ENDOCRINE DISORDERS
Why Are We Learning About Endocrine Disorders?
 Disruption of endocrine
systems tend to effect
numerous systems
throughout the body
 Hormones 
Communication
networks
 Influences how your heart
beats, bones & tissues
grow, pregnancy, stress
responses
 Contributes to diabetes, thyroid
disease, growth disease, sexual
dysfunction, etc.
 Thyroid condition = bulging eyes
Remember:

Endocrine disorders
influence many tissues &
organs (e.g., Metabolic
Syndrome)

Increases & decreases in
function lead to symptoms &
consequences

Tests are used to
determine
dysregulation

Treatments attempt to
restore homeostasis
Endocrine System:
 The endocrine system uses
hormones for
communication between
cells & tissues
 “Endocrine” denotes an
internal secretion of
biologically active
substances
 Subject to complex regulatory mechanisms that govern
o Hormone synthesis
o Release
o Transport
o Metabolism
o Delivery to the interior of the target cells
o Expression & activity of the hormone receptor & its downstream signaling machinery
Basic Endocrinology:

Endocrine:
hormones
entering the
blood stream &
acting on
distant
receptors
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Paracrine: hormones do

not enter the blood stream,
but act locally
Autocrine: hormones act
on the cells which produced
them
Hormone Receptors:
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Hormones can be water-soluble or lipidsoluble
Receptors are located on cell surface or
inside of the target cell
Diffuse into the cell to act because it is
lipid soluble & your member allows lipid
soluble in
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Hormones are divided into 3 categories:
o (1) Amines (from amino acids) - catecholamines
o (2) Peptides & Proteins – string together amino acids, you’ll
first get short proteins (peptides)
o (3) Steroids – cortisol, sex steroid hormones (estrogen,
testosterone)
Cells will only react if
they have the receptor
for the hormone
Different cells will
respond differently to
the effects of the same
hormone
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
Down-regulation vs. up-regulation of
receptors
o Down-regulation = when there is too
much of that hormone
o Up-regulation = where there is not
enough hormone; it makes more
receptors so it can catch every piece
of hormone it can
Classes of Hormones:
Amines/Amino
Acids:
 Dopamine
 Epinephrine
 Norepinephrine
 Thyroid Hormone
Peptides/Proteins: (Most
prominent category of hormones)
 Corticotrophin Release Hormone
(CRH)
 Thyrotropin-Releasing Hormone
(TRH)
 Insulin
Peptides/Proteins: (Most
prominent category of
hormones)
 Growth Hormone (GH)
 Luteinizing Hormone (LH)
 Follicle-Stimulating Hormone
(FSH)
Hypothalamus & Pituitary Gland:
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Hypothalamus = Master Coordinator
Pituitary = Master Gland
o Anterior Pituitary: hypothalamic stimulatory hormones regulate
o Posterior Pituitary: vasopressin/ADH & oxytocin synthesized in
hypothalamus
GH, TCH, ACTH, DSH are released to target hormone which releases
another hormone
Deficits in oxytocin will affect uterine contractions during childbirth
ACTH = stress system
LH & FSH = reproductive system
Stimuli interact with hypothalamus which releases primary hormone
& have negative feedback
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Steroids:
 Glucocorticoids
 Estrogens
 Testosterone
 Progesterone
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The negative feedback shuts it off. The hormone goes back & acts on the brain & pituitary gland to shut it off
Assessment of Endocrine Function & Hormone Levels:
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Autoantibody: is an antibody (a
type of protein) produced by the
immune system that is directed
against one or more of the
individual’s own proteins
o Many autoimmune disease,
notably lupus erythematous,
are caused by such
autoantibodies
Insulin Autoantibodies:
o Graves Disease
o Hashimoto Thyroiditis
o Addison Disease
Primary Cause: gland
producing hormone
 Originate in target
gland responsible
for producing the
hormone
 Cortisol = adrenal
glands (so if there
is a tumor at the
adrenal glands you
would say it’s a
primary cause)
 Hypofunction
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Stimulation Test: do something
that normally stimulates the
release of the hormone & look
for the release. See if not enough
or too much is being released &
compare it to normal levels
o Thyrotropin Releasing
Hormone
If you administer a hormone
that’s supposed to turn on the
system, but you take blood work
& its not turning on the system,
you know there is a hypofunction
problem
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Urine Test:
o Measures a hormone or metabolite
Genetic Tests:
o RET proto-oncogene in endocrine
neoplasia syndrome (endocrine
tumors)
Imaging:
o Isotopic & Nonisotopic
o MRI-hypothalamus, pituitary
o CT-adrenal, abdominal lesions
o Ultrasound-thyroid, parathyroid
o PET-endocrine tumors
Endocrine Disorders:
Secondary Cause: defective stimulating/releasing hormones
(pituitary)
 Target gland is normal “optimum”; function is altered by
defective levels of stimulating hormones or releasing
hormones
 Level of the pituitary
 Tumor at the level of the pituitary that affected ACTH
release so now you have too little ACTH release you’re not
going to have enough cortisol. So your blood work will show
whether its primary or secondary cause
 Removal of thyroid gland produces a primary deficiency;
removal of pituitary gland eliminates TSH stimulation of
thyroid, so secondary deficiency
Tertiary Cause: damage to
hypothalamus
 If the hypothalamus was
damaged, both pituitary and
target gland were
understimulated
 Top of the chain
 Brain injury, tumor, or some
other malfunction of the
hypothalamus
 Tertiary adrenal insufficiency =
problem was in the
hypothalamus
 Hyperfunction
Pituitary Gland:
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In adults, the most
common cause of
hypothalamic-pituitary
dysfunction is pituitary
adenoma
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In children, the most common cause of pituitary
dysfunction is hypothalamic tumors that manifest with
signs of pituitary hyposecretion
o Short stature due to low growth hormones levels &
delayed puberty due to gonadotropin deficiency
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Assessment: assess
anterior pituitary
hormone levels; MRI, CT
(looking for tumors in
hypothalamus &
pituitary)
Disorders of the Pituitary Gland:
Hyperpituitarism:
 Increased secretion of pituitary hormones
 Most common cause is adenoma arising from anterior
pituitary
 Lactotrophic adenomas are most frequent type of
hyperfunction pituitary adenoma (30%)
 Hyperprolactinemia inhibits the pulsatile secretion of
luteinizing hormone (LH)
o Amenorrhea, Galactorrhea, Infertility in females
Hypopituitarism:
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LH/FSH deficit 
Hypogonadism 
Amenorrhea, decreased
libido, erectile dysfunction
How would you treat LH/FSH
deficiency?

TSH deficit
 cold
intolerance,
dry skin,
mental
dullness
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Hypopituitarism:
 Decreased secretion of pituitary hormones
 Causes hypofunction of secondary organs
 ~70-90% of anterior pituitary must be destroyed before
clinically evident. Gradual, may take 10-20 years
 Cause may be congenital or from destruction of anterior
pituitary
 Classic order = GH, LH, FSH  TSH  ACTH 
prolactin
ACTH deficit  most serious
endocrine deficiency. Causes
secondary adrenal
insufficiency  weakness,
nausea, anorexia, fever &
postural hypotension
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Treatment:
o (1) Treat underlying
cause
o (2) Hormone
Replacement (cortisol
replacement with ACTH
deficiency)
Growth & Growth Hormone
Disorders:
 GH is essential for normal body growth &
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maturation
Regulated by GH releasing hormone (GHRH),
which increases GH & somatostain, which inhibits
GH release
GH is stimulated by hypoglycemia, fasting,
starvation, increased blood amino acids, stress (ex.
Trauma, heavy exercise, emotional stress)
GH is inhibited by increased glucose, free fatty acids, cortisol, & obesity
GH Deficiency  short stature or dwarfism
GH Excess  Gigantism, Enlargement of Heart, Metabolic Disturbances
o Prolonged GH excess increases blood glucose levels, & ultimately leads to insulin resistance
GH contributes to regulation of growth & metabolic functions
GHIN (GH-inhibiting hormone) inhibits the release of GH  Somatostatin
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Growth Hormone Deficiency (Short Stature):
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Attained height is
well below the 3rd
percentile
Assess GH & IGF-1
levels (by
stimulating with
insulin, GHRH,
levodopa or
arginine)
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Primary & Secondary
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GH deficiency, though a
number of causes for
short stature
Idiopathic GH deficiency
lack the hypothalamic
GHRH, normal

somatotropes
Pituitary tumors or agenesis
of the pituitary, lack of
somatotropes
o Agenesis – lack or failure
of development (as of a
body part)
GH replacement is
treatment

Obvious by 1-2 years old
o Normal intelligence
o Short stature
o Obesity with immature
facial features
o Delay in skeletal
maturity
o Delayed puberty
Growth Hormone Excess (Gigantism):

GH excess occurring
before puberty & the
fusion of the epiphysis of
the long bones results in
gigantism

GH excess in adulthood
Mean age 40-45years
Most common cause-GH
secreting adenomas
Enlarged hands/feet
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Excessive secretion of
GH by somatrope
adenomas
Adenomas – caused by
benign tumors
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High levels of IGF-1 stimulate
excessive skeletal growth
Abnormal lengthening of the
human form
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Treatment:
remove or
treat the
adenoma
Growth Hormone Excess (Acromegaly):
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Soft tissues and short bones
continue to grow (not long
bones)
Treatment:
o Correct metabolic
abnormalities
o Removal of tumor
o Somatostatin analogs
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Broad/bulbus nose,
protruding jaw,
slanting forehead
Vertebral changes
leading to
hunchback
Thyroid Gland:
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More than 12% of US population will develop a thyroid condition during their
lifetime
o ~20 million Americans have some form of thyroid disease…60% are unaware
Women are 5-8x more likely than men
o 1 in 8 women will develop a thyroid disorder in their lifetime
Most thyroid cancers respond to treatment
Thyroid disease may increase risk for CVD, osteoporosis, and infertility
Most thyroid diseases are life-long conditions that can be managed with medical attention
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Organs (i.e. heart) are
enlarged
GH-induced insulin
resistance (50-70%
have glucose
intolerance)
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The causes of thyroid problems are largely unknown
Prevalence and Impact of Thyroid Disease:
o More than 12 percent of the U.S. population will develop a thyroid condition during their lifetime.
o Up to 60 percent of those with thyroid disease are unaware of their condition
Most thyroid cancers respond to treatment, although a small percentage can be very aggressive
Undiagnosed thyroid disease may put patients at risk for certain serious conditions, such as cardiovascular diseases,
osteoporosis and infertility
Pregnant women with undiagnosed or inadequately treated hypothyroidism have an increased risk of miscarriage, preterm
delivery, and severe developmental
Function:
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Iodine is needed for
proper thyroid function
TRH is stimulated by cold
temperature, sleep, and
stress
Most major organs are
affected by thyroid
hormone
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Administration of T4
o Increase metabolic rate by 60-100%
o Enhance cardiovascular and respiratory
function
o Enhance gastric motility
o Increase appetite
o Weight loss
o Lead to muscle tremor
Disorders of the Thyroid Gland:
Hyperthyroidism:
• Increased thyroid
hormone
• Fine hair
• Nervousness, restlessness,
emotional instability,
insomnia
• Exophthalmos
• Muscle wasting
• Fine tremor
• Weight loss, increased
appetite
• Hypermetabolic state
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To test thyroid function:
o Measure T3, T4, TSH
levels
o Measure thyroid
autoantibodies
o 123I uptake, ultrasound
o FNA
Goiter:
Hypothyroidism:
• Decreased thyroid
hormone
• Coarse, brittle hair
• Lethargy and impaired
memory
• Puffy face
• Large tongue
• Muscle weakness
• Slow pulse
• Weight gain, peripheral
edema
• Hypometabolic state
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Abnormal enlargement of thyroid gland (not cancer)
Most common cause is lack of iodine in the diet (2
billion people).
Can be due to over or under production of thyroid
hormones to the nodules in gland
Symptoms:
o Swelling at base of neck
o Tight feeling in throat
o Coughing/hoarseness
o Difficulty breathing/swallowing
Also associated with Graves’ Disease and Hashimoto’s
Disease
Hyperthyroidism:
Graves’ Disease:
• Autoimmune Disorder characterized by
abnormal stimulation by thyroid stimulated
antibodies that act through TSH receptors
• Opthalmopathy, diffuse goiter, and increase in
•
•
Onset usually between 20-40 years old, women are 5x more likely
than men
Treatment:
o Removal of thyroid gland
o Radioactive Iodine
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sympathetic nervous system activity
o Surgery
• Bulging eyes, heat intolerance, anxiety
o Drugs to decrease thyroid function
Thyroid Storm:
• Rare, but extreme and life-threatening form of thyrotoxicosis
• Often precipitated by stress (infection), diabetic ketoacidosis, physical or emotional trauma or manipulation of
hyperactive thyroid gland during thyroidectomy.
• High fever (105°-106°), tachycardia, congestive heart failure, angina, agitation, restlessness, delirium.
• High mortality rate (90%)
• Treatment:
o Peripheral cooling with cold packs
o Supportive fluids (i.e. glucose)
o Beta-blockers
o Glucocorticoids
o Drugs to inhibit thyroid hormone synthesis & release
Hypothyroidism:
Treatment:
o Thyroid Hormone Replacement, most often T4
o Look for normalization of TSH
Congenital Hypothyroidism:
 Affects 1 in 5000 infants, newborn screening
 Lack of thyroid gland or abnormal synthesis of thyroid hormone or
deficient TSH secretion
 If untreated, causes mental retardation and impaired physical growth
Hashimoto Thyroiditis:
 An autoimmune disorder, thyroid gland may be destroyed
 Female to male ratio 5:1
 Detected by testing for anti-thyroid peroxidase antibodies
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Adrenal Gland:
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Medulla secretes epinephrine and
norepinephrine
Cortex secrets glucocorticoids,
mineralocorticoids and adrenal androgens
Cortisol release is influenced by stress,
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Acquired Hypothyroidism:
 Older children and adults
 Results from destruction or
dysfunction of the thyroid gland
(primary), or secondary disorder
caused by impaired pituitary
function, or tertiary disorder caused
by hypothalamic dysfunction
 Primary hypothyroidism may be
caused by thyroidectomy or ablation
of the gland with radiation, antithyroid drugs or large amounts of
iodine or radioactive iodine, or
iodine deficiency
Cortisol levels fluctuate throughout the day/night. Highest levels
are in early morning.
Stimulates gluconeogenesis by the liver
Required for effective anti-inflammatory action
Treatment with adrenal cortical hormones may alter behavior
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infection, pain, hypoglycemia, sleep,
hemorrhage & trauma
Adrenal cortical function is essential for life.
Loss of function is fatal within 4-14 days
Insufficiency is related mainly to
mineralocorticoid deficiency and
glucocorticoid deficiency

(abnormal to psychotic)
To test adrenal function: Blood levels of cortisol, aldosterone,
ACTH; 24h urine for metabolic end products; overnight
dexamethasone suppression test; insulin-induced hypoglycemic
test
Disorders of the Adrenal Gland:
Adrenal Excess:
 Hypercortisolism
 Altered deposition of fat:
protruding abdomen and
increased subclavicular fat
pad (buffalo hump)
 Glucose intolerance in 75%
 Diabetes in 20%
 Suppression of
inflammatory/immune
responses
 Hirsutism, acne, menstrual
irregularities
 “Moon” Face
 Extreme emotional
“swings”
o Euphoria to psychosis
Adrenal Insufficiency:
• Primary = Addison’s
Disease, destruction of
adrenal gland
• Secondary = disorder of
HPA system
• Anorexia/weight loss
• Fatigue/weakness
• GI symptoms, nausea
• Hyponatremia;
Hyperkalemia
• Hyperpigmentation (body
creases, mucous
membranes, etc.)
• Hypoglycemia
• Rapid withdrawal of
glucocorticoids, due to
suppression of HPA
adrenal atrophy
Adrenal Excess (Cushing Syndrome):
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Hypercortisolism
3 forms
1. Pituitary form (excess production of ACTH from tumor, Cushing disease)
2. Adrenal form (adrenal tumor, excess cortisol)
3. Ectopic form (non-pituitary ACTH secreting tumor)
Loss of diurnal fluctuations in cortisol secretion
5-25 cases occur per million people per year
It is most prevalent in adults between the ages of 20-50
Women account for 70% of cases
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Treatment:
o Surgical
o Irradiation
o Pharmacologic
Adrenal Insufficiency (Addison Disease):
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Adrenal cortical hormones are deficient
ACTH levels are elevated
o WHY?
Autoimmune destruction is most common cause
Before 1950, tuberculosis was the most common cause
Can be caused by HIV/AIDS
Not apparent until 90% of adrenal cortex is damaged
Mineralocorticoid deficiency increases excretion of sodium, chloride, water, and decreased excretion of potassium,
can lead to cardiovascular collapse
Abnormal appetite for salt
Poor tolerance to stress
Treatment = just trying to get them back to that normal
balance
o Chronic Disease
o Life-long Hormone Replacement
o Higher doses given during periods of stress
Cortisol is not able to do its main function
Maintaining blood glucose levels
For our muscles, our brain
If you don’t have it = weakness, will feel like crap
basically
Adrenergic diseases = caused by healthcare professionals
treatment
Giving someone too much replacement cortisol
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