Endocrine System

Types of Intercellular communication

Gap junctions: Through cytoplasm
Neurotransmitters: Through synaptic cleft
Paracrines: Through interstitial fluid
***Hormones: Through the blood

Principles of hormone communication

Hormones are released by endocrine glands (endocrine cells, neuroendocrine glands)
Hormones are picked up by the blood
Hormones travel throughout body
Hormones "diffuse" out of capillaries
Hormones stimulates "Target cells

Hormones are released by endocrine glands (endocrine cells, neuroendocrine glands)

When we produce a hormone the cells don't put it in the blood
The hormone is NOT going from the cell into the blood - The hormone leaves the cell and go into the interstitial fluid (the fluid surrounding cell)
We call these cells that are producing it end

Target cells

Target cells are those cells that have receptors for the hormone
Cells affected by hormones
Select cells that can hear the "signal" - they have receptors for the hormone
Hormones has specificity in their receptors

Hormones Chemistry: Classes of Hormones

Steroid hormones, Monoamines (Biogenic amines), & Peptides & Glycoproteins

Steroid hormones

Derived from cholesterol
Secreted by gonads and adrenal cortex

Monoamines (Biogenic amines)

Based on amino acids that have been tweaked and modified
Derived from tyrosine & tryptophan
Secreted by adrenal medulla, pineal, & thyroid glands
Norepinephrine is made in the medulla

Peptides & Glycoproteins

Secreted by pituitary, hypothalamus, and others

Hormones Receptors & Effects

Hydrophobic (doesn't care for water) hormones
Hydrophilic (water soluble) hormones

Hydrophobic hormones

Steroid hormones & TH
Travel thru the blood in certain way and we call them hydrophobic hormone
They don't flow around in the blood very easily
Require transport proteins
Penetrate plasma membrane and bind intracellular receptors
Affect gene transcription

Affect gene transcription

They turn on/off gene that were not previously turn on/off
They have a big effect primary because they affect which gene are on & off in a cell

Hydrophilic hormones

Do not require transport proteins
Do not pass into cells
Stimulate cells (2nd messengers)
Require transmembrane receptors
They affect which protein that are already present
Can change cell behavior (i.e. Make an osteoclast secrete more acids & dissolve mo

Stimulate cells (2nd messengers)

The extracellular signals are 1st messenger and then we have 2nd intracellular messenger
2nd messenger turn on & off proteins
The intercellular amplified product that tells a cell hormone

Peptides & Catecholamines

Hormone-receptor binding activates a G protein
G protein activates adenylate cyclase
Adenylate cyclase produces cAMP
cAMP activates protein kinases
Protein kinases phosphorylate enzymes. This activates some enzymes and deactivates others.
Activated enzyme

Endocrine Disorders: What are they?

Abnormal signals within the endocrine system

Endocrine Disorders: What's the cause?

Hyper- or hypo-secretion, or Hyper- or hypo-sensitivity of target cells

Endocrine Disorders: How does that happen?

Tumors, lesion, or autoimmune disorders

Pituitary Organ that control the Hypothalamus

Form floor and walls of the third ventricle of the brain
Controls water balance, thermoregulation, sex drive, childbirth & various autonomic functions
Many of its functions executed by the pituitary gland

Anatomy of the Pituitary

Anterior lobe (Adenohypophysis) &
Posterior lobe (Neurohypophysis)

Anterior lobe (Adenohypophysis)

Arises from the pharynx during development
Glandular epithelium tissue

Posterior lobe (Neurohypophysis)

Outgrowth of the brain
Nervous tissue

Posterior Pituitary (Make 0 hormones - Releases 2)

ADH & Oxytocin

What is ADH?

(Antidiuretic hormone) ? Produced in hypothalamus; transported by hypothalamo hypophyseal tract to posterior lobe

Neuroendocrine cells

Nervous tissues that produces hormones

What is Antidiuretic?

It makes you produce less urine
Effects of this is to raise the amount of water in your body
Two targets: Kidney & Brain
Causes us to gain more water
*High osmolality (salt concentration ? ADH ? Increase water retention; Increase thirst
High salt concentr

ADH

*High osmolality (salt concentration ? ADH ? Increase water retention; Increase thirst
High salt concentration makes the body secrete ADH to gain more water

What is Oxytocin?

Produced in hypothalamus; transported by hypothalamo hypophyseal tract to posterior lobe

Oxytocin

***Stimulate milk release
Neutral stimulus ? OT ? Smooth muscle contraction (uterus, reproductive ducts, & mammary glands); promotes emotional bonding
Causes smooth muscle contraction around the mammary gland

Anterior Pituitary Hormones

TSH, ACTH, PRL, GH

***TSH

(Thyroid stimulating hormone) -Tropic hormone
Stimulates secretion of thyroid hormone

***ACTH

(Adrenocorticotropic hormone) - Tropic hormone
Stimulate adrenal cortex to secrete glucocorticoids
Tropic hormone ? Hormones that cause the release of other hormone

***PRL

(Prolactin) - Tropic hormone
After birth stimulates mammary glands to synthesize milk, enhances secretion of testosterone by testes
Stimulate milk production

***GH

Growth Hormone)
Stimulate mitosis and cellular differentiation

Anatomy of Hypothalamus and Pituitary

Hypothalamic releasing & inhibiting hormones travel in the hypophyseal portal system to the anterior pituitary
Anytime hormone that ends in RH or IH means it is coming from the hypothalamus and it's affecting the pituitary
Gonadotropin, Thyrotropin, Corti

Gonadotropin

Releasing hormone
Comes from the hypothalamus and cause the anterior pituitary to release FSH and LH

Thyrotropin

Releasing hormone
Cause the release of TSH

Corticotropin

Releasing hormone

Prolactin

Inhibiting hormone

Growth Hormone

Releasing hormone & inhibiting hormone

Hypothalamo-Pituitary-Target Organ Relationships

Negative feedback inhibition
All hypothalamic and pituitary hormones are peptides

Pineal Gland

Pineal gland synchronizes physiological function w/ 24-hour circadian rhythms of daylight and darkness; Synthesize melatonin from serotonin during the night

What is the Thyroid Gland?

The thyroid is composed of follicles, simple cuboidal epithelium, filled with colloid; Thyroxine (T4) & Triiodothyronine (T3) are released from follicles

Thyroid hormone (T3 & T4) is composed of 2 tyrosines and 3 or 4 iodine ions.

Iodine absorption
We get iodine from salt
Thyroglobulin synthesis (tyrosine amino acid protein)
Iodine added to tyrosines of thyroglobulin
Thyroglobulin uptake and hydrolysis
Release of T4 and a small amount of T3 into the blood

Thyroid Gland

Decrease in temperature ? TH ? Increase Metabolic rate (temperature, O2 effects), Increase appetite, and Increase GH secretion

Thyroid Gland Disorders

Congeital Hypothyroidism, Myxedema, Goiter, Graves disease

Congeital Hypothyroidism (Low level of TH)

Hyposecretion present at birth (formerly cretinism)
Can be treated w/ oral thyroid hormone

Myxedema (decrease TH)

Adult/adolescent hypothyroidism

Goiter (Hypothyroidism)

Pathological enlargement of the thyroid gland
Dietary iodine deficiency, hyposecretion of TH
Symptoms: feeling cold, general activity is slower

Graves disease (hyperthyroidism)

Antibodies mimic the effect of TSH on the thyroid
Hypersecretion of TH

Increase Ca2+ ? Calcitonin ? Increase osteoblast activity & decrease PTH

High levels of Ca in the blood cause us to produce Calcitonin and that calcitonin comes from the thyroid gland
It elevate osteoblasts activity and we make more bone matrix
***We take Ca out of the blood and put it in the bone

C (parafollicular cells)

Makes Calcitonin

Parathyroid Glands

***Decrease Ca2+ ? PTH ? Increase osteoclast activity; Increase Ca2+ reabsorption from kidneys; Increase calcitriol (Vitamin D)
Increase calcitriol production, we absorb Ca from the food we've eaten, we are dissolving bone, and we are limiting ca loss fro

Parathyroid Disorders

Hypoparathyroidism & Hyperparathyroidism

Hypoparathyroidism

Accidental excision during surgery, decline in blood calcium, & fatal tetany in 3-4 days

Hyperparathyroidism

Parathyroid tumor
Ca2+ and phosphate blood levels increase
Spontaneous calcifications occur throughout body

Calcium Homeostasis - Decrease Ca2+ Hypocalcemia

Tingling sensations
Cardiac arrhythmias
Excitability of muscle, spasms, or tetany

Calcium Homeostasis - Increase Ca2+ Hypercalcemia

Sluggishness" of muscles
Depression
Slow reflexes

Calcium Homeostasis

*Blood-calcium levels are important to maintain, because the blood communicates with fluids all over our bodies

Pancreatic Islets

*Alpha cells secrete glucagon; Beta cells secrete insulin
Make sure glucose level are stable

Islet cells

Endocrine cells ? hormone produced by the cells of the islet that do not make their way into the duct/intestine but they go into the blood

Pancreatic Hormones: Insulin

Increase Glucose levels (hyperglycemia) ? Insulin ? Hypoglycemic effects

Hyperglycemia

High glucose level

Insulin's hypoglycemic effects:

Stimulates cells to absorb glucose
Promotes synthesis of glycogen
Suppresses use of stored fuels (fat)

Cause of Diabetes Mellitus?

Hyposecretion or inaction of insulin

Diagnosis of Diabetes Mellitus?

Revealed by elevated blood glucose, glucose in urine, polyuria & dehydration, and ketones in the urine

Type of Diabetes Mellitus

Type 1 (IDDM) & Type 2 (NIDDM)

Type 1 (IDDM)

5 to 10% of cases in US
Insulin is always used to treat Type I
Hereditary susceptibility
Autoantibodies attack and destroy pancreatic beta cells

Type 2 (NIDDM)

90 to 95% of diabetics in US
Insulin resistance
High level of insulin but cells are not responding
Risk factors are heredity, age (40+), obesity, and ethnicity (Native American, Hispanic, & Asian

Pancreatic Hormones: Glucagon

***Decrease Glucose levels (Hypoglycemia) ? Glucagon ? Hyperglycemic effects

Hypoglycemia

Low level of glucose

Glucagon's hyperglycemic effects:

-Stimulates gluconeogenesis & glycogenolysis in liver
Glycogenolysis
-Also stimulates fat catabolism and release of fatty acids to blood from adipose tissue

Glycogenolysis

Breaking down glycogen

Gluconeogenesis

Making new glucose

Liver ? IGF-I Growth Hormone (somatotropin)

Growth hormone = tropic hormone
Last for only a short time
GHRH ? High protein meals, hypoglycemia, sleep, exercise
GHIH ? High carbohydrate meals
IGF-I ? (somatomedin) Mediate the effects of growth hormone
Growth of cartilage, bone, muscle

Specific effects of GH & IGF-I on Proteins

Increase Production; Decrease Degradation

Specific effects of GH & IGF-I on Fats

Mobilized -take out of- " from adipocytes; preferentially used for energy

Specific effects of GH & IGF-I on Carbohydrates

Largely unused (glucose sparing effect), except for brain, kidney, liver RBCs

Gigantism

GH hypersecretion during childhood or adolescence

Acromegaly

Post-adolescent hypersecretion; thickening of bones and soft tissues

Pituitary dwarfism

GH hyposecretion; Made rare since GH supplementation became available

Adrenal Medulla

Neural stimulation ? Catecholamines (E & NE) ? Sympathetic effects; Other effects
Sympathetic effects ? Increases heart rate, eye dilation, decreases digestive activities

Other (non-sympathetic) effects of E & NE

Mobilize (making it available to all of our cells) fuels: lactate, fatty acids, & glucose (stored in the liver as glycogen)
Glucose is produced in the liver (glycogenolysis & gluconeogenesis)
Inhibit insulin secretion: "glucose-sparing effect

Inhibit insulin secretion: "glucose-sparing effect

Telling our body to use alternative fuel and to not use glucose

***CRH

Hyperthalamic hormone that causes the release of ACTH

Adrenal Cortex

Secretes 3 groups of steroid hormones (corticosteroids) from three layers of glandular tissue

Zona glomerulosa

Secretes mineralocorticoids: regulate the body's electrolyte balance
Primary hormone: aldosterone
Decrease Na+ or Increase K+ ? aldosterone ? Increase Na+ & Decrease K+ ; reabsorption by kidney

Zona fasciculata

Secrete glucocorticoids: regulate metabolism of glucose & other fuels
Primary hormone: cortisol
Physical or Mental Stress ? Cortisol ? Increase fat & protein breakdown; Increase gluconeogenesis

Cushing Syndrome

Hypersecretion of cortisol (could be pituitary in origin)
Symptoms: hyperglycemia, hypertension, edema, abnormal fat deposition, muscle & bone loss due to protein catabolism

Zona reticularis

Secretes sex hormones
Primary hormone: DHEA (dehydroepiandrosterone)
DHEA is not itself a hormone, but is the precursor to Testosterone

Adrenogeital syndrome (AGS)

Adrenal adrogen hypersecretion
Masculinizing effects are life stage-dependent:
Newborns girls exhibit masculinized genitalis
Early onset of puberty
Women experience increased body hair & beard, deepening of voice

General adaptation syndrome (GAS) "The Stress Response

Step 1: The Alarm Reaction
Step 2: Resistance
Step 3: Exhaustion