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PHGY 216 > Module 1: Endocrine Physiology > Flashcards

Module 1: Endocrine Physiology Flashcards

1
Q

what is the endocrine sys comprised of

A

many different glands

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2
Q

what do glands form

A

a coordinated system as they all secrete hormones, and many functional interactions take place between them

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3
Q

how is the endocrine system a major regulatory system

A

uses hormones to produce homeostatic adjustments

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4
Q

what are the 6 functions of the endocrine system

A
  1. maintain constant internal environment via regulation of metabolism and H2O/electrolyte balance
  2. adaptive stress response
  3. growth and development
  4. reproduction
  5. RBC production
  6. Integrating with autonomic nervous sys in regulating both circulation and digestive functions
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5
Q

what are hormones

A

chemical substances that are secreted directly into the blood at low quantities, and exert physiological effect at a distant target tissue

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6
Q

what are the 2 major classes of hormones

A
  1. hydrophilic (water loving)
  2. lipophilic (lipid loving)
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7
Q

what are hydrophilic hormones?

A
  • highly H2O soluble
  • low lipid solubility
  • can be found unbound to carrier molecules within the plasma
  • 1st group are mostly peptides or proteins (called peptide hormones), the 2nd are amines (hormones based on amino acid residues)
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8
Q

what are peptides

A

short chains of amino acids

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9
Q

what are proteins

A

longer chains of amino acids

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10
Q

2 types of hydrophilic hormones

A
  1. peptide hormones
  2. amines
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11
Q

2 types of amine hormones

A
  1. catecholamines (NE & E)
  2. thyroid hormones (note these are not hydrophilic)
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12
Q

where are catecholamines found

A

unique bc they are found both free and bound to carrier molecules

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13
Q

how are peptide hormones synthesized and secreted

A

by the same cellular machinery that makes proteins within cells

  1. synthesis: large precursor proteins called preprohormones are synthesized by ER ribosomes
  2. packaging: travel through ER and Golgi complex, then preprohormones are processed into active hormones and packaged into secretory vesicles
  3. storage: hormone-containing secretory vesicles can be stored until the cell receives the appropriate signal
  4. secretion: appropriate signal initiates exocytosis of vesicles and the hormones are released into the blood
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14
Q

what are lipophilic hormones

A
  • highly soluble in lipids
  • poorly soluble in H2O
  • generally require carrier molecules for transport throughout the body
  • include amine thyroid hormones and steroid hormones
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15
Q

what single molecule are steroid hormones synthesized from

A

cholesterol

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16
Q

how are different steroid hormones produced

A

depends on a particular tissue on the specific enzymes within that tissue

ex: enzyme leading to cortisol synthesis is only found in adrenal cortex which is why only that organ can make cortisol

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17
Q

how are steroid hormones stored and released

A

so lipophilic they are not stored, but rather released as they are synthesized

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18
Q

how do you regulate the amount of steroid hormone released

A

you need to regulate its synthesis!

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19
Q

what do you need for hormones to achieve their desired effect

A

only free, unbound hormone can interact w a receptor at its target cell

(not rly a problem for hydrophilic hormones and catecholamines mainly found in their unbound state, but lipophilic hormones need carrier molecules and the consideration of dynamic equilibrium of hormone binding to its carrier)

hormones are dynamically unbinding and rebinding, resulting in a small fraction of hormone that is unbound at a particular time. it is this unbound hormone that is active and able to act on target cells.

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20
Q

what happens when peptide hormones and catecholamines bind to their receptor?

A

produces effects within cells by activating 2nd messenger system. are able to amplify initial signal, as low concentrations of hormones trigger cellular responses.

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21
Q

how does cyclic AMP (cAMP) work as a secondary messenger

A
  1. extracellular messenger binds to receptor
  2. activates G protein
  3. shuttles to and activates several adenylyl cyclase
  4. these activated proteins convert many molecules of ATP to cAMP
  5. which activate protein kinase A
  6. the activate protein kinase A enzymes then phosphorylate and activate target proteins

which can bring about the desired result

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22
Q

how does Ca2+ work as a secondary messenger

A
  1. extracellular messenger binds to receptor activating G protein
  2. shuttles to activate several phospholipase C enzymes
  3. these proteins convert PIP2 to IP3 and DAG
  4. IP3 mobilizes intracellular Ca2+
  5. activating calmodulin
  6. Ca2+-calmodulin complexes and activates Ca2+-calmodulin complexes then activate Ca2+-calmodulin-dependent protein kinase
  7. which phosphorylate and activate target proteins bringing the desired response
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23
Q

what happens after steroid and thyroid hormones bind to their receptor

A
  • are able to pass through plasma membrane and the nuclear membranes of the cell
  • binding produces effects by regulating gene transcription and protein synthesis
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24
Q

how do lipophilic hormones exert their effects on cells

A

by regulating protein synthesis
*lipophilic hormone receptors can be found within the cytoplasm or the nucleus

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25
Q

what are the 6 steps of lipophilic hormones regulating protein synthesis

A
  1. free lipophilic hormone diffuse across the plasma membrane and/or the nuclear membrane to interact with intracellular receptors
  2. hormone-receptor complex (H-R) binds to the hormone response element (HRE) within the DNA
  3. DNA binding activates specific genes and produces messenger RNA (mRNA)
  4. mRNA leaves the nucleus
  5. mRNA binds to a ribosome and proteins are synthesized
  6. the newly synthesized proteins ultimately lead to the cellular response of the hormone
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26
Q

name some differences between neurotransmitters and hormones

A
  • neurotransmitters belong to the nervous system, hormones are endocrine system
  • neurotransmitters are transmitted across a synaptic cleft, hormones are transmitted by the blood
  • hormones are produced by endocrine glands, neurotransmitters are produced by neurons
  • neurotransmitters must travel a short distance to their target, hormones may travel a great distance
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27
Q

nervous control vs endocrine control for response time

A

nervous = rapid responses (milliseconds)
endocrine = slow responses (minutes to hours)

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28
Q

nervous control vs endocrine control for duration of effect

A

nervous = brief in duration (ends when stimulus stops)
endocrine = long in duration (effects persist after stimulus stops)

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29
Q

nervous control vs endocrine control for # of targets

A

nervous = hard-wired to one specific target (muscle or gland)
endocrine = many different targets in the body (blood circulates)

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30
Q

what is the pituitary gland

A
  • very small gland located in a bony cavity at the base of the skull
  • divided by the posterior and anterior pituitary gland
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31
Q

what is the posterior pituitary gland

A
  • comprised of neural-like tissues and is sometimes called neurohypophysis
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32
Q

what is the anterior pituitary gland

A
  • comprised of glandular epithelial tissues and is also called the adenohypophysis
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33
Q

what does the hypothalamus do

A

controls hormone release but does so in a different matter for either posterior/anterior lobe

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34
Q

What is the relationship between the hypothalamus and the posterior pituitary

A
  • hypothalamus is connected to the posterior pituitary by a neural pathway
  • in the hypothalamus there are 2 well-defined clusters of neurons, called supraoptic nucleus and the paraventricular nucleus, axons from these nuclei go down the pituitary stalk and terminate on blood vessels in the posterior pituitary
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35
Q

are hormones produced in the posterior pituitary gland itself

A

no

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35
Q

What is the relationship between the hypothalamus and the anterior pituitary

A
  • hypothalamus is connected to the anterior pituitary by a unique vascular link: the hypothalamic-hypophyseal portal system
  • hypothalamus secretes hormones into this portal system where they are carried directly to the anterior pituitary where they inhibit/promote the release of anterior pituitary hormones
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36
Q

where are hormones synthesized in the neuron cell bodies

A

the hypothalamus

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37
Q

what happens once hormones are synthesized by the hypothalamus

A
  • they are packed into small vesicles which are transported down the axons to the nerve endings in the posterior pituitary
  • once an appropriate stim reaches the hypothalamus, these neurons transmit an action potential that cause the release of hormone-containing vesicles into the blood
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38
Q

what is vasopressin

A
  • aka antidiuretic hormone (ADH)
  • enhances retention of water by the kidneys
  • causes contraction of arteriolar smooth muscle (vasoconstriction)
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39
Q

what is oxytocin

A
  • stim contraction of uterine smooth muscle cells during childbirth
  • promoting milk ejection during breastfeeding
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40
Q
  1. what 6 hormones does the anterior pituitary gland synthesize and release. 2. what do we call these hormones?
A
  1. GH, ACTH, LH, TSH, FSH, PRL
  2. tropic hormones
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41
Q

what is GH

A

growth hormone
- regulates overall body growth and is involved in metabolism

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42
Q

what is ACTH

A

stimulates secretion of cortisol by adrenal cortex (metabolic actions, stress response)

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43
Q

what is LH

A

luteinizing hormone

in females: responsible for ovulation and formation of corpus luteum, stim secretion of estrogen and progesterone in the ovaries

in males: stim release of testosterone from interstitial cells of Leydig

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44
Q

what is TSH

A

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

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45
Q

what is FSH

A

follicle-stimulating hormone

in females: stim growth and development of ovarian follicles and promotes secretion of estrogen by ovaries

in males: required for sperm production

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46
Q

what is PRL

A

prolactin

  • only anterior pituitary hormone that is not tropic!

in females: enhances breast development and milk production

in males: its physiological purpose is unclear

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47
Q

what is the hypothalamis-hypophyseal portal system

A

a vascular link between the hypothalamus and anterior pituitary

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48
Q

describe the steps of the hypothalamic-hypophyseal portal system

A
  1. hypophysiotropic hormones produced by neurosecretory neurons in the hypothalamus enter the hypothalamic capillaries
  2. the hypothalamic-hypophyseal portal system, a vascular link to the anterior pituitary
  3. portal system branches into the capillaries of the anterior pituitary
  4. the hypophysiotropic hormones, which leave the blood across the anterior pituitary capillaries, control the release of anterior pituitary hormones
  5. when stim by appropriate hypothalamic releasing hormone, the anterior pituitary secretes a given hormone into these capillaries
  6. anterior pituitary capillaries rejoin to form a vein, through which the anterior pituitary hormones leave for ultimate distribution throughout the body by systemic circulation
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49
Q

what does TRH release

A

thyrotropin-releasing hormone simulates the release of TSH and prolactin

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50
Q

what does GnRH stimulate

A

gonadotropin-releasing hormone stimulates the release of FSH and LH

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51
Q

what does GHIH stimulate

A

growth hormone inhibiting hormone inhibits the release of GH and TSH

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52
Q

what does CRH stimulate

A

corticotropin-releasing hormone stimulates the release of ACTH (corticotropin)

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53
Q

what does GHRH stimulate

A

growth hormone releasing hormone stimulates the release of growth hormone

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54
Q

what does PRH stimulate

A

prolactin-releasing hormone stimulates the release of prolactin

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55
Q

what does PIH stimulate

A

prolactin-releasing hormone stimulates the release of prolactin

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56
Q

hypothalamic neurons secrete hormones that receive a vast array of inputs, what are the 2 inputs?

A

neuronal and hormonal
they include both inhibitory and stimulatory inputs

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57
Q

do all sections of the hypothalamus have a blood-brain barrier?

A

no, some sections do not
bc of this the hypothalamus can monitor blood and respond to circulating chemicals o changes in plasma composition (osmolarity)

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58
Q

what are the hypothalamic hormones (for the most part) involved in

A

the 3 hormone hierarchic chain of command

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59
Q

what is the 3 hormone hierarchic chain of command

A

the hypothalamic hormone is released into portal sys, before traveling to pituitary gland to regulate output of a tropic hormone. this tropic hormone is transported by systemic circulation to its target endocrine gland where it regulates secretion of 3rd hormone producing a physiological effect

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60
Q

what hormone ultimately acts in negative-feedback fashion to reduce secretion of regulatory hormones higher in chain of command?

A

the hormone ultimately secreted by the target gland

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61
Q

in response to stress, the hypothalamus increases secretion of _______________

A

corticotropin-releasing hormone

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62
Q

corticotropin-releasing hormone then simulates the __________ pituitary to release ___________

A

anterior, adrenocorticotropic hormone

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63
Q

ACTH then acts on the adrenal ____________ to release ____________

A

cortex, cortisol

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64
Q

cortisol acts in a -‘ve feedback fashion to reduce secretion of regulatory hormones from the ___________ and _____________

A

hypothalamus, anterior pituitary

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65
Q

what is the thyroid gland?

A
  • located over the trachea just below the larynx
  • consists of 2 lobes connected by a thinner section of the gland known as the isthmus
  • no diff between lobes, the whole gland serves to produce and secrete thyroid hormones
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66
Q

what are the 2 thyroid gland hormones produced from

A

the amino acid tyrosine

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67
Q

what is a unique feature of both thyroid hormones

A

they contain iodine

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68
Q

what is the similarity and difference between the 2 thyroid hormones

A
  • they exert the same physiological effects
  • only differences in their speed and intensity of action
  • T3 is considered to be the more active thyroid hormone
  • T4 is converted to T3 in target tissues
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69
Q

what are the 2 thyroid hormones

A
  1. tetraiodothyronine (T4 or thyroxine)
  2. triiodothyronine (T3)
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70
Q

how many iodine molecules does tetraiodothyronine (T4 or thyroxine) contain

A

4, represents 90% of thyroid hormones secreted

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71
Q

how many iodine molecules does triiodothyronine (T3) contain

A

contains 3 iodine molecules and represents the remaining 10% of secreted hormones

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72
Q

how much iodine a week does the body require to ensure sufficient levels of thyroid hormone

A

1 mg

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73
Q

when ingested what does iodine circulate as

A

iodide

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74
Q
  1. what is an example a lipophilic hormone that (unlike others) are fully formed hormones and can be protected from secretion while they are stored?
  2. what are they bound too during this?
A
  1. thyroid hormones
  2. bound to thyroglobulin in the colloid of the thyroid gland
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75
Q

describe the 5 steps of thyroid hormone synthesis

A
  1. tyrosine-containing thyroglobulin is produced within the follicular cells by ER-golgi complex and transported to colloid by exocytosis
  2. iodide is taken in by follicular cells through iodide trapping. iodide is driven against its concentration gradient by using Na+-cotransporter that moves Na+ down its concentration gradient
  3. iodide is transferred into colloid of follicular lumen
  4. simultaneously to iodide moving into colloid, thyroperoxidase converts iodine which attaches to tyrosine residue on thyroglobulin molecule. called iodide organification. attachment of 1 iodine to tyrosine produces monoiodotyrosine (MIT) while the attachment of second iodine produces diiodotyrosine (DIT)
  5. coupling process occurs that combines MITs and DITs to form the thyroid hormones. 1 MIT and 1 DIT forms T3, 2 DITs form T4. there is no coupling for 2 MITs, and T3 and T4 remain bound to thyroglobulin molecule after chemical reactions
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76
Q

how are thyroid hormones released (3 steps)

A
  1. follicular cells engulf a portion of thyroglobulin-containing colloid by phagocytosis and create hormone-filled vesicles
  2. once inside follicular cell, lysosomes fuse with vesicles and digestive enzymes release all the MIT, DIT, T3, T4 from the thyroglobulin
  3. bc T3 and T4 are very lipophilic they immediately cross the plasma membrane to the blood where they bind to plasma proteins, mainly thyroid-binding globulin
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77
Q

what are the 5 actions of thyroid hormones

A
  1. metabolic rate and heat production
  2. intermediary metabolism
  3. sympathomimetic
  4. cardiovascular system
  5. growth
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78
Q

what do thyroid actions do on the metabolic rate and heat production

A

increases overall basal metabolic rate by increasing O2 consumption and energy expenditure. a consequence of increasing metabolic rate is an increased heat production.

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79
Q

what do thyroid actions do on the intermediary metabolism

A
  • influences enzymes flueling metabolism. - low concentrations of thyroid hormone = conversion of glucose to glycogen and protein synthesis are favoured
  • higher concentrations = causes breakdown of glycogen to glucose and degradation of proteins
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80
Q

how do thyroid actions cause sympathomimetic effects

A
  • increase target cell’s response to catecholamines
  • accomplished by increasing # of catecholamine receptors
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81
Q

what do thyroid actions do to the cardiovascular system

A

bc of sympathomimetic effect on heart, thyroid hormone can increase HR and strength of contraction to increase CO. also increases blood volume + flow

82
Q

what do thyroid actions do to growth

A

thyroid hormone is essential for normal growth. stim the release of both growth hormone and insulin-like growth factor, and also promotes their actions to stim the synthesis of new structural proteins and skeletal growth

83
Q

the hypothalamus secretes _____________ that acts on the anterior pituitary to secrete ______________

A

TRH, TSH

84
Q

what is TSH why is it important

A
  • most important regulator of thyroid hormone secretion, influences most of the stages of thyroid hormone synthesis and release
  • directly affects thyroid gland bc without it the gland shrinks in size, w too much the gland gets too large
85
Q

the release of both TSH and TRH are +’ve or -‘ve feedback control

A

-‘ve

86
Q

what does feeling stressed cause the hypothalamus to do to thyroid gland

A
  1. STRESS
  2. hypothalamus
  3. TRH release
  4. anterior pituitary
  5. TSH release
  6. thyroid gland
  7. T3 and T4 release
  8. increased metabolic rate, heat production, growth, CNS development, sympathetic activity
87
Q

what is hypothyroidism

A

low thyroid or underactive thyroid
- occurs when thyroid does not secrete enough hormone into the blood

88
Q

what is primary failure of thyroid gland

A

Hashimoto’s thyroiditis
- low levels of T3 and T4, but elevated levels of TSH
- no T3 or T4 being produced to provide -‘ve feedback and decreased production of TRH and TSH

89
Q

what is secondary failure of thyroid gland

A

hypothalamus and/or pituitary fail to secrete adequate TRH and/or TSH
- low levels of T3 or T4 (or both), as well as TRH and/or TSH depending on location of dysfunction

90
Q

what is the most common cause of hypothydroidism

A

inadequate dietary supply of iodine
- characterized by low T3 and T4, and elevated TSH

91
Q

common sympt of hypothyroidism

A
  • cold intolerance
  • slower reflexes
  • reduced mental alertness
  • easy to fatigue
  • slow, weak heart rate
  • weight gain due to decreased basal metabolic rate
92
Q

what is congenital hypothyroidism

A

(thyroid hormone deficiency acquired from birth)
called cretinism
- bc thyroid hormone is required for growth and development, this can cause dwarfism and intellectual disability

93
Q

hyperthyroidism due to secondary to excess hypothalamic or anterior pituitary secretions

A
  • when there is usually a tumour in either hypothalamus (secreting excess TRH) or in anterior pituitary (secreting excess TSH)
  • tumours generally ignore -‘ve feedback, resulting in elevated T3 and T4, w elevated TRH and/or elevated TSH
94
Q

what would you expect to see from a tumour in the thyroid gland itself

A
  • results in an increased secretion of thyroid hormones
  • elevated T3 and T4, decreased TSH
95
Q

what is grave’s disease

A
  • most common cause of hyperthyroidism
  • an autoimmune disease in which body produces long-acting thyroid stimulator (LATS), an antibody that targets and activates TSH receptors
  • LATs has same effect as too much TSH (causes follicles to grow larger and increase in number
  • LATs are not under -‘ve control, the hyperthyroid stim persists
  • T3 and T4 are high, while TSH levels are low
96
Q

hyperthyroidism symptoms

A
  • increased HR
  • excessive heat production
  • muscle weakness due to skeletal muscle protein degradation
  • mood swings due to increased CNS mental alertness
  • elevated basal metabolic rate that causes weight loss even with increased caloric intake
97
Q

what is goiter

A
  • hypothyroidism AND hyperthyroidism (a goiter)
  • an enlarged thyroid gland that is quite visible, results from increased TSH
98
Q

what are the adrenal glands

A
  • small and located at the top of the kidneys (2 endocrine organs)
  • outer layers are the adrenal glands called the cortex they secrete several steroid hormones
  • inner layer of adrenal gland is called medulla and secretes catecholamines
99
Q

what 3 zones can the adrenal cortex be divided into

A

zona glomerulosa
zona fasciculata
zona reticularis

100
Q

what are the 3 main categories of adrenal cortex hormones

A

mineralocorticoids
glucocorticoids
sex hormones

101
Q

what are mineralocorticoids

A
  • class of corticosteroids produced in adrenal cortex
  • influence salt & water balances in body
  • w/o them a person would die in days bc of circulatory shock
  • major one: aldosterone!
  • secretion is related to: electrolyte concentrations, blood volume, blood pressure, and is independent of anterior pituitary control
102
Q

what are the 2 primary stimuli for mineralocorticoid secretion

A
  • activation of RAAS sys in response to reduced Na+ and fall in blood pressure
  • direct stim of adrenal cortex by increased K+ concentration
103
Q

what is the primary glucocorticoid

A

cortisol

104
Q

what are the metabolic effects of cortisol

A

in liver, stimulates gluconeogenesis. (produces glucose from non-carbohydrate precursors like amino acids). cortisol stim protein degradation in muscle to get these amino acids. cortisol inhibits glucose uptake in most tissues minus the brain, and also breaks down lipid stores to mobilize free fatty acids that can be used as a fuel source.

105
Q

what is cortisols role in adaptation to stress?

A

not fully known why
- cortisol causes shift away from protein + fat stores while increasing carb stores
- w increased glucose this ensures good brain activity during times of fasting
- increased levels of amino acids, free fatty acids, and glucose provide building blocks for wound repair

106
Q

cortisol secretion from adrenal cortex is under _______ feedback involving the _________ and _________

A

-‘ve, hypothalamus, anterior pituitary

107
Q

describe cortisol secretion

A
  1. hypothalamus releases CRH, which stim the anterior pituitary to release ACTH
  2. ACTH stim adrenal glands to release cortisol
  3. plasma cortisol feeds back to hypothalamus and anterior pituitary to reduce CRH and ACTH release to maintain balance
108
Q

what 2 other influences help modulate cortisol secretion

A
  1. cortisol has a diurnal secretion pattern, w highest levels occurring in morning and lowest at night. this diurnal rhythm is intrinsic to hypothalamus and anterior pituitary control systems
  2. mental and physical stress can override normal patterns of cortisol secretion. stress leads to large increase in CRH release from hypothalamus
109
Q

what are androgens

A

male sex hormones (but are important for females too)

110
Q

whats estrogen

A

female sex hormones (but needed for males too)

111
Q

the adrenal cortex secretes _______ levels of androgens and estrogens

A

low

112
Q

how does the adrenal cortex release androgens and estrogens

A

release is stim by ACTH, which regulates cortisol secretion, so sex hormone secretion parallels cortisol secretion. amount of sex hormones secreted is considered insignificant to those secreted by gonads.

113
Q

what is the most important adrenal cortex sex hormone

A

dehydroepiandrosterone (DHEA)
- in males: plays little role (due to high testosterone
- in females: important for growth of pubic and armpit hair, enhancement of growth spurt at puberty, and maintenance of female sex drive

114
Q

what are catecholamines synthesized by

A

the adrenomedullary secretory cells

115
Q

what happens once catecholamines are synthesized

A

chromaffin granules, which are similar to neurotransmitter storage vesicles found in nerve ending. when stimulated they undergo exocytosis to release NE and E into bloodstream

20% if secreted catecholamines are NE, functionally we only consider actions of E

116
Q

general action of a1

A

excitatory!

117
Q

general action of a2

A

inhibitory

118
Q

general action of b1

A

excitatory

119
Q

general action of b2

A

inhibitory

120
Q

what does NE mainly bind with (what receptors)

A

a and b1 receptors

bc it is predominantly released from nerve endings, and those receptors are near postganglionic sympathetic nerve terminals

121
Q

what receptors does E bind w

A

can reach all a and b1 receptors, b2 are exclusively activated by E

122
Q

effects of E on organ systems

A
  • SNS mobilizes adrenomedullary E sys
  • increases HR, strength of contraction, increases CO, generalized vasoconstriction to increase total peripheral resistance and bp
123
Q

effects of E on metabolism

A

fight or flight!
- increases blood glucose
- increases liver gluconeogenesis (synthesis of new glucose) and glycogenolysis (breakdown of glycogen to release glucose)
- promotes lipolysis to increase circulating free fatty acids that can be used as an energy source by heart and skeletal muscles

124
Q

SNS & E

A

increased: muscle strength, mental activity, bp, cellular metabolism, blood flow to essential organs and decreased blood flow to non-essential organs

125
Q

stress with insulin & glucagon

A

these work to increase blood glucose
- increased glucagon secretion will break down glycogen stores to produce glucose and decreasing insulin secretion will reduce rate at which glucose is removed from circulation

126
Q

what is the CRH-ACTH-Cortisol sys

A

main sys involved in integrated stress response
- cortisol increases blood glucose levels, free fatty acids, and amino acids to provide energy to brain and repair damaged tissues

also recognized that ACTH may play a role in resisting stress
- during formation of ACTH from a larger molecule B-endorphin, a natural morphine like substance, is also produced and released w ACTH. B-endorphin can act like analgesia in case of physical injury

127
Q

what is RAAS sys

A

sympathetic sys increasing bp
- w stress there is an increase in vasopressin and angiotensin 2, both are vasoconstrictors that can help increase bp in an emergency

128
Q

steps of stress response

A
  1. hypothalamus receives input concerning physical and emotional stressors
  2. activates SNS
  3. secretes CRH to stim ACTH and cortisol release
  4. triggers release of vasopressin
129
Q

what is hyperadrenalism

A
  • adrenal glands secrete excessive amounts of hormones they produce
130
Q

what is cortisol hypersecretion

A

cushing’s syndrome
- due to overstim of adrenal cortex by CRh and/or ACTH
- adrenal tumours hypersecreting cortisol independent of ACTH, and ACTH-secreting tumours located somewhere other than pituitary
- causes buffalo hump (redistribution of at between shoulder blades) and moon face (cortisol causes excessive oedema in cheeks)

131
Q

adrenal androgen hypersecretion in adult females

A
  • develop masculine-like body hair, called hirsutism
  • usually an increase in male secondary sex characteristics
  • breasts shrink, and menstruation may cease
132
Q

adrenal androgen hypersecretion in adult males

A

little to no effects as the actions of DHEA are minor compared to that of testosterone

133
Q

adrenal androgen hypersecretion in newborn females

A
  • exhibit male-type external genitalia
  • during development, clitoris enlarges and takes on a penile-type appearance
134
Q

adrenal androgen hypersecretion in prepubertal males

A

early development of male secondary sex characteristics called precocious pseudo-puberty

135
Q

what is hyperaldosteronism

A

excessive mineralocorticoid secretion can be caused by an aldosterone-secreting tumour or by abnormally high activity of RAAS sys
- sympt are based on activity of aldosterone including hypernatremia, hypokalemia, and high bp

136
Q

primary adrenocortical insufficiency (addison’s disease)

A
  • occurs when all layers of adrenal cortex are under secreting, often caused by autoimmune destruction of cortex
  • typically aldosterone and cortisol deficient *can be fatal
  • pt’s display hyperkalemia and hyponatremia
137
Q

secondary adrenocortical insufficiency

A

occurs if there is a problem in hypothalamus or anterior pituitary characterized by reduced ACTH
- there is a cortisol deficiency but aldosterone levels are unaffected
- sympt depend on 3 factors: level of cortisol deficiency, rate of reduction in cortisol levels, underlying health of individual

causes: severe fatigue, loss of appetite, weight loss, nausea, vomiting, diarrhea, muscle weakness, irritability, and depression

aldosterone levels are usually unaffected
low bp and muscle spasms are not as likely as they are in primary insufficiency

138
Q

2 reactions within the cell related to metabolism

A
  1. intermediary metabolism
  2. fuel metabolism
139
Q

what are anabolic reactions (in metabolism)

A

leads to synthesis of larger organic macromolecules from smaller organic molecular subunits and are used for repair, growth, and storage of excess ingested nutrients

140
Q

what are catabolic reactions in metabolism

A

the breakdown of larger organic macromolecules either through the process of hydrolysis into smaller molecules, or oxidation of smaller molecules, such as glucose to yield ATP

141
Q

where is excess glucose stored?

A
  • in the liver and skeletal muscle as glycogen
  • when these are full any additional glucose is converted into free fatty acids and glycerol for synthesis of triglycerides which mainly occur in adipose tissue
142
Q

what are excess fatty acids stored as

A

triglycerides

143
Q

what are excess amino acids used for

A

they are not needed for protein synthesis and are not stored, but rather either used for structural proteins or converted to glucose and fatty acids for eventual storage as triglycerides

144
Q

how are most excess nutrients stored and why

A

most are stored as triglycerides in adipose tissue
when needed, this energy store can undergo catabolism to form free fatty acids and glycerol

145
Q

what is the body’s 2 functional metabolic states

A
  1. absorptive state
  2. postabsorptive state
146
Q

what is the absorptive state

A
  • anabolism dominates as ingested food is digested and absorbed into the circulation
  • ingested simple carbohydrates are converted in the liver to glucose, which is released to be available as fuel or stored as glycogen
  • ingested fats and proteins are also immediately used or stored
147
Q

what is the postabsorptive state

A
  • several hrs after ingesting food, catabolism dominates
  • glycogen stores in the liver and skeletal muscle become primary energy source
  • if postabsorptive state persists, glycogen alone cannot meet the body’s energy needs, so lipolysis occurs to break down triglycerides
148
Q

where does glycerol come from

A

the backbone of triglycerides when they are broken down and it can be converted to glucose by the liver

149
Q

what is lactic acid formed by

A

glycolysis, can be converted to glucose by the liver

150
Q

what are ketone bodies

A
  • group of compounds produced by liver in times of glucose shortages
  • liver uses free fatty acids as an energy source, they are oxidized to acetyl CoA, which does not produce any additional energy through citric acid cycle
  • this acetyl CoA is converted to ketone bodies and released into the blood
  • in times of starvation, the brain can use ketone bodies, instead of glucose, as an energy source
151
Q

what kind of organ is the pancreas

A

exocrine and endocrine
- exocrine functions are important for digestion
- endocrine functions are localized to the islets of Langerhans which are clusters of cells found throughout the pancreas

152
Q

alpha cells produce and secrete…

A

glucagon

153
Q

beta cells produce and secrete…

A

insulin

154
Q

delta cells produce and secrete…

A

somatostatin

155
Q

PP cells cells produce and secrete…

A

pancreatic polypeptide, which may play a role in reducing apettite

156
Q

what is somatostatin

A
  • delta cells secrete this
  • slows down digestive system to inhibit digestion and absorption of nutrients
  • -‘ve feedback manner, prevents too many nutrients being absorbed
  • found in pancreas, and is also produced in cells lining the digestive tract where it acts as a paracrine hormone to inhibit digestion
  • also released by hypothalamus where it inhibits the secretion of growth hormone and TSH
157
Q

what is insulin

A
  • small peptide hormone produced by beta cells of the pancreatic islets
  • dominant hormone in the absorptive state and plays a major role in anabolism
  • has been associated primarily w regulation of blood sugar, but has effects on fats and proteins as well
158
Q

factors that increase blood glucose

A
  • glucose absorption from digestive tract
  • hepatic glucose production: through glycogenolysis, through glycogenolysis of stored glycogen
159
Q

factors that decrease blood glucose

A
  • transport of glucose into cells: for utilization for energy production, for storage as glycogen through glycogenesis, for storage as triglycerides
  • urinary excretion of glucose (occurs only abnormally, when blood glucose level becomes so high it exceeds the reabsorptive capacity of kidney tubules during urine formation)
160
Q

Insulin has 4 main effects on carbohydrate metabolism to maintain blood glucose homeostasis what are they?

A
  1. inhibit the uptake of glucose into most cells
  2. inhibit glycogenolysis in the liver
  3. stimulate glycogenolysis in skeletal muscle and the liver
  4. inhibit gluconeogenesis in the liver
161
Q

4 effects of insulin on fats

A
  • enhances the entry of fatty acids into adipose tissue cells
  • increases GLUT-4 recruitment in adipose cells to increase glucose uptake for the synthesis of triglycerides
  • enhances the activity of enzymes involved in synthesizing triglycerides
  • inhibits lipolysis
162
Q

4 effects of insulin on proteins

A
  • promotes the uptake of amino acids in all tissues
  • enhances the activity of the enzymes involved in protein synthesis
  • inhibits the degradation of proteins
163
Q

insulin is directly related by the plasma glucose level with a ______ feedback system

A

-‘ve

164
Q

3 steps of regulation of insulin secretion

A
  1. elevation of blood glucose stim the islet b cells to secrete insulin. actions of insulin will lower blood glucose levels and secretion of insulin will stop. insulin promotes anabolism during absorptive state and lack of insulin promotes catabolism during postabsorptive state
  2. insulin release is caused by a feedforward state. GI hormones secreted by digestive tract stim insulin release to prepare for rise in blood glucose about to occur
  3. cells of the islets of langerhans are innervated by ANS. presence of food in digestive sys activates PSNS. the SNS has opposite effect to decrease insulin secretion. allows blood glucose levels to rise during fight-or-flight or when exercising
165
Q

what is glucagon

A
  • major pancreatic hormone involved during postabsorptive state
  • secretion is triggered by decrease in blood glucose levels
  • major site of action is liver, where its effects are direct opposite of insulin
166
Q

effects of glucagon on carbohydrates

A

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

167
Q

effects of glucagon on fats

A

promotes lipolysis while inhibiting fat storage. also enhances formation of ketone bodies in liver.

168
Q

effects of glucagon on proteins

A

promotes protein catabolism but only in liver

169
Q

a rise in blood amino acid concentration stimulates the release of both:

A

insulin and glucagon

170
Q

bones are the largest _________ store, and thus play a large role in preserving _____________ homeostasis

A

calcium

171
Q

when are the 2 main periods of rapid growth

A
  1. first 2 yrs of life
  2. puberty
172
Q

in both males and females pubertal growth is supported by __________ and ____________

A

GH, and androgens

173
Q

what are the 3 primary actions of growth hormone on intermediary metabolism?

A
  1. increased rate of protein synthesis
  2. increased fatty acid mobilization and use
  3. decreased rate of glucose use by body tissues
174
Q

what are the soft tissue actions of GH

A

GH can increase the # of cells (hyperplasia) through stimulating cell division, or stimulate cells to grow larger (hypertrophy) by promoting protein synthesis

175
Q

what do osteoblasts do

A

deposit new bone

176
Q

what do osteoclasts do

A

dissolve bone

177
Q

how do bones grow in thickness

A

achieved by adding new bone to outer layer of existing bone
- osteoblasts deposit new bone on outer surface of a bone
- osteoclasts on inside of bone are removing bone
- both the diameter of bone and marrow cavity will increase

178
Q

how do bones grow in length?

A
  • lengthening of long bones only occurs at its ends between the epiphysis and diaphysis in the epiphyseal plate
179
Q

what is the epiphysis

A

the knob at the end

180
Q

what is the diaphysis

A

shaft of the bone

181
Q

describe the process of bone growth in length

A
  1. cartilage forming cells called chondrocytes divide and stalk themselves into columns w newer cells towards the epiphysis and older cells near the diaphysis
  2. this division and increase in # of chondrocytes are what cause the long bones to elongate. as chondrocytes mature they hypertrophy, which pushes the epiphysis away from the diaphysis and the matrix around them calcifies
  3. the older chondrocytes are too far away from nutrient supply so they die. osteoclasts will now remove dead chondrocytes and the calcified matrix, allowing osteoblasts and their capillary supply, to invade this new space and start depositing bone through the process of ossification.
  4. formation of new chondrocytes is matched to the removal of dead chondrocytes such that the width of the epiphyseal plate remains fairly constant as the bone lengthens. end of adolescence, sex hormones cause the epiphyseal plate to completely ossify and linear bone growth ceases. thickening of bone can occur throughout life.
182
Q

how are the effects of GH mediated

A

through other peptides known as somatomedins also called insulin-like growth factors (IGFs). there are two IGFs: IGF-1 and IGF-2.

183
Q

describe what IGF-1 is

A
  • GH stim the synthesis and release of IGF-1 primarily in liver
  • do not get released into the blood, but rather IGF-1 might have paracrine actions
  • IGF-1 mediates mots of the growth promoting actions of GH
184
Q

describe what IGF-2 does

A

GH does not stim the production of this. this is important during fetal development. it is produced in adults but the role is not clear.

185
Q

what are GH 2 regulatory hormones from the hypothalamus

A
  1. growth hormone-releasing hormone (GHRH) stimulates its release
  2. growth hormone-inhibiting hormone (GHIH; aka somatostatin) inhibits its release
186
Q

what can deficiency of GH lead to?

A
  • can be a consequence of dysfunction either at level of the hypothalamus, the pituitary, or tissue level
  • if during childhood the result is dwarfism (this can be successfully treated w GH if seen early enough)
  • laron dwarfism, is caused by lack of response from tissues to GH. this type of dwarfism responds to IGF-1 treatment.
  • GH deficiency has less sympt in adults
187
Q

what happens with a growth hormone access

A
  • usually caused by a tumour in the anterior pituitary
  • to occur in children, GH excess would have a pronounced effect on the epiphyseal plates, causing rapid growth and producing gigantism
  • if it occured after epiphyseal plate closure then height is not affected
  • bones can thicken and cause the condition acromegaly
188
Q

how can calcium be regulated

A
  • under hormonal control to ensure proper concentration is maintained
  • Ca can be ingested thru diet to enter plasma and excess Ca is generally stored in bones
  • during high dietary intake periods of Ca, excess is avoided by decreasing absorption
  • when there is a need for increased Ca in plasma, Ca can be readily removed from the bones
189
Q

what 3 hormones regulate Ca2+ concentrations

A
  • parathyroid hormone (PTH)
  • calcitonin
  • vit D
190
Q

how is the parathyroid hormone (PTH) secreted

A

by parathyroid glands

191
Q

why is PTH essential

A

bc removing the parathyroid glands causes death due to hypocalcemia within a few days. the primary action of PTH is to raise plasma Ca2+ levels by its effects on bone, the kidneys, and intestines

192
Q

how is the parathyroid hormone and the bones interconnected

A
  • primary storage f Ca2+ is within bones
  • bone is constantly undergoing remodelling
  • this remodelling allows for very rapid changes in free Ca2+ just by regulating the activity of these cells
  • under the influence of PTH, osteoclast activity if slightly enhanced and osteoblast activity is slightly inhibited, meaning there is more breakdown of bone than build up, the net release is Ca2+ and PO4^3- into plasma
193
Q

how is the parathyroid hormone and kidneys interconnected

A

in kidneys, PTH stim reabsorption of Ca2+
- necessary otherwise the body would be forced to keep degrading bone to maintain plasma Ca2+ levels
- PTH also stim the kidneys to remove PO4^3-
is an important feature as high levels of plasma PO4^3- levels cause bone to increase hydroxyapatite precipitation, which would further remove Ca2+ from plasma
- PTH also stim kidneys to activate vit D

194
Q

as Ca2+ levels rise… PTH secretion __________

A

decreases

195
Q

describe the regulation of PTH release

A

decreased plasma Ca2+ concentration -> parathyroid glands -> increased PTH -> bone or activation of vit D or kidneys

  • if kidneys then to activation of vit D increases which moves to intestine, increased absorption of Ca2+ in intestine, increased plasma Ca2+
  • if kidneys and not to activation of vit D, then increased renal tubular Ca2+ reabsorption, to decreased urinary excretion of Ca2+, to increased plasma Ca2+
  • if bone then to mobilization of Ca2+ from bone which results in increased plasma Ca2+
    (all increase plasma Ca2+)
196
Q

what is calcitonin secreted from

A

the thyroid gland

197
Q

what are the actions of calcitonin

A
  • opposite to those of parathyroid hormone
  • secreted in response to increased plasma Ca2+ levels
  • acts on osteoclasts to decrease their activity, which prevents the release of Ca2+ and PO4^3- from the bone
  • C cells of the thyroid secrete calcitonin
198
Q

plasma Ca2+ concentration decreases what happens next

A
  • decrease in parathyroid glands
  • increase in PTH
  • increase in plasma Ca2+ concentration
199
Q

plasma Ca2+ levels increase what happens next

A
  • increase in thyroid C cells
  • increase in calcitonin
  • decrease in plasma Ca2+ concentration
200
Q
  1. what is vitamin D properly called
  2. how is vitamin D further hydroxylated
  3. how does vitamin D function
A
  1. cholecalciferol
  2. by the kidneys to form calcitriol, the biologically active form of vitamin D
  3. functions as a hormone as it can be produced by skin. main function is to increase intestinal absorption of Ca2+. vit D increases the responsiveness of bone cells to PTH
201
Q

describe the activation of vitamin D

A

1st - occurs in liver
2nd - occurs in kidneys
each step adds a hydroxyl group to the compound

202
Q

how does PTH play a role in the formation of vitamin D

A

by stim the enzymes in the kidney. end result is the formation of 1,25-(OH)2-vitamin D3 (calcitriol), which is the active form. PTH and vit D work together in Ca2+ homeostasis, although it is PTH that plays the primary role

203
Q

what is the most dramatic effect of activated vitamin D

A

to increase Ca2+ absorption in the intestine
- majority of ingested Ca2+ is typically not absorbed but is lost in feces
- vit D increases the responsiveness of bone to PTH
- vit D and PTH are closely independent

PHGY 216 (10 decks)

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