1. Clinical Anatomy Tony Serino, Ph.D.
Endocrine System
Clinical Anatomy
Tony Serino, Ph.D.

2. Endocrine: Topic Objectives
Be able to compare endocrine with neurological control
Be able to classify hormone types
Understand controlling factors in hormone response and effectiveness
Be able to compare and contrast hormone mechanism of action and the roll of second messengers
Be able to describe and explain entire GH reflex and contrast malfunctions

3. Endocrine System
Controls and modifies the internal environment by releasing chemicals (hormones) into the blood
Slower response time but longer duration of action compared to nervous system

4. Chemical Messengers (hormones)
Hormone –secreted by cell into blood and acts on another cell some distance away
Neurohormone –secreted by neuron into blood to affect a target cell some distance away
Local hormones –secreted by cell into interstitial fluid to affects cells nearby
Paracrines –affect neighboring cells
Autocrines –affect the secreting cell
Pheromones –secreted by cell onto body surface to affect cells of another individual

5. Hormones Chemical Classification
Amines –single or few amino acids, most water soluble
Epinephrine, Thyroxine (but water insoluble), Melatonin
Proteins –short to long chains of amino acids; water soluble
GH, FSH, LH, Insulin, Glucagon, ADH, etc.
Steroids –derivatives of cholesterol; water insoluble
Estrogen, Testosterone, Progesterone, Cortisol, Aldosterone

6. Steroid Hormones

7. Characteristics Common to all Hormones
Must have target cell with appropriate receptor molecules
Receptor-hormone complex must trigger events in target cell that changes its physiology
Mechanisms for deactivating the hormone response must be present

8. Controlling Hormone Response
Half-life of the hormone
Physiological range
Modifying target cell response
Up and down regulation
Turning off secretion
Negative feedback
Control by other hormones, neurons and metabolites

9. Control of Hormone Secretion

10. Mechanisms of Hormone Action
2nd messengers
Water Soluble
Water
Insoluble
Carrier protein

11. 2nd Messengers: cAMP

12. 2nd Messengers: IP3 and Ca++-Calmodulin

13. Steroid Hormone Transduction

14. Different Styles of Secretion
Prohormone –a hormone that is made as a larger (inactive form) that must be changed prior to secretion (allows for storage of hormone in secreting cell) Ex.: proinsulin, pro-opiomelanocortin
Prehormone –a hormone that is secreted in an inactive form that must be changed near or in the target cell Ex.: Thyroxine, Angiotensinogen

15. Proinsulin

16. Types of Endocrine Disorders
Hypersecretion
Too much secretion of the hormone
Hyposecretion
Too little secretion of hormone
Hyporesponsiveness
Normal secretion, but little to no response by target cells

17. Endocrine Glands

18. Control of Growth
Growth periods: prenatal and postnatal (consists of pre-puberal (especially the first 2 years –infancy) and puberty
Several factors influence growth: genetics, diet, health, and hormonal balance
Prenatal growth dominated by insulin secretion, post-natal dominated by GH, thyroxine, and sex hormones

19. GH secretion and effects
GH secretion stimulated by exercise, fasting, sleep (diurnal rhythm), stress on bones, decreased plasma glucose, increased plasma AA (such as after a high protein meal)
Increase protein synthesis
Increase differentiation
(increase mitosis)

20. GH interactions with other Hormones
Thyroxine: essential and permissive for GH
Needed to maintain energy levels for growth
Increases sensitivity of target cells to GH effects
Insulin: essential for GH effects
Dominant hormone for pre-natal growth
Estrogen and Testosterone: surge at puberty stimulates GH release, synergistic with GH anabolism; also trigger epiphyseal closure
Cortisol: anti-growth effects; decrease GH secretion, cell division, and increase catabolism

21. GH pathologies Hypersecretion:
Gigantism –in children with responsive epiphyseal plates
Acromegaly –in adults, with closed epiphyseal plates

22. GH pathologies Hypofunction: Dwarfism –in children
Pituitary –decreased GH secretion
Laron –decreased responsiveness due to lack of GH receptors
28 yo woman with pituitary dwarfism; 45” tall
Achondroplastic Dwarfism (genetic dwarf) due to failure of cartilage to form in epiphyseal plate