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