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PHGY 210 > Endo > Flashcards

Endo Flashcards

1
Q

2 functions of endocrine system

A
  • coordination of physiological processes
  • long distance communication
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2
Q

which 2 system are in charge of coordination of physiological processes

A

CNS and endocrine

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3
Q

endocrine signaling

A

involves hormone secretion into the blood by an endocrine gland, transported to a distant target site

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4
Q

neuroendocrine signaling

A

involves hormone secretion into the blood by a nerve cell, transported to a distant target site

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5
Q

2 types of systemic signaling (involving cascades)

A

endocrine and neuroendocrine signaling

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6
Q

local signaling

A

hormone does not have to enter systemic circulation

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7
Q

2 types of local signaling

A

paracrine and autocrine

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8
Q

paracrine signaling

A

substance released from 1 cell type interacts with neighbouring type 2 target cell

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9
Q

autocrine signaling

A

cell produces the hormone and has the corresponding receptor so will bind to itself

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10
Q

example of autocrine signaling

A

growth factor

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11
Q

6 steps of communication by hormones
*all applies to neurohormones too

A
  1. synthesis of hormone by endocrine cells
  2. release of hormone by endocrine cells
  3. transport of hormone to target site by bloodstream
  4. detection of hormone by specific receptor protein on target cells
  5. change in cellular metabolism triggered by hormone-receptor interactions
  6. removal of the hormone, which often terminates the cellular response
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12
Q

what is important about the 6 steps of communication by hormones

A

they can each be a point of control

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13
Q

9 classical endocrine organs

A
  • ovaries
  • testes
  • hypothalamus
  • anterior + posterior pituitary
  • thyroid gland
  • parathyroid gland
  • heart
  • adrenal gland
  • pancreas
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14
Q

how does hypothalamic-pituitary signaling occur

A

via blood vessels of pituitary stalk

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15
Q

hypothalamic-hypophyseal portal system

A

from hypothalamus to adenohypophysis (anterior pituitary)

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16
Q

how many hormone-producing cells in the anterior pituitary do hypothalamic neurohormones activate/inhibit

A

1/6

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17
Q

releasing hormones/factors

A

induce release of other hormones from pituitary

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18
Q

inhibiting hormones/factors

A

inhibit release of other hormones from pituitary

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19
Q

peptide and protein hormones (glycoproteins and polypeptides)

A

we have a gene in genome to build that hormone

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20
Q

steroid, amine and ionic calcium hormones

A

we have a gene that encodes enzymes that are necessary for biosynthesis of that hormone

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21
Q

why is ionic calcium considered a hormone

A

because we have a calcium-sensing receptor

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22
Q

where are protein hormones synthesized

A

on ribosomes as preprohormones

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23
Q

what characterizes preprohormones

A

extended N-terminal sequences

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24
Q

what is the purpose of the extended end-terminal sequences

A

directs them into secretory system

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25
Q

when is preprohormone sequence removed & why

A

removed during secretion, allows for mature hormone release

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26
Q

structure of steroid hormone

A

4 carbon ring structure

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27
Q

4 examples of steroid hormone

A

cortisol, aldosterone, testosterone, estradiol

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28
Q

what is a precursor for estradiol and how does it become that way

A

testosterone; aromatase burns off methyl group to turn it into an alcohol

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29
Q

where are thyroid hormones produced and what do they bind to

A

produced by thyroid, bind to thyroid hormone receptor

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30
Q

2 thyroid hormones

A

3,5,3’,5’-tetraiodothyronine (T4)
3,5,3’-triiodothyronine (T3)

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31
Q

why is 3,3’,5’-triiodothyronine (rT3) not considered a thyroid hormone

A

because it cannot bind to the thyroid receptor

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32
Q

what does T4/T3 refer to

A

the number of iodines on the thyroid hormone

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33
Q

percentage of T4 vs T3

A

T4 = ~90%
T3 = ~9%

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34
Q

lock and key mechanism

A

receptors are specific to the binding of only their corresponding hormone

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35
Q

4 properties of hormone receptors

A
  • specificity
  • affinity
  • saturability
  • measurable biological effect
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36
Q

specificity of hormone receptor

A

recognition of single hormone / family

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37
Q

affinity of hormone receptor

A

binding hormone at its physiological concentration

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38
Q

why is affinity crucial

A

because we need less binding when there is less hormone

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39
Q

saturability of hormone receptor

A

should have finite number of receptors

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40
Q

measurable biological effect of hormone receptor

A

measurable response due to interaction of hormone with its receptor

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41
Q

receptor upregulation

A

increased signaling/activity

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42
Q

how to upregulate a receptor (2)

A

increasing activity/responsiveness
increasing synthesis (no. of receptors)

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43
Q

receptor downregulation

A

decreased signalling/activity

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44
Q

how to downregulate a receptor (2)

A

decrease activity/responsiveness
decrease synthesis (no. of receptors)

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45
Q

3 ways for hormone to exert effects

A
  • direct effects on function at cell membrane
  • signalling via intracellular second messenger
  • intracellular genomic action
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46
Q

example of hormone having direct effects on function at cell membrane

A

insulin and glucose

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47
Q

which of the 3 ways of hormones exerting effects is least common

A

direct effects on function at cell membrane

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48
Q

which of the 3 ways of hormones exerting effects is most common and why

A

signalling via intracellular second messenger because so many G proteins

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49
Q

example of signalling via intracellular second messenger

A

G protein activation turns ATP into cAMP (secondary messenger) to activate protein kinase

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50
Q

what are the effects of signalling via intracellular second messenger

A

biological effects on protein transcription

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51
Q

intracellular genomic action

A

signalling by nuclear receptors, includes receptors for steroid hormones

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52
Q

how does intracellular genomic action work

A

steroids can enter cells (unlike glucose) and enter nucleus/cytoplasm directly to regulate transcription of specific genes

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53
Q

effect of intracellular genomic action

A

change cell protein content and the way the cell functions

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54
Q

what is hormone secretion regulated by

A

feedback mechanisms

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55
Q

what does excess of hormone lead to

A

diminution of hormone secretion

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56
Q

what does hormone deficiency lead to

A

increase of hormone secretion

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57
Q

2 examples of negative hormone feedback loops

A
  • Ca++ acts in negative feedback loop to regulate plasma calcium
  • CRH and ACTH work in negative feedback loop to regulate plasma cortisol levels
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58
Q

CRH name

A

corticotropin-releasing hormone

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59
Q

ACTH name and function

A

adrenocorticotropic hormone (stimulates cortisol release)

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60
Q

2 distinct tissues of pituitary gland

A

adenohypophysis and neurohypophysis

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61
Q

adenohypophysis

A

anterior pituitary/pars distalis = endocrine tissue

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62
Q

neurohypophysis

A

posterior pituitary/pars nervosa = neural tissue

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63
Q

what is pituitary gland protected by

A

bone

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64
Q

which of the pituitary hormones is different from the others and why

A

PIH/dopamine because it is an amine (we don’t have a gene for it)

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65
Q

what class do all pituitary hormones belong to except 1

A

peptides

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66
Q

2 posterior pituitary hormones

A

arginine vasopressin
oxytocin

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67
Q

what do the posterior pituitary hormones have in common

A

involved in smooth muscle tone but for physiologically diff conditions

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68
Q

arginine vasopressin

A

maintains BP

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69
Q

oxytocin

A

reproductive endocrinology

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70
Q

what is the posterior pituitary gland

A

outgrowth of hypothalamus connected by pituitary stalk

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71
Q

antidiuretic hormone (ADH) / vasopressin function

A

increases BP, leads to fluid retention and less peeing

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72
Q

where are oxytocin and ADH synthesized

A

supraoptic nucleus and paraventricular nucleus

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73
Q

where do the axons of the supraoptic nucleus and periventricular nucleus run down and terminate

A

axons run down pituitary stalk and terminate in posterior pituitary close to capillaries

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74
Q

when and where are the prohormones of oxytocin and ADH processed

A

processed in secretory granules during axonal transport

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75
Q

where are the mature forms of oxytocin and ADH liberated from

A

carrier molecules (neurophysins)

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76
Q

what are the circulating half lives of ADH and oxytocin

A

1-3 mins

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77
Q

3 functions of oxytocin in women

A

parturition
milk ejection
behavioural effects

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78
Q

oxytocin function in parturition

A

uterus sensitive to oxytocin at end of pregnancy; dilation of uterine cervix by fetal head causes oxytocin release to allow for uterine contraction

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79
Q

oxytocin function in milk ejection

A

infant suckling stimulates oxytocin production, causes milk filled ducts to contract and squeeze milk out

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80
Q

oxytocin function in behavioural effects

A

‘love hormone’; local release in brain reduces anxiety and enhances bonding and prosocial behaviour

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81
Q

2 functions of oxytocin in men

A

ejaculation
behavioral effects

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82
Q

oxytocin function ejaculation

A

oxytocin surge during sexual activity assists epidimial passage of sperm

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83
Q

typical thyroid gland size

A

15-20g

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84
Q

why does size of thyroid gland vary with (4)

A

sex, age, diet, reproductive state

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85
Q

how much thyroid do we really need to maintain euthyroid state

A

3g

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86
Q

who has larger thyroids

A

females

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87
Q

colloid

A

viscous fluid in the central cavity of thyroid follicles containing thyroglobulin

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88
Q

thyroglobulin

A

glycoprotein that contains tyrosine

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89
Q

what stores T3 and T4 prior to release

A

colloid

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90
Q

what happens to T3 and T4 once they leave colloid

A

split off thyroglobulin and enter blood where they bind to special plasma proteins

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91
Q

what controls synthesis of thyroglobulin

A

TSH

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92
Q

why can rT3 not bind to the thyroid hormone receptor

A

because it does not have the diiodination of proximal benzene ring

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93
Q

what is necessary for binding to thyroid receptor

A

iodine

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94
Q

what traps idodie and actively transports it across the cell against chemical gradient

A

thyroid follicular cells

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95
Q

why is it necessary to store iodide

A

the supply is limited to terrestrial vertebrates

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96
Q

what happens to iodide once in the thyroid (&how)

A

oxidized to iodine (I2) using ATP inside follicular cells

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97
Q

what happens to iodine once it is produced

A

binds to tyrosine of thyroglobulin

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98
Q

1 iodine + tyrosine =

A

MIT (monoiodotyrosine)

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99
Q

2 iodines + tyrosine =

A

DIT (diiodotyrosine)

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100
Q

oxidative coupling of 2 DIT =

A

T4

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101
Q

oxidative coupling of 1 DIT + 1 MIT =

A

T3

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102
Q

what happens when there is an increase in TSH

A

there is an increased rate of all the steps involved in T3 + T4 formation

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103
Q

what does low TSH mean

A

low turnover of thyroid homones

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104
Q

what is the synthesis and release of TSH controlled by

A

hypothalamic thyrotropin releasing hormone (TRH)

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105
Q

result of increased T3 + T4 in blood =

A

double negative feedback at hypothalamic and pituitary levels to decrease TRH and TSH release, and decrease T3 and T4 production

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106
Q

result of decreased T3 and T4 in blood =

A

TSH interacts with specific receptors located on follicular cells to increase T3 and T4 production

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107
Q

2 effects of iodine deficiency

A
  • decreased thyroid hormone synthesis (lower conc of T3 and T4 in circulation)
  • increased TSH release
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108
Q

result of increased TSH release

A

constant stimulation of thyroid follicular cells, leads to enlarged thyroid (may form goiter)

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109
Q

non toxic goiter

A

enlarged thyroid unable to synthesize biological active thyroid hormones due to iodine deficiency

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110
Q

3 effects of thyroid hormones on calorigenesis

A

increased cardiac output
increased blood oxygenation
increased breathing rate and number of circulating red blood cells

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111
Q

2 effects of thyroid hormones on carb metabolism

A

promotes glycogen formation in liver
increased glucose uptake into muscle and adipose tissue

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112
Q

effect of thyroid hormone on lipid turnover

A

increase lipid synthesis, mobilization and oxidation

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113
Q

effect of thyroid hormone on protein metabolism

A

stimulates protein synthesis

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114
Q

3 effects of thyroid hormones on normal growth

A

promotes normal branching and nerve myelination
promotes nervous system development and maturation
stimulates GH secretion, bone growth and IGF-1 production

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115
Q

lack of normal growth due to thyroid deficiency =

A

cretinism

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116
Q

2 most important thyroid hormone functions

A

increase basic metabolic rate
normal linear growth

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117
Q

what are 90% of molecular mechanisms of action of thyroid hormone

A

analogous to steroid hormones = T3 and T4 enter cell nucleus, bind to cognate nuclear receptor and alter specific gene transcription

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118
Q

2 other molecular mechanisms of action of thyroid hormone

A
  • may induce some effects by interactions with plasma membrane and mitochondria (specific T3/T4 receptor located in inner mitochondrial membrane)
  • act directly at plasma membrane and increase amino acid uptake
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119
Q

what do the 2 other molecular mechanisms of action of thyroid hormone have in common

A

they are independent of protein synthesis

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120
Q

how to protect yourself from nuclear power plant

A

excess stable iodine (127I) is used to protect thyroid gland from radioactive isotopes by saturating iodine transport system (isotopically dilutes amount of radioactive iodine entering gland)

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121
Q

what is used to treat thyroid cancer

A

radioactive iodine

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122
Q

hypothyroidism

A

low levels of thyroid hormones

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123
Q

primary hypothyroidism (myxedema)

A

inability to synthesize active thyroid hormones (thyroid level)

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124
Q

who is primary hypothyroidism more common in

A

women 40-60y

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125
Q

3 causes of primary hypothyroidism

A
  • thyroid atrophy (idiopathic)
  • autoimmune thyroiditis / Hashimoto’s disease
  • goitrous hypothyroidism / non-toxic goiter
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126
Q

autoimmune thyroiditis / Hashimoto’s disease

A

destruction by antibodies against cellular components of thyroid (more common in women, most common cause)

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127
Q

goitrous hypothyroidism / non-toxic goiter

A

blockage in a step of T3/T4 synthesis leading to growth of thyroid gland (decreased T3/T4, increased TRH and TSH)

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128
Q

secondary hypothyroidism

A

synthesis of little to no TSH (pituitary level)

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129
Q

tertiary hypothyroidism

A

synthesis of little to no TRH (hypothalamus level)

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130
Q

infantile hypothyroidism

A

absence of thyroid gland/ incomplete development of thyroid gland at birth

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131
Q

why are some babies normal at birth when they have infantile hypothyroidism

A

use mother’s T3/T4 but once born, can no longer produce their own therefore exhibit less physical growth and mental development

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132
Q

why does infantile hypothyroidism require immediate treatment

A

will exhibit dwarfism and cretinism

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133
Q

what can all forms of hypothyroidism be treated with

A

administration of thyroid hormones

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134
Q

hyperthyroidism

A

high levels of thyroid hormones

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135
Q

primary hyperthyroidism

A

at thyroid gland level

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136
Q

2 causes of primary hyperthyroidism

A

toxic diffuse goiter (Graves disease) and thyroid adenoma / thyroid cancer

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137
Q

toxic diffuse goiter (Graves disease)

A

autoimmune disease characterized by presence of substance produced by lymphocytes (LATS)

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138
Q

long acting thyroid stimulator / LATS

A

antibody that mimics TSH action, stimulates T3+T4 release

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139
Q

what does constant stimulation by LATS lead to (primary hyperthyroidism)

A

increased thyroid mass and toxic goiter formation

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140
Q

what makes a goiter toxic

A

in continues to synthesize biologically active T3/T4

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141
Q

does the negative feedback loop work in Graves disease

A

yes, the increase in thyroid hormones leads to less TRH and TSH, but LATS prevents reduction in T3/T4 synthesis

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142
Q

thyroid adenoma / thyroid cancer

A

synthesis of thyroid hormones independent of TSH stimulation (very curable)

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143
Q

secondary hyperthyroidism

A

no negative feedback from increased T3 and T4 (hormones synthesize independently of TSH (anterior pituitary level)

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144
Q

what is the most common cause of secondary hyperthyroidism

A

pituitary tumor

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145
Q

tertiary hyperthyroidism

A

no negative feedback of increased T3 and T4 to decreased TRH secretion (hypothalamus level)

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146
Q

what is the most common cause of tertiary hyperthyroidism

A

hypothalamic tumor

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147
Q

3 treatments for hyperthyroidism

A
  • surgery and administration of thyroid hormones
  • administration of radioactive iodide (131I) to destroy hormone-producing cells
  • administration of antithyroid drugs like propylthiouracil to block addition of iodine to thyroglobulin (block hormone synthesis)
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148
Q

what determines which hyperthyroidism treatment you pick

A

severity of disease

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149
Q

abnormalities of thyroid gland can be …

A

congenital or acquired

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150
Q

6 roles of calcium ions

A
  • skeletal structure
  • blood clotting
  • maintain transmembrane potentials
  • excitability of nervous tissue
  • muscle contraction
  • hormone and neurotransmitter release
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151
Q

where is 99% of our calcium found

A

loosely bound in bone

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152
Q

what is normal conc of calcium in cellular and extracellular fluid

A

~10mg/100 mL

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153
Q

what is the distribution of free calcium to calcium bound to albumin

A

50-50

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154
Q

where is calcium obtained

A

diet (dairy)

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155
Q

where is calcium absorbed from digestive tract into plasma

A

duodenum and upper jejunum

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156
Q

what 2 things increase absorption of calcium in intestine

A

vitamin D and PTH

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157
Q

where is some calcium excreted directly

A

feces

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158
Q

calcitonin function

A

deposits calcium in bone or tissue cells when concentration high

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159
Q

where does calcitonin cause some calcium to be lost

A

moves through kidney, lost in urine

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160
Q

what is the effect if calcitonin

A

decreased circulating calcium

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161
Q

what happens if calcium conc is less than 10mg/100mL (2)

A

PTH stimulates reabsorption of calcium from kidney and removal of calcium from bone and tissues (resorption)

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162
Q

what is calcium conc maintenance determined by

A

exchange between bone and plasms under hormonal influence

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163
Q

parathyroid hormone (PTH)

A

protein produced by parathyroid gland, increases circulating calcium

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164
Q

calcitonin

A

protein produced by thyroid gland C cells, lowers circulating calcium

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165
Q

vitamin D function

A

stimulates calcium uptake from digestive tract to increase circulating calcium conc

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166
Q

where is parathyroid hormone secreted from

A

parathyroid chief cells embedded in thyroid surface

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167
Q

how many parathyroid glands glands do we have and where are they

A

4 glands on back side of thyroid

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168
Q

what does removing the parathyroids do (2)

A

decrease plasma calcium levels, leading to tetanic convulsions and death

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169
Q

how big is PTH

A

84 amino acid polypeptide

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170
Q

how much of PTH do we need for full activity and why

A

N-terminal 34 amino acids (it is the receptor binding portion)

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171
Q

what is PTH synthesized as a part of, and how does it become PTH

A

preproparathyroid hormone undergoes proteolytic cleavage to produce PTH

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172
Q

what is PTH half life

A

3-18 min

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173
Q

PTH function

A

increase plasma Ca++ conc

174
Q

4 ways PTH increases plasma Ca++

A
  • bone resorption (increase bone demineralization)
  • kidney (increase reabsorption of Ca in proximal convoluted tubule)
  • vitamin D synthesis (stimulates conversion of 25-hydroxy D3 to 1,25 D3)
  • gut (facilitate absorption of Ca from gut to blood)
175
Q

what is PTH release controlled by

A

circulating Ca++ conc

176
Q

what does PTH bind to (&where)

A

cognate receptors on target cell exerts

177
Q

hypoparathyroidism

A

decreased levels of PTH in circ

178
Q

4 symptoms of hypoparathyroidism

A
  • hypocalcemia
  • decreased 1,25 D3 production
  • tetany/convulsions
  • if Ca++ < 7mg/100mL = increased neural overexcitability and muscle spasms
179
Q

why is severe hypoparathyroidism very dangerous

A

laryngeal muscle spasms can lead to death by asphyxiation

180
Q

hypoparathyroidism treatment

A

1,25D3 administration and calcium supplements

181
Q

hyperparathyroidism

A

increased levels of PTH in circ

182
Q

what is hyperparathyroidism often caused by

A

parathyroid adenoma of parathyroid. producing too much PTH

183
Q

3 effects of hyperparathyroidism

A
  • increased 1,25D3 production = calcium absorption from intestines
  • bone resorption & calcium reabsorption from kidney
  • kidney stones
184
Q

3 symptoms of severe hyperparathyroidism

A
  • cardiac arrhythmias
  • depressed neuromuscular excitability
  • calcium deposition on walls of blood vessels
185
Q

hyperparathyroidism treatment

A

removal of affected parathyroids and replacement therapy of 1,25D3 and Ca++

186
Q

where do we get vitamin D from (2)

A

limited dietary sources (cod liver oil, fatty fish) and can be synthesized from cholesterol metabolite (therefore not strictly a vitamin)

187
Q

when is vitamin D high

A

when Ca++ is low and PTH is high

188
Q

what is vitamin D depressed by

A

increased Ca++

189
Q

4 steps to vitamin D synthesis

A
  • UVB light + 7-dehydrocholesterol in skin
  • 25-hydroxylation in liver
  • 1-hydroxylation in kidney and tissues
  • 1,25D3
190
Q

3 physiological functions of vitamin D

A
  • increase Ca++ absorption from intestine
  • regulate immune system
  • anticancer properties
191
Q

why do northern countries have deficient bone mineralization

A

absence of UVB leads to vitamin D deficiency

192
Q

vitamin D deficiency in growing individuals

A

rickets

193
Q

who is more likely to be vitamin D deficient and why

A

dark-skinned individuals because make less vitamin D from given sun exposure

194
Q

vitamin D deficiency in adults

A

osteomalacia (soft bone)

195
Q

hereditary vitamin D-resistance rickets

A

due to inactivating mutation in vitamin D receptor

196
Q

3 symptoms ofhereditary vitamin D-resistance rickets

A

shortened clavicle
shortened ribcage
baldness

197
Q

which symptoms will be different in someone who lacks the enzyme for vitamin D, not the receptor

A

no baldness

198
Q

calcitonin structure

A

32 amino acid polypeptide (all 32 necessary)

199
Q

where is calcitonin produced

A

parafollicular / “C” cells of thyroid gland

200
Q

what controls calcitonin release

A

high plasma calcium = high calcitonin
low plasma calcium = low calcitonin release

201
Q

how do we know calcitonin is less important than PTH. and1,25 D3 for calcium regulation

A

can remove thyroid gland and maintain calcium homeostasis

202
Q

where are adrenal glands located

A

adjacent to upper surface of kidneys

203
Q

who has bigger adrenal glands

A

males

204
Q

2 distinct tissue types of adrenal glands

A

cortex and medulla

205
Q

what is adrenal cortex made of

A

large lipid-containing epithelial cells derived from mesoderm

206
Q

what does adrenal cortex produce

A

steroid hormones

207
Q

3 zones of adrenal cortex and their hormones

A
  • zona glomerulosa = mineralocorticoids (aldosterone)
  • zone fasciculata = glucocorticoids (cortisol)
  • zona reticularis = glucocorticoids, progestins, androgens and estrogens
208
Q

what is the adrenal medulla made of

A

chromaffin cells (fine brown granules when fixed with potassium bichromate) derived from neural crest

209
Q

what does adrenal medulla produce (2)

A

catecholamines (epinephrine and norepinephrine) and peptide hormones (enkephalins, dynorphins, atrial natriuretic peptides)

210
Q

what is the synthesis of adrenal steroids controlled by

A

adrenocorticotropin (ACTH)

211
Q

what produces ACTH

A

pituitary

212
Q

why is zona glomerulosa the only one that can synthesize mineralocorticoids

A

because it is the only zone with 18-hydroxylase

213
Q

why can zona glomerulosa no produce glucocorticoids

A

because it doesn’t have 17a-hydroxylase

214
Q

how big is ACTH

A

39 amino acid polypeptide

215
Q

2 ACTH functions

A
  • stimulates adenylyl cyclase to increase cAMP production
  • activates steroidogenic enzymes to increase synthesis and release of steroid hormones
216
Q

what 2 substances have circadian pattern and what does this mean for them

A

plasma cortisol and ACTH
have a built-in feedback loop delay
(lowest at midnight, max in morning but independent of sleep)

217
Q

what abolishes plasma cortisol and ACTH circadian pattern (2)

A

stress and Cushing’s disease

218
Q

steroid hormones

A

regulate the transcription of hormones or receptor-specific target genese

219
Q

2 adrenal hormones

A

aldosterone and glucocorticoids

220
Q

aldosterone function

A

sodium metabolism (increases reabsorption of Na+ by kidney)

221
Q

what must happen for aldosterone to affect sodium metabolism

A

coupled with Cl- during removal or replaced by K+/H+

222
Q

4 glucocorticoid functions

A
  • salt retention
  • protein and carb metabolism (PRIMARY FUNCTION)
  • lipid metabolism
  • anti-inflammatory and immunosuppressive actions
223
Q

which adrenal hormone is more effective at salt retention

A

aldosterone

224
Q

how are glucocorticoids involved in protein and carb metabolism (2)

A
  • stimulate synthesis of enzymes that break down tissue protein
  • decrease glucose uptake by muscle and adipose tissue and decrease glycolysis
225
Q

what happens when glucocorticoids stimulate synthesis of enzymes that break down tissue protein (2)

A
  • amino acids are converted to glucose and glycogen (gluconeogenesis) when they enter. the liver
  • can decrease protein matrix and lead to osteoporosis
226
Q

what happens when glucocorticoids decrease glucose uptake by muscle and adipose tissue and decrease glycolysis (3)

A
  • conserve glucose for other tissues
  • causes increased blood glucose (adrenal diabetes)
  • prolonged adrenal diabetes can lead to destruction of beta cells in pancreas and diabetes mellitus
227
Q

2 glucocorticoid effects on lipid metabolism

A
  • maintain or increase lipolitic enzyme levels in adipose tissue
  • increase lipolytic action of other hormones
228
Q

what does glucocorticoid excess lead to in terms of lipids (2)

A

hyperlipidemia and hypercholesterolemia

229
Q

3 glucocorticoid anti-inflammatory and immunosuppressive effects

A
  • decreased inflammatory response
  • atrophy of lymphatic system
  • decreased histamine formation = less allergic reactions
230
Q

why are glucoccorticoids used in organ transplantation

A

because decreases number of circulating lymphocytes and antiboy formation, therefore helps avoid organ rejection

231
Q

what is glucocorticoid secretion controlled by

A

ACTH

232
Q

what does the cortisol double negative feedback loop connect

A

hypothalamus (CRH) and anterior pituitary (ACTH)

233
Q

congenital adrenal hyperplasia

A

enzyme deficiency that leads to cortisol not being produced and ACTH secretion is unchecked

234
Q

congenital adrenal hyperplasia treatment

A

administer cortisol to correct deficiency and normalize ACTH secretion

235
Q

what does psychological and physical stress lead to

A

increased CRH, ACTH and cortisol synthesis and release

236
Q

advantage of increased cortisol

A

more energy and amino acids by tissue protein breakdown

237
Q

disadvantage of increased cortisol

A

inhibits wound healing

238
Q

Addison’s disease

A

hypofunction of adrenal cortex (failure to produce adrenocortical hormones cortisol and aldosterone)

239
Q

what is Addison’s disease mainly caused by

A

autoimmune attack on adrenal glands (or tuberculosis)
- may involve total gland destruction

240
Q

symptoms of cortisol/glucocorticoid deficiency (Addison’s disease) (6)

A

low blood sugar, low lipolysis, low gluconeogenesis
lack of energy, muscular weakness, inability to take stress

241
Q

treatment for cortisol/glucocorticoid deficiency (Addison’s disease)

A

cortisol to help carbohydrate metabolism

242
Q

symptoms of aldosterone/mineralocorticoid deficiency (Addison’s disease) (7)

A

low Na+, Cl-, H2O
low extracellular fluid, low cardiac output
increased K+, H+

243
Q

what happens after 7 day complete absence of mineralocorticoids

A

die

244
Q

treatment for aldosterone/mineralocorticoid deficiency (Addison’s disease)

A

aldosterone to control electrolyte blood levels

245
Q

Cushing’s disease

A

hyperfunction of adrenal cortex (increased production of glucocorticoids and mineralocorticoids)

246
Q

what is the cause of Cushing’s disease

A

increased circulating ACTH levels (pituitary/adrenal tumor), leads to hyperplasia/growth

247
Q

effects of increased glucocorticoid production (Cushing’s disease) (4)

A

increased blood glucose (adrenal diabetes), insulin secretion, protein breakdown = osteoporosis

248
Q

effects of increased mineralocorticoid production (Cushing’s disease) (6)

A

increased Na+, Cl-, H2O, plasma volume, extracellular fluid, hypertension

249
Q

why can Cushing’s disease lead to masculinization

A

increased sex hormones and androgens

250
Q

Cushing’s disease diagnosis (6)

A

puffy face, masculinization, hypertension that does not respond to BP medication, high blood glucose and steroid metabolites in urine, undetectable ACTH, high circulating cortisol

251
Q

Cushing’s disease treatment

A

subtotal removal of adrenal cortex

252
Q

what can sometimes happen after removing adrenal tumor

A

atrophy of other adrenal because loss of circulating ACTH (Addison’s diseasE)

253
Q

treatment after removing adrenal tumor

A

synthetic glucocorticoids and mineralocorticoids

254
Q

where is pancreas

A

behind stomach

255
Q

what is 99% of pancreas

A

exocrine = secretes digestive enzymes

256
Q

what is 1% of pancreas

A

islets of Langerhans

257
Q

islets of Langerhans

A

endocrine structure; compact cells with good vascularization

258
Q

60% islets of Langerhans

A

beta cells = synthesize insulin

259
Q

25% islets of Langerhans

A

alpha cells = synthesize glucagon

260
Q

insulin

A

only hormone that acts primarily to decrease blood glucose (IMPORTANT)

261
Q

fasting glucose level

A

80mg/100mL (always present in blood)

262
Q

why must glucose be transported into cells by membrane proteins

A

because it is hydrophilic

263
Q

what does stimulation of insulin receptors lead to

A

inserts glucose transport protein onto cell surfaces to increase glucose uptake

264
Q

what happens as we eat to induce insulin secretion before blood glucose increases

A

release of gastrin and vagal impulses to beta cells

265
Q

what does glucose become in liver and muscle cells

A

glycogen

266
Q

what does glucose become in adipose tissue

A

fat

267
Q

what does glucose become in other body cells

A

oxidized to produce ATP

268
Q

insulin deficiency

A

destruction of beta cells leads to diabetes mellitus

269
Q

diabetes mellitus

A

most tissues cannot take up glucose efficiently, glucose accumulates in circ

270
Q

will glucose accumulate in circ even if not ingested

A

yes because increased gluconeogenesis will occur (protein breakdown)

271
Q

what becomes main energy source in insulin deficiency

A

free fatty acids (FFA), but inefficently used

272
Q

what does incomplete FFA oxidation lead to (3)

A

increased circulating acetoacetic acid and metabolic acidosis, and acetone

273
Q

what is one way to tell someone has extreme untreated diabetes

A

smell acetone in breath

274
Q

what are consequences of incomplete FFA oxidation (3)

A

decreased blood pH, diabetic coma and death

275
Q

glucose >180mg% (3)

A

glucose in urine
loss of water in urine
dehydration and increased thirst

276
Q

treatment for diabetes mellitus

A

insulin administration (may also need to correct acidosis and electrolyte imbalance if extreme)

277
Q

type 1/insulin-dependent diabetes mellitus

A

insulin deficient

278
Q

2 causes of type 1 diabetes

A

beta cella destruction (no insulin synthesis) and defective insulin release

279
Q

treatment for beta cell destruction

A

insulin administration and proper diet

280
Q

treatment for defective insulin release

A

drugs stimulating insulin release and proper diet and exercise

281
Q

what is considered to be low blood glucose and why

A

20-30mg/100mL (not enough for brain use = insulin shock/hypoglycemic coma)

282
Q

type 2/insulin-independent diabetes mellitus

A

hypo-responsiveness of target cells to insulin

283
Q

what are insulin levels like in type 2 diabetes

A

normal to abnormally high

284
Q

what is insulin resistance in type 2 diabetes often due to

A

decreased no. of insulin receptors on target cells (downregulation)

285
Q

what is type 2 diabetes associated with

A

overeating / obesity

286
Q

treatment for type 2 diabetes

A

proper diet and exercise

287
Q

juvenile diabetes mellitus

A

insulin-dependent; beta cells don’t produce insulin

288
Q

treatment for juvenile diabetes mellitus

A

insulin administration

289
Q

glucose tolerance test

A

after overnight fast, administer 0.75-1.5g glucose per kg body weight, measure glucose before and every 30-60 mins for 3-4 hours
- glucose tolerance lower in diabetes, higher in hyperinsulinism

290
Q

how does blood glucose change in normal individual

A

from 80mg/100mL to 130mg/mL and after 2-3 hours, returns to normal

291
Q

how does blood glucose change in diabetic individual

A

increase in blood glucose is greater and returns to normal more slowly

292
Q

what type of hormone is glucagon

A

peptide hormone

293
Q

what synthesizes and releases glucagon

A

alpha cells of pancreas

294
Q

2 ways glucagon raises blood sugar

A

glycogenolysis (breakdown of glycogen) and gluconeogenesis (glucose synthesis)

295
Q

glucagon function in adipose tissue

A

increases rate of lipolysis -> increases FFA conc

296
Q

why is it less important than insulin

A

other hormones can have same function e.g. cortisol, epinephrine, norepinephrine

297
Q

what kind of hormone is growth hormone / somatotropin / STH

A

single chain polypeptide

298
Q

what produces growth hormone / somatotropin / STH

A

anterior lobe of pituitary

299
Q

2 growth hormone functions

A
  • increases protein synthesis in bone, muscle, kidney, liver (enhances amino acid uptake, accelerates transcription and translation of mRNA)
  • increases rate of lipolysis and utilisation of FFA as energy source
300
Q

what is growth hormone release controlled by

A

hypothalamic neurohormones:
- GRH = stimulates
- somatostatin = inhibits

301
Q

when and where are somatomedins produced

A

produced by liver under GH stimulation

302
Q

what are somatomedins structurally similar to

A

insulin, therefore called isunlin-like growth factors 1 and 2 (IGF-1 and IGF-2)

303
Q

somatomedin function

A

increase protein synthesis and stimulate growth

304
Q

GH deficiency

A

leads to decreased physical growth in the young

305
Q

excess GH in young individuals

A

gigantism

306
Q

excess GH in adults

A

acromegaly

307
Q

acromegaly

A

many bones (particularly cartilaginous regions) get longer a heavier, increased frontal bossing, brow furrow, enlargement of nose base, thickening of lips

308
Q

where do somatomedins act in their double negative feedback loop

A

hypothalamus and anterior pituitary

309
Q

primary reproductive organs

A

gonads
(testes = male)
(ovaries = female)

310
Q

2 gonad functions

A
  • gametogenesis (production of gametes - spermatozoa and ova)
  • secretion of sex hormones testosterone, estrogen and progesterone (male and female)
311
Q

where do females produce androgens (2)

A

ovaries and adrenals**

312
Q

role os estrogen in males

A

maintains bone density

313
Q

where is estrogen produced in males and how

A

testes; conversion by aromatase of testosterone to estradiol

314
Q

estrogen deficiency in males (2)

A
  • leads to decreased body fat
  • contributes to sexual desire and erectile function
315
Q

what secretes gonodotropin releasing hormone (GnRH)

A

hypothalamus

316
Q

where does GnRH travel to and how once secreted

A

travels to anterior pituitary via hypothalamo-pituitary portal vessels

317
Q

what does GnRH stimulate the release of

A

pituitary gonadotropins (follicle-stimulating hormone/FSH and luteinizing hormone/LH)

318
Q

what do FSH and LH do once secreted from anterior pituitary

A

stimulate development of spermatozoa/ova, and secretion of sex steroids (estrogens and androgens)

319
Q

2 locations sex steroids exert effects

A
  • gonads
  • other parts of reproductive system and body
320
Q

what do gonads produce, and what does it do

A

inhibin - feeds back on anterior pituitary

321
Q

spermatogenesis

A

production of mature germ cells

322
Q

where does spermatogenesis take place

A

seminiferous tubules

323
Q

testes principal functions (2)

A

spermatogenesis and steroidogenesis

324
Q

how long does the process of maturation from immature spermatogonia to mature spermatozoon take in humans

A

approx 60 days

325
Q

how come men have relatively constant supply of sperm throughout life

A

can renew pool of precursor germ cells (spermatogonia)

326
Q

what condition is spermatogenesis dependent on

A

androgen concentration in seminiferous tubules being 10x greater than in circulation

327
Q

what ensures the high androgen concentrations in seminiferous tubules

A

ABP synthesized by Sertoli cells

328
Q

2 types of cells involved for maturation of spermatozoa

A

Leydig cells and Sertoli cells

329
Q

where are Leydig cells located

A

outside seminiferous tubules

330
Q

Leydig cell function

A

synthesize androgens in response to LH binding to surface receptors

331
Q

where are Sertoli cells located

A

within seminiferous tubules

332
Q

Sertoli cell functions (2)

A
  • synthesize ABP and inhibin in response to FSH
  • envelop germ cells during maturation process
333
Q

2 negative feedback loop of testicular androgen regulation

A
  • hypothalamic-pituitary-Leydig cell axis
  • hypothalamic-pituitary-seminiferous-tubules-axis
334
Q

hypothalamic-pituitary-Leydig cell axis (4) DOUBLE NEGATIVE

A
  • GnRH stimulates release of LH and FSH
  • LH and FSH stimulate Leydig cells and Sertoli cells
  • Leydig cells produce androgens
  • Androgen inhibit release of GnRH (hypothalamus), LH and FSH (anterior pituitary)
335
Q

hypothalamic-pituitary-seminiferous-tubules axis

A
  • GnRH stimulates release of LH and FSH
  • LH and FSH stimulate Leydig cells and Sertoli cells
  • Sertoli cells secrete non steroidal inhibin
  • inhibin inhibits FSH release
336
Q

2 principal functions of ovary

A

production of mature eggs and steroid hormones

337
Q

function of steroid hormones in women (2)

A

regulate reproductive tract and influence sexual behaviour

338
Q

how many oocytes do women have at birth

A

2 mil (lifetime supply)

339
Q

how many oocytes are left at puberty

A

400,000 ova

340
Q

primordial follicles

A

oocyte surrounded by layer of granulosa cells and basement membrane

341
Q

what triggers development of primordial follicles into primary follicles

A

unsure

342
Q

what controls the growth of primary follicles once started (2)

A

gonadotropins and steroid hormones

343
Q

2 possible outcomes for primary follicle

A

ovulation or degeneration (atresia)

344
Q

first step of follicular growth

A

primordial follicle grows and develops zona pellucida

345
Q

zona pellucida

A

acellular layer rich in glycoproteins surrounding the oocyte

346
Q

what happens once primordial follicle has developed zona pellucida

A

granulosa cells divide and increase in layers to become primary follicles

347
Q

what influences primary follicle development

A

FSH and estrogens

348
Q

what is important for expression of LH receptors on granulosa cells

A

estrogens

349
Q

what happens after primary follicle is developed, and what influences it

A

FSH and LH cause primary follicle to develop into a secondary follicle that expresses receptors for FSH, estrogen and LH

350
Q

what happens after secondary follicle is developed

A

appearance of follicular antrum which contains secretions from granulosa cells

351
Q

what happens after appearance of follicular antrum and what influences it

A

FSH and LH cause granulosa cells to elaborate follicular fluid (large portion of preovulatory follicle)

352
Q

what also happens as follicle matures from primary to secondary follicle

A

cells from ovarian stroma surrounding follicle differentiate and become theca cells (steroid producing cells)

353
Q

what do theca and granulosa cells contribute towards

A

synthesis of higher amounts of estrogen

354
Q

what does the ruptured follicle transform into

A

corpus luteum

355
Q

what does corpus luteum secrete

A

progesterone

356
Q

what contributes to formation of corpus luteum (2)

A

theca and granulosa cells

357
Q

2 things corpus luteum synthesizes, and how much

A

progesterone and estrogens
- large amounts for few days following ovulation, then drop off unless implantation of fertilized ovum

358
Q

luteolysis

A

corpus luteum degenerates without implantation

359
Q

what can induce luteal regression and what effect may this have

A

prostaglandins; decrease LH binding and therefore steroidogenesis

360
Q

what may be the trigger for initiation of next reproductive cycle

A

decrease of plasma progesterone and estrogen

361
Q

what happens to corpus luteum upon implantation

A

transforms into corpus luteum of pregnancy

362
Q

what is corpus luteum of pregnancy responsible for

A

synthesis of progesterone and estrogen and creation of proper endocrine environment until placenta is established

363
Q

what causes endometrium to thicken prior to day 1 of menstrual cycle

A

estradiol

364
Q

what induces appearance of specialized glycogen-secreting glands

A

progesterone

365
Q

day 1 of menstrual cycle

A

1st day of detectable vaginal bleeding (deterioration of uterine endometrium)

366
Q

what causes menses/bleeding to begin on day 1

A

low estradiol and progesterone in circ; blood vessels supplying endometrium constrict to reduce blood supply

367
Q

what is the bleeding of menstrual cycle

A

endometrium deteriorates, flows through cervix into vagina

368
Q

how long does bleeding typically last

A

5 days (ovaries endocrinologically inactive)

369
Q

what leads to increased pituitary FSH secretion (2)

A
  • low estradiol and progesterone (lack of negative feedback loop)
  • decrease in inhibin
370
Q

what does the high FSH concentration lead to (days 1-7)

A

cohort of ovarian follicles develops and stimulates granulosa cells of follicles to proliferate

371
Q

what is another contributing factor of granulosa cell proliferation

A

granulosa cells produce estrogen

372
Q

what happens on day 8 of cycle

A

1 follicle becomes dominant and committed to further development, rest degenerate

373
Q

how does 1 follicle become dominant in humans

A

unknown

374
Q

what does the dominant follicle do

A

produces increasingly more estradiol to stimulate uterine endometrium proliferation

375
Q

what happens by day 13 of cycle

A

endometrium very thick, estradiol induces production of endometrial progesterone receptors

376
Q

3 sections of menstrual cycle (from day 1)

A

menstrual, proliferative, secretory

377
Q

2 phases of menstrual cycle

A

follicular and luteal

378
Q

3 effects of moderate estradiol concentrations

A
  • negative feedback on FSH
  • stimulates synthesis of LH by pituitary
  • increase sensitivity of pituitary to GnRH
379
Q

why does LH accumulate in pituitary at moderate estradiol concs

A

because it stimulates synthesis but inhibits release of LH

380
Q

what causes estrogen concentration to continue to build

A

developing follicle

381
Q

what do high estrogen concs do (and when)

A

stimulate LH release (LH surge) on day 14

382
Q

estrogen positive feedback control mechanism

A

stimulation of LH synthesis by estradiol + increased sensitivity of anterior pituitary to GnRH = increased LH synthesis

383
Q

what does LH surge do

A

causes follicle to rupture (mechanism unclear) and ovum is ejected

384
Q

what do oral contraceptive pills contain (2)

A

estrogen and progesterone

385
Q

why do oral contraceptives work

A

maintain moderate circulating levels of estrogen and progesterone to suppress release of LH and FSH from pituitary -> prevents ovarian follicles from maturing and being ovulated

386
Q

oral contraceptive success rate when taken correctly

A

99%

387
Q

luteal phase (& duration)

A

steroids produced by corpus luteum dominate (lasts 14 days)

388
Q

what happens after 14 days with no implantation and corpus luteum degenerates (4)

A
  • steroid levels drop
  • uterine endometrium degenerates
  • menstruation begins
  • pituitary starts to increase FSH secretion
389
Q

where is unfertilised egg taken to at ovulation

A

fallopian tube, propelled towards lumen of uterus

390
Q

up to what point will spermatozoa travel to fertilize the egg

A

oviduct

391
Q

when/where does egg start dividing into blastocyst

A

during its transport down the oviduct into uterine lumen

392
Q

what does blastocyst differentiate into (2)

A

trophoblast and inner cell mass

393
Q

what does trophoblast become

A

placenta

394
Q

what does inner cell mass become

A

embryo

395
Q

what does trophoblast do to embed developing embryo in endometrium

A

invades uterine mucosa

396
Q

what does trophoblast start to synthesize around the time of implantation

A

human chorionic gonadotropin (hCG)

397
Q

human chorionic gonadotropin (HCG) (2)

A

has LH-like properties, stimulates corpus luteum to continue secreting gonadal steroids

398
Q

what happens at 12th week of pregnancy

A

placenta takes over the endocrine function of corpus luteum

399
Q

what quickly appears in blood and urine, and what is this basis for

A

HCG; basis for immunological pregnancy test

400
Q

lactation

A

secretion of milk by breast (mammary glands)

401
Q

what is required for lactation

A

normal mammary development

402
Q

what happens for mature non-pregnant mammary gland (ductal) development

A

with puberty and increasing estrogen levels, duct growth enhancement and duct branching

403
Q

what stimulates growth of alveoli in mature non-pregnant mammary glands

A

alveoli

404
Q

what is most breast enlargement due to in mature non-pregnant mammary glands

A

fat deposition under glandular tissue

405
Q

what allows ductal and alveoli structures to fully develop (4)

A

estrogen, progesterone, prolactin and human placental lactogen

406
Q

what controls milk production during pregnancy

A

prolactin

407
Q

what inhibits milk secretion

A

high estrogen levels

408
Q

what happens to prolactin and estrogen levels after parturition

A

estrogen levels decrease, prolactin levels remain high

409
Q

what do the low estrogen and high prolactin levels allow for

A

milk synthesis, then alveoli secrete it to fill the ducts

410
Q

nursing

A

under action of oxytocin, ducts contract to cause milk ejection

411
Q

prolactin (what produces it & function)

A

anterior pituitary - milk production

412
Q

oxytocin (what produces it & function)

A

posterior pituitary - milk ejection

413
Q

what is milk made of (5)

A

water, protein, fat, carbohydrate lactose and antibodies

414
Q

lactational amenorrhea

A

maintained nursing stimulates prolactin production which inhibits the secretion of FSH and LH - blocks resumption of reproductive cycle therefore can be used as contraception

415
Q

menopause

A

loss of ovarian steroid production

416
Q

why can ovaries no longer produce estrogen and progesterone

A

most follicles depleted / disappeared through atresia

417
Q

4 symptoms of lack of estrogen

A

hot flashes, dry vagina, restlessness and bone loss

418
Q

what is indicative of menopause and why

A

high FSH conc; cessation of ovarian steroid hormone production eliminates negative feedback loop

419
Q

how to cure estrogen deficiency symptoms (but what is limitation)

A

estrogen replacement threapy, but fertility cannot be restored

420
Q

what is similar in structure to cholesterol

A

provitamin D3 (sensitive to UVB radiation)

421
Q

what is provitamin D3 converted to

A

vitamin D3

422
Q

what is vitamin D3 then converted to (& what does the conversion)

A

liver converts vitamin D into 25-hydroxy-vitamin D3

423
Q

what is major circulating form of vitamin D

A

25-hydroxy-vitamin D3

424
Q

what happens to 25-hydroxy-vitamin D3 in peripheral tissues

A

1-hydroxylation occurs - makes it 1,25-dihydroxy-vitamin D3 (active form that binds to receptors)

425
Q

what condition does the sun have to meet for UVB synthesis to occur

A

40 degress

426
Q

why is there vitamin D deficiency in the middle East

A

because it’s so hot that people avoid the sun

427
Q

3 conditions that have shown north-south gradients

A
  1. certain types of cancers
  2. autoimmune diseases
  3. infectious diseases
428
Q

what types of cancers show north-south gradient and why

A

digestive cancers and leukemias; places with elevation are more vitamin D sufficient therefore see reduction in colon cancer

429
Q

example of autoimmune disease with north-south gradient

A

multiple sclerosis

430
Q

what causes immune system cells (macrophages) to become responsive to 25D3

A

sensing presence of bacterial cell wall

431
Q

treatment of cells with 1,25 D3 induces what

A

secretion of antibacterial activity in the form of antimicrobial proteins

PHGY 210 (3 decks)

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