Download Name Chapter 18: Alterations of Hormonal Regulation I

PATHOPHYSIOLOGY
Name
Chapter 18: Alterations of Hormonal Regulation
I. Mechanisms of Hormonal Alterations
Elevated or depressed hormone levels can arise from:
A. Dysfunctions of Endocrine Secreting Tissues

Mechanisms that can cause this include:
1. Faulty feedback systems
o
Gland is not receiving signals for release of appropriate levels of hormone
2. Dysfunction of the gland
o
Secretory cells are unable to produce, obtain, or convert hormone precursors
o
Gland synthesizes or releases excessive amounts of hormone
3. Altered metabolism of hormones
o
Increased hormone degradation or inactivation
4. Production of hormones from nonendocrine tissues - ectopic hormone release
B. Target Cell Failure

Mechanisms that can cause target cells to fail to respond to hormones include:
1. Cell surface receptor-associated disorders
o
Decrease in number of receptors
o
Impaired receptor function
o
Presence of antibodies against specific receptors
o
Antibodies that mimic hormone action
o
Unusual expression of receptor function, for example on tumor cells
2. Intracellular disorders in messenger systems within the target tissue
3. Circulating inhibitors - generally antibodies that bind to the hormone and prevent binding
II. Alterations of the Hypothalamic-Pituitary System

Most commonly caused by interruption of the connection between the hypothalamus and pituitary,
the pituitary stalk (infundibulum).
A. Diseases of the Posterior Pituitary

Rare, usually related to abnormal secretion of antidiuretic hormone (ADH).

Antidiuretic hormone - controls serum osmolality, increases permeability of the renal tubules to
water, and causes vasoconstriction when administered pharmacologically in high doses.
1. Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
o
Hypersecretion of ADH
o
High ADH levels interfere with renal free water clearance, leading to abnormally concentrated
urine, and dilute blood plasma (hypoosmolality), especially sodium (hyponatremia).
2
o
Etiology – SIADH can be caused by:
 Cancer cells ectopically secreting ADH (Ex. small cell carcinoma) - most common
 Brain trauma or infection
 Infectious pulmonary diseases
o
Symptoms are due to the hyponatremia (low serum sodium).
 This can cause irreversible neurological damage.
2. Diabetes insipidus
o
Insufficiency of ADH
o
Causes partial or total inability to concentrate the urine
o
Low ADH levels cause formation of large quantities of dilute urine, and increased plasma
concentration (hyperosmolality). Dehydration results.
o
Symptoms - polyuria (excessive urination), thirst and polydipsia (excessive drinking)
o
Three types:
1. Neurogenic - caused by insufficient amounts of ADH
 Due to damage to the hypothalamus or pituitary.
2. Nephrogenic - caused by an inadequate response to ADH
 Due to diseases that damage renal tubules (example – pyelonephritis) or drugs such as
methoxyflurane anesthesia, lithium, or demeclocycline.
3. Psychogenic (primary polydipsia) – caused by excessive intake of fluids
 Due to psychological disorders
B. Diseases of the Anterior Pituitary
1. Hypopituitarism – insufficient secretion of one or more pituitary hormones.
o
Etiology – pituitary infarction, head trauma, infections, and tumors
o
Panhypopituitarism – decreased or absent secretion of all pituitary hormones
 ACTH deficiency – causes cortisol deficiency (life-threatening).
 TSH deficiency – causes thyroid hormone deficiency.
 FSH and LH deficiency – causes gonadal failure and loss of secondary sex characteristics.
 GH deficiency – causes pituitary dwarfism in children.
 ADH deficiency – causes diabetes insipidus.
2. Hyperpituitarism
o
Etiology – commonly caused by a benign slow-growing pituitary adenoma.
 Hypersecretes the hormone of the cell type from which it arose, independent of regulation.
o
Manifestations:
 Headache and fatigue
 Visual changes
 Hyposecretion of neighboring anterior pituitary hormones due to pressure atrophy
3
1. Hypersecretion of growth hormone (GH)
 Acromegaly - hypersecretion of GH during adulthood (after closure of epiphyseal plates)

Proliferation of connective tissue and bony matrix creates course facial features, large
hands and feet, etc.
 Gigantism - hypersecretion of GH in children and adolescents

Excessive skeletal growth, with some individuals becoming 8 or 9 feet tall.
 Long term hypersecretion of GH causes hypertension, renal, thyroid, and reproductive dysfunction.
2. Hypersecretion of prolactin
 Caused by prolactinomas – most common hormone-secreting pituitary tumor
 Manifestations:

In females - amenorrhea, galactorrhea (milk production), hirsutism, and osteopenia

In males - hypogonadism, erectile dysfunction, impaired libido, oligospermia, and
diminished ejaculate volume
III. Alterations of Thyroid Function
A. Hyperthyroidism
1. Thyrotoxicosis - general condition in which elevated thyroid hormone (TH; T3 and T4) levels cause
greater than normal physiologic responses.

Manifestations of thyroid hormone excess:
o
Enlarged thyroid gland
o
Increase in metabolic rate and heat production (causes flushed skin and perspiration)
o
Nervous excitability and insomnia
o
Increased heart rate and cardiac dysrhythmias; heart failure (in extreme cases)
o
Weight loss
o
GI hyperactivity, diarrhea & vitamin deficiencies
o
Thinning of hair and skin
2. Graves disease
o
Most common form of hyperthyroidism.
o
Tends to occur in women in their 30s and 40s.
o
Etiology - type II autoimmune hypersensitivity disorder involving stimulation of the thyroid
gland by antibodies against the TSH receptor (thyroid-stimulating immunoglobulins (TSI)).
 Antibodies stimulate enlargement of thyroid with goiter formation and hypersecretion of TH.
 Increased levels of thyroid hormone feed back on the pituitary to turn off TSH production.
o
Ocular symptoms - infiltration of the orbital contents causes orbital edema, which produces
protruding eyes (exophthalmos), muscle palsies, and damage to the optic nerve.
o
Pretibial myxedema - caused by infiltration of subcutaneous tissues of the anterior lower leg
which results in a “doughy” edema.
o
Treatment includes partial thyroidectomy or ablation of the gland with radioactive iodine.
4
3. Thyrotoxic crisis (thyroid storm)
o
Rare but dangerous worsening of the thyrotoxic state, in which death occurs within 48 hours
without treatment.
o
Usually occurs in individuals who have undiagnosed or partially treated Graves disease and are
subjected to excessive stress, Including:
 Surgery, infection, pulmonary or cardiovascular disorders, emotional distress, physical stress.
o
Manifestations:

Hyperthermia; tachycardia, especially atrial tachydysrhythmias; high-output heart failure;
agitation or delirium; and nausea, vomiting, or diarrhea contributing to fluid volume depletion.
o
Treatment is designed to:
a. Reduce circulating TH levels by inducing a block of TH synthesis.
b. Provide symptomatic and supportive care.
B. Hypothyroidism

Insufficient secretion of TH by the thyroid gland.

Manifestations of thyroid hormone deficiency:
o
Size of thyroid gland varies, depending on cause; may be small, normal or enlarged.
o
Decreased metabolic rate and body temperature; cold intolerance.
o
Weaker, more sluggish muscle contractions, which cause constipation and decreased
cardiac contractility
o
Slow heart rate and decreased cardiac output
o
Increased body weight
o
Rise in blood cholesterol levels (contributes to atherosclerosis)
o
Decreased sex drive, and menstrual irregularities
o
Depression of mental functioning and sleepiness
o
Course, brittle hair and hair loss
o
Severity is proportional to degree of hyposecretion.
o
Myxedema
 Characteristic sign of severe of long-standing hypothyroidism.
 Altered composition of the dermis and other tissues.
 Produces a nonpitting, boggy edema, especially around the eyes, hands, and feet.
1. Primary hypothyroidism
o
Loss of thyroid tissue leads to decreased production of TH (low T3 and T4), increased secretion of
TSH, and goiter.
o
Etiology – primary hypothyroidism can be due to:
 Congenital defects
 Defective hormone synthesis resulting from autoimmune thyroiditis, endemic iodine
deficiency, or antithyroid drugs
 Loss of thyroid tissue after surgical or radioactive treatment for hyperthyroidism
5
a. Acute thyroiditis - inflammation of the thyroid gland, often caused by a bacterium, that can result
in hypothyroidism.
b. Subacute thyroiditis - self-limiting nonbacterial inflammation of the thyroid gland.
 Inflammatory process damages follicular cells, causing leakage of T3 and T4.
 Hyperthyroidism then is followed by transient hypothyroidism, which is corrected by cellular
repair and a return to normal levels in the thyroid.
c.
Autoimmune thyroiditis (Hashimoto disease) – results in destruction of thyroid tissue by
circulating thyroid antibodies and infiltration of lymphocytes.
 May be caused by an inherited immune defect.
 Goiter formation is common.
 Most common cause of hypothyroidism in adults.
2. Secondary hypothyroidism
o
Usually caused by the pituitary's failure to synthesize adequate amounts of thyroid-stimulating
hormone (TSH).
o
Pituitary tumors are the most common cause.
o
Results in low levels of both TSH and TH (T3 and T4)
3. Myxedema coma
o
Diminished level of consciousness associated with severe hypothyroidism.
o
Often due to untreated hypothyroidism.
o
Symptoms include hypothermia without shivering, hypoventilation, hypotension,
hypoglycemia, and lactic acidosis.
o
Potentially fatal without treatment.
4. Congenital hypothyroidism
o
Absence of thyroid tissue during fetal development or defects in hormone synthesis.
o
Thyroid hormone is essential for embryonic growth, particularly of brain tissue.
o
Infant will be mentally retarded if there is no thyroxine during fetal life.
o
Overall growth is stunted.
o
This can be partially reversed if thyroxine is given immediately after birth.
o
If untreated this results in cretinism.
C. Thyroid carcinoma

Relatively rare.

Associated with exposure to ionizing radiation, especially in childhood.

T3 and T4 levels are usually normal.

Typically discovered as a small thyroid nodule or metastatic tumor in the lungs, brain, or bone.
6
IV. Alterations of Parathyroid Function

Cause profound effects on calcium homeostasis and bone health.

Parathyroid hormone (PTH) helps to maintain normal serum calcium levels by stimulating the
breakdown of bone and by increasing renal and gastric absorption of calcium.
A. Hyperparathyroidism

Excess secretion of PTH causes hypercalcemia and bone destruction.
1. Primary hyperparathyroidism
o
Excess secretion of PTH from one or more parathyroid glands
o
Usually caused by an adenoma of the chief cells in the parathyroid gland.
o
Manifestations:
 Very high serum levels of calcium cause neurologic, gastric, and muscular dysfunction.
 Bone resorption leads to osteopenia, osteoporosis, bone fragility, and pathologic fractures.
 Hypercalcemia and hypercalciuria can contribute to the formation of renal calculi.
2. Secondary hyperparathyroidism
o
Increase in PTH secondary to a chronic disease.
o
Usually a result of chronic renal failure.
 Kidney cannot activate vitamin D and cannot adequately reabsorb calcium from tubules.
 Persistent hypocalcemia results in increased PTH secretion, causing osteopenia
 They exhibit bone fragility but without the signs and symptoms of hypercalcemia.
B. Hypoparathyroidism

Abnormally low PTH level causes inability to maintain normal serum calcium levels.

Usually caused by parathyroid injury or removal during thyroid surgery

Lack of PTH causes depressed serum calcium levels, increased serum phosphate levels, decreased
bone resorption, and eventual hypocalciuria.

Manifestations associated with hypoparathyroidism are primarily those of hypocalcemia:
o
Lowered threshold for nerve and muscle excitation, causing muscle spasms, hyperreflexia,
clonic-tonic convulsions, laryngeal spasms, and, in severe cases, death by asphyxiation.
o
Also dry skin, alopecia, poor dentition, skeletal deformity.
V. Dysfunction of the Endocrine Pancreas: Diabetes Mellitus
A. Types of Diabetes Mellitus

Diabetes mellitus is a group of disorders characterized by glucose intolerance, chronic
hyperglycemia, and disturbances of carbohydrate, protein, and fat metabolism.

Classic signs and symptoms are often present as well (polyuria, polydipsia, polyphagia).
7
1. Type 1 Diabetes Mellitus
o
Insulin dependent diabetes mellitus (IDDM)
o
Results from a severe, absolute lack of insulin caused by loss of pancreatic beta cells.
o
Usually occurs in younger people.
o
About 10% of DM cases.
 Type 1A – immune-mediated (about 9%) ; Type 1B – idiopathic (about 1%)
o
Pathophysiology of Type 1A:
 In genetically vulnerable individuals an environmental trigger causes:

Production of autoantibodies against beta cells and insulin.

Cellular and cytokine-mediated injury (type IV hypersensitivity).

Destruction of insulin-secreting beta cells .
 Alpha cells produce excess glucagon (raises blood sugar).
 Low insulin and high glucagon causes hyperglycemia and ketoacidosis.
 Ketoacidosis - acidosis accompanied by the accumulation of ketone bodies in the body
tissues and fluids; caused by increased metabolism of fats and proteins.
o
Manifestations:
 Hyperglycemia, polydipsia, polyuria, polyphagia, weight loss, and fatigue.
o
Diagnosis is based on:
 Symptoms and family history.
 Elevated fasting plasma glucose levels and glucose tolerance tests.
 Elevated glycosylated hemoglobin (HbA1C) levels (indicates average glucose level to
which RBCs have been exposed).
o
Exercise allows uptake of glucose without insulin, so can cause hypoglycemia or reduce insulin
requirement.
2. Type 2 Diabetes Mellitus
o
Non-insulin dependent diabetes mellitus (NIDDM)
o
Results from a combination of insulin resistance and declining insulin secretion.
o
About 90% of DM cases.
o
Usually diagnosed later in life, although increasing in younger groups.
o
Strong genetic component; very common in certain ethnic groups.
o
Triggered by environmental factors, including obesity, poor diet, and lack of exercise.
o
Pathophysiology:
 In the obese, insulin has a diminished ability to influence glucose uptake and metabolism
(insulin resistance of target tissues).
 Some insulin production continues in type 2 diabetes mellitus, but the size and number of
beta cells decrease. Initially insulin secretion may be high, but it declines with time.
 Low insulin and high glucagon causes hyperglycemia, but usually not ketoacidosis.
 Increased lipid metabolism results in high levels of circulating lipids; risk of atherosclerosis.
8
3. Gestational diabetes
o
Occurs when a woman not previously diagnosed with diabetes shows glucose intolerance
during pregnancy.
o
Can cause potentially life threatening complications for both mother and fetus.
B. Acute Complications of Diabetes Mellitus
1. Hypoglycemia
o
Occurs in >90% of type 1 diabetics due to administration of too much insulin.
o
“Insulin shock”
o
Decreased blood glucose (45 to 60mg/dl) causes pallor, tremor, anxiety, tachycardia,
palpitations, sweating, headache, dizziness, irritability, fatigue, poor judgment, confusion,
visual disturbances, hunger, seizures, and ultimately coma.
o
Treatment - replacement of glucose.
2. Diabetic ketoacidosis (DKA)
o
Complication of type 1 diabetes.
o
Occurs when the body cannot use glucose as a fuel source because the body has no insulin or
not enough insulin, and fat is used instead.
o
Byproducts of fat breakdown, called ketones, build up in the body.
o
This leads to severe metabolic acidosis that, in association with hyperglycemia and
dehydration, can result in coma, shock, and even death.
3. Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
o
Complication of type 2 diabetes mellitus.
o
Occurs more often in the elderly, or those with infections or cardiovascular or renal disease.
o
Poor glucose control results in high levels of glucose (more than 500mg/dl) and high osmotic
pressures that lead to severe dehydration, low blood volume, and low perfusion pressures.
o
Ketosis is uncommon because there is enough insulin to prevent lipolysis and protein catabolism.
o
High overall mortality rate.
C. Chronic Complications of Diabetes Mellitus
1. Mechanisms of damage - alterations in carbohydrate, protein, and lipid metabolism (primarily
hyperglycemia) adversely affects tissue in three ways:
a. Glycation
o
Glycation - attachment of glucose to proteins, lipids, and nucleic acids in blood vessels,
nerves, lenses, and other tissues, forming advanced glycation end products (AGEs).
o
AGEs stimulate cellular injury, inflammation, oxidation of lipoproteins, dysfunction of the
endothelium (decreased vasodilators and anticoagulants) and thickening of the basement
membrane.
o
Contributes to immunologic deficiencies and autoimmunity.
9
b. Induction of the polyol pathway
o
Causes conversion of glucose to sorbitol (and then slowly to fructose).
o
Sorbitol increases intracellular osmotic pressure, causing cellular edema and tissue dysfunction.
o
This process is especially important in renal cells, red blood cells, eye lens, and nerves.
c. Activation of protein kinase C
o
Protein kinase C (PKC) - a family of different intracellular signaling proteins.
o
Inappropriately activated by hyperglycemia.
o
Contributes to insulin resistance, tissue inflammation and edema, and production of
mitogens and degradative enzymes.
o
These effects contribute to tissue remodeling and vascular dysfunction.
2. Sequelae of chronic diabetes mellitus – the mechanisms above cause:
a. Diabetic neuropathies – nerve degeneration and delayed conduction.
b. Microvascular disease – thickening and damage to the capillary wall.
o
Retinopathy – ischemia causes damage to retina.
o
Diabetic nephropathy – including end-stage renal disease; caused by damage to glomeruli.
c. Macrovascular disease – diabetes increases severity of atherosclerosis.
o
Coronary artery disease – high rate of CAD and myocardial infarction.
o
Stroke – twice as common for diabetics.
o
Peripheral arterial disease – results in gangrene and amputation.
d. Infection- increased risk due to poor circulation and immune deficiencies.
VI. Alterations of Adrenal Function
A. Hyperfunction Disorders of the Adrenal Cortex
1. Hypercortisolism – disorders that result from high levels of cortisol secretion.
o
Cushing disease – excessive anterior pituitary secretion of ACTH.

o
Usually due to a pituitary adenoma.
Cushing syndrome – excessive level of cortisol, regardless of cause.

Usually due to an adenoma of adrenal cortex (ACTH independent; low ACTH levels).

Could be from ectopic production of adrenocorticotropic hormone (ACTH) from a tumor
elsewhere in the body (e.g., small-cell lung cancer).

o
Prolonged glucocorticoid therapy.
Manifestations:

Obesity with fat deposition in face (“moon face”), neck and abdomen (truncal obesity).

Protein breakdown for gluconeogenesis causes muscle weakness, bone loss, and bruising.

High levels of glucocorticoids cause insulin insensitivity and impaired glucose tolerance.

At high levels, glucocorticoids mimic aldosterone, causing sodium and water retention
(hypertension) and potassium excretion.

Gonadocorticoids may also be in excess, causing menstrual dysfunctions and
masculinization in females.
10
2. Hyperaldosteronism
o
Primary hyperaldosteronism (Conn disease) - caused by an abnormality of the adrenal cortex.
o
Secondary hyperaldosteronism – caused by activation of the renin-angiotensin-aldosterone
system in conditions such as heart failure, renal failure, hypertension, and hepatic cirrhosis.
o
Aldosterone causes increased renal sodium and water retention with excess potassium
secretion.
o
Manifestations:

Hypertension - can lead to an increased risk for atherosclerosis and congestive heart failure.

Hypernatremia

Hypokalemia - can be severe enough to cause cardiac dysrhythmias and muscle weakness.
3. Hypersecretion of adrenal androgens and estrogens
o
Usually due to an adrenal tumor.
o
Feminization – can result in males.
o
Virilization – development of male characteristics can result in females.
B. Hypofunction Disorders of the Adrenal Cortex

Hypocortisolism - low levels of cortisol secretion.
o
Due to either:

Inadequate stimulation of the adrenal glands by ACTH.

Primary adrenal insufficiency - inability of the adrenals to produce and secrete the
adrenocortical hormones.

o
May be partial dysfunction so only synthesis of aldosterone or androgens is affected.
o
May affect glucocorticoid or mineralocorticoid secretion or both.
Primary adrenal insufficiency (Addison disease)
o
Inadequate production of cortisol and aldosterone.
o
Autoantibodies and cell-mediated immunity cause destruction of the adrenal cortex.
o
Associated with other autoimmune diseases such as Hashimoto thyroiditis and pernicious anemia.
o
Manifestations:
o

Metabolic abnormalities (e.g., hypoglycemia, hyponatremia, and hyperkalemia)

Hypovolemia and hypotension (can be life-threatening)

Orthostatic dizziness, weakness and fatigue

Anorexia, nausea, abdominal pain

Changes in mental status like confusion and apathy due to hypoglycemia
Addisonian crisis – in response to an acute stressor, the patient experiences fever, nausea,
vomiting, hyponatremia, hyperkalemia, hypotension, and dehydration, which could result
in circulatory shock.
o
In individuals with primary Addison disease, the lack of feedback on the pituitary results in
increased compensatory secretion of ACTH which can cause hyperpigmentation of the skin.
11
C. Disorders of the Adrenal Medulla

Adrenal medulla hyperfunction - usually caused by a:
o
Pheochromocytoma – a catecholamine-producing tumor of the adrenal medulla.

o
o
Most are benign, although 10% are malignant and may metastasize.
Symptoms of catecholamine excess are related to their sympathetic nervous system effects:

Hypertension

Tachycardia, palpitations

Glucose intolerance

Excessive sweating

Constipation

Weight loss
With exposure to certain foods (containing tyrosine) or excessive physiologic stress (e.g.,
surgery), episodes of extreme hypertension can occur with potential for cerebral and
cardiovascular complications.
Gland
Hypothalamus
THE PRINCIPLE ENDOCRINE GLANDS AND THEIR HORMONES
Hormone
Target Tissue
Primary Actions
Releasing and inhibiting hormones
Anterior lobe of pituitary
Stimulates or inhibits secretion of specific hormones
Anterior Lobe of Pituitary
Growth hormone (GH)
Most tissues in the body
Stimulates growth by promoting protein synthesis
Thyroid-stimulating hormone (TSH)
Thyroid gland
Increases secretion of thyroid hormone; increases the size
of the thyroid gland
Adrenocorticotropic hormone (ACTH)
Adrenal cortex
Increases secretion of adrenocortical hormones, especially
glucocorticoids such as cortisol
Follicle-stimulating hormone (FSH)
Ovarian follicles in females;
seminiferous tubules in males
Stimulates follicle maturation and estrogen secretion in
females; spermatogenesis in males
Luteinizing hormone (LH); also called
Ovary in females; testis in males
Stimulates ovulation and progesterone formation in
females; testosterone production in males
Prolactin
Mammary gland
Stimulates milk production
Antidiuretic hormone (ADH)
Kidney
Increases water reabsorption (decreases water lost in urine)
Oxytocin
Uterus; mammary gland
Increases uterine contractions; stimulates ejection of milk
from mammary gland
Thyroxine (T4) and
triiodothyronine (T3)
Most body cells
Increase metabolic rate; essential for normal growth and
development
Calcitonin
Primarily bone
Decreases blood calcium by inhibiting bone breakdown and
release of calcium; antagonistic to parathyroid hormone
Parathyroid hormone (PTH) or
Bone, kidney, digestive tract
Increases blood calcium by stimulating bone breakdown
and release of calcium; increases calcium absorption in the
digestive tract; decreases calcium lost in the urine
Insulin
General, but especially liver,
skeletal muscle, and adipose
Decreases blood glucose levels by facilitating uptake and
utilization of glucose by cells; stimulates glucose storage as
glycogen and production of fat
Glucagon
Liver
Increases breakdown of glycogen to increase blood glucose
levels
interstitial cell stimulating hormone (ICSH)
in males.
Posterior Lobe of Pituitary
Thyroid Gland
Parathyroid hormone
parathormone
Pancreas (Islets of Langerhans)
2
Gland
Hormone
Target Tissue
Primary Actions
Adrenal Medulla
Epinephrine, norepinephrine
Heart, blood vessels, liver,
adipose
Stimulates fight-or-flight response; increases heart rate and
blood pressure; increases blood flow into skeletal muscle;
increases blood glucose level
Adrenal Cortex
Mineralocorticoids (aldosterone)
Kidney
Increases sodium reabsorption and potassium excretion in
kidney tubules; secondarily increases water retention
Glucocorticoids (cortisol)
Most body tissues
Increases blood glucose levels; inhibits inflammation and
immune responses
Gonadocorticoids (androgens and
estrogens)
Most body tissues
Secreted in small amounts so that the effect is generally
masked by the hormones from the ovaries and testes
Testis
Testosterone
Most body cells
Promotes maturation and maintenance of the male
reproductive organs and secondary sex characteristics
Ovaries
Estrogens
Most body cells
Promotes maturation and maintenance of the female
reproductive organs and secondary sex characteristics;
helps regulate menstrual cycle
Progesterone
Uterus and breast
Prepares uterus for pregnancy and maintains pregnancy if
established; stimulates development of mammary gland;
helps regulate menstrual cycle
Pineal Gland
Melatonin
Hypothalamus
Regulates daily rhythms such as sleep and wakefulness
Thymus
Thymosin
Tissues involved in immune
response
Immune system development and function; maturation of
T-lymphocytes
Stomach mucosa
Gastrin
Gastric glands
Stimulates production of hydrochloric acid and pepsinogen
for digestion
Small intestine
Secretin
Pancreas
Stimulates production of bicarbonate-rich fluid to neutralize
stomach acid
Cholecystokinin
Pancreas and gallbladder
Stimulates secretion of digestive enzymes from pancreas
and release of bile from gallbladder
Heart
Atrial natriuretic peptide
Kidneys
Loss of sodium and water in urine to decrease blood
volume and blood pressure
Kidney
Erythropoietin
Bone marrow
Stimulates red blood cell production