypopituitarism: anterior lobe deficiency often involves deficiencies in
the
various hormone-producing cells (panhypopituitarism)
- deficiency of a particular tropic hormone results in target organ
deficiency (hypothyroidism, hypoadrenalism or deficits in sexual function)
- deficiency of prolactin-producing cells may cause failure of post partum
milk production
- deficiency of growth hormone in preadolescents produces dwarfism
- causes include:
- non-functioning adenoma, damage from ischemia, radiation or surgery,
or inflammatory conditions (e.g. tuberculosis); hypothalamic origin would be
indicated if
there is an accompanying posterior lobe dysfunction
• hyperpituitarism: anterior lobe hyperfunction involves adenomas of the
various hormone-producing cells, but usually only one cell type in any given
tumor
(figs. 20 - 1, 20 - 4 & ppt. 1); tumors may be functional (hormone-producing)
or silent
(no hyperfunction)
PMD 604, lec 10
- p. 2 - gigantism & acromegaly result from hypersecretion of growth hormone
from a tumor; gigantism is produced by elevated GH acting on long bone growth
(epiphysial discs); after adolescence (discs ossified), acromegaly (fig. 75 8 & ppt. 2)
results (coarse bony features due to excessive thickening); also possible
kyphosis
• pituitary tumors: may cause visual impairment due to pressure on optic
chiasma or headache due to increased intracranial pressure
PMD 604, lec 10
2.
- p. 3 Disorders of Posterior Pituitary: clinically important disorders involve
ADH hyposecretion or hypersecretion
• hyposecretion of ADH: caused by anaplastic tumor, infection, or trauma of
hypothalamohypophysial tract
- results in excessive urine output (diabetes insipidus); danger of
dehydration
unless sufficient polydipsia (increased water consumption) can compensate for
the
water loss
• hypersecretion of ADH: produced from non-endocrine tumors, or may result
from hypothalamic disturbance, neurohypophysial infarction or other brain
traumas
- resulting syndrome (SIADH - syndrome of inappropriate ADH release)
results from excessive water retention by kidneys; produces excessive
extracellular
fluid, with possible hyponatremia & osmotic swelling of brain tissues
3.
Disorders of Thyroid:
• Grave's disease: hypersecretion of thyroid hormones resulting from
autoantibodies that stimulate TSH receptors (TSI = thyroid stimulating
immunoglobulins); low TSH levels result from excessive inhibition by elevated
level of T3
&/or T4
• toxic goiter: hyperplasia of thyroid due to adenoma that secretes elevated
levels of thyroid hormones independent of usual TSH control mechanism;
depressed
TSH levels cause recession of normal thyroid tissue while tumor thrives
• signs of hyperthyroidism: exophthalmos (fig. 76 - 8 & ppt. 3) results from
edema & hyperplasia of retro-orbital tissues; other effects result from
elevated
metabolic rate (muscular wasting, extreme nervousness, hyperventilation,
tachycardia, insomnia, heat intolerance & excessive sweating)
• Hashimoto's thyroiditis: chronic granulomatous inflammation with
hyposecretion due to autoimmune condition (fig. 20 - 7 & ppt. 4); lack of
feedback
control of TSH leads to goiter (with reduced functional follicles)
• endemic goiter: caused by dietary iodine deficiency with resultant failure
of
thyroid hormone synthesis
- lack of inhibition of the endocrine axis results in elevated TSH &
hyperstimulation of thyroid
• idiopathic (non-toxic) goiter: impairment of iodine metabolism with
resultant failure of thyroid hormone synthesis
- lack of inhibition of the endocrine axis results in elevated TSH &
hyperstimulation of thyroid
• cretinism (ppt. 5) afflicts newborns (impaired growth & development)
PMD 604, lec 10
- p. 4 • myxedema (fig. 76 - 9 & ppt. 6) afflicts adults (caused by edematous
swelling
associated with glycoprotein deposit in dermis)
• signs of hyperthyroidism: fatigue, muscular sluggishness, mental
sluggishness, cardiac disturbances (HR & CO depressed), somnolence, weight
gain &
atherosclerosis
PMD 604, lec 10
4.
- p. 5 Disorders of Adrenal Cortex:
• cortical
hypersecretion: elevated levels of normal corticosteroids
- Cushing's syndrome: elevated glucocorticoid levels may result from
chronic ACTH or glucocorticoid therapy (iatrogenic Cushing's), an ACTH tumor
of
pituitary, an adrenal cortical tumor, or ectopic secretion of ACTH by tumor
of nonendocrine source, e.g. lung neoplasia (fig. 20 - 35 & ppt. 7)
- results in hyperglycemia (inhibited glucose utilization & stimulation of
gluconeogenesis in tissues) that may provoke 'adrenal diabetes' (not very
responsive to
insulin)
- Cushing's patients suffer from hypertension (mineralocorticoid action
of excessive cortisol), obesity (due to elevated lipids) & puffiness from
lipid deposits
in face (fig. 77 - 10 & ppt. 8), eyelids & upper torso ('moon face' &/or
'buffalo torso'),
muscle weakness & bone loss (protein catabolism due to excess cortisol),
masculinizing syndrome (hirsutism & acne) & menstrual disorders in women (due
to excess adrenal androgens) and susceptibility to infections (antiinflammatory action
of cortisol)
- hyperaldosteronism: tumor of aldosterone producing cells; main effect is
hypertension due to sodium and water retention
- adrenogenital syndromes: arise from excessive adrenal androgens
resulting from 'virilizing' carcinoma or congenital adrenal hyperplasia; also
may arise
with Cushing's
- masculinization of traits in females (hirsutism, menstrual disorders,
ambiguous genitalia); precocious sexual maturation in males (fig. 77 - 11 &
ppt. 9)
• cortical hyposecretion (rare): main condition is Addison's disease
(glucocorticoid & mineralocorticoid deficiency)
- caused by autoimmune destruction of cortex or sequel to TB, AIDS fungal
infection or metastatic cancer
- characterized by gastrointestinal disorders (nausea, vomiting, anorexia),
sodium & water losses (with risk of shock - severe hypotension), also
hyperkalemia
(polarized membrane disturbances) & acidosis; pigmentation disorder is
related to
excessive levels of ACTH that stimulate melanocytes (fig. 77 - 9 & ppt. 10)
- failure of stress response (low glucocorticoid levels) may exacerbate above
conditions
5.
Disorder of Endocrine Pancreas:
• diabetes mellitus (DM): two main forms -- IDDM (insulin dependent DM,
juvenile onset or type I) & NIDDM (non-insulin dependent DM, maturity onset
or type
II) (fig. 17 - 20)
- IDDM: arises as autoimmune condition probably provoked by
environmental assaults &/or genetic predisposition; lymphocytes & macrophages
attack 'self antigens' of  cells resulting in their destruction; insulin
deficiency
produces increased gluconeogenesis & glycogenolysis leading to hyperglycemia,
PMD 604, lec 10
- p. 6 glucosuria, polyuria & polydipsia; ketogenesis (from lipolysis & oxidation of
FFA
for energy) may lead to ketoacidosis (fig. 17 - 19)
- NIDDM (fig. 17 - 21): most often a genetically based defect, exacerbated
by obesity (products of adipocytes impede insulin receptor function), causing
insulin
resistance in target tissues accompanied by inadequate insulin response &
ensuing
progressive deterioration of  cells
- may involve protein (amylin) deposition
- chronic effects of DM: elevated glucose leads to non-enzymatic
glycosylation of protein (glycated protein, e.g., hemoglobin A1C)
- resultant complications include microangiopathy, which may
interfere with blood supply to various tissues (results in impaired healing,
kidney
damage, damage to lens & retina of the eye, hyperlipidemia and consequent
atherosclerosis and neuropathies)
- diagnosis: usual procedure is a glucose tolerance test (fig. 17 - 22)
- treatment: insulin injections and scrupulous dietary management of sugar
and caloric intake (IDDM); regular exercise, weight loss & sulfonyl urea
(NIDDM)
PMD 604, lec 10
5.
- p. 7 Disorders of Parathyroid:
• hyperparathyroidism: occurs more frequently in females (3:1)
- produces loss of bone mineral matrix, which leads to hypercalcemia;
hypercalcemia may cause kidney stones, muscular cramps, depressed nerve
function,
pain & metastatic calcification
- results from benign or malignant tumor (usually confined to one gland)
or from hyperplasia (usually affects all four glands); hyperplasia
characterizes
secondary hyperparathyroidism (sequel to renal failure & loss of calcium in
urine, or
sequel to GI malabsorption or to vitamin D deficiency)
• hypoparathyroidism: rarely occurring diminished output of PTH
- formerly a consequence of inadvertent surgical removal of parathyroids
(during thyroidectomy); autoimmune attack of parathyroid tissue is now the
more
important cause
- results in hypocalcemia (due to excessive renal loss of calcium), which, in
turn, causes muscular tetany (may lead to respiratory failure), weakness &
altered
mental processes, including seizures
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