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Physiology 210 > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

Endocrine system

A

cells of endocrine produce chemical messengers within glands that influence tissues separated from the gland by some distance

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2
Q

2 main regularity systems

A
  • nervous system: precise, rapid, short term regulation
  • endocrine system: slower, more sustained over long term processes
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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
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4
Q

Glands of endocrine system

A

pituitary gland, hypothalamus, thyroid gland, parathyroid glands, adrenal glands, pancreas, gonads

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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
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6
Q

Paracrine signaling

A

hormone is released from cell but it will act on neighboring cells rather than on distant target cells

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7
Q

Autocrine signalling

A

hormone is released into extracellular space and acts on cell which it was released

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8
Q

Endocrine signalling

A

hormone is released into bloodstream and acts on distant target sites

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9
Q

Neuroendocrine signalling

A

nerve cells release neurotransmitter to neuroendocrine cells which release hormone into bloodstream

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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
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11
Q

2 main groups of hormones

A
  • steroid: derived from cholesterol
  • protein: amines (derived from tyrosine), peptides, proteins
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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
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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
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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
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15
Q

2 types of hormones in plasma

A
  • bound to binding protein - inactive
  • free - active
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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
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17
Q

Hormones are released

A

episodically
- increased level of hormones in blood can be achieved by increase in frequency or amplitude of release

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18
Q

Negative feedback

A
  • more common
  • inhibits hormone secretion when levels are high
  • increases hormone secretion when levels are low
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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
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20
Q

Hormone receptor pattern

A

lock (receptor) in key (hormone) interaction

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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
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22
Q

Signal amplification

A
  • allow for amplification of response following binding of a hormone to its receptor
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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
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24
Q

Up-regulation

A
  • more receptors
  • occurs at low hormone concentrations to increase activity
  • increased receptor synthesis or decreased receptor degradation
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25
Q

Sensitization

A
  • more affinity
  • occurs at low hormone concentrations to increase activity
  • conformation changes in lock structure to make stronger interactions
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26
Q

Down-regulation

A
  • 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
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27
Q

Densitization

A
  • less affinity
  • occurs at high hormone concentrations to decrease activity
  • conformation changes in lock structure to make weaker interactions
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28
Q

3 endocrine dysfuction

A
  • 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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29
Q

What/where is the hypophysis

A
  • pituitary gland
  • found in ventral part of base
  • lie just below the hypothalamus
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30
Q

Posterior pituiary

A
  • neural tissue
  • down-growth from hypothalamus
  • neurohypophysis
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31
Q

Anterior pituitary

A
  • non-neural tissue
  • andenohypophysis
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32
Q

Intermediate pituitary

A
  • between anterior and posterior pituitary
  • lost before birth in humans
  • scattered endocrine cells remain
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33
Q

2 hypothalamus nuclei

A
  • paraventricular nuclei
  • supraoptic nuclei
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34
Q

How are nuclei hormones produced and transported

A
  • 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
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35
Q

2 neural secretions from posterior pituitary

A
  • Antidiuretic hormone/vasopressin
  • Oxytocin
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36
Q

How is ADH produced in nerve

A
  • 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
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37
Q

2 ADH actions

A
  • vasoconstriction action
  • anti-diuretic action
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38
Q

Vasoconstriction action

A
  • causes contraction of blood vessels
  • causes increase in blood pressure
  • only occurs at high concentrations of hormones such as blood loss/hemorrhage
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39
Q

Anti-diuretic action

A
  • 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
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40
Q

Mechanism of ADH action

A
  • 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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41
Q

2 factors affecting ADH secretion

A
  • plasma volume
  • plasma osmolarity
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42
Q

What receptors are in hypothalamus

A
  • osmoreceptors
  • SON and PVN
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43
Q

Baroreceptors

A
  • 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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44
Q

Main stimuli for ADH decrease

A

decrease in blood volume or increase in blood osmolarity

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45
Q

ADH response to dehydration steps

A

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

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46
Q

ADH response to overhydration steps

A

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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47
Q

With an ____ in plasma osmolarity, there is ____ in plasma ADH levels

A
  • increase
  • increase
    linear
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48
Q

With an ____ in mean arteriole pressure, there is ____ in plasma ADH levels

A
  • decrease
  • increase
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49
Q

Other factors that increase ADH secretion

A
  • stress/emotion
  • heat
  • nicotine
  • caffeine
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50
Q

Other factors that decrease ADH secretion

A
  • cold
  • alcohol
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51
Q

ADH deficiency

A
  • diabetes insipidus
  • hypothalamic/central - problem of ADH production
  • nephrogenic - problem of ADH action
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52
Q

ADH excess

A
  • syndrome of inappropriate ADH (SIADH)
  • problem of ADH production and feedback failure
  • low blood sodium levels
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53
Q

Polyuria

A

produce large amounts of dilute urine

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54
Q

Polydipsia

A

excessive thirst and fluid intake

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55
Q

Treatment for diabetes insipidus

A
  • hypothalamic/central - ADH
  • nephrogenic - other antidiuretics
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56
Q

Oxytocin release and production

A
  • released from posterior pituitary
  • produced in paraventricular nuclei (PVN) in hypothalamus
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57
Q

Oxytocin actions

A
  • 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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58
Q

Effect of oxytocin in parturition

A
  • positive feedback loop
  • initial mild contractions lead to oxytocin release and further uterine contractions, putting more pressure against the cervix
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59
Q

Effect of oxytocin in milk let-down

A
  • 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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60
Q

Other functions of oxytocin

A
  • released during sexual intercourse to stimulate orgasm
  • social bonding
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61
Q

Regulation of oxytocin secretion

A
  • genital tract or nipple stimuli
  • stress lowers secretion
  • psychogenic/physical
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62
Q

Oxytocin deficiency

A
  • impaired delivery
  • impaired lactation
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63
Q

Oxytocin excess

A
  • no problems associated
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64
Q

Anterior pituitary

A
  • produced hormones essential for growth and reproduction
  • controlled by hypothalamus through blood supply
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65
Q

Median eminence-capillary bed

A
  • receives axons from nuclei in hypothalamus
  • gives rise to hypothalamo-hyposphyseal portal vessels
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66
Q

Hypothalamo-hyposphyseal portal vessels

A
  • venous or portal blood vessels which run into anterior pituitary
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67
Q

Short portal vessel

A
  • blood vessel which comes from capillary bed into posterior pituitary
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68
Q

Parvocellular neurons

A
  • 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
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69
Q

Magnocellular neurons

A
  • neuroendocrine cells located in hypothalamus
  • largest cells in brain
  • synthesize oxytocin and ADH
  • PVN and SON
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70
Q

5 secretions of anterior pituitary

A
  • 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
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71
Q

7 hypothalamic releasing hormones

A
  • 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
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72
Q

TSH

A
  • stimulates thyroid gland
  • secrete T3 and T4
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73
Q

ACTH

A
  • stimulates adrenal cortex
  • secrete cortisol
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74
Q

LH and FSH

A
  • stimulate gonads
  • secrete sex hormones and regulate growth and development of gamete production
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75
Q

Negative feedback in hypothalamic-anterior pituitary control system

A
  • hormones released from target endocrine gland will have negative feedback on anterior pituitary and hypothalamus
  • anterior pituitary hormones exert feedback on hypothalamus
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76
Q

Effect of growth hormone (GH)

A
  • 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
Q

Control of growth hormone (GH)

A
  • 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
Q

3 inhibitory GH effects

A
  • somatomedins from liver
  • GH inhibits own release
  • inhibited by products of lipolysis and glucose
79
Q

Diurnal pattern of GH release

A
  • 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
Q

Deficiency of GH

A
  • dwarfism in juveniles
  • somatopause in adults
81
Q

Types of dwarfism

A
  • 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
Q

Somatopause

A
  • increase fat production
  • decrease lean body mass
  • metabolic disturbances
  • impaired immune function
  • thymic atrophy
83
Q

Excess of GH in childhood

A
  • pituitary gigantism
84
Q

Excess of GH in adults

A
  • 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
Q

Prolactin

A
  • released from anterior pituitary
  • gonadal modulator
  • mammary gland development
  • involved in lactation or milk production
86
Q

Prolactin releasing factors

A
  • stimulate prolactin secretion
  • TRH and oxytocin
  • estrogen and testosterone increases prolactin secretion
  • progesterone inhibits prolactin secretion
  • mammary stimulation - suckling
87
Q

Excess prolactin

A
  • hyperprolactinemia
  • gonadal dysfunction, amenorrhea, reduced libido
  • treated with dopamine agonist
88
Q

Prolactin deficiency

A
  • hypoprolactinemia
  • gonadal dysfunction, lactation impairment
89
Q

Pituitary diabetes

A
  • excess of all anterior pituitary hormones
  • hyperglycemia
90
Q

Hypopituitarism

A
  • deficiency in pituitary hormone production
91
Q

Panhypopituitarism

A
  • affects all pituitary hormones
92
Q

Hypothalamic-pituitary-thyroid axis

A
  • 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
Q

Thyroid hormone effects

A
  • increase metabolic rate and heat production
  • enhance growth and CNS development
  • enhance sympathetic activity
94
Q

What inhibits the axis

A
  • T3 and T4 at mainly at pituitary and at hypothalamus
  • stress
95
Q

What stimulates the axis

A

cold in infants

96
Q

Thyroid stimulating hormone (TSH)

A
  • 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
Q

Thyroid gland

A
  • 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
Q

Colloid

A
  • consists of glycoprotein called thyroglobulin
  • thyroglobulin is synthesized in follicular cells and secreted into colloid
  • colloid is site of thyroid hormone biosynthesis
99
Q

Thyroglobulin

A
  • precursor for thyroid hormones
  • contains tyrosine residues which provide template
100
Q

2 thyroid hormones

A
  • 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
101
Q

Synthesis of thyroid hormones

A
  • 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
Q

Enzyme responsible for thyroid hormone production

A

thyroid peroxidase

103
Q

Thyroid hormones are ____ soluble

A
  • lipid
  • need to be carried by binding protein in blood
  • TBG - thyroid binding globulin
104
Q

Thyroid hormone receptors

A
  • found everywhere on most cells
105
Q

Thyroid hormone action

A
  • 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
Q

3 thyroid hormone receptors

A
  • 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
107
Q

Thyroid hormone excess

A
  • hyperthyroidism
  • increased basal metabolic rate
  • most common type is Grave’s disease - autoimmune disease which antibodies develop against TSH receptors
108
Q

3 causes of hyperthyroidism

A
  • 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
Q

Grave’s disease

A
  • large swelling in neck, overstimulation of thyroid gland
  • exophthalmos, eye bulging
  • heart palpitations
  • increased sympathetic nervous system action
110
Q

Thyroid hormone deficiency

A
  • hypothyroidism
  • decreased metabolic rate
111
Q

5 causes of hypothyroidism

A
  • 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
Q

Hypothyroidism in utero

A
  • cretinism
  • severely stunted mental and physical development
  • irreversible
113
Q

Hypothyroidism in adults

A
  • myxedema
  • accumulation of hyaluronic acid and mucus edema under skin
  • slow mentation and slow speech
  • lethargic
  • bradycardia
114
Q

Only hormone that provides feedback inhibition on adrenal cortex

A
  • cortisol
115
Q

Adrenal cortex release mechanism

A
  • hypothalamus releases CRH
  • stimulates anterior pituitary to produce ACTH
  • stimulates steroidogenesis in all zones of adrenal cortex
116
Q

ACTH

A
  • peptide hormone
  • produced by cell called corticotrophs
  • trophic hormone stimulates adrenal blood floow, adrenal growth, adrenal steroidogenesis
117
Q

POMC processing

A
  • make ACTH –> alpha-MSH (pigmentation)
  • make beta-LPH –> beta-MSH (pigmentation) or beta-endorphin (opiate) –> met-enkephalin (opiate)
118
Q

Adrenal cortex zones

A
  • glomerular zone - aldosterone - salt/water retention
  • fascicular zone - cortisol - sugar metabolism
  • reticular zone - androgens - sex characteristics
119
Q

Steroidogenesis in glomerular zone

A
  • all steroids produced from cholesterol
  • cholesterol –> pregnenolone –> progesterone –> corticosterone –> aldosterone
120
Q

Aldosterone action

A
  • 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
Q

Aldosterone secretion regulation

A

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
Q

Renin

A
  • enzyme secreted by juxtaglomerular cells of juxtaglomerular apparatus sensory for low Na+ concentrations
123
Q

Excess aldosterone

A
  • 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
Q

Steroidogenesis in fascicular zone

A
  • cholesterol –> pregnenolone –> cortisol
125
Q

Cortisol actions

A
  • 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
Q

Cortisol actions in stress

A
  • prevents inflammation
  • prevents autoimmunity
  • mobilizes glucose during stress
127
Q

Control of cortisol secretion

A

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
Q

Primary cortisol deficiency

A
  • Addison’s disease
  • defect in adrenal cortex, no feedback inhibition
  • levels of ACTH are very high leading to skin pigmentation
129
Q

Secondary cortisol deficiency

A
  • defect at level of pituitary
  • pituitary does not produce ACTH and adrenal cortex will not be stimulated by cortisol
  • no skin pigmentation
130
Q

Addison’s disease

A
  • reduced cortisol secretion
  • hypoglycemia
  • low Na+/high K+ levels in blood
  • hypotension/hyperkalemia
131
Q

Cortisol excess

A
  • Cushing’s syndrome
  • moon face, buffalo hump, hirsutism
  • 3 causes: pituitary tumor, adrenal tumor, ectopic tumor
132
Q

Cushing’s syndrome - pituitary tumor

A
  • high production of ACTH stimulates adrenal cortex to produce too much cortisol
133
Q

Cushing’s syndrome - adrenal gland tumor

A
  • produces high levels of cortisol
  • cortisol inhibits production of ACTH from pituitary through feedback regulation
134
Q

Cushing’s syndrome - ectopic tumor

A
  • 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
Q

Steroidogenesis in reticular zone

A
  • cholesterol –> pregnenolone –> DHEA
136
Q

Adrenal androgens/DHEA

A
  • weak androgen converted to testosterone/estrogen
  • secondary sexual characteristics
137
Q

Adnrenogenital syndrome

A
  • biosynthetic pathways that make aldosterone and cortisol are deficient and all precursors go to make DHEA
  • excess androgens in adrenal cortex
138
Q

Symptoms of adrenogenital syndrome in females

A
  • masculinization of genitals
  • male-pattern hair growth (hirsutism)
  • male-type balding
  • heavy arms and legs
  • involution of breasts
139
Q

Symptoms of adrenogenital syndrome in males

A
  • pseudopuberty - sperm dysfunction
140
Q

Calcium metabolism roles

A
  • neurotransmission
  • muscular contraction
  • blood clotting
  • cell cytoskeleton
  • cell metabolism
  • skeletal support
141
Q

Phosphate metabolism roles

A
  • glycolysis
  • energy transfer
  • cofactor for enzymes and skeletal support
142
Q

3 hormones that regulate calcium and phosphate

A
  • 2 hypercalcemic hormones: parathyroid hormone (PTH) and vitamin D3 (VD)
  • 1 hypoglycemic hormone: calcitonin (CT)
143
Q

Parathyroid gland

A
  • embedded in thyroid gland
  • 4 glands, 2 on each lobe of thyroid gland
144
Q

PTH action

A
  • increase plasma calcium
  • decrease plasma phosphate
145
Q

3 PTH target sites

A
  • kidney: increase Ca2+ reabsorption, decrease PO43- reabsorption, increase vit D3 activation
  • bone: increase bone resorption/breakdown
  • GIT: indirect increase vit D3 formation
146
Q

Feedback regulation of PTH

A
  • hypercalcemia inhibits PTH
  • hypocalcemia simulates PTH
  • 1,25 (OH2) D3 inhibits PTH
147
Q

Relationship of PTH

A
  • linear
  • low levels of plasma calcium stimulates
  • high levels of plasma calcium inhibits
148
Q

Where is PTH synthesized in

A
  • parathyroid gland by chief cells
149
Q

Main stimulus for PTH

A
  • low plasma calcium
150
Q

Hyperparathyroidism

A
  • bones, stones, abdominal groans
  • soft tissue calcification (kidney stones)
  • weak bones and fractures
  • GIT dysfunction
151
Q

Primary hyperparathyroidism

A
  • 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
Q

Secondary hyperparathyroidism

A
  • consequence of low blood calcium that would stimulate PTH release
  • rickets in children and osteolmalacia in adults
  • renal failure
153
Q

Primary hypoparathyroidism

A
  • 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
Q

Trousseau’s sign

A
  • hypoparathyroidism
  • involuntary contraction of carpal muscles due to hypocalcemia and tetany
155
Q

Chvostek’s sign

A
  • hypocalcemia
  • tap trigeminal nerve which runs along cheek
  • tetany and snarl
156
Q

Pseudohypoparathyroidism

A
  • high PTH, low Ca2+, high PO43-, low 1,25 (OH2) D3
  • tissue insensitivity to PTH action
  • PTH receptors do not work
157
Q

Calcitonin

A
  • peptide hormone
  • opposes action of PTH
  • made in parafollicular cells (C-cells) in the thyroid gland adjacent to thyroid follicles
158
Q

Calcitonin action

A
  • decrease plasma calcium
  • decrease plasma phosphate
159
Q

3 calcitonin target sites

A
  • kidneys: decrease Ca2+ reabsorption, decrease PO43- reabsorption, decrease vit D3 activation
  • bone: decrease bone resorption/break down
  • GIT: decrease Ca2+ absorption main site**
160
Q

As plasma calcium increases, ____ release of calcitonin

A
  • increase
161
Q

Calcitonin clinical use

A
  • 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
Q

Vitamin D3

A
  • 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
Q

Vitamin D3 synthesis

A
  • 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
Q

1,25 vitamin D3 action

A
  • increase plasma calcium
  • increase plasma phosphate
165
Q

3 1,25 vitamin D3 target sites

A
  • kidney: increase Ca2+ reabsorption, increase PO43- reabsorption
  • bone: promote PTH action
  • GIT: increase absorption of Ca2+ and PO43-
166
Q

GIT actions of vitamin D3

A
  • 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
Q

Vitamin D3 stimulus

A
  • increase PTH
  • low Ca2+
168
Q

Vitamin D3 deficiency

A
  • rickets in juveniles
  • osteomalacia in adults
  • low vit D, low Ca2+, high PTH = poor bone formation and increased bone breakdown
169
Q

Vitamin D3 excess

A
  • toxicity
  • hypercalcemia
  • soft tissue calcification –> blood vessel calcification –> aneurysm –> death
170
Q

2 pancreas gland

A
  • exocrine - pancreatic juice for digestion, ducts
  • endocrine - regulated blood sugar and found in Islet of Langerhans or pancreatic islets
171
Q

3 cells pf pancreatic islets

A
  • alpha - secrete glucagon
  • beta - secrete insulin
  • delta - somatostatin
172
Q

Pancreatic islets hormones are ____

A
  • paracrine
173
Q

Somatostatin effects

A
  • inhibit glucagon and insulin
174
Q

Insulin effects

A
  • inhibit glucagon
175
Q

Glucagon effects

A
  • stimulates insulin and somatostatin
176
Q

Neural innervation of pancreatic islets

A
  • sympathetic system through splanchnic nerve: increase glucagon and decrease insulin
  • parasympathetic system through vagus nerve: increase insulin and decrease glucagon
177
Q

Insulin structure

A
  • 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
Q

Insulin action

A
  • lower blood glucose
  • anabolic - builds up tissues
  • storage hormone - store glucose in cells, increase fat deposition in tissues, increase protein synthesis
179
Q

Factors affecting insulin

A
  • 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
Q

Insulin regulation

A
  • 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
Q

Glucagon action

A
  • catabolic peptide hormone - break down, fasting
  • glucose: decrease glycogenesis, increase gluconeogenesis, increase glycogenolysis
  • lipid: increase lipolysis, decrease lipogenesis
  • protein: minor increase of degradation
182
Q

Factors affecting glucagon

A
  • nutrients: decrease glucose, increase amino acids
  • GIT hormones: increase gastrin/CCK, decrease secretin
  • neural stimuli: increase stress (sympathetic), increase food (parasympathetic)
183
Q

Diabetes mellitus

A
  • 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
Q

Symptoms of diabetes mellitus

A
  • polyuria - large amounts of dilute urine
  • polydipsia - excessive thirst
  • polyphagia - excessive hunger
185
Q

Type 1 diabetes mellitus

A
  • insulin dependent and juvenile onset
  • autoimmune disease attacks beta cells causing loss of insulin secretion
  • treated with insulin injections
  • 10-20%
186
Q

Type 2 diabetes mellitus

A
  • insulin independent and adult onset
  • insulin resistance - decreased receptor response
  • normal or high plasma insulin levels
  • receptor downregulation
  • associated with obesity
  • 80-90%
187
Q

Complications of diabetes mellitus

A
  • cardiovascular disease (atherosclerosis, gangrene, hypertension)
  • nephropathy, retinopathy, dermopathy, neuropathy, ulcers/infections
188
Q

Insulin excess

A
  • causes: insulin-secreting tumor, insulin overdose, reactive hypoglycemia
  • symptoms: hypoglycemia, sympathetic activation, insulin shock
  • treatment: glucose for diabetes, low carbohydrates for reactive hypoglycemia

Physiology 210 (12 decks)

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