D’YOUVILLE COLLEGE
BIOLOGY 307/607 - PATHOPHYSIOLOGY
Lecture 18 - ENDOCRINE DISORDERS
Chapter 17
1.
Endocrine Glands:
• endocrine vs. exocrine (fig. 17 - 1 & ppt. 1):
- exocrine (= to secrete externally) glands secrete products into a duct system
that conveys products to an external surface, e.g. salivary glands, sweat glands,
digestive portion of pancreas
- endocrine (= to secrete internally) glands secrete products directly into
bloodstream, e.g. pituitary gland, thyroid gland, adrenal gland, etc.; products are
called hormones, which travel in bloodstream to exert effects at distant targets
• neuroendocrine control (fig. 17 - 2 & ppt. 2):
- many endocrine organs are regulated by the nervous system via releasing
or inhibiting hormones secreted by specialized neurons (called neurosecretory cells) of
hypothalamus
- these act upon the anterior pituitary (via a hypophyseal portal system) to
control release of tropic hormones that act on 'target' endocrine glands to regulate
their activities, e.g., thyroid stimulating hormone, adrenocorticotropic hormone
(ACTH)
• hormone receptors & target cell specificity:
- hormones exert their effects by binding to receptors in the target endocrine
gland or target tissue; any tissue lacking the specific receptor for a hormone will be
insensitive to that hormone's effect
- receptors may be intracellular or on the surface of the plasma membrane
(fig. 17 - 3 & ppt. 3) & many tissues may bear receptors (intracellular or membrane
bound) for several different hormones (fig. 17 - 4 & ppt. 4)
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• hormonal effect & second messengers:
- hormone-receptor binding sets in motion metabolic changes within the
target cell that may vary from cell type to cell type; the result of metabolic changes is
the 'hormonal effect'
- some hormones bind to receptors that interact with the cell's DNA, e.g.
steroids, thyroid hormone, whereas most others bind to surface receptors that activate
a 'second messenger' inside the cytoplasm that then instigates the 'hormonal effect' (fig.
17 - 5 & ppt. 5)
• regulation of hormonal levels in blood:
- clearance of hormone from blood (accomplished by target tissue
inactivation, liver inactivation, or kidney excretion) is usually at a constant rate, so
variations in blood level are usually tied to rate of secretion (fig. 17 - 6 & ppt. 6)
- secretion of a hormone is most often regulated by feedback mechanisms, e.g. in
the neuroendocrine axis (fig. 17 - 7 & ppt. 7)
2.
Selected Hormonal Disorders:
• altered endocrine function:
- causes of hypofunction may reside with the endocrine gland or its target
tissue's response (fig. 17 - 8 & ppt. 8); hyperfunction may often result from excessive
secretion
• thyroid disorders
- anatomy & physiology: bowtie-shaped gland located at base of neck (fig.
17 - 9 & ppt. 9); thyroid hormone stored as protein (colloid) within follicles; active
hormone (T3 or T4) is iodinated amino acid derivative (fig. 17 - 10 & ppt. 10)
- hormone secretion regulated by hypothalamo-hypophyseo-thyroid axis (fig. 17 11 & ppt. 11)
- primary hormonal effect is stimulation of numerous aspects of
metabolism, especially overall metabolic rate; many secondary effects derive from
this (table 17 - 1)
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- hypothyroidism: when mild, produces conditions related to lowered
metabolic rate (weakened muscular activity, depressed sex drive, depressed mental
activity, etc.)
- caused by dysfunction of various components of the endocrine axis
(fig. 17 - 15 & ppt. 12) or Hashimoto's thyroiditis, an inflammatory condition which
has an autoimmune basis
- if hypofunction originates in the thyroid itself, swelling of the gland
(goiter) develops from hyperstimulation by endocrine axis
- more severe dysfunction causes myxedema, which produces
exaggeration of above conditions & produces puffiness from widespread edema (due
to deposit of glycoprotein in dermis)
- thyroid hypofunction in newborns causes cretinism, a severe
disturbance of various aspects of development
- hyperthyroidism (thyrotoxicosis): multiple effects from accelerated
metabolism, e.g., excessive metabolic heat production, weight loss, neural irritability,
accelerated heart rate & possible dysrhythmias, muscle atrophy from protein
breakdown (table 17 - 4)
- signs include exophthalmos & toxic goiter
- Graves' disease: mostly affecting young women, is an autoimmune
condition that involves autoantibodies against TSH receptors, which stimulate thyroid
hypersecretion
• pancreatic islet disorders
- endocrine pancreas: isolated islands of endocrine tissue (islets) are
surrounded by much more abundant exocrine tissue; two main cell types secrete
insulin ( cells) & glucagon ( cells) (fig. 17 - 17 & ppt. 13)
- functions of insulin: promotes function of glucose carriers in cell
membrane to facilitate glucose uptake; also stimulates glycogenesis & lipogenesis in liver,
to promote glucose & fat storage
- glucagon: along with growth hormone (from pituitary) & epinephrine
(from adrenal medulla), glucagon acts antagonistically to insulin (table 17 - 5)
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- diabetes mellitus: two main forms -- IDDM (juvenile onset or type I) &
NIDDM (maturity onset or type II) (fig. 17 - 20 & ppt. 14)
- IDDM: arises as autoimmune condition with probable genetic
predisposition (fig. 17 - 18 & ppt. 15); resulting insulin deficiency produces
hyperglycemia, glucosuria, diuresis, increased gluconeogenesis and ketogenesis
(from lipolysis & oxidation of FFA for energy) (fig. 17 - 19 & ppt. 16)
- NIDDM: most often a genetically based defect of  cells accompanied by
progressive insulin resistance in target tissues (exacerbated by obesity); progressive
deterioration may involve protein (amylin) deposition (fig. 17 - 21 & ppt. 17)
- chronic effects of DM: elevated glucose leads to incorporation into
protein (glycated protein); resulting 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 &
ppt. 18)
• adrenal disorders
- adrenal glands: located upon superior pole of kidney (fig. 17 - 23 & ppt.
19), divided into medulla (secretes catecholamines) (fig. 17 - 26 & ppt. 20) and cortex
(secretes corticosteriods) (fig. 17 - 24 & ppt. 21); regulation involves hypothalamohypophyseo-adrenal axis (fig. 17 - 25 & ppt. 22), renin-angiotensin system & sympathetic
nervous system
- general adaptation syndrome (GAS): response to stressors entails adrenal
responses to prepare body for dealing with stressful situation (fig. 17 - 27 & ppt. 23)
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- disorders of cortical hypersecretion: include Cushing's syndrome (table
17 - 11), hyperaldosteronism, & adrenal virilism
- Cushing's patients suffer from hypertension (excess aldosterone),
obesity & puffiness from lipid deposits in face & eyelids (elevated lipids due to
excess cortisol), muscle weakness & bone loss (protein catabolism due to excess
cortisol) and masculinizing syndrome in women (due to excess adrenal androgens)
- disorders of cortical hyposecretion: main condition is Addison's disease,
characterized by inability to effectively deal with stress (response with nausea,
vomiting, fever, electrolyte and water losses, with risk of shock); pigmentation
disorder is related to excessive levels of ACTH from the feedback system
• parathyroid disorders
- located on posterior surface of thyroid gland, parathyroids regulate
calcium balance (fig. 17 - 29 & ppt. 24)
- hypersecretion leads to excessive bone loss (vulnerability to fracture),
hypercalcemia (kidney stones, metastatic calcification, muscular cramps)
- hyposecretion leads to hypocalcemia (muscular cramps, tetany in
muscles, which may lead to respiratory failure)
• pituitary disorders
- pituitary (hypophysis): located immediately inferior to hypothalamus in
sella turcica of sphenoid bone (fig. 17 - 30 & ppt. 25)
- anterior lobe, controlled by releasing/inhibiting hormones, secretes several
tropic hormones responsible for regulating other endocrines (thyroid, adrenals,
gonads) as well as prolactin and growth hormone
- posterior lobe, represents site of release for hormones elaborated by NS
cells of hypothalamus (oxytocin & antidiuretic hormone)
- hypersecretion usually results from benign tumor resulting in various
conditions involving hyperactivity of endocrine targets, e.g., Cushing's disease from
hyperstimulated adrenal cortices; prolactin excess may produce impotence in males,
and breast milk production (galactorrhea) & menstrual disturbances in females;
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growth hormone excess is responsible for gigantism (when present in preadult
years) or acromegaly (when present in adults)