Endocrine

1. Introduction to Anatomy and
Physiology II
Bio 132
Professor Peter Smith D.P.T, ATC
Smithpr@sunysuffolk.edu
http://www2.sunysuffolk.edu/smithpr/
Spring 2013

2. Overview of Anatomy and
Physiology
• Anatomy – The study of the structure of body
parts and their relationships to one another.
• Physiology – the study of the function of the
body’s structural machinery.
• Understanding both the anatomy and physiology
of the human body is critical to all health care
providers.
• You can’t diagnose disease (Pathology) if you
don’t understand both the underline anatomy
and physiology.

3. Homeostasis
• A great deal of energy is spent trying to maintain
homeostasis.
– the ability to maintain a relatively stable internal
environment in an ever-changing world.
• The internal environment of the body is in a
dynamic state of equilibrium
• Chemical, thermal, and neural factors interact to
maintain homeostasis
– As we age these mechanisms become less efficient.
• Makes us more susceptible to disease and less resilient
once we have one.

4. Negative Feedback
• In negative feedback systems, the output shuts
off the original stimulus
– This makes up 99% of the homeostatic
feedback loops.
• Examples include regulation of : body
temperature, body pH, blood glucose levels,
blood pressure, body calcium levels.
– Prevents large fluctuations and keeps the internal
environment relatively stable

5. Negative Feedback
Figure 1.5

6. Positive Feedback
• In positive feedback
systems, the output
enhances or
exaggerates the
original stimulus.
• Less than 1% of the
feedback loops.
Figure 1.6

7. Positive Feedback

8. Endocrine System: Overview
• Endocrine system – controlling system which
influences metabolic activities of cells by means
of hormones.
• Hormones
– chemical messenger secreted into bloodstream,
stimulates response in another tissue or organ
• Endocrine glands – produce hormones
– pituitary, thyroid, parathyroid, adrenal, pineal, testes,
ovaries and the hypothalamus.
• Other tissues and organs that produce hormones include:
adipose cells, cells in the walls of the small intestine,
kidneys, and heart.

9. Endocrine System

10. Hormones
• Hormones:
– Regulate the metabolic function of other cells
• Alter plasma membrane permeability ( insulin)
• Stimulate protein synthesis (GH)
• Activate or deactivate enzyme systems
(GHRH,GHIH)
• Induce secretory activity (Prolactin)
• Stimulate mitosis (FSH)
– Tend to have prolonged effects
– Are classified as amino acid-based hormones, or steroids ( lipid
based)
• Eicosanoids – leukotrienes and prostaglandins

11. Amino Acid Based Hormones
• Most hormones belong to this
class, including:
– Glucagon, Insulin
• are functional
polypeptides
– Specificity of hormone is
determined by 3-D
configuration.
– Polar molecules: water
soluble allowing them to be
transported in the blood.
– They exert their effects on
extracellular receptors.

12. Steroids (Lipid Based Hormones)
• Steroids – derived from
cholesterol
– Non polar molecules:
are hydrophobic
therefore require a
protein carrier to be
transported in the blood.
• Adrenocortical hormones
• Aldosterone
• Gonadal
• Estrogen,
Testosterone

13. Hormone Action
• Hormones alter target cell activity by one of two
mechanisms
– Second messengers involving:
• Amino acid–based hormones cannot pass through
the membrane.
– They attach to a specific regulatory G protein on
surface of cell membrane.
– This sets off a series of steps that can activate or inhibit
numerous functioning enzymes in the cell.
– Direct gene activation involving steroid hormones
• Since steroid based hormones are lipophillic they
can diffuse through the cell membrane and enter
the nucleus where they can alter gene expression.

14. Amino Acid-Based Hormone Action: cAMP
Second Messenger
Figure 16.2a

15. 1. Hormone (first messenger) binds to its
receptor, which then binds to a G protein
2. The G protein is then activated as it binds
GTP, displacing GDP
3. Activated G protein activates the effector
enzyme adenylate cyclase
4. Adenylate cyclase generates cAMP
(second messenger) from ATP
– cAMP activates protein kinases, which then
cause cellular effects
Amino Acid-Based Hormone Action:
cAMP Second Messenger

16. Figure 16..3
Steroid Hormones

17. 1. Steroid hormones and thyroid hormone are
hydrophobic, therefore require a carrier protein to
circulate in the blood.
2. To exert their effects they separate from their carrier
proteins and diffuse easily into their target cells.
3. Once inside, they bind and activate a specific
intracellular receptor
4. The hormone-receptor complex travels to the nucleus
and binds a DNA-associated receptor protein
5. This interaction prompts DNA transcription to produce
mRNA
– The mRNA is translated into proteins, which bring about a
cellular effect.
– What’s the significance of having both lipid and amino acid
based hormones.
Steroid Hormones

18. • The nervous system modifies the stimulation of
endocrine glands and their negative feedback
mechanisms.
• Nervous system is fast acting/short duration while the
endocrine is slow starting/long lasting.
• The nervous system can override normal endocrine
controls.
– For example, control of blood glucose levels are
normally maintained by the endocrine system.
• Under stress when the body needs more glucose
the hypothalamus and the sympathetic nervous
system are activated to supply ample glucose.
Nervous / Endocrine System
Interrelationship

19. Communication by the Nervous
and Endocrine Systems

20. Endocrine vs. Exocrine Glands
• Exocrine glands
– Ducts carry secretion to a surface or organ
cavity which exert extracellular effects.
• (food digestion) Amylase is released to hydrolyze
polysaccharides into di and monosaccharides
• Endocrine glands
– no ducts, release hormones into tissue fluids
such as the blood.
• Rich blood supply to distribute hormones.
• intracellular effects, alter target cell metabolism

21. • Blood levels of hormones:
– Are controlled by negative feedback systems
– Vary only within a narrow desirable range
• Hormones are synthesized and released in response to
three basic mechanisms.
• Humoral: changes and substances in the blood (glucose or
K+)
• Neural: stimulation from the nervous system via
neurotransmitters.
• Hormonal stimuli: organ or gland releases a hormone
that stimulates the release of another hormone from another
glands or organ.
Control of Hormone Release

22. Endocrine Organs

23. Hypothalamus
• Controls many endocrine glands:
– regulates the endocrine system through it’s direct
connection to the pituitary gland
• The hypothalamus controls basic functions such
as:
– body temperature, blood pressure, growth and
development ,reproduction, electrolyte balance and
water regulation.
• It accomplishes this by producing both releasing
and inhibiting hormones that influence the
anterior pituitary gland.
• Produces ADH and Oxytocin which are
transported to the posterior pituitary where they
will ultimately be released.

24. Pituitary Gland (Hypophysis)
• Suspended from
hypothalamus by the
pituitary stalk
(infundibulum)
– housed in sella turcica
of sphenoid bone
• Adenohypophysis
(anterior pituitary)
– arises from glandular
tissue
• Neurohypophysis
(Posterior Pituitary)
– arises from brain
(neural tissue)

25. Histology of Pituitary Gland

26. Neurohypophysis
Posterior Pituitary
• Neurohypophysis –
posterior lobe (neural
tissue) and the
infundibulum
– Receives hormones
from the hypothalamus.
– Hormones are stored,
and released
• Oxytocin and ADH

27. • Oxytocin is a strong stimulant of uterine
contraction
– During labor increasing levels leads to
increased intensity of uterine contractions.
• Regulated by a positive feedback mechanism
– PITOCIN is a synthetic form used to induce labor
• Oxytocin triggers milk ejection (“letdown” reflex)
in women producing milk.
– Baby suckling of breast causes ejection of
milk.
– It’s considered the pair bonding hormone
Oxytocin

28. Oxytocin

29. • AKA. Vasopressin is released in response to low
blood pressure, dehydration and high solute
concentration in the hypothalamus.
• ADH helps to prevent dehydration by:
– ADH stimulates thirst
– ADH targets aquaporins in the kidney to
increase water permeability.
• This will increase blood volume which increases
BP
– Causes small arteries to constrict thus
increasing BP
– Reduces secretory activity of sweat glands
preventing additional water loss
Antidiuretic Hormone

30. Antidiuretic Hormone (ADH)
• Alcohol inhibits ADH release and causes
many unwanted trips to the bathroom.
– Hang over symptoms primarily result of
dehydration .
• Diabetes insipidus is a condition where
there is a hyposecretion of ADH
– What effect will this have on urinary output
and hydration status?

31. Figure 16.5
Anterior Pituitary-Hypothalamic Connection:

32. • Adenohypophysis – anterior lobe, made up of
glandular tissue derived from the oral mucosa
during embryologic development.
– Synthesizes and secretes a 6 major
hormones
• There is a vascular connection via the
hypophyseal portal system
– The vascular anatomical connection provides an a
means of delivering hypothalamic hormones directly
to the anterior pituitary.
– Hypothalamic hormones avoid general circulation
allowing smaller amounts of hormones to be
delivered in a fraction of the time.
Anterior Pituitary

33. • The hypothalamus sends a chemical stimulus to
the anterior pituitary in the form of releasing
hormones :
– Releasing hormones stimulate the synthesis
and release of hormones from the anterior
pituitary.
• example TRH (Thyrotropin Releasing
Hormone) causes the production and
release of TSH( Thyroid Stimulating
Hormone)
– Inhibiting hormones shut off the synthesis and
release of hormones.
– PIL( Prolactin inhibiting Hormone)
• inhibits the synthesis and release of
Prolactin
Activity of the Adenophypophysis

35. • Releasing hormone (GHRH) from the hypothalamus
stimulates GH release in response to low blood sugar,
increased levels of stress i.e. exercise and increases in levels
of some amino acids.
• GH: causes cells in the liver, muscle, cartilage, bones and
other tissues to release (IGF’s):
• Insulin like growth factors. (Anabolic)
– Skeletal muscle: increase uptake of A.A to build more
protein and inhibits protein catabolism.
– Facilitates bone and cartilage growth by absorbing
building blocks such as sulfur.( i.e. glucoseamine sulfate,
Chondroitin sulfate)
– Promotes sodium, potassium and chloride retention by the
kidneys and enhances calcium absorption by the small
intestine.
Metabolic Action of Growth Hormone

36. Metabolic Action of Growth
Hormone
• Anti-insulin effects include
– Liver: reduces the formation of glycogen and
promotes lipolysis of adipose cells. (the
hydrolysis triglycerides for energy).
• Decreased rate of glycogen production in
the liver makes more available for
structures rely on sugar exclusively. (brain)
– :Growth hormone–inhibiting hormone (GHIH)
inhibits GH release

37. Gigantism
• Excessive growth
hormone before the
growth plates fuse.
– Good for basketball
– Bad for horse racing.

38. Acromegaly
• To much GH usually
after the growth
plates have fused.
– Results in great
wrestlers.
• Beware the Pituitary
Tumor.

39. Dwarfism
• Hyposecretion of GH
• May require GH
replacement therapy

40. Thyroid Gland
• The largest endocrine
gland, located in the
anterior neck, consists of
two lateral lobes
connected by a median
tissue mass called the
isthmus
• Its rich blood supply reflect
its importance.

41. Thyroid Stimulating Hormone
• Triggered by hypothalamic secretion of thyrotropin-
releasing hormone (TRH )
• TSH stimulates the normal development and secretory
activity of the thyroid gland (Thyroxin)
• Rising blood levels of thyroid hormones act on the
pituitary and hypothalamus to block the release of TSH

42. Thyroid Gland
• Thyroid follicles
– lined with simple cuboidal epithelial (follicular
cells) that secretes two hormones, T3 and T4
• T4 : 98% and relatively inactive.
• T3 :cells convert T4 into this form which is much more
active.
– Colloid: incorporates iodine and thryoglobulin to
produce thyroid hormone
– thyroid hormone is stimulated by conditions that
increase the bodies need for ATP.
• A ↓in body temperature, hypoglycemia, high altitude
and pregnancy all increased thyroid hormone

43. Figure 16.8
Synthesis of Thyroid Hormone

44. Thyroid Hormone
• Thyroid hormone (TH) action is like turning up the
thermostat.
• TH causes:
↑ body’s metabolic rate and O2 consumption
– Calorigenic effect - ↑ heat production with increased ATP
consumption.
↑ heart rate, contraction strength blood pressure and
respiratory rate
» by enhancing norepinephrine and epinephrine
actions.
∀↑ stimulates many things necessary for growth and
devolvement.
∀↑in appetite and breaking down of CHO, lipids and
proteins for energy

45. Endemic goiter
• Goiter = enlarged thyroid
gland
– results from dietary iodine
deficiency.
– Can’t produce TH,
– no feedback to Pituitary ↑
TSH
– This causes hypertrophy of
the thyroid gland.

46. Toxic goiter (Graves disease)
• Antibodies mimic TSH
causing ↑’d TH to be
released,
• Excessive Thyroxin levels
– elevated metabolism
– heart rate
– weight loss
– nervousness
– exophthalmos (bulging
eyes)
– ANS induced sweating.

47. Thyroid Histology

48. • Parafollicular cells produce calcitonin:
– ↓ blood Ca2+
and promotes Ca2+
deposition in bone.
• Calcitonin:
– Inhibits osteoclast activity (breaks down bone
releasing calcium from the bone matrix)
– Stimulates calcium uptake and incorporation
into the bone matrix by increasing osteoblast
activity.
• Regulated by a blood (calcium ion concentration
in the blood) negative feedback mechanism
• Antagonist to parathyroid hormone (PTH)
Calcitonin

49. Parathyroid Glands
• Tiny glands
embedded in the
posterior aspect of
the thyroid
– Chief (principal) cells
secrete PTH
(parathyroid hormone)
– PTH regulates calcium
balance in the blood

50. Figure 16.11
Effects of Parathyroid Hormone

51. Figure 16.12a
Adrenal Cortex

52. • Adrenal glands – paired, pyramid-shaped
organs on top of the kidneys structurally and
functionally they are two glands in one.
• Adrenal Cortex releases a variety of hormones
that allow the body to deal stress blood pressure
changes with development of secondary sex
characteristics.
• Adrenal medulla – nervous tissue that is the
hormonal branch of the sympathetic nervous
system (fight/flight)
Adrenal (Suprarenal) Glands

53. • Different corticosteroids are produced in
each of the three layers
– Zona glomerulosa – mineralocorticoids
(chiefly aldosterone)
– Zona fasciculata – glucocorticoids
(chiefly cortisol)
– Zona reticularis – gonadocorticoids
(chiefly androgens) testosterone in males and
estrogen in females
Adrenal Cortex

54. • Produced by the Anterior Pituitary.
– Triggered by hypothalamic corticotropin-
releasing hormone (CRH)
– Stimulates the adrenal cortex to release
corticosteroids and mineralocorticoids.
• ACTH is stimulated by
–fever,
–hypoglycemia,
–various stressors
Adrenocorticotropic Hormone
(ACTH) (Corticotropin)

55. • Regulate the electrolyte concentrations of
extracellular fluids
– Aldosterone – most important mineralocorticoid
– Maintains Na+
balance by reducing excretion of Na+
from the body while increasing K+
excretion.
Aldosterone secretion is stimulated by:
– Rising blood levels of K+
– Low blood Na+
– Decreasing blood volume or pressure
Mineralocorticoids

56. Glucocorticoids (Cortisol)
• Stress on body causes hypothalamus to release
CRH→ACTH → targets adrenal cortex to release
Cortisol: Cortisol
– targets liver and muscle cells:
– Increases levels of the following in the blood to
ensure there is enough available fuel to deal with
stress.
• glucose
• fatty acids
• amino acids
– Gluconeogenesis (formation of glucose from non-
carbohydrates)
• Inhibit inflammation
• Depressed the immune system

57. Cushing Disease
• Cushing Disease :hyper secretion of ACTH or Cortisol
– Results in moon face hunch back appearance.
– Muscle wasting
– Hyperglycemia
• Depress cartilage and bone formation
• Promote diseases of the cardiovascular, nervous and
gastrointestinal systems.
• Increased blood pressure
• Often medically induced as a result of patient given high dose
corticosteroids
– For treatment of inflammatory, autoimmune and allergic medical
condition.

58. Cushing Disease

59. Cushing Disease

60. Adrenal Medulla
• The adrenal medulla functions as an extension
of the sympathetic nervous system.
• Under periods of stress a neuron from the
hypothalamus directly stimulates as the adrenal
medulla.
• Since this is a direct neural connection the
adrenal medulla can release the catecholamines
(epinephrine and norepinephrine) immediately.
– Catecholamines are the hormonal portion of the SNS
• Functionally their effects on the body are the same.

61. Figure 16.15
Stress and the Adrenal Gland

62. Addison's Disease
• Results from a
hyposecretion of ACTH or
an autoimmune disease
that damages the
adrenals.
• Results in decreased
glucocorticoids and
mineralocorticoid release.
• Results in hypotension
and hypoglycemia
• Corticosteroid
replacement therapy

63. A patient 16 y/o male with complaints of tunnel vision
and HA comes into your office. He is 6ft 11inches in
height and weighs 295 lbs. The patients parents are
both over 6 feet. What is a possible diagnosis for his
condition.
A. A tumor causing increased thyroid function.
B. Genetic ( follow up with ophthalmologist for
tunnel vision.)
C. A hyperactive pancreas
D. A pituitary tumor
E. Under active hypothalamic secretions

64. Clinical Question
What actions would be appropriate.
• A) Order a head CT to observe any anomalies in
the cranium.
• B) Blood work to look at levels of GH, LH,
insulin, ETC
• C) Send him to an ophthalmologist for further
examination.
• D) Set him up with your 6ft 2 sister and tell him
not to walk into any walls.
• E) All of the above.

65. A 48 female presents to the doctor with the
following complaints. She reports excessive
fatigue recent weight gain and depression.
She has recently been loosing her hair and
has become very forgetful.
•Is this an endocrine problem?
•If so what hormone might explain these
symptoms.

66. A patient was in a car accident five years
ago. Since then he has been in chronic pain
managed by opiate painkillers. The patient
reports that the medication is no longer
working. The doctor responds by increasing
the dose.
Why did the patient require a higher dose of
medication to get the same therapeutic
effect?

67. Hormones and Target Cell Sensitivity
• Cells respond to hormonal levels of stimulation differently. When signaling is
low the target cell will make more receptors. When stimulation is high the cell
will reduce the number of receptors.
• What is the clinical applications to the cells intrinsic homeostatic
mechanisms?

68. Endocrine Screen
• Hyperglycemia / Hypoglycemia
• Poly /glucosurea
• Temp. intolerance (hot vs. cold)
• Changes in heart rate / palpitations
• Changes in physical features
– Skin changes, excessive abnormal hair growth, Body Fat
distribution
• Deep Rapid Breathing
• Changes in Body WT.
• Fatigue /weakness
• Goiter
• Irradiation exposure