Clinical Anatomy Tony Serino, Ph.D.

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Presentation transcript:

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

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

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

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

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

Steroid Hormones

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

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

Control of Hormone Secretion

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

2nd Messengers: cAMP

2nd Messengers: IP3 and Ca++-Calmodulin

Steroid Hormone Transduction

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

Proinsulin

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

Endocrine Glands

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

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)

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

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

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