Endocrine glands include

the hypothalamus, pituitary,

thyroid, parathyroids,
adrenals, pancreas, ovaries,
testes, and pineal gland

Exocrine glands are not

part of the endocrine system.
They secrete their substances
into ducts that then empty
into a body cavity or onto a
surface.

• Hormones are
chemical substances
produced in the body
that control and
regulate the activity
of certain target cells
or organs.
• Hormones act only on
cells that have
receptors specific to
that hormone, since
the shape of the
receptor determines
which hormone can
react with it.
• This is an example of
the lock-and key
model of biochemical • Simple Feedback o Negative feedback
reactions. relies on the blood level of a hormone or
other chemical compound regulated by the
• Lipid-soluble hormones are synthesized hormone (e.g., glucose).
from cholesterol and are produced by the o Positive feedback is also used to
adrenal cortex, sex glands, and thyroid. o regulate hormone synthesis and
Lipid-soluble hormones (steroids, thyroid) release. The female ovarian hormone
are relatively small molecules that estradiol operates by this type of
cross the target cell membrane by feedback.
simple diffusion. • Nervous System Control: endocrine
• Water-soluble hormones (insulin, growth glands are directly affected by the activity
hormone [GH], and prolactin) have receptors of the nervous system. Pain, emotion,
on or in the cell membrane. o Water-soluble sexual excitement, and stress can
hormones circulate freely in the blood to their stimulate the nervous system to modulate
target tissues, where they act. hormone secretion.
o Water-soluble hormones are not
dependent on plasma proteins for CIRCADIAN RHYTHM
transport.
• This is an endogenous 24-hour rhythm
that can be driven and altered by sleep-
wake or dark-light 24hour (diurnal) cycles.

REGULATION OF HORMONAL SECRETION

 • Hormone levels fluctuate predictably
during these cycles. For example, cortisol

declinestoward evening,and rises againtoward the

end of sleepto peakby morning.GH, thyroid-
stimulatinghormone(TSH), and prolactin
secretions peakduringsleep.
 The menstrualcycle is an exampleof a body
rhythm that is longerthan 24 hours (ultradian).
These rhythms must be consideredwhen
interpreting laboratory results for hormonelevels.

DISORDERSOF ANTERIOR PITUITARY GLAND

ACROMEGALY

 Acromegalymost often occurs as a result of a

benignpituitary tumor (adenoma
).
DISORDERSOF PITUITARY GLAND
 The excessivesecretion of GH results in an
rises early in the day, Acromegaly is a
rare condition characterized by an
overproduction of growth hormone (GH).

overgrowth of soft tissues and bones in the

hands, feet, and face.
• Because the problem develops after
epiphyseal closure, the bones of the arms
and legs do not grow longer.

Clinical Manifestations

Skeletal & Soft Tissue Changes

• Enlargement of hands and feet

• Joint pain (mild to crippling)
• Thickening and enlargement of bony and
soft tissues on the face, feet, and head
• Enlargement of the tongue → speech
difficulties
• Deepened voice due to hypertrophy of
vocal cords

Neurological & Sensory Effects

• Carpal tunnel syndrome

• Peripheral neuropathy
• Proximal muscle weakness
• Visual changes due to pressure on the
optic nerve from a pituitary adenoma
• Frequent headaches
Respiratory & Skin Changes • Sleep apnea due to upper airway
narrowing and obstruction from increased
pharyngeal soft tissues
• Thick, leathery, and oily skin

Endocrine & Metabolic Effects

• Menstrual disturbances in women

• GH antagonizes insulin action →
hyperglycemia
• Glucose intolerance leading to diabetes
mellitus
• Symptoms: Polydipsia (increased thirst) and
polyuria (increased urination)
• Mobilization of stored fat → Increased free
fatty acid levels → Higher risk of
atherosclerosis

Complications & Prognosis

• Reduced life expectancy by 5–10 years Higher

risk of:

• Cardiac disease
• Respiratory disease
• Diabetes mellitus  Colorectal cancer
• Even with treatment, joint pain and
deformities often persist.

• Despite enlarged tissues muscle weakness is DISORDERS OF POSTERIOR PITUITARY GLAND

common, and hypertrophied joints become
painful and stiff. • The hormones secreted by the posterior
• Osteoporosis of the spine and joint pain pituitary, antidiuretic hormone (ADH) and
develop. oxytocin, are produced in the hypothalamus
and then transported and stored in the
• Many men experience erectile dysfunction,
posterior pituitary gland.
and women may have amenorrhea, increased
facial hair. • ADH, also referred to as arginine vasopressin
(AVP) or vasopressin, plays a major role in the
and deepened voices.
regulation of water balance and osmolarity.
DIAGNOSTICS:

• Skull radiograph, MRI & CT reveals pituitary

enlargement. The two primary problems associated with ADH
• Bone radiographs show thickened long bone secretion are a result of either overproduction or
and skull. underproduction of ADH.
• Radioimmunoassay shows increased plasma • Overproduction or oversecretion of ADH
level of GH. results in a condition known as syndrome of
inappropriate antidiuretic hormone (SIADH).
• Results of glucose tolerance test show the
• Underproduction or undersecretion of
same or increased levels of GH.
ADH results in a condition referred to as
MANAGEMENT: diabetes insipidus (DI).

• HYPOPHYSECTOMY removal of the Pituitary

Gland
• Consequent destruction of the pituitary by
Radiation Therapy.
• DOC: Bromocriptine Mesylate (Parlodel) o
Inhibits the release of GH
o Used in conjunction with Pituitary
Irradiation or surgery to reduce
the serum GH level
 • Urinary & Weight Changes:

o Low urine output

o Increased body weight

• Severe Symptoms (Serum Sodium <

120 mEq/L):

o Vomiting o

Abdominal cramps o

Muscle twitching o

Seizures

• Neurological Effects (Progressive

Hyponatremia & Cerebral Edema):
o Lethargy

o Confusion

Headache
o Seizures sustained secretion of ADH
o Coma plasma osmolarity
SYNDROME OF INAPPRPRIATE ANTIDIURETIC
HORMONE (SIADH)
•
• SIADH results from abnormally high production or
• In SIADH, ADH is released despite normal or low

• This disorder is characterized by fluid retention,

serum hypoosmolality, dilutional hyponatremia,
hypochloremia, concentrated urine in the presence
of normal or increased intravascular volume, and
normal renal function.

Clinical Manifestations

• Early Symptoms:

o Thirst

o Dyspnea on exertion

o Fatigue

• Fluid & Electrolyte Imbalance:

o Increased permeability of renal distal tubule &

collecting duct → water reabsorption
Expansion of extracellular fluid volume Expansion of extracellular fluid volume

DIABETES INSIPIDUS

o Expansion of extracellular fluid volume  Diabetes insipidus (DI) is caused by a deficiency

of production or secretion of ADH or a decreased
o Decline in plasma osmolality renal response to ADH.

o Increased glomerular filtration rate  The decrease in ADH results in fluid and
electrolyte imbalances caused by increased urine
o Dilutional hyponatremia (low sodium levels) output and increased plasma osmolality

→ muscle cramping, pain, weakness  Depending on the cause, DI may be transient or a

chronic, lifelong condition.
 Central DI (caused by head trauma, intracranial
surgery, or brain tumors):

• Acute onset with excessive fluid loss

• Triphasic pattern after intracranial surgery:
• Acute phase: Abrupt onset of polyuria
• Interphase: Temporary normalization of urine
output
• Permanent phase: Central DI becomes
permanent
(occurs 10–14 days post-op)
• DI caused by head trauma is often self-limiting,
while DI from cranial surgery is more likely to
be permanent.

Nephrogenic DI (caused by renal insensitivity

to ADH):

• Clinical manifestations similar to central DI

• Less dramatic onset and lower fluid loss
compared to central DI

Complications of
Severe DI

•
If oral fluid intake cannot compensate for
urine loss:
• Severe dehydration:
o Poor skin turgor o
Hypotension o Tachycardia o
Hypovolemic shock

Neurological Symptoms (due to

hypernatremia & increased serum
osmolality):

• Irritability
• Mental dullness
• Coma
Clinical Manifestations:

• Polydipsia (excessive thirst) DISORDERS OF THYROID GLAND

• Polyuria (excretion of large amounts of urine, 2–20
L/day)  Alterations in thyroid function are among the most  Compensatory Mechanism: common endocrine
disorders.

o Most patients drink large amounts of  The thyroid hormones, thyroxine (T4) and water,
helping maintain normal or triiodothyronine (T3), regulate energy metabolism moderately
elevated serum osmolality and growth and development.
• Disorders of the thyroid gland include goiter,
General Symptoms:
benign and malignant nodules, inflammation,
• Fatigue (due to nocturia) hyperthyroidism, and hypothyroidism
• Generalized weakness
HYPERTHYROIDISM • Other causes include toxic nodular goiter,
thyroiditis, excess iodine intake, pituitary
• Hyperthyroidism is hyperactivity of the tumors, and thyroid cancer.
thyroid gland with sustained increase in • The term thyrotoxicosis refers to the
synthesis and release of thyroid hormones. physiologic effects or clinical syndrome of
 The most common form of hypermetabolism that results from excess
hyperthyroidism is Graves’ disease. circulating levels of T4, T3, or both.
 • Hyperthyroidism and thyrotoxicosis usually o Ocular muscle changes → muscle

weakness and diplopia (double

vision)

occur together, as seen in Graves’ disease.

Clinical Manifestations
Early & Systemic Symptoms 
General Effects of Excess Thyroid Hormone
Early signs: o Weight loss o
• Increased metabolism
Increased nervousness
• Enhanced tissue sensitivity to sympathetic
• Cardiovascular & Neuromuscular
nervous system stimulation Thyroid Gland Symptoms:
Examination Findings  Goiter: o Palpitations o Tremors Advanced &
o Palpable enlargement of the Severe Symptoms
thyroid gland o May be visible if
• Acropachy: Clubbing of the digits (advanced
excessively large  Bruits on disease)
auscultation: Complications
o Indicates increased blood supply to
Thyrotoxicosis (also called Thyrotoxic Crisis or
the Thyroid
thyroid Storm)
Ophthalmopathy (Eye Abnormalities) • Is Acute, severe, and rare condition caused
• Exophthalmos (Classic in Graves’ by excessive thyroid hormone release

Disease): o Bilateral protrusion of the • Life-threatening emergency but rarely fatal if

treated early
eyeballs o Due to increased fat deposits
and fluid (edema) in orbital tissues and • Common triggers (stressors):

muscles o Increased pressure forces the o Infection o Trauma

eyeballs outward o Surgery (especially thyroidectomy, due
• Eye-Related Complications: to
gland manipulation)
o Upper eyelid retraction and
elevation → visible sclera above PRIMARY HYPERTHYROIDISM
the iris

o Incomplete eyelid closure → dry • A toxic nodule is a thyroid nodule that becomes
independent of the pituitary and secretes excess
and irritated corneas
thyroid hormone.
o Risk of corneal ulcers and vision • Graves' disease is an autoimmune disorder
that causes hyperthyroidism. In autoimmune
loss
 disorders, the body produces antibodies
against some part of itself.

SECONDARY & TERTIARY HYPOTHYROIDISM

• Secondary hypothyroidism can result from

SECONDARY & TERTIARY HYPERTHYROIDISM
pituitary pathology such as infection,
inflammation, infiltration. hemorrhage, or tumor
• A pituitary tumor that secretes TSH, (either a non-functioning tumor within the
amiodarone toxicity, and struma ovarii, an pituitary or a brain tumor impinging upon it).
ovarian tumor that secretes thyroid • Tertiary hypothyroidism can be caused by
hormone. hypothalamic under-activity or tumor.
• Other causes include toxic nodular goiter,
Clinical Manifestations
thyroiditis, excess iodine intake, pituitary
tumors, and thyroid cancer. • Fatigue, lethargy
• Thyrotoxicosis refers to the physiologic • Impaired memory, slowed speech, decreased
effects or clinical syndrome of initiative
hypermetabolism that results from excess • Somnolence (excessive sleepiness)
circulating levels of T4, T3, or both. • Depression
• Weight gain due to a decreased metabolic rate
HYPOTHYROIDISM
• Decreased cardiac contractility & output
• Hypothyroidism is a deficiency of thyroid • Low exercise tolerance
hormone that causes a general slowing of • Shortness of breath on exertion
the metabolic rate. • Risk of cardiovascular complications, especially
• Hypothyroidism is more common in women in patients with preexisting heart disease
than men. • Anemia (low or normal erythropoietin levels)
• Hypothyroidism can be classified as primary • Easy bruising
or secondary • Increased serum cholesterol & triglycerides →
Risk of coronary atherosclerosis
PRIMARY HYPOTHYROIDISM • Myxedema (Severe Hypothyroidism) o
Physical changes: o Puffiness o Facial &
periorbital edema o Masklike appearance
• Primary hypothyroidism is caused by
destruction of thyroid tissue or defective
hormone synthesis.
DISORDERS OF ADRENAL MEDULLA
• A Hashimoto's Thyroiditis is an
autoimmune disease. It occurs with other
PHEOCHROMOCYTOMA
autoimmune disease.
• Iodine Deficiency causes hypothyroidism • Pheochromocytoma, which is a rare condition
because Iodine is necessary for thyroid caused by a tumor in the adrenal medulla affecting
hormone synthesis. the chromaffin cells, results in an excess production
of catecholamines (epinephrine, norepinephrine).
• The most dangerous immediate effect of the
disease is severe hypertension.
• If left untreated, it may lead to hypertensive • Androgens contribute to growth and development
encephalopathy, diabetes mellitus, in both genders and to sexual activity in adult
cardiomyopathy, and
death.
• The most striking
clinical features of
pheochromocytoma
are severe, episodic
hypertension
accompanied by the
classic manifestations
of severe, pounding
headache;
tachycardia with
palpitations; profuse
sweating; and
unexplained
abdominal or chest
pain.
women.
• The term corticosteroid refers to any one of these
DISORDERS OF ADRENAL CORTEX three types of hormones produced by the adrenal
cortex.
• Adrenal cortex steroid hormones have three CUSHING SYNDROME
main
classifications: glucocorticoids, • Cushing syndrome is a clinical condition that
mineralocorticoids, and androgens. results from chronic exposure to excess
• Glucocorticoids regulate metabolism, corticosteroids, particularly glucocorticoids.
increase blood glucose levels, and are critical in • Several conditions can cause Cushing syndrome.
the physiologic stress response. • The most common cause is iatrogenic
• The primary glucocorticoid is cortisol. administration of exogenous corticosteroids (e.g.,
• Mineralocorticoids regulate sodium and prednisone).
potassium balance. • Other causes of Cushing syndrome include adrenal
tumors and ectopic ACTH production by tumors
(usually of the lung or pancreas) outside of the
hypothalamicpituitary-adrenal axis.
• Cushing disease and primary adrenal tumors are
more common in women in the 20- to 40-year-old
age-group.  Ectopic ACTH production is more
common in men.

Clinical Manifestations

• The first indication of Cushing syndrome may be the

clinical presentation, including
• (1) centripetal (truncal) obesity or generalized
obesity;
• (2) “moon face” (fullness of the face) with facial
plethora;
• The primary mineralocorticoid is aldosterone.
• (3) purplish red striae (usually depressed below • Over-stimulation of the adrenal glands by an ectopic
the skin surface) on the abdomen, breast, or ACTH producing tumor.
buttocks • The most common site of ectopic production is a
• (4) hirsutism in women; small cell lung cancer, though other cancers can
• (5) menstrual disorders in women;  (6) produce ACTH as well.
hypertension; and • Cushing's syndrome is any state which creates
• (7) unexplained hypokalemia. pathologic hypercortisolism. Cushing's disease is
the specific case of hypercortisolism resulting from
an ACTH-secreting pituitary adenoma.

ADDISON’S DISEASE

• Adrenocortical insufficiency (hypofunction

of the adrenal cortex) may be from a primary
cause (Addison’s disease) or a secondary cause
(lack of pituitary ACTH secretion).
• In Addison’s disease, all three classes of adrenal
corticosteroids (glucocorticoids,
mineralocorticoids, and androgens) are reduced.
• In secondary adrenocortical insufficiency,
corticosteroids and androgens are deficient but
mineralocorticoids rarely are.
• ACTH deficiency may be caused by pituitary
disease or sup pression of the
OTHER Causes: hypothalamicpituitary axis because of the
administration of exogenous corticosteroids.
• Decreased ACTH secretion in either scenario decreases cortisol secretion from the adrenal gland, but the rest
of the adrenal still functions normally. Thus, there is no hyperkalemia in secondary and tertiary adrenal
insufficiency.

DISORDERS OF PARATHYROID GLANDS

HYPERPARATHYROIDISM

• Hyperparathyroidism is a condition involving an increased secretion of parathyroid hormone (PTH).

 • PTH helps regulate serum calcium and phosphate levels by stimulating bone resorption of calcium, renal
tubular reabsorption of calcium, and

activationof vitaminD.
PRIMARYADRENALINSUFFICIENCY
PRIMARY HYPERPARATHYROIDISM

• Autoimmune
Disease

• Polyglandularautoimmune
syndromeType 1
(HAM : hypoparathyroidism,
adrenalinsufficiency,
mucocutaneous
candidiasis)
• Polyglandularautoimmune
syndromeType 2:
(Adrenal insufficiency with either autoimmune
thyroid diseaseor insulin-dependent
diabetes
mellituswith possiblevitiligo, prematureovarian
failure, and/or perniciousanemia)

• Waterhouse
Friedrichsen
Syndrome

SECONDARY& TERTIARY ADRENALINSUFFICIENCY  The parathyroidglandsare not undercontrol of

the pituitary. PTH secretion is regulatedentirely
• Pituitary lesionsor tumorscan lead to secondary
by calciumcon centration.So secondary
adrenalinsufficiency due to decreasedACTH

• Excess secretion of PTH by the parathyroid glands.

Increase PTH will raise blood Calcium level.

• Because PTH induces release of calcium from bone,

alkaline phosphatase can be elevated, as in any cause of
bone breakdown.

SECONDARY & TERTIARY HYPERPARATHYROIDISM

 hyperparathyroidism is not related to the pituitary
secretion. as with other secondary endocrine diseases, but
• Hypothalamic lesions or tumors can cause rather to
blood calcium concentration.
tertiary adrenal insufficiency due to decreased
• Vitamin D deficiency or renal failure (which causes
CRII stimulation of ACTII release from the hypocalcemia secondary to decreased vitamin D
pituitary. activation.
• Tertiary Hyperparathyroidism occurs when
secondary hyperparathyroidism persists
inappropriately after the resolution of the
renal failure or after renal transplantation.

HYPOPARATHYROIDISM

• Hypoparathyroidism is an uncommon condition

associated with inadequate circulating PTH. It is
characterized by hypocalcemia resulting from a
lack of PTH to maintain serum calcium levels.
• PTH resistance at the cellular level may also occur
(pseudohypoparathyroidism). This is caused by a
genetic defect resulting in hypocalcemia in spite
of normal or high PTH levels and is often
associated with hypothyroidism and
hypogonadism.
• Surgical damage I removal of the parathyroids,
for example from thyroid surgery
• Magnesium (a 2+ ion like calcium), which
affects the parathyroids' secretion of PTH;
hypo- or hypermagnesemia can lead to
hypocalcemia.
• Infiltrative disease of the parathyroids (e.g.,
Wilson's disease)
• Metastases to the parathyroids

HUNGRY BONE SYNDROME

• Congenital absence of the parathyroids (e.g.,

DiGeorge Syndrome is a problem with the third
and fourth branchial pouches in which the thymus
and parathyroids are absent).
• Autoimmune destruction of the parathyroids in
rare diseases such as HAM (hypoparathyroidism,
adrenal insufficiency, mucocutaneous candidiasis)
and APECED (autoimmune polyendocrinopathy
candidiasis, ectodermal dystrophy).
• Familial (i.e., genetic) hypoparathyroidism.
VITAMIN D DEFICIENCY