UNIT A CHAP 13 – ENDOCRINE SYSTEM

HORMONE TYPE AND STRUCTURE MINI QUIZ STUDY NOTES

Endocrine system
- Uses ductless glands that secret hormones to various parts of body, slower process than
nervous system but effects last longer

Types of glands:
- Exocrine glands secrete products to body via ducts -> sweat, mucus, digestive enzymes
- Endocrine glands secrete hormones into bloodstream where they travel to specific
target cells
o Endocrine cells are grouped into ductless organs called glands

Endocrine system:
- Hypothalamus (endocrine center), pituitary gland (master gland), pancreas (dual gland),
adrenal glands (deals with stress hormones, mineral and water balance, sex hormone),
pineal gland (sleep), thymus (immunity)
- Endocrine cell ejects hormone into bloodstream and then is received by a target cell

Hormone types:
- Polypeptides, amines, steroids
- Water soluble -> polypeptides and amines (receptor on outside of cell, cannot pass
through phospholipid bilayer)
- Lipid soluble -> steroids and thyroid hormones (receptors must be on inside of cell, can
pass through phospholipid bilayer)

Water soluble hormones:

- Polypeptide/amine hormones are usually water soluble
- If glandular dysfunction present, hormones cannot be taken orally as proteins are
digested in the stomach. Must be injected intravenously
- Water soluble hormones unable to cross lipid bilayer, must interact with cell surface
signal receptors
o Norepinephrine, insulin are water soluble
- Bind to cell surface receptors, then alters gene code transcription (the code for
synthesis of a particular protein)
- Also could cause:
o Activation of an enzyme
o Change in uptake/secretion of a specific molecule
o Changes in membrane permeability, increases protein synthesis, or
rearrangement of the cytoskeleton

Lipid soluble hormones:

- Steroids and some larger nonpolar molecules (amines)
 - Made from cholesterol, a lipid synthesized by the liver
- May be taken orally or intravenously in case of glandular dysfunction
- Can cross the lipid bilayer of target cells and interact with intracellular or nuclear
membrane receptors
- Steroid hormones have 4 carbon rings
- Alters gene code transcription
- Also could cause DNA to trigger production of certain hormones

Multiple effects of hormones:

- Many hormones elicit more than one response in the body
- The effects vary depending on type of receptor molecule on target cells

Regulating the regulators:

- Control is done through NEGATIVE FEEDBACK MECHANISMS
o Goes against the stimulus to reduce the effect
o End product interacts with the initiating stimulus-response gland
- Stimulus -> hypothalamus -> hormone 1 (tropic hormone) -> pituitary gland -> hormone
2 (stimulating hormone) -> target cells -> hormone 3 (negative feedback hormone) ->
target cells + pituitary gland + hypothalamus (negative feedback)

Tropic hormones:
- causes the release of other hormones from various endocrine glands
- many are released from anterior pituitary gland
o thyroid stimulating hormone TSH -> T4, T3
o adrenocorticotropic hormone ACTH -> stress
o luteinizing hormone LH -> estrogen, progesterone, testosterone
o follicle stimulating hormone FSH -> estrogen, follicles
- hypothalamus controls release of tropic hormones via releasing or inhibiting hormones
PITUITARY MINI QUIZ STUDY NOTES

Hypothalamus:
- Big role in integration of nervous and endocrine systems
- Signals the pituitary gland via releasing or inhibiting hormones and neurons that run
through a connecting stalk

Pituitary gland:
- Releases at least 8 hormones involved in metabolism, growth, development, and
reproduction
- releases several tropic hormones
- consists of 2 lobes
o posterior
o anterior

Posterior pituitary:
- also part of nervous system
- does not produce any hormones, just releases the hormones (produced by
hypothalamus) into the body
- oxytocin OCT – usually in females, stimulates uterine muscle contractions, release of
milk by the mammary glands
- antidiuretic hormone ADH – promotes retention of water by kidneys when dehydrated
- Neurosecretory cells in hypothalamus make ADH and OCT, transported to posterior
pituitary by neuronal axons, nerve signals from brain trigger the release of these
hormones in response to stimuli

Posterior: Antidiuretic Hormone ADH:

- Regulates blood osmolarity (solute in blood, e.g. ions)
- Is secreted in response to changing blood osmotic pressure
- Regulates kidney function, increases water retention, reducing urine output
- Osmoreceptor cells in the hypothalamus monitor osmolarity of the blood and regulate
release of ADH from posterior pituitary
- More dehydrated -> high blood osmolarity -> hypothalamus -> more water -> pituitary
-> ADH -> target cells -> negative feedback when body is hydrated again
- Diabetes insipidus – production of excessive amounts of urine caused by the failure of
kidney to respond to ADH

Posterior: Oxytocin OCT:

- Stimulates smooth muscle to contract
- Facilitates uterine contraction and regulates milk release during nursing
- Stimulus (birth or suckling) -> hypothalamus -> posterior pituitary -> oxytocin released
-> uterine wall or mammary glands smooth muscle contract
- POSITIVE FEEDBACK – wouldn’t want the oxytocin to stop and thus stop releasing
milk/stop contracting the uterine wall
 - cuddle chemical

Anterior pituitary:
- true hormone synthesizing gland
- produces and releases at least 6 major hormones
o Human growth hormone hGH
o Thyroid stimulating hormone TSH
o Adrenocorticotropic hormone ACTH
o Prolactin (PRL)
o Follicle stimulation hormone (FSH)
o Leutinizing hormone (LH)
- Blood vessels called a portal system
o Carries releasing hormones from hypothalamus -> to the anterior pituitary,
which stimulates or inhibits release of hormones from gland
o Every anterior pituitary hormone (tropic) is controlled by at least one releasing
hormone (from hypothalamus, not tropic)
hGH AND THYROID GLAND MINI QUIZ STUDY NOTES

Human growth hormone hGH:

- Affects every body tissue (via direct stimulation or tropic effects)
- Stimulates the liver to release growth factors (IGF’s) insulin-like growth factor
(regulatory protein)
- Releases:
o Protein synthesis
o Cell division and growth
o Metabolic breakdown and release of fats stored in adipose tissue

Conditions associated with hGH:

- Gigantism (excessive hGH), pituitary dwarfism (overproduction of hGH in adulthood),
and acromegaly (bones and soft tissue widen, leading to cardiovascular diseases,
diabetes, respiratory problems, muscle weakness, colon cancer)

Thyroid hormones:
- Thyroid gland
- Thyroxine
- Thyroid, calcitonin, parathyroid

Thyroid gland:
- Below the larynx in the throat
- Made of 2 lobes
- Secretes Thyroxine T4 and Triiodothyronine T3
o Regulates bioenergetics
o Helps maintain normal blood pressure
o Heart rate
o Muscle tone
o Regulates digestive and reproductive function

Thyroxine release mechanism:

- Hypothalamus (TRH, releasing hormone) -> pituitary (TSH, tropic hormone) -> thyroid
gland (T4 and T3)
- Higher levels of T4 and T3 and TSH inhibit the release of TRH from hypothalamus
(negative feedback) thus turning off the production of TSH from pituitary

T4 primary role:
- Increase rate of which the body metabolizes fats, proteins, and carbohydrates for
energy
- Stimulates cells of heart, skeletal muscle, liver, and kidney to increase the rate of cellular
respiration

Thyroid conditions:
 - Cretinism due to failure of thyroid to develop in childhood (no negative feedback) low
levels of thyroxine
o Stocky and short, slow pulse rate, puffy skin, hair loss, tired, weight gain
- Hyperthyroidism due to over-production of thyroxine
o Anxiety, insomnia, heat intolerance, irregular heartbeat, weight loss

Graves Disease:
- Severe hyperthyroidism resulting when body’s immune system creates antibodies that
attack/bind to TSH receptors on the thyroid
- Overstimulation of thyroid, enlargement
o Swelling of muscles around eye, interferes with vision
o Treated with medication or irradiation of part of thyroid
- Iodine needed to make T4
o Insufficient iodine -> insufficient T4 -> less inhibition of TSH -> no negative
feedback -> goitre

Calcium metabolism: Thyroid – calcitonin: -ve

- Calcium is crucial in blood clotting, nerve conduction, muscle contraction, development
of teeth and bones
- Calcium levels are regulated in small part by calcitonin
- When calcium levels in blood are too high, calcitonin stimulates uptake of calcium into
bones

Parathyroid glands – calcium homeostasis: -ve

- Low levels of calcium -> blood PTH release -> inhibits release of calcitonin from thyroid
o Breaks down bone material
o Stimulates kidneys to reabsorb calcium, activates vitamin D
o Vitamin D stimulates absorption of calcium from food in intestine
o Release of PTH is inhibited by increased blood calcium levels
PTH AND CALCITONIN SUMMARY:
- Low levels of calcium in blood -> PTH -> inhibits calcitonin from thyroid -> kidneys
reabsorb calcium -> breakdown of bone to release calcium into blood -> increased
absorption of calcium in intestine -> blood calcium increased -> negative feedback, PTH
stopped (thyroid)
- High levels of calcium in blood -> thyroid releases more calcitonin -> stimulates uptake
of calcium into bones (parathyroid)
- Homeostasis

Conditions of PTH:
- Deficiency of PTH -> low blood calcium and causes tetany (neurons depolarize without
stimulus)
- Overproduction of PTH -> high blood calcium and causes bones to soften and weaken,
kidney stones
Antagonistic hormones:
- Homeostasis by control of calcium is a good example by the action of 2 antagonistic
hormones
o Decrease of blood calcium -> PTH ^
o Increase in blood calcium -> calcitonin ^
ADRENAL GLANDS MINI QUIZ STUDY NOTES

Adrenal gland:
- Medulla (nervous system, short term stress responses)
- Cortex (endocrine control, long term stress response stimulated by ACTH)
o Corticoids
 Glucocorticoids
 Mineralocorticoids
 gonad corticoids
- Adrenal cortex (outer layer)
o True endocrine cells
o Long term stress response
- Adrenal medulla (inner layer)
o Involved in short term stress response
o Secretory cells derived from neural tissue

Adrenal Medulla:
- Produces two closely related hormones
o Epinephrine (adrenaline)
o Norepinephrine (noradrenaline)
- Both are catecholamines – synthesized from amino acid tyrosine
- These hormones regulate short term stress response -> fight or flight response
- Under the control of the nerve cells from sympathetic division of autonomic nervous
system
- Stress stimulus -> preganglionic neurons -> release acetylcholine (neurotransmitter) in
the adrenal medulla
- Acetylcholine combines with receptors on cells -> epinephrine and norepinephrine are
released into blood as hormones

Functions of Epinephrine and Norepinephrine:

- Increase metabolic rate
- Release is quick because under the nervous system control
- Glycogen breakdown in the liver and skeletal muscle cells, increase glucose into blood
from liver and stimulate the release of fatty acids
- Cardiovascular and respiratory system effects
o Heart rate and stroke volume ^ , dilate bronchioles in lungs
o Constriction of some vessels
- Epinephrine acts quickly, used to counteract the effects of life threatening situations ->
anaphylactic shock (epi pen)

Adrenal cortex:
- Regulating long term stress response
- Adrenal cortex responds to endocrine signals
 - Stressful stimuli signal hypothalamus to release corticotropic-releasing hormone (CRH)
-> ACTH from anterior pituitary -> adrenal cortex -> cortex signals the release of a group
of hormones called corticosteroids
- Hormones produced in the adrenal cortex are steroid hormones (cholesterol)
o Glucocorticoids -> glucose metabolism, promote glucose synthesis from non-
carbohydrate sources such as proteins, more glucose for fuel
o Mineralocorticoids
o Gonadocorticoids

Cortisol: (CORTEX)
- Raises blood glucose levels
o Skeletal muscle break down -> amino acids -> moves to liver and kidneys ->
converted in glucose -> more glucose available
o Fat cells also broken down -> glucose
- Most abundant glucocorticoid
- Works in conjunction with epinephrine but is longer lasting
- Negative feedback on hypothalamus and anterior pituitary -> suppresses ACTH -> stops
cortisol release

Long term exposure to Glucocorticoids:

- Impaired thinking, damage the heart, high blood pressure, diabetes
- Cortisol is a natural anti-inflammatory -> infections

Mineralocorticoids: (CORTEX)
- Mostly water balance
- Aldosterone, principle mineralocorticoid, functions in ion and water homeostasis of the
blood
o low blood volume/pressure -> angiotensin II -> aldosterone -> kidneys to
reabsorb sodium ions and water from filtrate, raising blood pressure and volume
o stress -> ACTH -> aldosterone + glucocorticoids
o negative feedback loop: heart atria stretched -> cardiac cells release ANH ->
aldosterone secretion inhibited

Inadequate secretion of corticoids -> Addison’s Disease:

- hypoglycemia – lack of cortisol
o weight loss, mental fatigue, weakness
- decrease in sodium and water absorption due to a lack of aldosterone
o low blood pressure and dehydration

Over secretion of corticoids -> Cushing’s Disease:

- high blood sugar hyperglycemia
- fat deposits resulting from excess glucose in body

Gonadocorticoids (sex hormones): (CORTEX)

- Androgens (testosterone) and Estrogens are produced in small amounts in adrenal
glands by both sexes, most in gonads (testes and ovaries)
o Potentially supplements sex hormones produced in the gonads
o May be involved in onset of puberty
o Androgens thought to influence sex drive
PANCREAS MINI QUIZ STUDY NOTES

Pancreas:
- Mainly exocrine tissue (ducts) that produces digestive enzymes
- Secrets enzymes via pancreatic ducts into duodenum

Islet of Langerhans:
- Scattered among exocrine tissue
- Endocrine cells
- Secretes 2 hormones which have opposite effects
o Insulin
o Glucagon

Pancreas:
- Beta cells: secrete insulin
o Decrease blood glucose
- Alpha cells: secrete glucagon
o Increase blood glucose

Homeostasis of blood glucose: 90mg/100mL

- when blood glucose levels fluctuate away from 90mg/100mL, hormonal action:
- both insulin and glucagon are regulated by negative feedback mechanisms

Increase in blood glucose levels:

- pancreatic beta cells secrete insulin
- insulin -> all body cells except brain -> target cells more permeable to glucose,
promotes conversion of glucose to glycogen in liver, inhibits conversion of amino acids
and fatty acids to sugars -> net result, lower blood glucose concentration

Decrease in blood glucose levels:

- pancreatic alpha cells secrete glucagon
- only liver cells are sensitive to glucagon
- glucagon -> liver cells increase glycogen hydrolysis (breakdown) -> liver converts amino
acids and fatty acids to glucose and starts to release glucose to blood stream -> net
result, increase blood glucose levels

Antagonistic effects of glucagon and insulin are vital to glucose homeostasis

- hGH, epinephrine, and cortisol play roles in glucose homeostasis as well

Glucose imbalance:
- Diabetes mellitus – body unable to produce enough insulin or does not respond
properly to insulin
- After a meal, blood glucose levels will rise and remain high due to insulin deficiency
o Hyperglycemia
 - In diabetes, glucose is excreted in the urine
- Dehydration, constant thirst

Effects of hyperglycemia:
- Without insulin -> glucose cannot enter cells -> no cellular respiration -> fatigue
- protein and fat metabolism -> acidic metabolites -> lowers pH -> could lead to tissue
damage (denaturing of proteins, coagulation, etc.)
- long run:
o blindness, kidney failure, circulatory problems, nerve damage, infection

Types of diabetes mellitus:

- type 1 diabetes:
o juvenile diabetes or insulin dependent diabetes
o caused when immune system produces antibodies that attach and destroy beta
cells (insulin) of pancreas (an autoimmune disease) -> no insulin
o daily insulin injections
- type 2 diabetes:
o develops over time, insulin receptors in body stop responding to insulin, beta
cells produce less insulin over time due to poor lifestyle
o obesity, diet, and genetics are causes of type 2 diabetes
 90% of diagnosed diabetes cases are type 2

Treatment:
- Type 1: insulin injection
- Type 2: exercise, diet, medication
- Synthetic insulin produced from genetically engineered bacteria
- Islet cell transplants