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X Physiology 1B > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

define endocrinology

A

study of communication within a living organism by means of hormones

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2
Q

in homeostasis what is a hormone used as?

A

effector

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3
Q

define homeostasis

A

the process by which a living thing or cell keeps the conditions inside it the same despite changes in the conditions around it

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4
Q

what is hemocrine function referred to as?

A

endocrine

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5
Q

what is hemocrine communication?

A

vesicles containing hormones leave cell and diffuse into the blood stream where they travel to their target cell which has the correct receptor and has biological effect

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6
Q

define autocrine hormonal communication

A

has effect on the same cell which secreted the hormone

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7
Q

define paracrine hormonal communication

A

hormone that is released affects nearby cells

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8
Q

what is paracrine hormonal communication known as in neuronal cells?

A

neurocrine

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9
Q

what is solinocrine hormone communication?

A

where hormone is released into a duct

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10
Q

what are the 4 methods of hormone communication?

A

hemocrine
autocrine
paracrine (nerocrine)
solinocrine

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11
Q

in what 2 states may hormones circulate?

A

free or bound to binding protein

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12
Q

what is the purpose of binding hormone to a binding protein?

A

provides reservoir/pool of hormones to avoid fluctuations
extends the half life of the hormone
allows insoluble hormones to circulate

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13
Q

how do hormones affect the target cell?

A

by binding to unique recognition receptors on the target tissue

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14
Q

where are hormone receptors found?

A

in the cytosol
on the cell surface
in the nucleus

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15
Q

what are the 3 classifications of hormones?

A

peptide and protein hormones
small amino acid hormones
steroids

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16
Q

where do peptide and protein hormones originate from?

A

protein synthesis in endocrine cells

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17
Q

what are peptide and protein hormones often synthesised as?

A

pro-hormones (inactivated hormones) that are then processed

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18
Q

where are peptide and protein hormones stored?

A

in vesicles within endocrine cells

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19
Q

what amino acid are small amino acid hormones based on?

A

the amino acid tyrosine

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20
Q

what are 3 examples of peptide and protein hormones?

A

insulin, oxytocin and parathyroid hormone

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21
Q

how are small amino acid hormones stored?

A

have specialised storage and secretory mechanisms

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22
Q

what is an example of a small amino acid hormone?

A

thyroid hormone - iodinated tyrosine

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23
Q

what are steroid hormones a modification of?

A

cholesterol

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24
Q

are steroid hormones soluble?

A

no

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25
Q

give an example of a steroid hormone

A

cortisol produced in the adrenal gland

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26
Q

what do peptide and protein hormones act at?

A

cell surface receptors

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27
Q

what does activation of a cell surface receptor by peptide and protein hormones cause?

A

down stream signalling

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28
Q

what types of cells does peptide and protein hormones act on?

A

only cells with an appropriate receptor but these can be widespread with simultaneous actions on widespread tissues

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29
Q

describe the G-protein signalling pathway

A

signal molecule binds - activates second messenger - leads to phosphorylation of proteins - change in cell behavior

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30
Q

what receptor do steroids act at?

A

cytoplasmic or nuclear receptor

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31
Q

why do steroids circulate with a binding protein?

A

insoluble in water and hydrophobic

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32
Q

why can steroids diffuse through the cell membrane?

A

they are lipophillic

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33
Q

where are steroid receptors found around the body?

A

widespread - have simultaneous actions on widespread organs and tissues

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34
Q

where is the receptor for amino acid derived hormones always located?

A

in the nucleus

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35
Q

describe the process of steroid hormones effecting a target cell

A

steroid diffuses into cell and binds to a receptor in the cytosol or nucleus. The conformational change which results from this promotes transcription and translation of different/required proteins

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36
Q

are there storage pools of steroid and peptide hormones?

A

steroid - none

peptide - secretory vesicles

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37
Q

how does interaction with the cell membrane differ between steroid and peptide hormones?

A

steroid - diffusion through cell membrane

peptide - binding to receptor on cell membrane

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38
Q

where is the receptor for steroid and peptide hormones located?

A

steroid - in cytoplasm or nucleus

peptide - on cell membrane

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39
Q

what is the actions of steroid and peptide hormones?

A

steroid - regulation of gene transcription

peptide - signal transduction cascades affect a variety of processes

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40
Q

what is the response time of steroid and peptide hormones?

A

steroid - hours to days

peptide - seconds to minutes

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41
Q

how is release of hormones controlled?

A

feedback mechanisms
tropic hormones
neuronal control

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42
Q

what are the main feedback mechanisms in the body used for?

A

homeostasis uses many negative feedback loops

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43
Q

describe the feedback loop associated with glucose

A

eating increases glucose concentration leads to stimulation of beta cells to produce insulin. Insulin encourages glucose storage which reduces circulating glucose and so reduces insulin production by beta cells

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44
Q

what do tropic hormones do?

A

stimulate release of another hormone from other endocrine glands

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45
Q

what do trophic hormones do?

A

have a growth effect on cells and tissues (hyperplasia - increasing cell numbers, hyper trophy - increasing cell size)

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46
Q

describe an example of tropic hormones

A

hypothalamus releases TRH which stimulates the anterior pituitary to release TSH which stimulates the thyroid gland to release T3 and T4 leading to increase BMR, protein synthesis and sympathetic tone

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47
Q

what is an example of neuronal control of hormones?

A

release of adrenaline by adrenal medulla

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48
Q

where is the pituitary gland located?

A

at the base of the brain below the hypothalamus

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49
Q

what is the role of the hypopophyseal portal circulation?

A

direct route for hormones down to the pituitary lobe

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50
Q

what is tissue is the anterior lobe of the pituitary gland made of?

A

glandular tissue

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51
Q

what is tissue is the intermediate lobe of the pituitary gland made of?

A

glandular tissue

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52
Q

what is tissue is the posterior lobe of the pituitary gland made of?

A

neuronal tissue

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53
Q

what happens during the anterior pituitary pathway of the hypothalamus pituitary axis (HPA)?

A

hypothalamus secretes hypothalamic hormone which binds to glandular cells in the anterior lobe of the pituitary gland causing it to release anterior lobe hormone which then diffuses into the circulation

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54
Q

what happens during the posterior pituitary pathway of the hypothalamus pituitary axis (HPA)?

A

neuroendocrine cells in hypothalamus transport information via axonal transport into posterior lobe which causes posterior lobe hormone to be released into the blood stream

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55
Q

where do neuroendocrine cells reside in the hypothalamus?

A

nuclei

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56
Q

what does the hypothalamus monitor?

A

levels of circulating hormones, metabolites, nutrients and electrolytes

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57
Q

what does the hypothalamus respond to?

A

stress, cold, trauma, hunger, pain, neuronal reflex

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58
Q

what is the hypothalamus the focus point for?

A

information on internal well being

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59
Q

how may hormones are released from the hypothalamus?

A

many

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60
Q

what do hypothalamus hormones bind to and cause?

A

target cells in anterior pituitary which leads to the production of pituitary hormone

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61
Q

what 2 effects can hypothalamus hormones have?

A

inhibitory or stimulatory

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62
Q

what are the 2 main actions of oxytocin?

A

during labor to cause contraction of the uterus

during lactation essential for milk let down

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63
Q

how is oxytocin release stimulated?

A

stretch receptors feeds back to hypothalamus via spinal cord (neural feedback) causing release of oxytocin

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64
Q

how does oxytocin release lead to further oxytocin release?

A

stretch receptors cause release of oxytocin which causes further contractions and so stimulates stretch receptors more

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65
Q

how is ADH release stimulated?

A

secretory stimulus through 2 mechanisms:
increased plasma osmolarity
decreased plasma volume

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66
Q

what is decreased plasma volume detected by?

A

volume receptors in veins, atria and carotids

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67
Q

what clinical abnormalities can lead to lack of ADH production

A

diabetes insipidus - leads to chronic excretion of large volumes of dilute urine and thirst caused by hyperosmolarity

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68
Q

what else can cause disruption of ADH production?

A

pituitary tumors and traumatic skull injury

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69
Q

where does ADH originate from?

A

posterior pituitary gland

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70
Q

where is the thyroid located in humans?

A

adjacent to the larynx

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71
Q

what is the name for the fluid found in the follicles of the thyroid?

A

colloid

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72
Q

what is thyroid hormone derived from?

A

the amino acid tyrosine

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73
Q

what is incorporated into the thyroid hormone along with tyrosine?

A

iodine

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74
Q

what is the first form of thyroid hormones?

A

thyroglobuline

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75
Q

what is thyroglobuline?

A

polymer containing tyrosine

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76
Q

where is thyroglobuline stored?

A

in the colloid of the follicle

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77
Q

what is the backbone of thyroglobuline formed of?

A

peptide

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78
Q

what are the 2 released thyroid hormones?

A

T4 (thyroxine) and T3 (triodothyronine)

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79
Q

how many iodides are attached to thyroxine?

A

4

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80
Q

how many iodides are attached to thyroglobuline?

A

3

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81
Q

describe the process of thyroid hormone synthesis

A

follicular cell synthesizes enzymes and thyroglobulin from colloid
iodine is co-transported into the cell with Na+ and transported into colloid
enzymes add iodine to thyroglobulin to make T3 and T4
thyroglobulin is taken back into the cell
intracellular enzymes separate T3 and T4 from the protein
free T3 and T4 enter the circulation

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82
Q

what proportion of total hormone released from thyroid gland is made up of T3?

A

10%

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83
Q

what proportion of total hormone released from thyroid gland is made up of T4?

A

90%

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84
Q

how much receptor affinity (activity) does T3 have?

A

5x more affinity than T4

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85
Q

how much receptor affinity (activity) does T4 have?

A

low

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86
Q

does T3 circulate freely in the blood?

A

no - is protein bound

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87
Q

does T4 circulate freely in the blood?

A

no - is protein bound

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88
Q

is T3 or T4 more tightly protein bound

A

T4

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89
Q

how long is the half-life of T3?

A

1 day

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90
Q

how long is the half life of T4?

A

6 days

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91
Q

why is the half life of T4 so much longer than that of T3?

A

due to it’s tight protein binding

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92
Q

what are most of the physiological effects of thyroid hormone due to?

A

T3

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93
Q

what is the role of T4?

A

acts as a pool for T3 as it can be converted easily but lasts longer due to it’s half life

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94
Q

what regulates secretion of thyroid hormone?

A

hypothalamus-pituitary-thyroid axis

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95
Q

describe the regulation of thyroid secretion

A

hypothalamus releases TRH which moves via the hypopophyseal portal circulation to thyrotrophs in the anterior pituitary which is stimulated to release TSH. TSH enters circulation and arrives at the thyroid gland where it stimulates the release of T3 and T4

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96
Q

what is TRH?

A

thyrotropin releasing hormone

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97
Q

what is TSH?

A

thyroid stimulating hormone

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98
Q

what factors stimulate the release of TRH and so the release of thyroid hormones?

A

sympathetic activation and cold

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99
Q

what factors inhibit the release of TRH and so the release of thyroid hormones?

A

cortisol and growth hormone

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100
Q

what does TSH bind to in the thyroid?

A

TSH receptor on thyroid follicular cell

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101
Q

what does binding of TSH to TSH receptor on thyroid follicular cell stimulate?

A

all functions of thyroid gland increase - iodine uptake, protein synthesis, re-uptake of colloidal thyroglobulin

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102
Q

what are the functions of the thyroid gland?

A

iodine uptake, protein synthesis, re-uptake of colloidal thyroglobulin

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103
Q

what do the increased thyroid gland functions lead to?

A

increased size, number and secretory activity of thyroid cells

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104
Q

what does increased size, number and secretory activity of thyroid cells lead to?

A

increased synthesis and release of T3 and T4

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105
Q

how do unstimulated thyroid gland cells appear?

A

cuboidal epithelium with follicles full of colloid

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106
Q

how do stimulated thyroid gland cells appear?

A

columnar epithelium with follicles depleted/collapsed and hypertrophy of follicle cells

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107
Q

what is hypertrophy of follicle cells due to?

A

increased uptake of colloid for T3/T4 production

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108
Q

how is T3/T4 production slowed when necessary?

A

negative feedback

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109
Q

how does negative feedback of T3/T4 production impact T3/T4 production?

A

if T3/T4 production is high TRH and TSH are suppressed

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110
Q

what are the 3 main effects of thyroid hormone on the body?

A

cardiovascular
growth
basal metabolic rate

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111
Q

what are the physiological actions of thyroid hormone on the cardiovascular system?

A

increased manufacture and incorporation of beta1 adrenergic receptors

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112
Q

what does increased manufacture and incorporation of beta1 adrenergic receptors do to the cardiovascular system?

A

increased responsiveness

sets sensitivity of heart rate to adrenaline/noradrenaline

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113
Q

what is the long term sensitivity of cardiac cells to thyroid hormone regulated by?

A

plasma levels of thyroid hormone

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114
Q

what is thyroid hormone essential for in childhood?

A

normal growth

development of CNS

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115
Q

how does thyroid hormone support growth in childhood?

A

action is unclear - possibly through supporting the action of growth hormone

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116
Q

what can lack of T3/T4 in late foetal/early neonatal period lead to?

A

irreversible failure of CNS development. Reduced number of neurons and reduced mylination

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117
Q

define basal metabolic rate (BMR)

A

the rate at which the body uses energy to maintain vital functions whilst at rest

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118
Q

what is increased oxidative metabolism measured by?

A

increased heat production

increased oxygen consumption

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119
Q

what do reduced thyroid production rates lead to?

A

hypothyroid

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120
Q

what do increased thyroid production rates lead to?

A

hyperthyroid

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121
Q

what is the effect of increased thyroid hormone on BMR?

A

increases BMR

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122
Q

what is the effect of increased BMR?

A

increased oxidative metabolism
stimulates catabolic and anabolic reactions in pathways affecting fats, carbohydrates and proteins
stimulates synthesis of enzymes and structural proteins
more glucose made available to meet elevated metabolic demand
increased lipid metabolism

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123
Q

what is increased oxidative metabolism associated with?

A

increased Na/K activity

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124
Q

describe the action of thyroid hormone on target cells

A

T3/T4 enter the target cell
most of T4 is converted into T3
T3 enters the nucleus and binds to the thyroid hormone receptor (THR)
binding of THR to promoter elements activates gene transcription

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125
Q

how does T3/T4 enter the target cell?

A

through membrane/transporter

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126
Q

what is hyperthyroidism caused by?

A

overproduction of thyroid hormones

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127
Q

what diseases can cause hyperthyroidism?

A

Grave’s disease

tumors of follicular cells

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128
Q

what are the effects of hyperthyroidism on the thyroid gland?

A

thyroid gland increased in size (Goiter)
hyperplasia (cells increase in size)
increased rate of TH secretion
increased metabolic rate

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129
Q

what are the systemic effects of hyperthyroidism?

A

cardiovascular - increased force of contraction, increased weight of contraction
weight loss
CNS - nervousness, irritability, sleeplessness
fatigue
heat tolerance
sweating
moist skin

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130
Q

what is LATS?

A

long acting thyroid stimulator

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131
Q

what is the effect of LATS?

A

over-stimulation of thyroid leading to increased T4/T3 synthesis and secretion

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132
Q

what do the LATS immunoglobulins stimulate as well as the thyroid follicles?

A

connective tissue - leads to exophthalmus (bulging of eyes)

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133
Q

what is the treatment for Grave’s disease?

A

anti-thyroid drugs
thyroidectomy
radioactive iodine

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134
Q

how does Grave’s disease lead to gland enlargement?

A

LATS directly stimulates thyroid gland and is outside the normal feedback loop so there is continued stimulation of T3/T4 formation so gland enlarges

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135
Q

what is hypothyroidism caused by?

A

low T3/T4 secretion

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136
Q

what are the causes of hypothyroidism?

A

iodine deficiency - iodine cannot be synthesised

Hashimoto’s disease - autoimmune destruction of thyroid cells

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137
Q

what effect does hypothyroidism have on metabolic rate?

A

decreased metabolic rate

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138
Q

what is the treatment for hypothyroidism?

A

increase iodine

replacement TH

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139
Q

what are the systemic effects of hypothyroidism?

A

increased weight
decreased appetite
myxedema
cold intolerance
Goiter
cardiovascular - decreased cardiac output, decreased force of contraction, decreased rate of contraction
CNS - mental sluggishness, fatigue, cognitive dysfunction (in children)

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140
Q

how does iodine deficiency lead to gland enlargement?

A

no feedback control of TSH, no T3/T4 formation. TSH level remains high which leads to continued stimulation by TSH, the gland enlarges

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141
Q

define growth

A

increase in size

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142
Q

what is hypertrophy?

A

increase in cells size

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143
Q

what is hyperplasia?

A

increase in cell number

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144
Q

what do hypertrophy and hyperplasia lead to?

A

over all size increase of the organism

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145
Q

what does growth require?

A

fuel and building blocks

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146
Q

what manages the presence of fuel and building blocks?

A

hormones and growth factors

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147
Q

what does IGF-1 stand for?

A

insulin like growth factor

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148
Q

what is the hormone involved in growth?

A

growth hormone

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149
Q

what is the growth factor involved in growth?

A

IGF-1

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150
Q

what sort of hormone is growth factor?

A

peptide

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151
Q

what does growth hormone bind to?

A

growth hormone receptor in target tissues

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152
Q

what is the effect of growth hormone?

A

causes growth in almost all tissues of the body that can grow

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153
Q

what does growth hormone promote?

A

differentiation of some cell types

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154
Q

what are the short term effects of growth hormone?

A

metabolic

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155
Q

what does growth hormone circulate bound to?

A

growth hormone binding protein

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156
Q

how tight is the binding of growth hormone to the binding protein?

A

weak - allows rapid release into tissues

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157
Q

what cells is growth hormone secreted by?

A

somatotrophs in the anterior pituitary

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158
Q

what is released from the hypothalamus to stimulate GH release from the anterior pituitary?

A

growth hormone releasing hormone (GHRH)

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159
Q

what factors increase GHRH release and so GH release from the anterior pituitary?

A 
decreased blood glucose
decreased free fatty acids
starvation
protein deficiency 
trauma
stress
excitement
excersise 
sleep
testosterone
oestrogen
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160
Q

what is Ghrelin?

A

growth hormone release inducing

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161
Q

what is the effect of Ghrelin?

A

affects somatotrophs directly and stimulates GHRH release and so GH release

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162
Q

what is the effect of somatostatin?

A

inhibition of release of GH

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163
Q

what conditions cause release of somatostatin?

A

increased blood glucose
increased free fatty acids
obesity
aging

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164
Q

what types of peptides are somatostatin and GHRH?

A

hypothalamic peptide

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165
Q

what are the 2 ways GH is secreted?

A

pulsatile and diurnal

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166
Q

what happens during pulsatile GH secretion?

A

small amounts of GH released over time

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167
Q

what happens during diurnal GH secretion?

A

large increase in GH release overnight

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168
Q

what is GH secretion regulated by?

A

neurons in hypothalamus

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169
Q

what evidence is there for the importance of pulsatile GH secretion?

A

in hypophysectomized rats the only rats with normal weight gain (as a measurement of growth) were those who received pulsatile GH. Continuous GH did not provide the environment required and weigh increase was low

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170
Q

describe the secretion of GH

A

arcuate nucleus in hypothalamus secretes GHRH into the hypophyseal portal circulation and delivers it to the somatotrophs of the anterior pituitary which release growth hormone

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171
Q

how does feedback control of GH release work?

A

GH inhibits it’s own release when it reaches a certain level. It also stimulates somatostatin release which inhibits GHRH

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172
Q

what are the short term and long term effects of GH?

A

acute - metabolic

long term - growth promotion

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173
Q

what are the acute effects of GH on protein metabolism?

A

increased amino acid uptake and utilization
increased protein synthesis
reduced protein catabolism

174
Q

what are the acute effects of GH on lipids?

A

reduced lipogenesis (fat storage)

175
Q

what are the acute effects of GH on carbohydrates?

A

reduced glucose uptake and oxidation

increased gluconeogenesis/glycogenolysis leading to increased blood glucose

176
Q

what additional effect does GH have on protein - glucose relationship?

A

increased glucose is not made at the cost of protein. GH protects protein

177
Q

what factor mediates the effects of GH?

A

IGF-1

178
Q

where is IGF-1 released?

A

into the serum by GH

179
Q

what is IGF-1 produced by?

A

the liver and locally in tissues

180
Q

what is IGF-1 secretion dependent on?

A

GH

181
Q

what does IGF-1 mediate?

A

local growth

182
Q

how does IGF-1 cause bone growth?

A

GH binds to receptor on prechondrocytes which stimulates release of IGF-1. This leads to hypoplasia and maturation

183
Q

when does IGF-1 peak in the human?

A

at puberty and corresponds with peak in rate of heigh increase

184
Q

what are the direct effects of GH?

A

anti-insulin, diabetogenic effects

185
Q

what are the direct effects of GH on adipocytes?

A

reduced lipogenesis

reduced fat accumulation

186
Q

what are the direct effects of GH on liver and skeletal muscle?

A

increased; gluconeogenesis, glycogenolysis, blood glucose, protein synthesis

187
Q

what are the indirect effects of GH?

A

IGF-1 mediated local effects leading to growth in multiple tissues
IGF-1 mediated endocrine effects causing the liver to release IGF-1 into circulation to feedback on GH levels to hypothalamus

188
Q

what is plasma IGF-1 level a measure of?

A

GH secretion

189
Q

why is IGF-1 a better measure of GH levels?

A

IGF-1 does not fluctuate as widely throughout the day as GH does

190
Q

what are the feedback effects of IGF-1?

A

directly inhibits GHRH and stimulates somatostatin release which inhibits GH release

191
Q

what is excess GH caused by?

A

often pituitary tumors

192
Q

what is excess GH known as in children before epiphyseal plate has closed?

A

giantism

193
Q

what is excess GH known as in adults after epiphyseal plate has closed?

A

acromegaly

194
Q

what are the characteristics of acromegaly?

A 
soft tissue swelling resulting in visible enlargement of hands, feet, nose and lips with visible thickening of skin
soft tissue swelling of internal organs
generalised expansion of skull
pronounced brow protrusion
pronounced lower jaw protrusion
insulin resistance
195
Q

what is insulin resistance in acromegaly caused by?

A

excess GH

196
Q

what is deficit of GH known as in children?

A

dwarfism

197
Q

what are characteristics of dwarfism?

A

short stature but body develops in appropriate proportions

Delayed physical maturation (bones and puberty)

198
Q

what is dwarfism caused by?

A

pituitary malformation/tumor

GH-R or GHRH-R mutation

199
Q

what effect does pituitary malformation/tumor have on GH?

A

reduction in production of GH due to hypopituitarism

200
Q

what effect does GH-R or GHRH-R mutation have on GH?

A

not sensitive to GH as the receptors are damaged/do not work so cannot be activated

201
Q

what is used in GH therapy in children?

A

given bolus injections of recombinant hGH

202
Q

what is the issue with bolus injection of GH?

A

pulsatile release of GH is prefurrable and so there is investigation into compounds which could regulate GH secretion more naturally

203
Q

what causes decline in GH secretion?

A

age

204
Q

what can be achieved by giving older individuals hGH?

A

modest increase in muscle mass
modest increase in bone density
decreases in body fat

205
Q

what does hGH not do?

A

increase muscle strength, functionality or cellular metabolism and so performance.

206
Q

what complications arise in over 50% of people receiving hGH?

A

diabetes, hypertension, CV disease, arthritis, tissue edema or carpal tunnel syndrome

207
Q

what effect can inciting cellular growth when it is naturally slowing have?

A

increase cancer risk

208
Q

what are the 2 separate tissues of the adrenal gland?

A

cortex and medulla

209
Q

what hormones are produced by the cortex?

A

corticosteroids

210
Q

what hormones are produced in the medulla?

A

adrenaline and noradrenaline

211
Q

what are the 3 layers of the cortex?

A

glomerulosa
fasiculata
reticularis

212
Q

how many adrenal glands are there in the body?

A

2 on the superior aspect of the kidney

213
Q

what is produced by different zones of the cortex?

A

different hormones

214
Q

what hormones are produced in the glomerulosa?

A

mineralocorticoids

215
Q

what is an example of a mineralocorticoid?

A

aldosterone

216
Q

what hormones are produced in the fasciculata?

A

glucocorticoids

217
Q

what are examples of glucocorticoids?

A

cortisol

corticosterone

218
Q

what hormones are produced by the reticularis?

A

androgens and oestrogens

219
Q

is there enough androgen/oestrogen produced by the reticularis of the adrenal gland to replace loos of gonadal steroids?

A

no

220
Q

what are all corticosteroids generated from?

A

cholesterol

221
Q

where does the body gain cholesterol from?

A

absorbed from GI tract (from the diet) or synthesised from acetate within the cell

222
Q

what is cholesterol transported around the body with?

A

LDL

223
Q

why must cholesterol be transported around the body with LDL?

A

it is insoluble in water

224
Q

are steroids stored in cortical cells?

A

no - it is synthesised and released straight away

225
Q

what is stored within cortical cells to enable creation of hormones from cholesterol?

A

precursor (cholesterol esters)

226
Q

how does cholesterol enter the cell?

A

binds to cell surface receptor

227
Q

where is the receptor located for steroid hormones?

A

in the cytoplasm of target tissues

228
Q

what happens the the steroid hormone on biding with receptor?

A

steroid receptor complex translocates to the nucleus

229
Q

what is the effect of steroid hormone on the nucleus?

A

modulates transcription of genes leading to creation of new/altered proteins which can alter cell function

230
Q

give an example of glucocorticoids

A

cortisol/corticosterone

231
Q

where is cortisol/corticosterone secreted from?

A

zona fasiculata in adrenal cortex

232
Q

what is the ratio of cortisol/corticosterone secretion in the human?

A

7:1

233
Q

what does cortisol/corticosterone circulate with?

A

bound to plasma proteins

234
Q

what plasma protein is cortisol/corticosterone bound to in circulation?

A

transcortin

235
Q

what is the half-life of cortisol/corticosterone?

A

60-90 minutes

236
Q

what is release of cortisol/corticosterone controlled by?

A

tropic hormones of the hypothalamus/pituitary axis

circadian release

237
Q

what factors stimulate release of glucocorticoid from the adrenal cortex?

A

acute and long term stress - trauma, heat, cold, pain, fright, disease
hypothalamic circadian rhythm generator

238
Q

describe the release of glucocorticoid from the adrenal cortex

A

hypothalamus is stimulated by external factors to release CRH. This stimulates release of ACTH from corticotrophs in the anterior pituitary. ACTH then stimulates adrenal cortex fasciciulata cells to release cortisol into the circulation to reach target cells in the peripheral tissues

239
Q

what is CRH?

A

corticotrophin releasing hormone

240
Q

what is ACTH?

A

adrenocorticotrophic hormone

241
Q

how is cortisol release stopped/managed?

A

cortisol itself inhibits release of ACTH and CRH

ACTH directly inhibits the release of CRH

242
Q

what is the name of cells which release ACTH?

A

corticotrophs

243
Q

what are the main physiological effects of glucocorticoids seen in?

A

metabolism of glucose

244
Q

what are the physiological effects of glucocorticoids on metabolism?

A

stimulation of glyconeogenesis
inhibition of effects of of insulin
stimulation of catabolism of proteins to aid gluconeogenesis
shifting metabolism from glucose to fat to increase lipolysis and glucose sparing

245
Q

what is the effect of inhibition of effects of insulin due to glucocorticoids?

A

reduced tissue uptake of glucose

246
Q

what is gluconeogenesis?

A

synthesis of glucose from amino acids

247
Q

what state do the physiological effects of glucocorticoids on metabolism lead to?

A

hyperglycemic

248
Q

how have we discovered the physiological effects of glucocorticoids on muscle and the nervous system?

A

by observing effects on those with reduced/no glucocorticoids

249
Q

what effect does insufficient glucocorticoids have on the cardiac, skeletal and vascular smooth muscle?

A

muscle fatigue leading to cardiac insufficiency/failure, loss of vasomotor tone and general skeletal muscle weakness

250
Q

what effect does insufficient glucocorticoids have on the nervous system?

A

affects on mental function, lethargy, apathy and inability to concentrate

251
Q

what effect does excess glucocorticoids have on the nervous system?

A

hyperactivity, insomnia, euphoria and increased sensory activity

252
Q

what are the responses to stress produced by glucocorticoids?

A

metabolism increases to increase the availability of glucose
cardiac, skeletal and smooth muscle become primed for escape
nervous system increases alertness

253
Q

what are the physiological effects of glucocorticoids on inflammatory and immune responses?

A

anti-inflammatory and immunosuppressive effects leading to:
inhibition of secretion of cytokines
inhibition of proliferation of immune cells
inhibition of synthesis of antibodies
increased susceptibility to infection

254
Q

what can glucocorticoids be used for?

A

therapeutic effects due to their anti-inflammatory effect

255
Q

how potent is dexamethasone in comparison to cortisol?

A

30x more potent

256
Q

where are mineralocorticoids released from?

A

zona glomerulosa

257
Q

what are mineralocorticoids bound to in circulation?

A

plasma protein transcortin

258
Q

what is the half life of mineralocorticoids?

A

15-30 mins

259
Q

what is the role of mineralocorticoids?

A

regulate concentration of sodium and potassium in the extracellular fluid

260
Q

what is the main stimuli for secretion of mineralocorticoids?

A

changes in electrolyte levels and water balance

261
Q

describe the release of mineralocorticoid (aldosterone0 from the adrenal cortex

A

juxtaglomerular cells secrete renin in response to low blood pressure, Na+ and blood volume. The liver secretes angiotensinogen which is broken into angiotensin 1 (by renin) and then angiotensin 2 (by ACE - produced in the lungs and kidney). angiotensin 2 causes release of aldosterone from adrenal cortex and is delivered to the kidney tubules

262
Q

what is the effect of aldosterone on the kidney tubule?

A

activation of Na/K pumps
increased Na+ retention and K+ excretion
leading to blood volume and blood pressure increase

263
Q

what does hypercorticism lead to?

A

overproduction of cortisol

264
Q

what is the cause of primary hypercorticism?

A

andrenomas of the adrenal cortex

265
Q

what is the cause of secondary hypercorticism?

A

pituitary tumors leading to uncontrolled ACTH levels

266
Q

what is the cause of iatrogenic hypercorticism?

A

widespread use of synthetic glucocorticoids

267
Q

what are symptoms of hypercorticism?

A 
upper body obesity
rounded face
increased fat around neck
slender extremities
fragile/thin skin
weak bones
hyperglycemia
268
Q

why must there be careful withdrawal and reduction of therapeutic glucocorticoids?

A

to avoid hypocorticism as there is negative feedback on endogenous cortisol release by exogenous/synthetic cortisol

269
Q

what is hypoadrenocorticism?

A

undersecretion of glucocorticoids and/or mineralocorticoids

270
Q

what are the causes of primary hypoadrenocorticism?

A

atrophy of adrenal cortex due to autoimmune attack

271
Q

what are the causes of secondary hypoadrenocorticism?

A

pituitary malfunction (e.g. reduced ACTH release affects only cortisol, aldosterone is still produced)

272
Q

what are the causes of iatrogenic hypoadrenocorticism

A

abrupt withdrawal of steroid therapy

273
Q

in what type of hypoadrenocorticism is ACTH high due to no steroid providing negative feedback ?

A

primary

274
Q

what are the main symptoms of hypoadrenocorticism

A

muscle weakness
poor cardiovascular function
low blood pressure (lack of gluco- and mineralocorticoids)

275
Q

what is another name for adrenaline and noradrenaline?

A

cateholamines

276
Q

what are adrenaline and noradrenaline secreted from?

A

adrenomedullary cells

277
Q

what do adrenaline and noradrenaline bind to?

A

receptors on adipose, cardiovascular, muscular and pancreatic tissue and CNS

278
Q

what is the response of cells to adrenaline and noradrenaline related to?

A

adrenergic receptors

279
Q

what is the primary source of adrenaline?

A

adrenal medulla

280
Q

what is noradrenaline synthesised by?

A

chromaffin cells and noroadrenergic neurons

281
Q

how does acetylcholine stimulate secretion of cateholamines?

A

cell is depolarized, calcium influx causes granules containing adrenaline/noradrenaline to fuse with chromaffin cell membrane. They exit the cell by exocytosis

282
Q

what is the response of cells to adrenergic receptors related to?

A

the nature of adrenergic receptors

283
Q

how are adrenergic receptors regulated?

A

hormone binding properties (affinity)
receptor concentration on the cell surface
receptor signalling and activation of second messengers

284
Q

what does the nature and regulation of adrenergic receptors do?

A

regulate responsiveness of the target cell to cateholamines

285
Q

what does stress lead to?

A

activation of ANS and release of adrenal cateholamines

286
Q

what effect does activation of ANS and release of adrenal cateholamines have on the body?

A

shunting of blood to heart and respiring tissues through vasodilation/constriction
glycogenolysis leading to liberation of fuel for muscles
increased force and rate of constriction of the heart with little effect on blood flow to the CNS

287
Q

what can cause hyperfunction of the adrenal medulla?

A

pheochromocytomas (tumors in chromaffin cells) - rare and benign but secrete large amounts of cateholamines

288
Q

what are the signs of pheochromocytomas?

A

elevated blood pressure and increased heart rate

289
Q

what can too much blood glucose cause?

A 
dehydration
microvascular damage (e.g. blindness)
290
Q

what can too little blood glucose cause?

A

CNS issues as it is glucose dependent

291
Q

what is the normal range of blood glucose?

A

5.5 is normal but can go up to 8 postprandial

292
Q

what are the 2 distinct phases of fuel metabolism?

A

anabolic phase

catabolic phase

293
Q

what does the anabolic phase begin with?

A

food ingestion

294
Q

how long does the anabolic phase last?

A

a few hours

295
Q

what happens during the anabolic phase?

A

caloric intake exceeds caloric demand
glucose levels in plasma increase
energy storage occurs

296
Q

when does the catabolic phase begin?

A

4-6 hours after food intake

297
Q

what happens during the catabolic phase?

A

caloric demand exceeds caloric intake
glucose levels in plasma decrease
endogenous fuels mobilized from liver, muscle and adipose tissues

298
Q

what happens during glycogenesis?

A

glucose is converted to glycogen in order to be stored

299
Q

what happens during glycogenolysis?

A

glycogen is broken down into glucose to be released

300
Q

what happens during glycolysis?

A

glucose is converted to pyruvate

301
Q

what happens during glyconeogenesis?

A

pyruvate is broken back down into glucose to allow glucose release

302
Q

what hormones are released from the endocrine pancreas?

A

glucagon

insulin

303
Q

what is the role of glucagon?

A

mobilizes fuel in the catabolic phase

304
Q

what is the role of insulin?

A

stores fuel in the anabolic phase

305
Q

what cells release glucagon in response to low blood glucose?

A

alpha cells of pancreas

306
Q

what cells release insulin in response to high blood glucose?

A

beta cells of pancreas

307
Q

what do glucagon and insulin both work to achieve?

A

normal blood glucose levels

308
Q

what is the endocrine pancreas formed of?

A

Islets of Langerhans which release glucagon and insulin

309
Q

what is the role of the exocrine pancreas?

A

produces digestive enzymes and releases them into the gut

310
Q

what type of hormone is insulin?

A

peptide

311
Q

how many amino acids is insulin formed from?

A

51

312
Q

what is the insulin receptor?

A

a receptor tyrosine kinase

313
Q

what is insulin released from?

A

secretory granules within beta cells

314
Q

what is insulin released in response to?

A

increased plasma glucose

315
Q

describe the process of glucose stimulated insulin secretion from beta cells

A

glucose enters the cell and glycolysis takes place leading to an increase in ATP concentration within the cell. ATP acts on K+ channels and blocks K+ exit from the cell. The cell is then depolarized and Ca2+ channels are opened. The influx of calcium increases the concentration within the cell and causes granules containing insulin tot fuse with the cell membrane and insulin exits by exocytosis

316
Q

what is the main factor which stimulates insulin secretion?

A

glucose

317
Q

what are the 3 other stimulators of insulin secretion/

A

amino acids
GI hormones
parasympathetic nervous system (activated when eating begins)

318
Q

what is the inhibitor of insulin secretion?

A

sympathetic nervous system

319
Q

what are the 3 main insulin target tissues?

A

liver
muscle
adipose tissue

320
Q

what does insulin bind to?

A

insulin receptor on target issues

321
Q

how does insulin affect processes within tissues?

A

stimulation or inhibition of key enzymes

322
Q

how does insulin affect the liver?

A

increases glucose storage
increased lipogenesis
increased proteogenesis

323
Q

how does insulin increase glucose storage within the liver?

A

increases glycogenesis
decreases glyconeogenesis
increases glycolysis

324
Q

what is lipogenesis?

A

movement of fatty acids into lipid storage

325
Q

what is proteogenesis?

A

increase in protein formation

326
Q

how does glucose enter the hepatocyte?

A

through GLUT2 transporters

327
Q

what are the actions of insulin on muscle?

A

increase in glucose storage
increased amino acid uptake
increased glycogenesis

328
Q

how does insulin increase glucose storage within muscles?

A

increased glucose uptake
increased glycolysis
increased glycogenesis

329
Q

how does insulin increase glucose uptake in the muscles?

A

binds to a receptor causing GLUT4 transporter to fuse with membrane and so increase glucose uptake

330
Q

what are the actions of insulin on adipose tissue?

A

increased glucose removal from blood
increased synthesis of fatty acids
increased lipogenesis

331
Q

how does insulin increase glucose storage within adipose tissue?

A

increased glucose uptake

increased glycolysis

332
Q

what do all actions of insulin result in in blood?

A

reduced blood concentration of glucose, amino acids and fatty acids

333
Q

where is glucagon released from?

A

alpha cells in the pancreatic islets of Langerhans

334
Q

what type of hormone is glucagon?

A

peptide

335
Q

how many amino acids is glucagon formed from?

A

31

336
Q

what effect does glucose have on glucagon?

A

inhibits release

337
Q

what do the actions of glucose antagonise?

A

those of insulin

338
Q

what is glucagon primarily regulated by?

A

plasma glucose concentration

339
Q

what is glucagon’s principle target tissue?

A

the liver

340
Q

what is the main effect of glucagon on the liver?

A

increased glucose output

increased lipolysis

341
Q

how does glucagon increase glucose output from the liver?

A

increased gluconeogenesis

increased glucogenolysis

342
Q

what does increased lipolysis due to the action of glucose on the liver lead to?

A

increased fatty acids

increased ketone bodies

343
Q

what can ketone bodies be used for?

A

fuel by muscle and the CNS when glucose is too low

344
Q

what are the other regulators of blood glucose?

A

growth hormone - inhibition of insulin induced glucose utilization
glucocorticoids - protect form hypoglycaemia during times of stress
adrenaline - maintain glucose supply to brain

345
Q

what causes type-1 diabetes?

A

auto-immune disease which destroys insulin producing beta cells in pancreatic islets

346
Q

what percentage of diagnosed diabetic cases are type 1?

A

5-10%

347
Q

what causes type-2 diabetes?

A

reduced beta cell function and insulin resistance in target tissues

348
Q

what percentage of diagnosed diabetic cases are type 2?

A

90-95%

349
Q

what are the symptoms of diabetes?

A 
dehydration
thirst
excessive urination
tiredness
weightloss/hunger
ketoacidosis (type-1)
350
Q

how would a type 2 diabetic perform on a glucose tolerance test?

A

high fasting glucose
greater rise in glucose once glucose is administered
increased glucose levels persist

351
Q

what does the reduced ability of beta cells to produce insulin cause?

A

increased blood glucose leading to hyperglycaemia due to reduced glucose uptake and utilisation due to lack of insulin

352
Q

what is the effect of glucagon action remaining intact in type 1 diabetics?

A

cells end up in catabolic state leading to breakdown of glycogen, fat and proteins in order to provide glucose.
there is glucose and ketone production in massive excess of what will be used

353
Q

what is the effect of glucose and ketone bodies in the blood due to type 1 diabetes?

A

osmolality of blood increases and pH becomes more acidic

354
Q

what do ketoacidosis and osmotic stress lead to?

A

dehydration - glucose spills into urine and takes water with it (glucosuria)

355
Q

what is the treatment of type 1 diabetes?

A

recombinant insulin (careful monitoring of blood glucose)

356
Q

what are target tissues resistant to in type 2 diabetes?

A

insulin - is increased to compensate

357
Q

what has happened to beta cell function in type 2 diabetes?

A

impaired so there is decreased insulin production

358
Q

what body codition is insulin resistance associated with?

A

obesity

359
Q

how many type 2 diabetic patients are obese?

A

55%

360
Q

what else can lead to type 2 diabetes?

A

genetic predisposition

361
Q

what is the treatment of type 2 diabetes?

A

lifestyle changes: diet and exercise

bariatric surgery and caloric restriction - restores insulin sensitivity

362
Q

what are the 2 main antidiabetic drugs?

A

metformin

sulfonylureas

363
Q

what is the action of metformin?

A

reduces live glyconeogenesis and glycogenolysis

increases insulin sensitivity

364
Q

what is the action of sulfonylureas?

A

increase insulin release by inhibiting K+ channels in beta cells

365
Q

what is calcium used for?

A

essential for normal physiological function

366
Q

what is calcium the essential mineral component of?

A

skeleton and teeth

367
Q

what are 6 other roles of calcium in the body?

A 
muscular contractions
blood coagulation
enzyme activity
neuronal activity
hormone secretion
cell adhesion
368
Q

where is most calcium located in the body?

A

bone - 99%

369
Q

in what form is calcium found in the blood?

A

inorganic - mineralized matrix of bone as hydroxyapatite

370
Q

where is intracellular calcium found?

A

endoplasmic reticulum

371
Q

how much calcium is found in the extracellular fluid?

A

0.1%

372
Q

how much calcium is free in the cytosol?

A

a very tiny amount! 0.000002%

373
Q

what 3 parts is the calcium in the cytoplasm?

A

ionised
complexed calcium salts
protein bound

374
Q

which is biologically active calcium?

A

ionised Ca

375
Q

what are the main functions of calcium?

A

second messenger and regulatory ion

376
Q

what is calcium influx into the cell controlled by?

A

Ca2+ channels

377
Q

what does influx of Ca2+ into the cell permit?

A

Ca2+ to function as a signaling ion to activate intracellular processes

378
Q

what is the concentration gradient between extracellular and intracellular?

A

10,000 fold concentration gradient between ECF and ICF which provides driving force for Ca2+ influx

379
Q

what is cellular function regulated by?

A

interaction with intracellular calcium binding proteins and calcium sensitive protein kinases

380
Q

what does interaction with intracellular calcium binding proteins and calcium sensitive protein kinases cause?

A

biological responses such as neurotransmitter release, contraction or secretion

381
Q

what is calcium balance regulated by?

A

parathyroid hormone
calcitionin
activated vitamin D (1,25 DHCC)

382
Q

what type of hormone is parathyroid hormone?

A

peptide

383
Q

what causes release of parathyroid hormone?

A

responds to falling levels of circulating calcium

384
Q

where is parathyroid hormone released from?

A

chief cells of the parathyroid gland

385
Q

where is parathyroid hormone stored within chief cells?

A

secretory granules

386
Q

what controls release of parathyroid hormone?

A

concentration of circulating calcium

387
Q

what effect does high calcium have on parathyroid hormone release?

A

inhibits secretion

388
Q

what effect does low calcium have on parathyroid hormone release?

A

allows secretions

389
Q

describe the mechanism of inhibition of secretion of parathyroid hormone

A

calcium binds to receptor (all become filled) and activation leads to the inhibition of PTH secretion

390
Q

describe the mechanism of secretion of parathyroid hormone

A

calcium does not bind to receptors so no inhibition and PTH is secreted

391
Q

what does PTH cause in bone?

A

Ca2+ salts in bone ECF
breakdown of hepoxyapatite crystals
leading to efflux of calcium from bone

392
Q

what cells immediately break down Ca2+ salts in bone?

A

osteoblasts

393
Q

what cells breakdown hepoxyapatite crystals in bone?

A

osteoclasts (long term)

394
Q

what effect does PTH have on kidneys?

A

increase kidney tubular reabsorption of Ca2+
promote formation of active vitamin D
decreased loss of calcium in urine

395
Q

what effect does PTH have on the gut?

A

promote formation of active vitamin D

enhanced absorption of calcium from intestine

396
Q

what is the overall effect of PTH on blood calcium levels?

A

increase

397
Q

What is fast exchange of Ca2+ in bone?

A

release from labile pool

398
Q

what is slow exchange of Ca2+ in bone?

A

bone dissolution through osteoclast activity

399
Q

describe the slow exchange effect of parathyroid hormone on bone

A

PTH causes osteoblast to release RANK ligand which acts on oseteoclasts causing them to mature. This leads to bone reabsorption

400
Q

what type of hormone is activated vitamin D?

A

steroid

401
Q

where is activated vitamin D produced from?

A

cholesterol or diet

402
Q

what is activated vitamin D produced in response to?

A

falling levels of blood calcium via PTH

403
Q

how is cholecalciferol (vitamin D3) produced?

A

UV light on the skin interacts with cholesterol

404
Q

where can cholecalciferol (vitamin D3) be gained?

A

cholesterol interacting with UV

through the diet

405
Q

what are the biological actions of active vitamin D?

A

longer term regulation of Ca2+ homeostasis
Increase absorption of Ca2+ from intestine
prevents calcium stripping from bone so bones are protected

406
Q

how does cholecalciferol (vitamin D3) become active vitamin D (1,25 DHCC)?

A

enters the liver where it becomes 25-hydroxycholecalciferol. From the liver this moves to the kidneys where, under the regulation of PTH, renal 1 alpha-hydroxylase becomes active vitamin D (1,25 DHCC)

407
Q

what hormone is conversion of 25-hydroxycholecalciferol to active vitamin D (1,25 DHCC) regulated by?

A

PTH

408
Q

once active vitamin D (1,25 DHCC) enters the cell what effects does it have?

A

increases protein synthesis of Ca channels, Calbindin, Ca pumps and exchangers (proteins involved in calcium absorption/regulation)

409
Q

what sort of hormone is calcitonin?

A

peptide

410
Q

what does secretion of calcitonin increase in response to?

A

elevation of blood Ca2+

411
Q

what is calcitonin secreted by?

A

endocrine cells in the thyroid gland known as C-Cells

412
Q

what are the main roles of calcitonin?

A

reduce blood Ca2+

prevent hypercalcaemia

413
Q

what are the primary target tissues of calcitonin?

A

bone and kidney

414
Q

what effect does calcitonin have in the bone?

A

inhibits bone resorption (reduces entry of Ca2+ into plasma from skeleton) by shrinking osteoblasts

415
Q

what effect does calcitonin have in the kidneys?

A

reduces Ca2+ absorption so more is lost in urine

416
Q

what is the major factor concerned with minute to minute regulation of blood Ca2+ levels?

A

PTH - protects from hypocalcaemia

417
Q

what is the emergency hormone used to prevent post-prandial hypercalcaemia and excessive loss of Ca2+ from skeleton during pregnancy?

A

calcitonin

418
Q

what is vitamin D deficiency known as in adults?

A

osteomalacia

419
Q

what is vitamin D deficiency known as in children?

A

rickets

420
Q

what causes vitamin D deficiency?

A

diet deficient in vitamin D and lack of sunlight

renal 1alpha-hydroxylase deficiency (genetic)

421
Q

what does reduced active vitamin D lead to?

A

reduced calcium uptake in gut
increased PTH
increased calcium resorbed from bone as little/none being absorbed from gut
cartilage improperly mineralised. Weak, malformed bones

422
Q

what is hyperparathyroidism?

A

excessive PTH secretion by parathyroid glands

423
Q

what happens during primary hyperparathyroidism?

A

parathyroid cells secrete unregulated, excessive amounts of PTH (e.g. adenomas of chief cells)

424
Q

what effect does increased PTH due to hyperparathyroidism have?

A

calcium resorption from bone increases
calcium uptake in kidney increases
decrease in bone density leading to multiple fractures

425
Q

what causes secondary hyperparathyroidism?

A

renal: chronic renal failure leading to increased (excessive) PTH secretion

426
Q

how does a reduction in kidney function/hyperparathyroidism cause hypocalcaemia?

A

active vitamin D production is reduced and Ca2+ retention in kidney is reduced. Calcium absorption in the gut is reduced leading to hypocalcaemia and increased PTH release

427
Q

what does secondary hyperparathyroidism cause?

A

bone deformation and fractures due to resorption of bone

428
Q

what causes hypoparathyroidism?

A

inadequate PTH secretion (can be caused by inadvertent removal of parathyroid gland during thyroid surgery)

429
Q

what does hypoparathyroidism cause?

A

increased neuromuscular excitability (due to decreased threshold of excitation), paresthesia and tetany

430
Q

how does reduced/no PTH lead to hypocalcaemia?

A

reduced: active vitamin D production, bone reabsorption, Ca retention in kidney, Ca absorption in gut leading to hypocalcaemia

X Physiology 1B (5 decks)

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