Endocrine Physiology Flashcards
(188 cards)
1
Q
Endocrine system
A
cells of endocrine produce chemical messengers within glands that influence tissues separated from the gland by some distance
2
Q
2 main regularity systems
A
- nervous system: precise, rapid, short term regulation
- endocrine system: slower, more sustained over long term processes
3
Q
2 glandular systems in the body
A
- exocrine glands: glands that empty their secretions into body cavities through tubular ducts
- endocrine glands: ductless system composed of glands that release secretions internally into bloodstream
4
Q
Glands of endocrine system
A
pituitary gland, hypothalamus, thyroid gland, parathyroid glands, adrenal glands, pancreas, gonads
5
Q
2 reasons why they are highly vascularized
A
- all hormones are made from dietary precursors so they need a large blood supply
- rely on bloodstream to transport hormones to target sites
6
Q
Paracrine signaling
A
hormone is released from cell but it will act on neighboring cells rather than on distant target cells
7
Q
Autocrine signalling
A
hormone is released into extracellular space and acts on cell which it was released
8
Q
Endocrine signalling
A
hormone is released into bloodstream and acts on distant target sites
9
Q
Neuroendocrine signalling
A
nerve cells release neurotransmitter to neuroendocrine cells which release hormone into bloodstream
10
Q
7 hormone characteristics
A
- regulate homeostasis
- high potency
- specific receptors
- act with a delay
- have limited storage
- secreted irregularly in phases
- carried in blood by binding proteins
11
Q
2 main groups of hormones
A
- steroid: derived from cholesterol
- protein: amines (derived from tyrosine), peptides, proteins
12
Q
Steroid hormone synthesis
A
- cholesterol enters cell bound to LDL
- can be stored in cell as lipid droplets
- cholesterol can also be synthesized within cell from acetate
- moved to mitochondria where formed into pregnenolone intermediate
- further modified into steroid hormones
- lipid soluble so can diffuse out of cell
13
Q
Protein hormone synthesis
A
- made from translation of messenger RNA in nucleus
- mRNA –> pre-hormone –> pro-hormone –> hormone
- hormones packaged into secretory vesicle after passage through Golgi and move to plasma membrane to release contents
14
Q
Role of secretory vesicle
A
- protect hormone from proteolytic degradation
- provide a reservoir in sites of synthesis
- provide a transport mechanism along microtubules and microfilaments to site of release
- provide a release mechanism - exocytosis
- provide a quantal release
15
Q
2 types of hormones in plasma
A
- bound to binding protein - inactive
- free - active
16
Q
4 roles of binding protein
A
- increase solubility and concentration of lipid-soluble hormones
- increase size, protecting hormone from clearance and degradation
- inactive free hormones, providing a buffer against large and sudden hormone changes
- dynamically regulated with rate of secretion, rate of degradation, and rate of hormone binding to receptors
17
Q
Hormones are released
A
episodically
- increased level of hormones in blood can be achieved by increase in frequency or amplitude of release
18
Q
Negative feedback
A
- more common
- inhibits hormone secretion when levels are high
- increases hormone secretion when levels are low
19
Q
Positive feedback
A
- rare
- allows events to be rapidly attained after catastrophic collapse of system
- hormone acts on target cell to product another hormone which will stimulate original target cell to release more
20
Q
Hormone receptor pattern
A
lock (receptor) in key (hormone) interaction
21
Q
Importance of cAMP second messenger system
A
- protein hormones are not lipid soluble and cannot cross cell membrane and must bind to membrane bound receptors to produce a response
22
Q
Signal amplification
A
- allow for amplification of response following binding of a hormone to its receptor
23
Q
2 receptors for steroid hormones
A
- nuclear: binds to receptors in nucleus and alter protein synthesis
- cytoplasmic: involved in intracellular transport and provide a reservoir of hormone
24
Q
Up-regulation
A
- more receptors
- occurs at low hormone concentrations to increase activity
- increased receptor synthesis or decreased receptor degradation
25
Sensitization
- more affinity
- occurs at low hormone concentrations to increase activity
- conformation changes in lock structure to make stronger interactions
26
Down-regulation
- less receptors
- occurs at high hormone concentrations to decrease activity
- decreased receptor synthesis, increased degradation, internalized membrane receptors, dislocation of receptor and signal transduction system
27
Densitization
- less affinity
- occurs at high hormone concentrations to decrease activity
- conformation changes in lock structure to make weaker interactions
28
3 endocrine dysfuction
- primary defects in synthesis - problem of endocrine gland
- defect in regulation of hormone - problem in hormone action
- defect in hormone action - problem with target tissue
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What/where is the hypophysis
- pituitary gland
- found in ventral part of base
- lie just below the hypothalamus
30
Posterior pituiary
- neural tissue
- down-growth from hypothalamus
- neurohypophysis
31
Anterior pituitary
- non-neural tissue
- andenohypophysis
32
Intermediate pituitary
- between anterior and posterior pituitary
- lost before birth in humans
- scattered endocrine cells remain
33
2 hypothalamus nuclei
- paraventricular nuclei
- supraoptic nuclei
34
How are nuclei hormones produced and transported
- hormones synthesized in cell bodies of nuclei
- long axons pass down the infundibulum (contains neuron axons and blood vessels)
- end in posterior pituitary gland
- stored there until stimulus propagates to axon terminals and triggers release by exocytosis
- hormones will enter blood stream
35
2 neural secretions from posterior pituitary
- Antidiuretic hormone/vasopressin
- Oxytocin
36
How is ADH produced in nerve
- first product is called pro-pressophysin
- converted to ADH and bound to neurophysin protein
- neurophysin transports small hormone down axon and release
- after release neurophysin dissociates from hormone and has no action
37
2 ADH actions
- vasoconstriction action
- anti-diuretic action
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Vasoconstriction action
- causes contraction of blood vessels
- causes increase in blood pressure
- only occurs at high concentrations of hormones such as blood loss/hemorrhage
39
Anti-diuretic action
- control fluid balance in body by reducing urination
- increases permeability of the renal collecting duct
- increases number of water channels in collecting duct
- reduces glomerular filtration rate
- causes contraction of glomerulosa cells reducing surface area for filtration
40
Mechanism of ADH action
- ADH in circulation will travel to kidneys
- ADH binds to its receptor on collecting cell
- binding of ADH induces synthesis of second messenger (cAMP)
- cAMP causes up-regulation of aquaporin 2 protein via gene transcription
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2 factors affecting ADH secretion
- plasma volume
- plasma osmolarity
42
What receptors are in hypothalamus
- osmoreceptors
- SON and PVN
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Baroreceptors
- blood volume affects blood pressure
- changed in blood volume affect stretching of blood vessel walls
- found in aortic arch and carotid sinus
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Main stimuli for ADH decrease
decrease in blood volume or increase in blood osmolarity
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ADH response to dehydration steps
dehydration --> decrease blood volume --> decrease stretch of blood vessels --> decrease activity of baroreceptors --> decrease inhibition of inhibit afferents to hypothalamus --> increase neuron activity in hypothalamus --> increase release of ADH --> ADH acts on collecting ducts in kidneys to increase water reabsorption from urine
46
ADH response to overhydration steps
increased water --> increase extracellular fluid volume --> increase blood volume --> stimulate cardiovascular baroreceptors --> increases activity if inhibitory affects to hypothalamus --> decrease ADH release --> decrease water reabsorption --> increase water excretion and reduce blood volume
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With an ____ in plasma osmolarity, there is ____ in plasma ADH levels
- increase
- increase
linear
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With an ____ in mean arteriole pressure, there is ____ in plasma ADH levels
- decrease
- increase
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Other factors that increase ADH secretion
- stress/emotion
- heat
- nicotine
- caffeine
50
Other factors that decrease ADH secretion
- cold
- alcohol
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ADH deficiency
- diabetes insipidus
- hypothalamic/central - problem of ADH production
- nephrogenic - problem of ADH action
52
ADH excess
- syndrome of inappropriate ADH (SIADH)
- problem of ADH production and feedback failure
- low blood sodium levels
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Polyuria
produce large amounts of dilute urine
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Polydipsia
excessive thirst and fluid intake
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Treatment for diabetes insipidus
- hypothalamic/central - ADH
- nephrogenic - other antidiuretics
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Oxytocin release and production
- released from posterior pituitary
- produced in paraventricular nuclei (PVN) in hypothalamus
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Oxytocin actions
- uterine myometrium: parturition, prevent hemorrhage, restoration of pre-pregnancy uterine size, stimulation of sperm movement in female tract, movement of cervix
- mammary myometrium: stimulates milk letdown
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Effect of oxytocin in parturition
- positive feedback loop
- initial mild contractions lead to oxytocin release and further uterine contractions, putting more pressure against the cervix
59
Effect of oxytocin in milk let-down
- suckling causes release of oxytocin
- acts on receptors of myoepithelial cell which contract
- milk that is already synthesized is released into lumen
- positive feedback loop
- conditioned response - visual and auditory stimuli
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Other functions of oxytocin
- released during sexual intercourse to stimulate orgasm
- social bonding
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Regulation of oxytocin secretion
- genital tract or nipple stimuli
- stress lowers secretion
- psychogenic/physical
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Oxytocin deficiency
- impaired delivery
- impaired lactation
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Oxytocin excess
- no problems associated
64
Anterior pituitary
- produced hormones essential for growth and reproduction
- controlled by hypothalamus through blood supply
65
Median eminence-capillary bed
- receives axons from nuclei in hypothalamus
- gives rise to hypothalamo-hyposphyseal portal vessels
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Hypothalamo-hyposphyseal portal vessels
- venous or portal blood vessels which run into anterior pituitary
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Short portal vessel
- blood vessel which comes from capillary bed into posterior pituitary
68
Parvocellular neurons
- neurons with small cell bodies with short axons
- nuclei who axons end in median eminence
- product neural secretions that are released into blood vessels which carry secretions down to anterior pituitary
69
Magnocellular neurons
- neuroendocrine cells located in hypothalamus
- largest cells in brain
- synthesize oxytocin and ADH
- PVN and SON
70
5 secretions of anterior pituitary
- gonadotropins - stimulate gonad activity
- growth hormone (GH) - stimulate growth
- thyroid-stimulating hormone (TSH) - stimulate thyroid gland
- prolactin (PRL) - acts on mammary glands to affect milk formation
- adrenocorticotropin (ACTH) - acts on adrenal gland
71
7 hypothalamic releasing hormones
- GnRH - stimulates release of LH and FSH
- GHRH - stimulates release of GH
- TRH - stimulates release of TSH and prolactin
- PRFs - stimulates release of prolactin
- CRH - stimulates release of ACTH
- SRIF - inhibits release of GH and TSH
- PIFs - inhibits release of FSH and PRL
72
TSH
- stimulates thyroid gland
- secrete T3 and T4
73
ACTH
- stimulates adrenal cortex
- secrete cortisol
74
LH and FSH
- stimulate gonads
- secrete sex hormones and regulate growth and development of gamete production
75
Negative feedback in hypothalamic-anterior pituitary control system
- hormones released from target endocrine gland will have negative feedback on anterior pituitary and hypothalamus
- anterior pituitary hormones exert feedback on hypothalamus
76
Effect of growth hormone (GH)
- effects muscle, liver, adipose tissue
- induces protein synthesis on muscle and liver
- increases lipolysis
- induces production of somatomedins (insulin-like growth factors) to increase tissue growth
- hyperglycemia and hyperlipidemia
77
Control of growth hormone (GH)
- GHRH stimulates
- GHIH/somatostatin inhibits
- increased by deep sleep, stress, reduced blood glucose levels, increased blood amino acids, decreased blood fatty acids
- pronounced diurnal rhythm of GH release
78
3 inhibitory GH effects
- somatomedins from liver
- GH inhibits own release
- inhibited by products of lipolysis and glucose
79
Diurnal pattern of GH release
- 24 hour cycle
- number and amplitude of GH release episodes increased in dark, sleep and fasting
- frequent meals high in glucose and fatty acids suppress GH release
- frequent meals high in amino acids increase GH relrease
80
Deficiency of GH
- dwarfism in juveniles
- somatopause in adults
81
Types of dwarfism
- isolated growth hormone deficiency (Type 1) - defect in GH production
- Laron-type dwarfism - defect in GH action because receptor problems
- GH dwarfs - normal body proportions for people their age, just shorter in height
- thyroid dwarfs - have body proportions of individual much younger than themselves
82
Somatopause
- increase fat production
- decrease lean body mass
- metabolic disturbances
- impaired immune function
- thymic atrophy
83
Excess of GH in childhood
- pituitary gigantism
84
Excess of GH in adults
- acromegaly
- growth in face bones, hands, feet, cartilage
- protruding jaw
- internal organs increase
- increased glucose release leading to diabetes
- due to GH secreting tumor on pituitary
85
Prolactin
- released from anterior pituitary
- gonadal modulator
- mammary gland development
- involved in lactation or milk production
86
Prolactin releasing factors
- stimulate prolactin secretion
- TRH and oxytocin
- estrogen and testosterone increases prolactin secretion
- progesterone inhibits prolactin secretion
- mammary stimulation - suckling
87
Excess prolactin
- hyperprolactinemia
- gonadal dysfunction, amenorrhea, reduced libido
- treated with dopamine agonist
88
Prolactin deficiency
- hypoprolactinemia
- gonadal dysfunction, lactation impairment
89
Pituitary diabetes
- excess of all anterior pituitary hormones
- hyperglycemia
90
Hypopituitarism
- deficiency in pituitary hormone production
91
Panhypopituitarism
- affects all pituitary hormones
92
Hypothalamic-pituitary-thyroid axis
- hypothalamus releases thyrotropin - releasing hormone (TRH) into hypothalamohypopshyeal portal vessels
- TRH acts on anterior pituitary to release thyroid-stimulating hormone
- TSH acts on thyroid gland to product T3 and T4 which acts on target cells
93
Thyroid hormone effects
- increase metabolic rate and heat production
- enhance growth and CNS development
- enhance sympathetic activity
94
What inhibits the axis
- T3 and T4 at mainly at pituitary and at hypothalamus
- stress
95
What stimulates the axis
cold in infants
96
Thyroid stimulating hormone (TSH)
- peptide hormone produced by anterior pituitary
- stimulates growth of thyroid gland
- trophic hormone: affects growth, nutrition, function of thyroid gland
- stimulates biosynthesis of thyroid hormones
- glycoprotein hormones - contains sugar residues
97
Thyroid gland
- vascular structure - good blood supply
- capsule of connective tissue covering the thyroid gland which is made up of secretory parts called follicles
- follicles have cavities lined with epithelial cells and are filled with viscous protein rich substance called colloid
98
Colloid
- consists of glycoprotein called thyroglobulin
- thyroglobulin is synthesized in follicular cells and secreted into colloid
- colloid is site of thyroid hormone biosynthesis
99
Thyroglobulin
- precursor for thyroid hormones
- contains tyrosine residues which provide template
100
2 thyroid hormones
- have tyrosine amino acids residues with iodine attached to them
- thyroxine (T4) has 4 iodine
- triiodothyronine (T3) has 3 iodine
- T4 is degraded by deiodinase to T3
- T3 is more biologically active but more T4 is produced
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Synthesis of thyroid hormones
- iodide is cotransported with sodium ions across basolateral membrane in follicle cell
- iodide diffuses to apical membrane of follicle cell
- thyroglobulin is made in follicle cells and released into colloid by exocytosis
- iodide is oxidized to iodine at luminal surface of follicle cell and attached to rings or tyrosine residues on TG
- addition of 1 iodine - MIT, addition of 2 iodine - DIT
- coupling of MIT to DIT (T3) or DIT to DIT (T4)
- thyroid hormone secreted into blood
102
Enzyme responsible for thyroid hormone production
thyroid peroxidase
103
Thyroid hormones are ____ soluble
- lipid
- need to be carried by binding protein in blood
- TBG - thyroid binding globulin
104
Thyroid hormone receptors
- found everywhere on most cells
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Thyroid hormone action
- latent period
- long lasting responses
- increases oxygen and glucose uptake by most tissues
- increases basal metabolic rate - calorigenesis - heat
- promotes neural activity
- cardiovascular action
- intermediary metabolism
- growth and development
106
3 thyroid hormone receptors
- membrane bound receptors - linked to glucose channels to allow glucose to enter
- cytoplasmic receptors - reservoir of hormone, stimulate ATP production
- nuclear receptors - affect gene transcription and protein synthesis
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Thyroid hormone excess
- hyperthyroidism
- increased basal metabolic rate
- most common type is Grave's disease - autoimmune disease which antibodies develop against TSH receptors
108
3 causes of hyperthyroidism
- primary problem with thyroid gland: excess T3 and T4 and toxic goiter
- secondary problem with pituitary gland: increased TSH and goiter
- tertiary problem with hypothalamus: increased TRH and goiter
109
Grave's disease
- large swelling in neck, overstimulation of thyroid gland
- exophthalmos, eye bulging
- heart palpitations
- increased sympathetic nervous system action
110
Thyroid hormone deficiency
- hypothyroidism
- decreased metabolic rate
111
5 causes of hypothyroidism
- deficiency of dietary iodine: increased TSH and goiter
- primary problem with thyroid gland: increased TSH and goiter
- Hashimoto's thyroiditis: autoimmune disease where antibodies developed against T3 and T4 and goiter
- secondary problems with pituitary gland: low levels of TSH, no goiter
- tertiary problems with hypothalamus: low levels of TRH, no goiter
112
Hypothyroidism in utero
- cretinism
- severely stunted mental and physical development
- irreversible
113
Hypothyroidism in adults
- myxedema
- accumulation of hyaluronic acid and mucus edema under skin
- slow mentation and slow speech
- lethargic
- bradycardia
114
Only hormone that provides feedback inhibition on adrenal cortex
- cortisol
115
Adrenal cortex release mechanism
- hypothalamus releases CRH
- stimulates anterior pituitary to produce ACTH
- stimulates steroidogenesis in all zones of adrenal cortex
116
ACTH
- peptide hormone
- produced by cell called corticotrophs
- trophic hormone stimulates adrenal blood floow, adrenal growth, adrenal steroidogenesis
117
POMC processing
- make ACTH --> alpha-MSH (pigmentation)
- make beta-LPH --> beta-MSH (pigmentation) or beta-endorphin (opiate) --> met-enkephalin (opiate)
118
Adrenal cortex zones
- glomerular zone - aldosterone - salt/water retention
- fascicular zone - cortisol - sugar metabolism
- reticular zone - androgens - sex characteristics
119
Steroidogenesis in glomerular zone
- all steroids produced from cholesterol
- cholesterol --> pregnenolone --> progesterone --> corticosterone --> aldosterone
120
Aldosterone action
- steroid hormone
- upregulate/synthesize proteins that move Na+ into collecting ducts on kidneys
- acts on receptors in nucleus and cytoplasm
- activates mitochondrial enzymes that provide energy for Na+/K+ ATPase
121
Aldosterone secretion regulation
low plasma volume, low plasma Na+, acts on kidneys to release renin, renin converts angiotensinogen to angiotensin I, angiotensin I converted to angiotensin II by ACE, angiotensin II acts on adrenal cortex to promote aldosterone production, Na+ retention and K+ excretion
122
Renin
- enzyme secreted by juxtaglomerular cells of juxtaglomerular apparatus sensory for low Na+ concentrations
123
Excess aldosterone
- Conn's syndrome
- increased Na+ retention and decreased K+ uptake, water retention and volume excess, hypertension
- decreased K+ uptake, increased urinary loss of K+, alkalosis, tetany, muscular weakness, dysrhythmia
124
Steroidogenesis in fascicular zone
- cholesterol --> pregnenolone --> cortisol
125
Cortisol actions
- increases blood glucose
- anabolic effects on liver
- catabolic effects on peripheral tissue (adipose tissue, skin, connective tissue, muscle)
- fatty acids, glycerol, amino acids used for glucogenesis
126
Cortisol actions in stress
- prevents inflammation
- prevents autoimmunity
- mobilizes glucose during stress
127
Control of cortisol secretion
stress/diurnal rhythm
- stimulates hypothalamus to release CRH, anterior pituitary to release ACTH, ACTH acts on adrenal cortex to make cortisol, increased plasma levels of cortisol
- levels are low at end of day and high during sleep
128
Primary cortisol deficiency
- Addison's disease
- defect in adrenal cortex, no feedback inhibition
- levels of ACTH are very high leading to skin pigmentation
129
Secondary cortisol deficiency
- defect at level of pituitary
- pituitary does not produce ACTH and adrenal cortex will not be stimulated by cortisol
- no skin pigmentation
130
Addison's disease
- reduced cortisol secretion
- hypoglycemia
- low Na+/high K+ levels in blood
- hypotension/hyperkalemia
131
Cortisol excess
- Cushing's syndrome
- moon face, buffalo hump, hirsutism
- 3 causes: pituitary tumor, adrenal tumor, ectopic tumor
132
Cushing's syndrome - pituitary tumor
- high production of ACTH stimulates adrenal cortex to produce too much cortisol
133
Cushing's syndrome - adrenal gland tumor
- produces high levels of cortisol
- cortisol inhibits production of ACTH from pituitary through feedback regulation
134
Cushing's syndrome - ectopic tumor
- can produce ACTH which stimulates cortisol production from adrenal cortex
- high levels of cortisol inhibit ACTH production from pituitary
- tumor is not inhibited from producing ACTH and cortisol levels remain high
135
Steroidogenesis in reticular zone
- cholesterol --> pregnenolone --> DHEA
136
Adrenal androgens/DHEA
- weak androgen converted to testosterone/estrogen
- secondary sexual characteristics
137
Adnrenogenital syndrome
- biosynthetic pathways that make aldosterone and cortisol are deficient and all precursors go to make DHEA
- excess androgens in adrenal cortex
138
Symptoms of adrenogenital syndrome in females
- masculinization of genitals
- male-pattern hair growth (hirsutism)
- male-type balding
- heavy arms and legs
- involution of breasts
139
Symptoms of adrenogenital syndrome in males
- pseudopuberty - sperm dysfunction
140
Calcium metabolism roles
- neurotransmission
- muscular contraction
- blood clotting
- cell cytoskeleton
- cell metabolism
- skeletal support
141
Phosphate metabolism roles
- glycolysis
- energy transfer
- cofactor for enzymes and skeletal support
142
3 hormones that regulate calcium and phosphate
- 2 hypercalcemic hormones: parathyroid hormone (PTH) and vitamin D3 (VD)
- 1 hypoglycemic hormone: calcitonin (CT)
143
Parathyroid gland
- embedded in thyroid gland
- 4 glands, 2 on each lobe of thyroid gland
144
PTH action
- increase plasma calcium
- decrease plasma phosphate
145
3 PTH target sites
- kidney: increase Ca2+ reabsorption, decrease PO43- reabsorption, increase vit D3 activation
- bone: increase bone resorption/breakdown
- GIT: indirect increase vit D3 formation
146
Feedback regulation of PTH
- hypercalcemia inhibits PTH
- hypocalcemia simulates PTH
- 1,25 (OH2) D3 inhibits PTH
147
Relationship of PTH
- linear
- low levels of plasma calcium stimulates
- high levels of plasma calcium inhibits
148
Where is PTH synthesized in
- parathyroid gland by chief cells
149
Main stimulus for PTH
- low plasma calcium
150
Hyperparathyroidism
- bones, stones, abdominal groans
- soft tissue calcification (kidney stones)
- weak bones and fractures
- GIT dysfunction
151
Primary hyperparathyroidism
- high PTH, high Ca2+, low PO43-, high 1,25 (OH2) D3
- problem with thyroid gland
- soft tissue calcification
- calcification of blood vessels - aneurysm - death
152
Secondary hyperparathyroidism
- consequence of low blood calcium that would stimulate PTH release
- rickets in children and osteolmalacia in adults
- renal failure
153
Primary hypoparathyroidism
- low PTH, low Ca2+, high PO43-, low 1,25 (OH2) D3
- increase neuromuscular activity
- tetany - muscle spasms
- asphyxia and death
- poor teeth and regular fillings
154
Trousseau's sign
- hypoparathyroidism
- involuntary contraction of carpal muscles due to hypocalcemia and tetany
155
Chvostek's sign
- hypocalcemia
- tap trigeminal nerve which runs along cheek
- tetany and snarl
156
Pseudohypoparathyroidism
- high PTH, low Ca2+, high PO43-, low 1,25 (OH2) D3
- tissue insensitivity to PTH action
- PTH receptors do not work
157
Calcitonin
- peptide hormone
- opposes action of PTH
- made in parafollicular cells (C-cells) in the thyroid gland adjacent to thyroid follicles
158
Calcitonin action
- decrease plasma calcium
- decrease plasma phosphate
159
3 calcitonin target sites
- kidneys: decrease Ca2+ reabsorption, decrease PO43- reabsorption, decrease vit D3 activation
- bone: decrease bone resorption/break down
- GIT: decrease Ca2+ absorption main site**
160
As plasma calcium increases, ____ release of calcitonin
- increase
161
Calcitonin clinical use
- no excess or deficiency syndromes
- treatment of postmenopausal osteoporosis - absence of estrogen, PTH action is not antagonized
- treatment of Padget's disease - excessive osteoclast (bone breakdown) activity
162
Vitamin D3
- steroid hormone that regulates plasma calcium and phosphate levels
- 90% synthesized in the skin - photoisomerized by UV
- 10% synthesized by diet/supplements - D2 from plants
163
Vitamin D3 synthesis
- cholesterol --> liver --> 7-dehydrocholesterol --> skin --> vitamin D3
- vitamin D3 --> liver --> 25 hydroxyvitamin D --> kidney
- activating --> 1,25 dihydroxyvitamin D
- inactivating --> 24,25 vitamin D
- all through enzymes
164
1,25 vitamin D3 action
- increase plasma calcium
- increase plasma phosphate
165
3 1,25 vitamin D3 target sites
- kidney: increase Ca2+ reabsorption, increase PO43- reabsorption
- bone: promote PTH action
- GIT: increase absorption of Ca2+ and PO43-
166
GIT actions of vitamin D3
- promotes absorption of calcium from lumen to blood by genomic effects that synthesize proteins
- vit D diffuses across cell membrane and binds to nucleus receptors to impact gene transcription
- increase calcium channels, calcium binding proteins and calcium ATPase
167
Vitamin D3 stimulus
- increase PTH
- low Ca2+
168
Vitamin D3 deficiency
- rickets in juveniles
- osteomalacia in adults
- low vit D, low Ca2+, high PTH = poor bone formation and increased bone breakdown
169
Vitamin D3 excess
- toxicity
- hypercalcemia
- soft tissue calcification --> blood vessel calcification --> aneurysm --> death
170
2 pancreas gland
- exocrine - pancreatic juice for digestion, ducts
- endocrine - regulated blood sugar and found in Islet of Langerhans or pancreatic islets
171
3 cells pf pancreatic islets
- alpha - secrete glucagon
- beta - secrete insulin
- delta - somatostatin
172
Pancreatic islets hormones are ____
- paracrine
173
Somatostatin effects
- inhibit glucagon and insulin
174
Insulin effects
- inhibit glucagon
175
Glucagon effects
- stimulates insulin and somatostatin
176
Neural innervation of pancreatic islets
- sympathetic system through splanchnic nerve: increase glucagon and decrease insulin
- parasympathetic system through vagus nerve: increase insulin and decrease glucagon
177
Insulin structure
- proinsulin - single amino acid chain connected by C-peptide
- C-peptide cleaved off to produce bioactive insulin
- insulin has 2 polypeptide chains: A chain and B chain
178
Insulin action
- lower blood glucose
- anabolic - builds up tissues
- storage hormone - store glucose in cells, increase fat deposition in tissues, increase protein synthesis
179
Factors affecting insulin
- increasing concentrations of glucose, amino acids, fatty acids in blood
- hormones released by GIT in response to food
- ingesting food - parasympathetic stimulation
- stress - sympathetic inhibition
180
Insulin regulation
- increase plasma glucose levels --> stimulate beta cells to secrete insulin --> increase uptake of glucose by adipose tissue and muscle --> net uptake of glucose my liver --> decrease plasma glucose levels
181
Glucagon action
- catabolic peptide hormone - break down, fasting
- glucose: decrease glycogenesis, increase gluconeogenesis, increase glycogenolysis
- lipid: increase lipolysis, decrease lipogenesis
- protein: minor increase of degradation
182
Factors affecting glucagon
- nutrients: decrease glucose, increase amino acids
- GIT hormones: increase gastrin/CCK, decrease secretin
- neural stimuli: increase stress (sympathetic), increase food (parasympathetic)
183
Diabetes mellitus
- insulin deficiency and glucagon excess syndrome
- hyperglycemia --> osmotic diueresis --> cellular dehydration/volume depletion --> circulatory failture and renal function
- protein catabolism --> wasting syndrome
- ketogenesis --> acidosis --> diabetic coma and fruity breath
184
Symptoms of diabetes mellitus
- polyuria - large amounts of dilute urine
- polydipsia - excessive thirst
- polyphagia - excessive hunger
185
Type 1 diabetes mellitus
- insulin dependent and juvenile onset
- autoimmune disease attacks beta cells causing loss of insulin secretion
- treated with insulin injections
- 10-20%
186
Type 2 diabetes mellitus
- insulin independent and adult onset
- insulin resistance - decreased receptor response
- normal or high plasma insulin levels
- receptor downregulation
- associated with obesity
- 80-90%
187
Complications of diabetes mellitus
- cardiovascular disease (atherosclerosis, gangrene, hypertension)
- nephropathy, retinopathy, dermopathy, neuropathy, ulcers/infections
188
Insulin excess
- causes: insulin-secreting tumor, insulin overdose, reactive hypoglycemia
- symptoms: hypoglycemia, sympathetic activation, insulin shock
- treatment: glucose for diabetes, low carbohydrates for reactive hypoglycemia
