ENDOCRINE SYSTEM
ENDOCRINE SYSTEM
◦consists of glands, specialized cell clusters, and
hormones
◦chemical transmitters secreted by the glands in
response to stimulation.
◦Regulates body’s metabolic activities and
maintains homeostasis.
HORMONES
PROTEIN HORMONE LIPID HORMONE
WATER-SOLUBLE LIPID-SOLUBLE
INSULIN ALDOSTERONE
GLUCAGON CORTISOL
SEX HORMONE
HORMONE REGULATION
HORMONE REGULATION
HYPOTHALAMUS
◦“THE HEART OF THE ENDOCRINE SYSTEM”
◦integrative center for the endocrine
and autonomic (involuntary) nervous
systems. It helps control some
endocrine glands by neural and
hormonal pathways.
ANTERIOR PITUITARY
◦ Hypothalamic hormones stimulate the anterior pituitary gland
to release four types of trophic (gland-stimulating) hormones:
◦ adrenocorticotropic hormone (ACTH), also called
corticotropin
◦ thyroid-stimulating hormone (TSH)
◦ luteinizing hormone (LH)
◦ follicle-stimulating hormone (FSH)
ANTERIOR PITUITARY
◦ The secretion of trophic hormones stimulates their respective
target glands, such as the adrenal cortex, the thyroid gland,
and the gonads.
◦ Hypothalamic hormones also control the release of effector
hormones from the pituitary gland. Examples are growth
hormone (GH) and prolactin.
ANTERIOR PITUITARY
ANTERIOR PITUITARY
◦If the pituitary stalk is damaged, all
anterior pituitary hormones will be
decreased EXCEPT: Prolactin
POSTERIOR PITUITARY
◦an extension of the hypothalamus
◦Antidiuretic hormone (ADH)/V______ and
oxytocin—produced in the Hypothalamus
but are stored in the posterior pituitary.
◦They're released from the posterior pituitary
by neural stimulation.
POSTERIOR PITUITARY
POSTERIOR PITUITARY
◦Vasopressin and Oxytocin are synthesized by the
nerve cell bodies in the Supraoptic and
Paraventricular nuclei. (POSA)
◦When ADH is secreted, the body retains water.
◦Oxytocin stimulates uterine contractions during
labor and milk secretion in lactating women.
ADRENAL
GLANDS
MNEMONICS:
G-F-R
Glomerulosa, Fasciculata, Reticularis
“The deeper you go, the sweeter it gets.”
“Salt, Sugar, Sex”
Aldosterone, Cortisol, Weak Sex Hormones
ENDOCRINE PANCREAS
◦ The pancreas produces glucagon (from Alpha cells) and insulin (from Beta
cells).
◦ Glucagon is a hormone released when a person is in a fasting state. It
stimulates the release of stored glucose from the liver to raise blood glucose
levels. (Main stimulus: Low blood glucose)
◦ Insulin is a hormone released during the postprandial (nourished) state. It aids
glucose transport into the cells and promotes glucose storage. It also
stimulates protein synthesis and enhances free fatty acid uptake and storage.
Insulin deficiency or resistance causes diabetes mellitus. (Main stimulus: High
blood glucose)
THYROID GLAND
◦Necessary for normal growth and
development
◦Increasing metabolic activity and
protein synthesis
THYROID GLAND
◦Diseases of the thyroid are caused by thyroid
hormone overproduction or deficiency and
gland inflammation and enlargement.
PARATHYROID GLANDS
◦There are ____ parathyroid glands located
behind the thyroid gland.
◦These glands secrete PTH, which helps
regulate calcium levels and control bone
formation.
PARATHYROID GLANDS
ENDOCRINE
DISORDERS
HYPER- VS. HYPOTHYROIDISM
HYPERTHYROIDISM
HYPOTHYROIDISM
CAUSES
HYPERTHYROIDISM HYPOTHYROIDISM
Graves disease: Most Iodine deficiency: Most
common cause of common cause of
primary congenital
hyperthyroidism (85%) hypothyroidism
Autoimmune e.g.,
Hashimoto: Most
common cause of
hypothyroidism In
iodine-sufficient areas
GOITER
◦ Thyroid enlargement, caused by impaired thyroid
hormone synthesis
◦ Clinical presentation: symptoms referable to mass effect
◦ Most common cause: Iodine deficiency
◦ Multinodular goiters can produce very large glands that can
be mistaken for malignancy
◦ Incidence of malignancy is low
GOITER: PATHOPHYSIOLOGY
HYPERPARATHYROIDISM
PRIMARY Hyperfunctioning of the parathyroid gland
Adenoma (most common) > Hyperplasia >
Carcinoma
SECONDARY As compensation to chronic hypocalcemia
Renal failure (most common), steatorrhea, Vitamin
D deficiency, inadequate dietary Ca2+
TERTIARY Persistent PTH secretion after correction of
hypocalcemia (post-renal transplant)
CLINICAL MANIFESTATIONS
◦Nephrolithiasis, nephrocalcinosis,
gallstones, Aortic and/or Mitral valve
calcifications
HYPOPARATHYROIDISM
Causes:
◦ Surgically induced (Most common)
◦ Genetics
◦ May have normal PTH levels with symptoms of PTH
deficiency
CLINICAL MANIFESTATIONS
◦Tetany (neuromuscular
irritability) Chvostek
and Trousseau sign
◦Calcification of lens,
cataract formation
CUSHING’S SYNDROME
◦ Most common cause overall:
Exogenous steroids (“Iatrogenic”)
◦ Most common endogenous cause:
ACTH-secreting pituitary adenoma
(Cushing disease)
◦ Common clinical presentation:
abdominal striae, obesity,
dorsocervical fullness (buffalo hump),
moon facies
CUSHING’S SYNDROME
◦When glucocorticoid excess is caused by
pituitary-dependent conditions, it’s called
Cushing’s disease.
CUSHING’S SYNDROME
◦Frequent infections or slow wound healing
due to decreased lymphocyte production,
hyperglycemia, and suppressed antibody
formation may occur.
◦Hypertension due to sodium and water
retention is common in Cushing’s syndrome.
It may lead to ischemic heart disease and
heart failure.
CUSHING’S SYNDROME
ADDISON’S DISEASE
◦Addison’s disease, also called adrenal
hypofunction or adrenal insufficiency,
occurs in two forms: primary and
secondary.
◦Either primary or secondary Addison’s
disease can progress into adrenal crisis.
ADDISON’S DISEASE
◦ The primary form of Addison’s disease originates within the adrenal glands.
◦ It’s characterized by decreased mineralocorticoid, glucocorticoid, and androgen
secretion.
◦ The secondary form of Addison’s disease is caused by a disorder outside the gland,
such as a pituitary tumor with corticotropin deficiency.
◦ In secondary forms of the disorder, aldosterone secretion may be unaffected.
ADDISON’S DISEASE
◦ Adrenal crisis (acute adrenal insufficiency) is the most serious complication of Addison’s
disease. AKA Addisonian crisis which is a critical deficiency of mineralocorticoids and
glucocorticoids. It’s a medical emergency that requires immediate, vigorous
treatment.
◦ This potentially lethal condition usually develops in patients who:
◦ don’t respond to hormone replacement therapy
◦ undergo extreme stress without adequate glucocorticoid replacement
◦ abruptly stop hormone therapy
◦ undergo trauma
◦ undergo bilateral adrenalectomy
◦ In adrenal crisis, destruction of the adrenal cortex leads to a rapid decline in the steroid
hormones cortisol and aldosterone. This directly affects the liver, stomach, and kidneys.
ADDISON’S DISEASE
ADDISON’S DISEASE
◦ These signs and symptoms may
indicate Addison’s disease:
◦ confusion
◦ fatigue
◦ GI disturbances and weight loss
◦ hyperkalemia
◦ hyperpigmentation
◦ hypoglycemia
◦ hyponatremia
◦ hypotension
◦ muscle weakness.
DIABETES INSIPIDUS
DIABETES MELLITUS
DIABETIC KETOACIDOSIS
CLINICAL MANIFESTATIONS
