Transcript The Endocrine System

The Endocrine System
Chapter 13
Endocrine
• to interstitial fluid circulation
• exocrine- secreted to ducts  lumen or outside the
body
• Endocrine glands:
– Pituitary, thyroid, parathyroid, adrenal & pineal
• Hormone secretion + other functions:
– Hypothalamus, thymus, pancreas, ovaries, testes,
kidneys, stomach, liver, small intestine, skin, heart,
adipose tissue & placenta
Figure 13.1
Hormone Operation
• General chemical signal in circulation
• Slower than nerve responses
• Target cells must have a specific receptor
– Response determined by responding
cell, i.e. different cells may respond
differently to the same hormone
• Cell may respond to more than one
hormone,
– i.e. has more than one type receptor
Hormone Chemistry
• Soluble in lipids = Hydrophobic
– steroids, e.g. testosterone, estrogens, etc.
– thyroid hormones, e.g. T3, T4
– Nitric oxide (NO)
• Water soluble= Hydrophillic
– Amino acid derivatives, e.g. epinephrine, norepinephrine
– Peptides, e.g. antidiuretic Hormone (ADH), oxytocin
– Proteins, e.g. insulin & growth hormone
• General Action depends on chemistry
Lipid Soluble Action
• Hormone detaches from carrier in blood stream
• Diffusion through interstitial fluid & cell
membrane into cell
• Binds to & activates receptor
• Receptor-hormone complex alters gene expression
• If new mRNA protein synthesis
• New proteins alter cell activity
Figure 13.2
Water-Soluble Action
• Diffuses from blood and binds to receptor in
plasma membrane
• Starts reaction inside cell forming second
messenger
– Cyclic AMP is a common one
• Second messenger causes activation of several
proteins (enzymes)
• Activated proteins produce physiological
responses
• Second messenger is inactivated
Figure 13.3
Control of Secretions
• Release occurs in short bursts
• Regulated by:
– Signals from nervous system, e.g. adrenal
medulla release of epinephrine
– Chemical changes in blood, e.g Blood Ca2+
affects parathyroid hormone
– Other hormones, e.g. ACTH from pituitary
stimulates cortisol release from adrenal cortex
Hypothalamus & Pituitary
• Major link between nervous & endocrine
systems
• Hypothalamic Cells synthesize at least 9
hormones
• Pituitary synthesizes 7
• Regulate growth, development, metabolism
& homeostasis
Pituitary
• Two lobes; anterior & posterior
• Hypophyseal portal veins
– Connect capillaries in hypothalamus to
capillaries in anterior pituitary
Hypothalamus  Pituitary
• Axons of hypothalamic neurons
(neurosecretory cells) end near capillaries of
hypothalamus
• Secrete Releasing hormones or Inhibiting
hormones  portal veins
• Regulate release of anterior pituitary
hormones
Figure 13.4
Human Growth Hormone (hGH)
• Promotes synthesis of IGFs = somatomedins
– in liver, muscle, cartilage & bone
• Released in bursts (~2 hour intervals)
• Hypothalamus Growth Hormone Releasing
Hormone (GHRH) & Growth Hormone Inhibiting
Hormone (GHIH )
– Regulated by blood glucose levels
Thyroid Stimulating Hormone
• Stimulates the formation & secretion of
Thyroid hormones from thyroid gland
• Hypothalamus Thyrotropin Releasing
Hormone (TRH)- no TIH
– Regulated by circulating thyroid hormone
levels
Follicle Stimulating Hormone (FSH) &
Luteinizing Hormone (LH)
• In females:
– FSH starts follicle development
– LH stimulates formation of corpus luteum & secretion of
progesterone
• In males:
– FSH stimulates sperm production in testes
– LH stimulates release of testosterone
• Gonadotrophin releasing Hormone (GnRH) from
hypothalamus is suppressed by high levels of
estrogen in females and testosterone in males
Prolactin (PRL)
• Initiates & maintains milk production by
mammary glands
• Ejection of milk depends on oxytocin
• Prolactin inhibiting hormone (PIH) suppresses
prolactin release
• High levels of Estrogens  PRH prolactin
release
• Unknown function in males
– Hypersecretion  impotence
Adrenocortcotrophic Hormone
(ACTH)
• Controls production & secretion of
glucocorticoids from adrenal cortex
• Corticotrophin Releasing Hormone (CRH)
from hypothalamus stimulates secretion of
ACTH
• Stress related stimuli can also stimulate ACTH
release
• Glucocorticoids inhibit CRH & ACTH release
Melanocyte Stimulating Hormone
(MSH)
• Small circulating amounts
• Excess causes skin darkening
Posterior Pituitary
• axon terminals from hypothalamus• Release hormones
• Oxytocin- enhance smooth muscle contraction
during birth & milk ejection
– may play role in emotional bonding
• Antidiuretic Hormone (ADH) = vasopressin
– Causes kidney to retain more water
– Vasoconstriction increase in blood pressure
– high blood osmotic pressure increase secretion
Figure 13.5
Figure 13.6
Thyroid Gland
• Below larynx- two lobes
– follicular cells surround follicles
–  thyroxin (T4) & triiodothyronine (T3)
– Stored in follicle
• Parafollicular cells (C-cells)
– calcitonin
Figure 13.7a
Figure 13.7b
Thyroid Hormones
• T4 & T3 increase basal metabolic rate, protein
synthesis & growth
• Blood level is controlled via feedback through
hypothalamus
– Increased body ATP demand can also raise blood levels
• Calcitonin inhibits osteoclasts  decrease in
blood Ca2+
– Feedback control on blood levels
Figure 13.8
Parathyroid Glands
• Small round masses in posterior of thyroid
gland
• Chief cells release parathyroid hormone (PTH)
• Regulator of Ca2+, Mg2+ & HPO42– Increases number & activity of osteoblasts
– Slows loss of Ca2+ & Mg2+ in urine
– Promotes production of calcitriol  increases rate
of Ca2+, Mg2+ & HPO42- absorption in GI tract
Figure 13.9
Figure 13.10
Pancreas
• Fattened organ in curve of duodenum
• Mostly an exocrine organ for digestion
• Endocrine cells in pancreatic islets
• Several cell types:
• alpha cells glucagon
• beta cells insulin
Figure 13.11a
Figure 13.11b
Figure 13.11c
Actions of Insulin & Glucagon
• Low blood glucose stimulates glucagon release
• Glucagon stimulates liver glucose release  increased blood
glucose
• High glucose levels stimulate insulin release
• Insulin increase glucose transport into skeletal muscle and
adipose cells  decreased blood glucose
• Insulin promotes Amino Acid uptake, protein synthesis & lipid
storage
• ANS also modulates hormone release
Figure 13.12
Adrenal Gland
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Near kidneys
Two separate gland structuresAdrenal cortex and adrenal medulla
3 zones in Cortex-3 steroid hormones
– Outer zone  mineralocorticoids
– Middle zone  glucocorticoids
– Inner Zone  androgens
Figure 13.13a
Figure 13.13b
Mineralocorticoids
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•
•
•
Aldosterone is the major form
Stimulates Na+ reabsorption from urine to blood
Stimulates excretion of K + into urine
Part of renin-angiotensin-aldosterone pathway
– Decreased BP  release of renin from kidney
– Renin causes angiotensinogen angiotensin I
– In lungs Angiotensin converting enzyme (ACE) causes
Angiotensin I  angiotensin II
– Angiotensin II causes Aldosterone release
Figure 13.14
Glucocorticoid action
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•
•
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Increase rate of protein breakdown
Stimulate liver formation of glucose
Breakdown of triglycerides in adipose
Anti-inflammatory effects– Inhibit white blood cells
• Depresses immune system
• Regulated by negative feedback through
hypothalamus
Androgens
• Small amount secreted from adrenal cortex
• Contribute to libido in females
• Converted to estrogens by other body
tissues
• Stimulate axillary hair growth in both boys
& girls
• Contribute to adolescent growth spurt
Adrenal Medulla
• Consists of sympathetic post ganglionic cells
• stimulated by preganglionic sympathetic
neurons
• Releases Epinephrine and norepinephrine
• gives systemic sympathetic effects
• occurs during strong physiological stress
Gonads
• Produce gametes
• Release sex steroids (testosterone or estrogen &
progesterone)
• Also hormone inhibin
– Inhibits FSH release
• hormones from pituitary (FSH & LH)
• Ovaries also produce a hormone relaxin during
pregnancy
• details later in course
Pineal
• Small gland attached to roof of third
ventricle of brain
• Produces melatonin
• Sets bodies biological clock
– More released in darkness
Other hormones
• Prostaglandins (PG) & leukotrienes (LT)
• Derived from fatty acids
• Act locally in most tissues & released from most
body cells
• LTs stimulate white blood cells & mediate
inflammation
• PGs affect many visceral functions & also
modulate inflammation, promote fever & intensify
pain
Stress Responses
• Part of homeostatic responses
• When successful leads to extra
physiological capacity and long term
adaptation
• Initial “fight-or-flight” response
– Nerve mediated response-sympathetic
Stress- Resistance Reaction
Slower & longer Than initial response
– Hypothalamus  Increased CRH, GHRH, TRH
• CRHACTHCortisol  mobilize metabolites
(amino acids, glucose & fat)
• GHRHhGH mobilize fats & glucose for energy
and promote tissue growth & repair
• TRHTSHthyroid hormones increased
Metabolic capacity
Aging
• Some decrease in function with aging
• Loss of negative feedback sensitivity, e.g. decline
in circulating thyroid hormones
• PTH levels rise loss of bone mass
• Less glucocorticoid production
• Slower release of insulin
• Thymus declines after puberty
• Ovary response to gonadotrophins stops
• Slow decline in testosterone production