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PHGY 216 > Endocrine Physiology - Mod 1 > Flashcards

Endocrine Physiology - Mod 1 Flashcards

1
Q

what are glands?

A

a specialized cell, group of cells, or organ that secretes substances to be used by or eliminated from the body

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2
Q

what are the 6 functions of the endocrine system?

A
  1. maintain constant internal environment
  2. adaptive stress response
  3. growth and development
  4. reproduction
  5. red blood cell production
  6. works with ANS for circulation and digestive functions
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3
Q

hydrophilic hormones

A
  • highly water soluble, not lipid soluble
  • unbound in the plasma
  • peptides, proteins, or amines (catecholamines like NE and EPI)
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4
Q

synthesis of peptide hormones (simple)

A
  1. synthesis
  2. packaging
  3. storage
    4, secretion
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5
Q

synthesis of peptide hormones (detail)

A
  1. preprohormones are synthesized by ER ribosomes
  2. processed into active hormones and packaged into secretory vesicles in the ER or golgi
  3. vesicles stored until cell receives signal
  4. exocytosis of vesicles and hormones are released into blood
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6
Q

lipophilic hormones

A
  • highly soluble in lipids, not water soluble
  • require carriers
  • thyroid and steroid
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7
Q

synthesis of lipophilic hormones

A
  • steroids all synthesized from cholesterol
  • cell specific enzymes determine which hormones are produced
  • released as they are synthesized
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8
Q

how do peptide hormones and catecholamines bind to receptors on the plasma membrane surface?

A
  • activated second messenger systems
  • pathways amplify initial signal because low conc. of hormones will trigger cellular responses
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9
Q

how does cAMP work as a secondary messenger?

A
  • binds to receptor that can activate G protein which will activate adenylyl cyclase molecules
  • activated proteins convert ATP to cAMP which activates protein kinase A
  • protein kinase A enzymes phosphorylate and activate target proteins
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10
Q

how does Ca2+ work as a secondary messenger?

A
  • binds to receptor that activates G protein which will activate phospholipase C enzymes
  • proteins convert PIP2 to IP3 and DAG
  • IP3 mobilizes intracellular Ca2+ to activate calmodulin
  • Ca2+-calmodulin complex activates. Ca2+-calmodulin-dependent protein kinase which will phosphorylate and activate target proteins
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11
Q

how to steroid and thyroid hormones bind to receptors?

A
  • inside the cells
  • pass through plasma and nuclear membranes
  • when they bind they regulate gene transcription and protein synthesis
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12
Q

lipophilic hormones and protein synthesis

A
  1. free lipophilic hormones diffuse across plasma membrane to interact with receptors
  2. hormone-receptor complex binds to hormone response element in DNA
  3. DNA binding activates specific genes to produce mRNA
  4. mRNA leaves nucleus
  5. mRNA binds to ribosome so proteins can be synthesized
  6. synthesized proteins lead to cellular response of hormone
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13
Q

nervous control - HPA

A
  • rapid responses
  • effects only last while the stimulus is going
  • hard-wired to one specific target
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14
Q

endocrine control - HPA

A
  • slow responses
  • effects persist after stimulus stops
  • many targets in the body
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15
Q

where is the pituitary gland?

A

base of the skull

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16
Q

pituitary gland lobes

A

2 unrelated and uninteracting lobes

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17
Q

posterior pituitary gland structure

A
  • made of neural-like tissues (neurohypophysis)
  • connected to hypothalamus by neural pathways (supraoptic and paraventricular nucleus)
  • axons from nuclei go down pituitary stalk to terminate on posterior pituitary
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18
Q

anterior pituitary gland structure

A
  • made of glandular epithelial tissue (adenohypophysis)
  • connected to hypothalamus by vascular link (hypothalamic- hypophyseal portal system)
  • hypothalamus secretes hormones into the portal system and brings them to the anterior pituitary
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19
Q

how do posterior pituitary hormones work?

A

synthesized in hypothalamus and transported down axons, action potentials cause vesicles to be released into blood

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20
Q

what are the posterior pituitary hormones?

A

vasopressin and oxytocin

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21
Q

vasopressin (aka ADH)

A

enhances retention of water by kidneys and causes contraction of arteriolar smooth muscle

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22
Q

oxytocin

A

stimulates contraction of uterine smooth muscle cells during child birth, and promotes milk ejection during breastfeeding

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23
Q

what does it mean if a hormone is tropic? (like in the anterior pituitary)

A

once they are released they stimulate other endocrine glands to release hormones

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24
Q

what are the 6 hormones of the anterior pituitary?

A

GH (somatotropin), ACTH, LH, TSH, FSH, PRL

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25
Q

what is the hormone GH?

A

Growth Hormone
- regulates body growth and metabolism

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26
Q

what is the hormone ACTH?

A

adrenocorticotropic hormone
- stimulates adrenal cortex to secrete cortisol

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27
Q

what is the hormone LH?

A

luteinizing hormone
- responsible for ovulation and formation of corpus luteum in females
- stimulates release of testosterone from interstitial cells of Leydig in males

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28
Q

what is the hormone TSH?

A

thyroid-stimulating hormone
- stimulates release of thyroid hormones from thyroid gland

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29
Q

what is the hormone FSH?

A

follicle-stimulating hormone
- stimulates growth and development of ovarian follicles and promotes secretion of estrogen in females
- required for sperm production in males

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30
Q

what is the hormone PRL?

A

prolactin
- enhances breast development and milk production in females
- present in males with no purpose
- only non-tropic anterior pituitary hormone

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31
Q

6 stages of hypothalamic-hypophyseal portal system

A
  1. hypophysiotropic hormones are produced by neurosecretory neurons in hypothalamus then go through hypothalamic capillaries
  2. hypothalamic capillaries join to form HHPS
  3. HHPS branches into anterior pituitary capillaries
  4. hypophysiotropic hormones leave the blood through ant.pit. capillaries and control the release of hormones
  5. ant.pit. secretes a hormone into capillaries when stimulated by a releasing hormone
  6. capillaries rejoin to form a vein so hormones can be distributed to the body
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32
Q

what are the 7 hormones produced in the hypothalamus?

A

TRH, GnRH, GHIH, CRH, GNRH, PRH, PIH

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33
Q

what is hormone TRH?

A

thyrotropin-releasing hormone
- stimulates release of TSH and prolactin

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34
Q

what is hormone GnRH?

A

gonadotropin-releasing hormone
- stimulates release of FSH and LH

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35
Q

what is hormone GHIH?

A

growth hormone inhibiting hormone
- inhibits release of growth hormone and TSH

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36
Q

what is hormone CRH?

A

corticitropin-releasing hormone
- stimulates release of ACTH

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37
Q

what is hormone GNRH?

A

growth hormone releasing hormone
- stimulates release of GH

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38
Q

what is hormone PRH?

A

prolactin-releasing hormone
- stimulates release of prolactin

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39
Q

what is hormone PIH?

A

prolactin-inhibiting hormone
- inhibits the release of prolactin

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40
Q

what type of inputs do hormones from the hypothalamic neurons receive?

A

neuronal and hormonal
inhibitory and stimulatory

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41
Q

blood barrier in the hypothalamus

A

some sections dont have - means that it can monitor blood and respond to changes

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42
Q

where is the thyroid gland?

A

over the trachea, just below the larynx

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43
Q

describe the cellular structure of the thyroid gland

A
  • follicular cells arranged to form hollow spheres
  • C cells that secrete calcitonin
  • the middle of the hollow spaces is called the colloid and it is made up of thyroglobulin where the hormones are synthesized and stored
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44
Q

what are the 2 thyroid hormones?

A

T4 (tetraiodothyronine or thyroxine)
T3 (triiodothyronine)

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45
Q

what is the composition and function of T4?

A

4 iodine molecules
makes up 90% of thyroid hormones secreted
converted to T3 in target tissues

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46
Q

what is the composition and function of T3?

A
  • 3 iodine molecules
  • 10% of thyroid hormones secreted
  • more active
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47
Q

why is iodine important?

A
  • required to keep the thyroid hormone at sufficient level
  • circulates as iodide once ingested
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48
Q

5 steps to the synthesis of thyroid hormones

A
  1. tyrosine-containing thyroglobulin is produced by ER-golgi complex and is transported into colloid by exocytosis
  2. follicular cells take up iodide by trapping it against the gradient (uses Na+ cotransporter that moves Na+ down the gradient)
  3. iodide transferred into colloid
  4. thyroperoxidase converts iodide into iodine (more reactive) which attaches to a Tyr residue on a thyroglobulin
    - process called iodide organification
    - produces MIT or DIT
  5. coupling process combines MITs and DITs to form thyroid hormones that are then bound to the thyroglobulin
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49
Q

3 steps to the release of thyroid hormones

A
  1. follicular cells engulf part of the thyroglobulin-containing colloid by phagocytosis and create vesicles
  2. lysosomes fuse with vesicles and digestive enzymes release all MIT, DIT, T3, T4
  3. T3 and T4 cross plasma membrane and bind to plasma thyroid-binding protein
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50
Q

how fast do thyroid hormones act

A

very slowly

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51
Q

what are the 5 main actions of thyroid hormones? (no description)

A
  • metabolic rate and heat production
  • intermediary metabolism
  • sympathomimetic
  • cardiovascular system
  • growth
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52
Q

thyroid hormones - metabolic rate and heat production

A

thyroid hormone increases BMR
- increases oxygen consumption and energy expenditure resulting in increased heat production

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53
Q

thyroid hormone - intermediary metabolism

A

influences enzymes involved in fuel metabolism
- effects differ depending on how much thyroid hormone present
- in low conc. glucose is converted to glycogen
- in high conc. glycogen breaks down into glucose

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54
Q

thyroid hormone - sympathomimetic

A

increase target cell’s response to catecholamines
- increases number of catecholamine receptors

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55
Q

thyroid hormone - cardiovascular system

A

have sympathiomimetic effects on the heart
- can increase HR and strength of contraction which will increase blood volume and flow

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56
Q

thyroid hormone - growth

A

essential for normal growth
- stimulates release of GH and insulin-like growth factor
- promotes actions to stimulate synthesis of new structural proteins and skeletal growth

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57
Q

hypothalamic-pituitary-thyroid axis

A
  • hypothalamus secretes TRH which acts on the anterior pituitary to secrete TSH
  • TSH regulates thyroid hormone secretion, acting on most stages of synthesis and release
  • TSH directly affects thyroid gland
  • release of TRH and TSH are under negative feedback control
58
Q

what is hypothyroidism?

A

when the thyroid gland does not secrete enough thyroid hormone into the blood

59
Q

hypothyroidism - primary failure

A

hashimoto’s thyroiditis
- autoimmune disorder in which antibodies target the thyroid gland in a way that it can no longer produce thyroid hormone
- results in low levels of T3 and T4, but elevated levels of TSH because the negative feedback loop which decreases TRH and TSH can’t happen

60
Q

hypothyroidism - secondary failure

A

when hypothalamus and pituitary don’t secrete adequate TRH and TSH
- low levels of T3 and T4
- potential low levels of TRH and TSH

61
Q

hypothyroidism - inadequate dietary supply of iodine

A

most common cause
- low T3 and T4, elevated TSH

62
Q

hypothyroidism - cretinism

A

congenital hypothyroidism
- causes dwarfism and intellectual disability

63
Q

symptoms of hypothyroidism

A
  • cold intolerance
  • slow reflexes
  • reduced mental alertness
  • easy to fatigue
  • slow, weak heart rate
  • weight gain b/c decreased BMR
64
Q

what is hyperthyroidism?

A

increased levels of thyroid hormone

65
Q

hyperthyroidism - secondary to excess secretions

A

tumor in the hypothalamus or anterior pituitary
- ignore negative feedback resulting in elevated T3, T4, TRH, and TSH

66
Q

hyperthyroidism - thyroid tumor

A

results in increased secretion of thyroid hormones
- elevated T3 and T4
- decreased TSH

67
Q

hyperthyroidism - Graves’ Disease

A

most common cause
- autoimmune disease that produces long-acting thyroid stimulator (LATS) that targets and activates TSH receptors on follicular cells
- LATS has the same effect as excessive TSH causing follicles to grow
- no negative feedback so elevated T3 and T4, low TSH

68
Q

symptoms of hyperthyroidism

A
  • increased HR
  • excessive heat production
  • muscle weakness (skeletal muscle protein degradation)
  • mood swings (CNS alertness)
  • weight loss from elevated BMR
69
Q

goiter

A

visibly enlarged thyroid gland
- from increased TSH
- common symptom between hypo and hyperthyroidism

70
Q

where are the adrenal glands?

A

small glands on top of the kidney

71
Q

layers of the adrenal glands

A

outer layer - cortex (secretes steroid hormones)
inner layer - medulla (secretes catecholamines)

72
Q

adrenal cortex zones

A
  • zona glomerulosa
  • zona fasciculata
  • zona reticularis
73
Q

zona glomerulosa

A

produces mineralocorticoids that influence mineral (electrolyte) balance

74
Q

zona reticularis

A

produces glucocorticoids that influence glucose, lipid, and protein metabolism

75
Q

zona fasciculata

A

produces sex hormones in low quantities, similar to the ones produces in gonads
- also produced in zona reticularis

76
Q

mineralocorticoids

A

main one is aldosterone which is essential for sodium conservation
- secretion is related to electrolyte conc., blood volume, BP
- would die from circulatory shock without them

77
Q

2 primary stimuli of mineralocorticoids

A
  1. activation of renin-angiotensin-aldosterone system in response to reduced Na+ and a fall in BP
  2. direct stimulation of adrenal cortex by increased K+ concentration
78
Q

glucocorticoids

A

main one is cortisol
- roles in metabolism and stress adaptation

79
Q

glucocorticoids in metabolism

A

cortisol stimulates gluconeogenesis in the liver which produces glucose from amino acids
- stimulates protein degradation in muscle and inhibits glucose uptake by tissues
- breaks down lipid stores to mobilize free fatty acids that can be used as a fuel source

80
Q

glucocorticoids in stress adaptation

A

if under severe stress, cortisol will cause a shift away from protein and fat stores while increasing carb stores
- increased glucose availability ensures adequate brain activity and wound repair

81
Q

cortisol secretion

A

negative feedback
- hypothalamus releases corticotropin-releasing hormone that stimulates anterior pituitary to release ACTH
- diurnal secretion pattern which means highest levels in morning and lowest at night

82
Q

sex hormones

A

androgens for males, estrogens for females
- secretion parallels cortisol secretion

83
Q

dehydroepiandosterone (DHEA)

A

most important adrenal cortex sex hormone (more so in females)
- causes growth of pubic and armpit hair, enhancement of puberty growth spurt, maintenance of female sex drive

84
Q

adrenal medulla

A

synthesizes catecholamines
- epi and noepi stored on chromaffin granules that can undergo exocytosis to release epi and noepi into the blood (only really have to consider actions of epi though)

85
Q

effects of epinephrine on organ systems

A

sympathetic nervous system can use it during stress
- causes increased HR and contractile strength which increases CO and vasoconstriction to increase TPR and BP
- decreases digestive activites

86
Q

effects of epinephrine on metabolism

A

affects carbohydrates, fats, and lipids
- increases blood glucose by enhancing liver gluceoneogenesis and glycogenolysis
- promotes lipolysis to increase circulatory free fatty acids that can be used as an energy source

87
Q

sympathetic nervous system and epinephrine as an integrated stress response

A

permits body to overcome anything from preventing escape from a stressful situation

88
Q

insulin and glucagon as an integrated stress response

A

works to the same purpose as cortisol
- increased blood glucose
- increased glucagon secretion will break down glycogen stores to produce glucose
- decreased insulin secretion will reduce the rate that glucose is removed from circulation

89
Q

CRH-ACTH-Cortisol System as an integrated stress response

A

main system involved
- increases levels of blood glucose, free fatty acids, and amino acids
- provides energy substrate to brain to facilitate repair of damaged tissues
- B-endorphin is a precursor molecule that helps form ACTH that can act like analgesia in physical injury

90
Q

renin-angiotensin-aldosterone system as an integrated stress response

A

increase vasopressin and angiotension II which are vasoconstrictors that can increase BP

91
Q

hyperadrenalism

A

adrenal glands secrete excessive amounts of hormones

92
Q

cortisol hypersecretion (cushing’s syndrome)

A
  • overstimulation of adrenal cortex by CRH or ACTH, adrenal tumors hypersecreting cortisol independent of ACTH, and ACTH-secreting tumors somewhere else
  • increased plasma glucose
  • buffalo humps and moon face
93
Q

adrenal androgen hypersecretion

A

adult females - masculine-like body hair, decreased breasts and menstruation, more male secondary sex characteristics
adult males - little to no effects
newborn females - male-type external genitalia
prepubertal males - early development of secondary sex characteristics

94
Q

hyperaldosteronism

A

symptoms based on activity of aldosterone and include excessive Na+ retention, K+ depletion, and high bp

95
Q

when does adrenocortical insufficiency occur

A

when both adrenal glands aren’t working
- if one stopped functioning the other would hypertrophy to make up for it

96
Q

adrenocortical primary insufficiency (addision’s disease)

A

when all layers of the adrenal cortex are under-secreting
- caused by autoimmune destruction of the cortex
- a deficiency of aldosterone and cortisol
- have hyperkalemia and hyponatremia
- affects cardiac rhythms and reduced EDF and blood volumes (causes hypotension)
- poor stress response and low blood glucose and hyperpigmentation of skin

97
Q

adrenocortical secondary insufficiency

A

problem in the hypothalamus or anterior pituitary causing reduced ACTH
- deficiency of cortisol, normal aldosterone
- symptoms depend on level or cortisol deficiency, rate of reduction in cortisol levels, underlying health of individual
- loss of appetite, weight, fatigue, nausea, vomiting, diarrhea, muscle weakness, irritability, depression

98
Q

anabolic reactions

A

leads to synthesis of larger organic macromolecules from smaller organic molecule subunits
- for repair, growth, and storage of excess ingested nutrients

99
Q

catabolic reactions

A

break down of larger organic macromolecules either through hydrolysis into smaller molecules or oxidation of smaller molecules to yield ATP

100
Q

excess glucose storage

A

stored in liver and skeletal muscle as glycogen
- when stores are full, excess glucose is converted into free fatty acids and glycerol for synthesis of triglycerides occurring in adipose tissue

101
Q

excess fatty acid storage

A

stored as triglycerides

102
Q

excess amino acids

A

not needed for protein synthesis
- used for structural proteins or converted to glucose and fatty acids for eventual storage as triglycerides

103
Q

absorptive metabolic state

A

anabolism dominated as ingested food is digested and absorbed into circulation
- ingested simple carbs are converted to glucose in liver which is released as fuel or stored as glycogen
- ingested fats and proteins are used immediately or stored

104
Q

postabsorptive metabolic states

A

catabolism dominates hours after food is ingested
- glycogen stored in liver and muscle becomes primary energy source
- after time glycogen is not sufficient so lipolysis uses triglycerides to meet energy needs

105
Q

glycerol

A

comes from triglycerides when they are broken down
- can be converted to glucose by the liver

106
Q

lactic acid

A

formed by glycolysis
- can be converted to glucose by the liver

107
Q

ketone bodies

A

produced in the liver when there are glucose shortages
- when liver uses free fatty acids they are oxidized to acetyl CoA which doesn’t produce energy through citric acid cycle
- acetyl CoA converted to ketone bodies and released into blood

108
Q

the pancreas functions

A

endocrine and exocrine organ
- exocrine functions are important for digestion
- endocrine functions are localized to islets of langerhans

109
Q

alpha cells

A

produce and secrete glucagon (in pancreas)

110
Q

beta cells

A

produce and secrete insulin (in pancreas)

111
Q

delta cells

A

produce and secrete somatostatin (in pancreas)

112
Q

PP cells

A

secrete pancreatic polypeptide which can play a role in reducing appetite

113
Q

somatostatin

A

released by delta cells
- slows down digestive system to inhibit digestion and absorb nutrients to prevent overabsorption
- produced in pancreas and celling lining of digestive tract
- acts as a paracrine hormone
- released by hypothalamus where it inhibits secretion of GH and TSH

114
Q

insulin

A

small peptide hormone produced by beta cells of pancreatic islets
- dominant hormone in absorptive state
- major role in anabolism
- associated with regulation of blood sugar

115
Q

2 factors that increase blood glucose

A
  1. glucose absorption from digestive tract
  2. hepatic glucose production
    - through glycogenolysis of stored glycogen
    - through gluconeogenesis
116
Q

2 factors that decrease blood glucose

A
  1. transport of glucose into cells
    - utilization for energy production
    - storage as glycogen through glycogenesis
    - storage as triglycerides
  2. urinary excretion of glucose
117
Q

4 main effects of insulin on carbohydrates

A
  1. increase uptake of glucose into most cells
    - causes movement of GLUT-4 glucose transporters from intracellular pool to plasma membrane
    - brain doesn’t need insulin bc it always has GLUT-1 and GLUT-3 transporters and liver doesn’t need bc it has GLUT-2
  2. inhibit glycogenolysis in the liver
    - prevents catabolism of glycogen and further promotes glucose storage
  3. stimulate glycogenesis in skeletal muscle and liver
    - promotes storage of glucose as glycogen
  4. inhibit gluconeogenesis in liver
    - prevents formation of glucose from amino acids
118
Q

4 main effects of insulin on fats

A
  1. enhances entry of fatty acids into adipose tissue cells
  2. increases GLUT-4 recruitment in adipose cells to increase glucose uptake for synthesis of triglycerides
  3. enhances activity of enzymes involved in synthesizing triglycerides
  4. inhibits lipolysis
119
Q

3 main effects of insulin on proteins

A
  1. promotes uptake of amino acids into all tissues
  2. enhances activity of enzymes involved in protein synthesis
  3. inhibits degradation of proteins
120
Q

3 steps to the negative feedback system of insulin secretion regulation

A
  1. elevation of blood glucose stimulates islet beta cells to secrete insulin which lowers blood glucose levels and secretion of insulin stops
  2. insulin released in a feedforward system
    - GI hormones secreted by digestive tract stimulate insulin release to prepare for rise in blood glucose that is about to occur
  3. cells of islets of Langerhans are innervated by ANS
    - presence of food in digestive system activates PNS in feedforward manner and SNS decreases insulin secretion
121
Q

glucagon

A

major pancreatic hormone in the postabsorptive state
- secretion of glucagon triggered by decrease in blood glucose levels
- effects are opposite to insulin in the liver

122
Q

effects of glucagon on carbohydrates

A

glucagon increases hepatic glucose production by decreasing glycogen synthesis, enhancing both glycogenolysis and gluconeogenesis

123
Q

effects of glucagon on fats

A

glucagon promotes lipolysis while inhibiting fat storage and enhances formation of ketone bodies in liver

124
Q

effects of glucagon on proteins

A

glucagon promotes protein catabolism in liver

125
Q

growth periods in the body

A
  • before puberty there is very little difference between male and female height and weight
  • pubertal growth is supported by growth hormone and androgen
126
Q

3 main metabolic actions of GH

A
  1. increased rate of protein synthesis
  2. increased fatty acid mobilization and use
  3. decreased rate of glucose use by body tissues
127
Q

soft tissue actions of GH

A

can increase number of cells through cell division, stimulate cells to grow larger by promoting protein synthesis
- promotes thickness and length of bone
- effects are mediated through other peptides known as somatomedins called insulin-like growth factors

128
Q

IGF-I on GH

A

release and synthesis stimulated by GH in the liver
- other tissues can produce IGF-I when stimulated by GH, but don’t release it into the blood because it has paracrine actions
- mediates most growth promoting actions of GH

129
Q

IGF-II on GH

A

production not stimulated by GH
- important during fetal development, not adults

130
Q

bone growth - thickness

A

achieved by adding new bone to outer layer
- as osteoblasts are depositing new bone on outer surface, osteoclasts remove bone on the insides
- diameter of bone and marrow cavity increases

131
Q

bone growth - length

A

only occurs between epiphysis and diaphysis
- chondrocytes divide and stack below the epiphysis
- below that are older chondrocytes that hypertrophy which pushes epiphysis away from diaphysis and matrix calcifies
- older chondrocytes die and get removed at the same rate that new ones form

132
Q

regulation and secretion of GH

A
  1. diurnal pattern of secretion
    - reaches peak levels half an hour after entering deep sleep
  2. deficiency is because of dysfunction at hypothalamus, pituitary, or tissue level
    - causes dwarfism
  3. excess is caused by an anterior pituitary tumor
    - causes gigantism
133
Q

how is calcium regulated?

A
  • under hormonal control to ensure proper concentration is maintained
  • can be ingested through diet and is stored in bones
  • can be removed from bones if there is more needed in plasma
134
Q

what 3 hormones regulate the plasma concentration of Ca2+?

A

parathyroid hormone
calcitonin
vitamin D

135
Q

what are the 5 physiological processes that involve calcium?

A
  1. neuromuscular excitability
  2. secretion of vesicles
  3. excitation-contraction coupling
  4. release of neurotransmitters
  5. role as a second messenger
136
Q

where are the parathyroid glands

A

4 small glands on the back of the thyroid gland

137
Q

how does the parathyroid effect the bones?

A
  • primary storage area of Ca2+ where it is stored as hydroxyapatite crystals which are precipitated Ca3(PO4)2
  • bone remodelling allows for rapid changed in free Ca2+ by regulating activity of cells
  • osteoclast activity is enhanced by osteoblast activity inhibited by PTH
  • with PTH there is release of Ca2+ and PO4 3+ into plasma
138
Q

how does the parathyroid affect the kidneys?

A
  • PTH stimulates reabsorption of Ca2+, without it the body would have to degrade bone
  • PTH stimulates kidneys to remove PO4 3+
  • PTH stimulates kidneys to activate vitamin D
139
Q

calcitonin

A
  • secreted from thyroid gland
  • actions opposite to parathyroid hormone
  • secreted in response to increased plasma Ca2+ levels
140
Q

activation of vitamin D

A

2 steps to be activated
- 1st in liver, 2nd in kidneys
- each step adds a hydroxyl group to compound

PHGY 216 (2 decks)

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