Endocrine System PA 544: Clinical Anatomy Tony Serino, Ph.D. Biology Department
Download
Report
Transcript Endocrine System PA 544: Clinical Anatomy Tony Serino, Ph.D. Biology Department
Endocrine System
PA 544: Clinical Anatomy
Tony Serino, Ph.D.
Biology Department
Misericordia Univ.
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
nd
2
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
Increase protein
synthesis
(increase mitosis)
Increase
differentiation
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)
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