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53 Cards in this Set

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Define endocrinology.
def. the study of the control of the physiological processes of systems of cells, tissues, organs, and glands that secretes hormones
Define hormone.
def. chemicals produced by one cell which enters the bloodstream, is transported to a different body location, and then binds to a specific receptor on a target cells, altering function of the target
2 major control system of the human body
1) nervous system
a. rapid, short term signaling
b. precies, direct interconnection

2) endocrine system
a. slower acting, longer lasting signal
b. diffuse, indirect connection (via the blood)
Sequence of Endocrine Signaling
endocrine gland -> hormone -> receptor binding -> postreceptor events -> response
General Functions of the Endocrine System
1) homeostasis
2) Reproduction
3) Growth & Development
4) Behavior
2 Types of Hormones
1) tropic hormone: stimulate and maintain their endocrine target tissues; ex TSH

2) non-tropic hormone - hormones exert effects on non-endocrine target tissues
3 Classes of Hormones
1) Peptides & Proteins
a. hydrophobic
b. small chains of a.a.
c. synthesized via transcription & translation
d. processed in the Golgi/ER
e. mature hormone stored in secretory granules and exocytose when matured

2) Amines
a. derived from naturally occuring a.a.

3) Steroids
a. derived from cholesterol
b. lilophilic
c. after synthesis, diffuse thru PM into blood
d. body can't degrade steroids so they can be taken orally
Postreceptor Events Mechanism for the Classes of Hormone
1) Peptides - G coupled protein pathway

2) Steroids - DNA txn
Regulation of Hormone Levels
1) negative-feedback control
2) neuroendocrine reflexes
3) circadian rhythm
Regulation of Hormone Responsiveness
1) down regulation of hormone receptors
2) permissiveness
3) synergism
4) antagonism
types of endocrine disorder
1) insufficient activity -
a. hyposecretion
b. increased removal from blood
c. abnormal target responsiveness

2) overactivity
a. hypersecretion
b. reduced plasma carriers
c. decreased removal from blood
Features of the Pineal Gland
- tiny structures located in the center of the brain
- releases melatonin
- works in conjunction w/SCN to entrain circadian rhythm w/external cues
- additional fx: shuts down ovulation, highly effective anti-oxidant, induces natural sleep, enhances immunity
Circadian Rhythm
- regular fluctuation in physiological or performance parameters that occur with a roughly 24 hour period
- rely on an endogenous generator and entrainment
- focal ablation of the SCN eliminates circadian rhythm ,
- mammalian SCN integrates mult. inputs, but light is the dominant cue for entrainment
- animals placed in cts darkness exhibit "free run' which reflects the period of endogenous generator
- phototransduction apparatus for photentrainment in mammals is located in the eye. Genetic "knockout" of specialized photoreceptors located in the retina, in combination with rods and cones, together completely abolish photoentrainment
H-P axis; hypothalamus & Pituitary axis
- integratin of both neural and endocrine pathway:
a. produces both tropic and non-tropic hormone
b. controls growth, dvlpmnt, reproduction, stress response, water reabsorption, lactation, contractions during childbirth
- from the hypothalamus:
a. large # input
b. integrates signals from internal and external envir. to coordinate an endocrine response
c. directly controls the pituitary

- from the pituitary
a. anterior & posterior
b. collectively secretes 8 hormones
Hormones released by H-P axis
1) vasopressin - enhances water retention in kidney. causes contraction of arteriolar smooth muscle

2) oxytocin - stimulates contraction of uterine smooth muscle during childbirth, influences bonding
Hormones released by Anterior Pituitary
1) Growth Hormone (GH)
2) Thyroid-stimulating hormone (TSH)
3) Adrenocorticotropic hormone (ACTH)
4) Follicle Stimulating Hormone (FSH)
5) Prolactin (PRL)
6) Luteinizing Hormone (LH)
What is a hypophysiotropic hormone?
- Hypothalamus secretes hypophysiotropic hormone to control secretion of anterior pituitary hormone
2 feedback mechanism by target gland hormones
- long loop negative feedback: hormones produced by the target endocrine gland feeback on either the hypothalamus or anterior pituitary
FActors affecting growth
1)genetic determination
2)adequate diet
3)stress-free, disease-free envir.
4) growth hormones
Features of GH
- promote cell growth via hyperplasia or hypertrophy
- metabolic fx: mobilize fat stores as a major energy source while conserving glc
Factors of Bone Growth
- epiphyseal plate cartilage: active growing region of bone
- chondrcytes cartilage cells whose hyperplasia and hypertrophy trigger long bone growth
- osteoclasts bone breakers
- osteoblasts bone formers
osteocytes entrapped osteoblasts important for Ca exchange
- some actions mediated by somatomedins
- mult factors control of GH secretion
other hormones affecting growth
- thyroid hormone: permissive for GH, hypothyroidism leads to stunting, hyper nothing
- insulin: bidirectional effect on growth
- androgens & estrogens: stimulate linear growth and wiegh gain & increased muscle mass, then ultimately lead to closure of epiphyseal plate
Growth Hormone Disorder
1) GH deficiency occuring in childhood -> dwarfism

2) excess GH in childhood -> gigantism

3) excess GH excretion after adolescence -> acromegaly, condition in which bones thicken especially in extremeties and face
Anatomy of Thyroid Gland
- follicular gland: secrete T4 (thyroxin) & T3 (triiodothyronine)
- colloid: thyroglobulin produced by follicular cell
Requirement for thyroid hormone synthesis
Tyrosin & Iodine
Steps in Synthesis of Thyroid Hormones
1) Thyroglobulin produced in Golgi/ER of follicular cell and then secreted into colloid
2) iodine actively transported from blood to colloid
3) in colloid, tyrosine become mono- or di-iodinated
4) tyrosine couple together while still on the thyroglobulin producing T3 & T4
5) upon stimulation, follicular cells phagocytize a piece of the colloid
6) endocytotic vesicl fuses with lysosome & lysosomal nz cleaves colloid releasing t4 & t3 into the blood
7) iodine reuptook from dit & mit
relative percentage of release of t3 to t4
90% t4, other t3
80% of t3 comes from t4
what percentage of t3 and t4 are free in the blood
1% t3; 0.1% t4
name some carriers for t3 & t4
- thyroxin-binding globulin
- albumin
- thyroxine-binding prealbumin
Effects of thyroid hormone
1) primary determinant of BMR
a. slow onset, long duration
b. calorigenic
2) permissive for GH, epinephrine, norepinephrine
a. increases receptor to increase responsiveness to catecholamines
b. stimulates GH secretion and increases effectiveness of somatomedins
Regulation of thyroid hormone
- hpothalamus-pituitary-thyroid axis
- activated by stress, cold in infants
Abnormalies of thyroid Function
1) Hypothyroidism
- Caused by failure of thyroid gland, failure of H-P axis, or lack of dietary iodine.
- Leads to myxedema in adults, cretinism in children.
- Treatment is replacement therapy with exogenous thyroid hormone or iodine.
2) Hyperthyroidism
- Caused by autoimmunity (Graves disease Figure 19-4), excess in H-P axis, or thyroid tumor.
- Graves disease often accompanied by exopthalmos (bulging eyes Figure 19-5).
- Treatment is partial removal of oversecreting thyroid, radioactive iodine, or antithyroid drugs.
3) Goiter can occur with either hypo- or hyper-thyroidism, depending on the etiology
Anatomy of the Adrenal Gland
- Adrenal cortex - zonas glomerulosa, fasciculate and reticularis. Secretes steroids (below).
- Adrenal medulla - secretes catecholamines
Cortisol (glucocorticoids)
- Metabolic effects of cortisol:
a) increase blood glucose by decreasing uptake everywhere except the brain and by increasing
hepatic gluconeogenesis.
b) increase free fatty acids (lipolysis).
c) increase blood amino acids (proteolysis).
- Permissive for catecholamines to induce vasoconstriction.
- Stress adaptation.
- Anti-inflammatory and immunosuppressive
- Regulated by hypothalamus-pituitary-adrenal cortex axis (CRH, ACTH) (Figure 19-8)
- Cortisol hypersecretion: Cushing’s syndrome
DHEA
- Weak masculinizing hormone
- In males, more abundant but weaker than testosterone
- In females, significant role in pubertal growth spurt, sex drive
- Hypersecretion in childhood results in adrenogenital syndrome (Figure 19-10; 19-11)
males: precocious pseudopuberty (no sperm production)
females: pseudohermaphroditism
Abnormalities of adrenal cortex
1) Aldosterone hypersecretion
- Conn’s syndrome, caused by tumor
- hypernatremia, hypokalemia, high blood pressure

2) Cortisol hypersecretion
- Cushing’s syndrome, caused by tumor or excess CRH/ACTH
- hyperglycemia, muscle weakness, hippocampal atrophy

3) DHEA hypersecretion
- Adrenogenital syndrome, caused by defect in cortisol pathway
- masculinization, sterility, symptoms of cortisol deficiency

4) Adrenocortical hyposecretion
- Addison’s disease, caused by autoimmune destruction of adrenal cortex
- aldosterone symptoms: hyperkalemia, hyponatremia, low blood pressure
- cortisol symptoms: hypoglycemia, poor stress response
Catecholamines
1) Secreted by adrenal medulla under influence of sympathetic nervous system (Figure 7-4)

2) Effects of catechoamines
- reinforce sympathetic response “fight or flight”
- increased cardiac output
- generalized vasoconstriction
- vasodilation of vessels supplying heart, muscles and lungs
- increased glucose and fatty acids in blood
- increased alertness

3) Secretion is part of a generalized stress response (Figure 19-11; 19-12)
Reaction in fuel metabolism
- glycogensis: glucose is stored as glycogen, blood glucose goes down
- glycogenolysis: glycogen is broken down to glucose, blood glucose goes up
- gluconeogenesis: amino acids are interconverted to glucose, blood glucose goes up
- protein synthesis and degradation
- fat synthesis and degradation
Major pathways in fuel metabolism
Food intake -> digestion -> absorbable units -> usable metabolic pool in body <-> storage
Absorptive state (fed)
- preferred fuel (glucose) is plentiful, used by most cells
- rapid anabolism of absorbed fuel subunits
- lasts about 4 hours following a mea
Postabsorptive state (fasting)
- glucose sparing at non-neural tissue
- gluconeogenesis is activated
- anabolism of amino acids and fatty acids is curtailed
Pancreatic hormones insulin and glucagon regulate fuel metabolism
islets of Langerhans:
- beta cell secretes insulin
- alpha cell secretes glucagon
Effects of insulin on cho's, fat, and pro's
carbohydrate: insulin lowers blood glucose levels
- facilitates glucose transport into most cells
- stimulates glycogenesis, inhibits glycogenolysis, inhibits gluconeogenesis
fat: insulin lowers blood fatty acid levels and promotes triglyceride storage
protein: insulin lowers blood amino acid levels and enhances protein synthesis
Factors controlling insulin secretion
- major factor: negative feedback between beta cells and plasma glucose level
- amino acid levels in blood
- gastrointestinal hormones (feedforward control)
- autonomic nervous system
Diabetes mellitus (too little insulin activity)
Most common endocrine disorder
Results from inadequate insulin action
Most prominent feature is elevated blood glucose levels, leading to “sweetened” urine
Type I: lack of insulin secretion
- childhood onset
- treated with insulin injections
Type II: normal or increased insulin secretion but reduced sensitivity of target tissue
- adult onset
- treated with diet control
Short-term consequences of insulin deficiency
- hyperglycemia causes dehydration, can lead to renal and/or circulatory failure
- switch to fats as main energy source, can lead to ketosis and acidosis
Long-term consequences
- on average, reduced life span due to degenerative disorders of the vasculature and nervous system
- heart disease, stroke, kidney and retinal lesions, neuropathies and circulatory problems, sometimes
requiring amputation
Effect of glucagon on cho's, fats, and pro's
carbohydrate: increase blood glucose levels
- inhibits glycogenesis
- stimulates glycogenolysis
- stimulates gluconeogenesis
fat: increase blood fatty acid levels
protein: promotes protein catabolism, but little effect on blood amino acid levels
Fuel metabolism following a high protein meal
The effects of insulin and glucaogon counteract one another to keep blood glucose levels within normal
range
Calcium in the body
99% in bone, 0.9% inside cells, <0.1% in ECF
The concentration of freely diffusible calcium found in ECF is critical for:
Neuromuscular excitability
Excitation-contraction coupling in cardiac and smooth muscle
Stimulus-secretion coupling
Maintenance of tight junctions between cells
Clotting of blood
ECF [Ca] is regulated by hormonal control of Ca exchange between the ECF and
three compartments: bone, kidney and intestine. Involves
Calcium homeostasis
- maintenance of constant ECF [Ca] on minute-to-minute basis
- primarily accomplished by exchange with bone
Calcium balance
- maintenance of constant total amount of Ca in body
- balances intake with excretion over long term (months)
ACtion of parathyroid hormone on ECF [Ca]
1) raises ECF [Ca]
Actions on bone
- “bone bank” consists of Ca stored in hydroxyapatite crystals
- PTH induces fast Ca efflux into ECF from the small labile Ca pool in bone fluid
- PTH promotes a slow transfer of Ca (and phosphate) to the ECF (bone resorption)
- osteoporosis involves an altered balance of osteoclast/osteoblast activity.
Actions on kidneys: stimulates Ca conservation
Action on the intestine: indirect, by stimulating kidney enzymes that activate vitamin D
Negative feedback regulation of PTH by ECF [Ca]
PTH hypersecretion – hypercalcemia - “bones, stones and abdominal groans”
PTH hyposecretion – hypocalcemia - accidental removal of parathyroid leads to death
Action of CAlcitonin of ECF [Ca]
Calcitonin lowers ECF [Ca] by decreasing Ca efflux into ECF, decreasing bone resorption
Interxn of PTH & Vit D
Vitamin D increases Ca absorption in the intestine
Vitmain D deficiency - demineralized bone (Rickets)