phys endocrine (5) - mt. san antonio college · 2012-01-24 · relationship between endocrine and...
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Endocrine SystemEndocrine SystemEndocrine System
Dr. Carmen RexachDr. Carmen RexachPhysiologyPhysiology
Mt San Antonio CollegeMt San Antonio College
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Relationship between endocrine and neural physiology
• Both neurons and endocrine cells can secrete into the blood stream
• Endocrine cells and neurons generate electrical potentials when depolarized
• Peptides produced by endocrine cells have neurotransmitter function & can act as hormones
• A single cell can produce biogenic amine neurotransmitters and peptide hormone molecules
• A single gene can be transcribed/translated to produce either peptide neurotransmitter or hormone
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Structural classification of hormones
• Amino Acid derivatives• Peptide hormones• Lipid derivatives
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Amino Acid Derivatives
• Derivatives of Tyrosine– Catecholamines
• epinephrine and norepinephrine(adrenal medulla)
• dopamine (hypothalamus)– Thyroid hormones
• T3, T4
• Derivatives of Tryptophan– Melatonin (pineal gland)
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Peptide Hormones
• Short polypeptides (<200 amino acids)– ADH, ACTH, insulin, PTH, Calcitonin,
ANF, GI tract hormones and others• Proteins
– TSH,LH, FSH, erythropoietin, renin, inhibin
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Lipid derivatives
• Steroid hormones – cholesterol derivatives– androgens, estrogens, progestins, hormones of adrenal
cortex, and others
• Eicosanoids– arachadonic acid derivatives– prostaglandins, leukotrienes, thromboxanes,
prostacyclins, etc.
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Lipid derivatives
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Prohormones and prehormones
• Prohormones– long chained precursor– cut and spliced to produce endproduct(s)
• Prehormones– produced in inactive form– require modification to become active– examples
• T4 T3 at target cell• testosterone• Vitamin D3
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Response at the target cell
• Hormone must be recognized by specific cell receptor
• Hormone/receptor complex must be coupled to signal-transduction mechanism
• The generated signal must cause a change in intracellular processes by changing the activity or concentration of enzymes, carrier proteins, etc.
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Hormone interactions• Synergistic and permissive effects
– synergistic: working together• additive (epinephrine, norepinephrine on heart)• complementary (FSH/LH on spermatogenesis)
– permissive: potentiation• increased response of target cell to a 2nd
hormone• increased activity of second hormone
• Antagonistic effects: opposition– insulin/glucagon
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Hormone concentration• Half-life of hormone
– Time required for the blood [hormone] to be reduced to ½ reference level
• Minutes to days
• Concentration– physiological level
• amount necessary for normal function– pharmacological level
• too much– incidental binding to protein receptors with
similar structure but less affinity– secondary conversion into other products– Results: varying effects in body
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Upregulation and downregulation
• Upregulation (Priming effect)– chronically low levels of hormone in ECF
leads to increase of number and sensitivity of protein receptors for that hormone
• Downregulation (Desensitization)– chronically high levels of hormone in the ECF
leads to decrease in the number and sensitivity of protein receptors for that hormone
– Prevented by pulsatile secretions
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Relationship to NIDDM• Non-insulin dependent diabetes
mellitus– obesity– increased sugar consumption leads to increase
in circulating insulin– chronic increase in insulin levels leads to
downregulation of insulin receptors on cell surfaces
– cells become refractory to insulin– can result in atrophy of the β cells and insulin
dependence
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Mechanisms of hormone action
• Same category = similar mechanism• Determined by:
– location of receptor– cellular response to receptor activation
• Location of Receptor– Nonpolar hormones
• in nucleus of target cell• in cytoplasm of target cell
– Polar hormones• on outer surface of plasma membrane
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Steroid and thyroid hormones
• Nonpolar– into plasma attached to carrier proteins– dissociate in blood near target– hormone into target
• moves into cell and binds to intracellular receptor
• alterations allow for direct binding to DNA• Result: genetic transcription (mRNA
synthesis)
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Steroid hormones
Result: turn a keymetabolic pathwayon or off
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Steroid Hormones: In nucleus
• DNA-binding domain of receptor binds to specific HRE of the DNA.
• Dimerization occurs.– Process of 2 receptor
units coming together at the 2 half-sites.
• Stimulates transcription of particular genes.
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Thyroid hormones
T4
T3
Result: turn key enzymesin a metabolicpathway on oroff
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Mechanism of Thyroid Hormone Action
• T4 passes into cytoplasm and is converted to T3.
• Receptor proteins located in nucleus.– T3 binds to ligand-binding
domain. – Other half-site is vitamin
A derivative (9-cis-retinoic) acid.
• DNA-binding domain can then bind to the half-site of the HRE.
– Two partners can bind to the DNA to activate HRE.
• Stimulate transcription of genes.
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Peptide hormones• Polar = restricted to cell surface• Utilize second messenger system
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Second messenger = cAMP
α
Adenylate cyclase
ATP cAMP +Pi
PO43-Protein kinase
G-protein
Result: Turn key enzyme in a metabolicpathway on or off
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Second messenger = Ca++
α adrenergic receptor
epi
PLC
PIP2 IP3DAG
Ca++
Ca++
Protein kinase
calmodulin
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Epi Can Act Through Two 2nd Messenger Systems
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Remember• Different hormones have different
effects on same target cell• Response of target cell to same
second messenger can differ in different cells
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Endocrine glands and their products
Endocrine glands and Endocrine glands and their productstheir products
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Pituitary gland
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structure
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Anterior pituitary
• Trophic effects:– High blood
[hormone] causes target organ to hypertrophy.
– Low blood [hormone] causes target organ to atrophy.
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Hormones of anterior pituitary• GH = somatotropin
– Generalized growth promoting effects• TSH = thyrotropin
– Regulates activity of thyroid gland• ACTH = corticotropin
– Regulates activity of adrenal cortex• PRL = prolactin
– Mammary growth, development, lactogenesis• Gonadotropins
– FSH = folliculotropin– LH = leutotropin
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Pituitary hormones: pars intermedia & posterior
• Pars intermedia– MSH– Beta (β)-endorphins
• Posterior pituitary– ADH– oxytocin
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Hypothalamic Control of Posterior Pituitary
• Hypothalamus neuron cell bodies produce:– ADH: supraoptic
nuclei.– Oxytocin:
paraventricularnuclei.
• Transported along the hypothalamo-hypophyseal tract.
• Stored in posterior pituitary.
• Release controlled by neuroendocrinereflexes.
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Hypothalamic control of anterior pituitary
• Hypothalamopituitary portal vessel• releasing hormones: polypeptides released by
the hypothalamus– TRH TSH– CRH ACTH– GnRH FSH/LH– GHRH GH
• inhibiting hormones– PIH PRL– Somatostatin GH
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Negative feedback loops
HypothalamusIncreased secretion hormone #1
Anterior pituitaryIncreased secretion hormone #2
3rd Endocrine glandIncreased secretion hormone #3
Target cells of hormone #3Respond to hormone #3
stimulus
Increased plasma hormone #1
Increased plasma hormone #2
Increased plasma hormone #3
-
-
-
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Positive feedback effect• Amplifies initial biological effect of
hormone
estradiol LH
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Pituitary gland disorders
Acromegaly
Identical twins
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Acromegaly vs. Gigantism
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Influence of higher brain functions
• Emotions• Stress• Circadian rhythms
– somatotropin released in greatest quantities during first 90 minutes of sleep
– estradiol on GnRH response
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Adrenal gland
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Functions of the adrenal cortex• Mineralocorticoids
– zona glomerulosa– aldosterone = Na+/K+ regulation
• Glucocorticoids– zona fasciculata– cortisol and corticosterone– protein and carbohydrate
metabolism• Sex steroids
– zona reticularis– androgens and estrogens =
maintenance of secondary sex characteristics
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Adrenal Cortex
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Stress and the adrenal gland
• Stimulate pituitary-adrenal axis due to chronic controlled stress– increased secretions of ACTH– increased secretions of glucocorticoids
• Sympathetic response– stimulation of adrenal medulla– response to physical challenge or
physically challenging stressors
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Stress and the Adrenal Gland• Three phase
response– 1) Alarm phase
• Adrenal glands activated.
– 2) Stage of resistance
• Stage of readjustment.
– 3) Stage of exhaustion
• Sickness and/or death if readjustment is not complete.
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Adrenal gland disorders: Cushing’s syndrome
Caused by excess production of ACTHClassic symptoms seen in this 23 y.o. female
hirsutism (face)central obesityhyperpigmentation & striae
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Cushing’s syndrome
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Thyroid gland
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Thyroid Hormones
• located just below the larynx
• largest of the pure endocrine glands
• Follicular cells secrete thyroxin
• Parafollicular cellssecrete calcitonin
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Production of thyroid hormones
• 2I- + H2O2 I2– iodide enters cell by secondary cotransport with Na+
• I2 + HO CH2CHCOOH
• DIT + DIT T4• MIT + DIT T3
MIT
DITTyrosine
Tetraiodothyronine(thyroxine)
triiodothyronine
NH2
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Production and release
• T3 and T4 produced.• TSH stimulates pinocytosis into the
follicular cell.– Enzymes hydrolyze T3 and T4 from
thyroglobulin.• Attached to TBG and released into
blood.
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Secretion of T3/T4
• T4 circulates bound to protein• Protein allows for transport in the
plasma and through the cytosol in the cell for access to nuclear receptors
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Binding proteins
• three major binding proteins produced in the liver– thyroxine-binding pre-albumin (TBPA)
• binds 70-75% of T4– thyroxine-binding globulin (TBG)
• binds 15-20% of T4– albumin
• 5-10% of T4
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T3 vs T4
• Both of these are water insoluble, but certain binding proteins have greater affinity for T4
• T4 concentrations in humans 50x’s greater than T3
• Functions– T3 physiologically relevant hormone– T4 involved in negative feedback loop on pituitary
production of TSH & production of TRH by the hypothalamus
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Effects • Protein synthesis• maturation of nervous system• increased BMR
– during prolonged fasting plasma T3 levels decrease (ever wonder why it is harder to loose weight when you start dieting?? Your body is prolonging your survival by minimizing its energy usage!)
• Thyroid diseases– Goiter– Graves disease– Cretanism/myxedema
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Diseases of the Thyroid
• 1) Iodine-deficiency (endemic) goiter
• 2) Abnormal growth of the thyroid gland.
• 3) In the absence of sufficient iodine, cannot produce adequate amounts of T4 and T3.
• 4) Lack of negative feedback inhibition.
• 5) Stimulates TSH, which causes abnormal growth.
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Goiter
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Graves disease: hyperthyroidism
exopthalmos Digital clubbing
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Myxedematous cretinism20-year-old African male with three cretin women of the same age
Characteristics:Mental retardationSevere growth retardationDelayed sexual maturationIncomplete maturation of featuresPuffy, thickened skin
hypothyroidism
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Parathyroid gland
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Parathyroid hormone• Major regulator of Ca++ metabolism• Effect
– increase plasma Ca++ by• stimulation of bone resorption• renal tubular Ca++ reabsorption• synthesis of 1,25-(OH)2-D3
– decrease plasma PO43-
• Regulated by plasma Ca++
concentration
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RICKETS OSTEOMALACIA: 25 YO FEMALE
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Pancreas: Islets of Langerhans
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Islets of Langerhans• Four major cell types
– Alpha (α) cells = glucagon– Beta (β) cells = insulin– Delta (δ) cells = somatostatin (inhibition of
insulin, glucagon, and assimilation rate of nutrients in GI tract)
– F cells = pancreatic polypeptide (inhibits pancreatic exocrine secretion)
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Pineal gland• Located in brain in
roof of 3rd ventricle
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Pineal gland• Major site of melatonin synthesis
– highest levels of secretion at night• Controversial effects
– Alleviation of jet lag after transmeridialflights
– Antigonadal effects = inhibition of melatonin is trigger for puberty onset• Continuous light leads to early onset of
sexual development
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Thymus
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Thymus• Location: behind manubrium of
sternum• attains weight of approximately 40
grams at puberty, then begins to involute
• Function: development of immune response
• Hormone: thymosin– T cell education
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GI tract, gonads, placenta• GI tract• Gonads
– Androgens– Estrogens– Progestones
• Placenta– Estrogens– Progesterone– Human chorionic gonadotropin– somatomamotropin