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HOM > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

what is a hormone?

A

any substance formed in very small amounts in 1 specialised organ or group of cells, carried to another organ or group of cells upon which it has a specific physiological effect

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2
Q

what are the main hormone producing glands in the body?

A

hypothalamus, pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, ovaries, testes

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3
Q

what are the main 3 ways hormones act on the body?

A

enable and promote development of physical, sexual and mental characteristics; keep certain physiological parameters constant; enable and promote adjustment of physiological adaptations

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4
Q

what are the 4 main structural types of hormone?

A

peptide and protein hormones, steroid hormone, amine hormones, arachidonic acid derivatives

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5
Q

what are steroid hormones?

A

lipid hormones derived from cholesterol

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6
Q

how are steroid hormones mainly transported in the blood?

A

bound to plasma proteins as aren’t water soluble

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7
Q

what must happen before bound steroid hormones can interact with the target cell?

A

must be released

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8
Q

what are amine hormones derived from?

A

tyrosine or tryptophan

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9
Q

what sort of hormones are thyroid hormones?

A

amine hormones

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10
Q

what sort of hormones are catecholamines?

A

amine hormones

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11
Q

what sort of hormone is thyroxine?

A

thyroid hormone which is an amine hormone

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12
Q

what sort of hormone is adrenaline?

A

catecholamine which is an amine hormone

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13
Q

what is an example of a hormone that can act as both a neurotransmitter and hormone?

A

dopamine

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14
Q

what are arachidonic acid derivatives synthesised from?

A

linoleic acid

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15
Q

what do arachidonic acid derivative hormones play a role in?

A

mediation of inflammatory responses

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16
Q

how do some non-steroidal anti-inflammatory drugs (NSAIDs) interact with arachidonic acid derivatives?

A

inhibit their mediation of inflammatory responses

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17
Q

what do peptide hormones contain that directs the protein to the secretory pathway in the cell?

A

an N terminal sequence

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18
Q

what does signal recognition complex binding of peptide hormones cause?

A

translational arrest

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19
Q

what happens when peptide hormones bind to the signal recognition complex?

A

translational arrest, signal recognition complex binds to docking protein in ER, signal peptide sequence cleaved from hormone in ER, re-initiation of translation, sometimes additional cleavages required to generate mature hormone from prohormone

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20
Q

difference between prohormone and preprohormone?

A

preprohormones have multiple cleavage sites

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21
Q

what group do some peptide hormones require the addition of?

A

an amide group at the carboxy terminus

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22
Q

where is kisspeptin produced?

A

arcuate and anteroventral periventricular regions of the hypothalamus

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23
Q

what does kisspeptin do?

A

stimulates secretion of gonadotrophin releasing hormone (GnRH)

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24
Q

what does gonadotrophin releasing hormone do?

A

inhibits release of gonadotropic hormones from pituitary

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25
Q

where is gonadotrophin inhibitory hormone produced?

A

paraventricular and dorsomedial regions of the hypothalamus

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26
Q

what sort of hormone are kisspeptin and GnIH?

A

peptide hormones

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27
Q

what is the general mechanism of action of peptide/protein hormones?

A

bind to cell surface receptors and activate intracellular signalling mechanisms that result in alteration of protein and enzyme activities

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28
Q

what is the general mechanism of action of steroid hormones?

A

bind to intracellular receptors and alter gene transcription

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29
Q

how do hormones signal via tyrosine kinase activation?

A

bind to receptor tyrosine kinases -> dimerisation and auto-activation of tyrosine kinase activity -> protein phosphorylation and biological response

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30
Q

how do hormones signal via the G protein/adenylyl cyclase pathway?

A

hormones bind to specific cell surface receptors and activate G proteins to stimulate (Gs) or inhibit (Gi) adenylyl cyclase- adenylyl cyclase increases intracellular cAMP levels, activates PKA to alter protein activities by phosphorylation

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31
Q

how do hormones signal using the DAG/IP3 pathway?

A

hormones bind to cell-surface receptors and activate G-proteins (Gq) which stimulate phospholipase C to convert PIP2 to IP3 and DAG. IP3 stimulates Ca2+ release from internal stores, DAG activates PKC. Calmodulin activated protein kinase activated, increases protein phosphorylation. Enzymatic activities altered

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32
Q

how do hormones signal via cytoplasmic/nuclear receptors?

A

nuclear receptors have common domain structure consisting of an activation domain (AF1), Zn finger DNA binding domain, and a ligand binding/dimerisation domain. Lipid soluble hormones (steroid or thyroid) cross plasma membrane, bind to nuclear receptors in cytoplasm- allows receptor to dissociate from heat shock proteins and enter nucleus as hormone-receptor complex which brings about changes in gene transcription by binding to a specific hormone response element

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33
Q

how is hypothalamus linked to anterior pituitary gland?

A

prominent blood vessel portal system, no direct neural connection

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34
Q

how is the hypothalamus linked to the posterior pituitary gland?

A

nerve fibres from paraventricular and supraoptic nuclei in hypothalamus pass directly to posterior pituitary where they secrete the hormones they contain into the bloodstream

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35
Q

what neurons does the paraventricular nucleus contain?

A

oxytocin and vasopressin neurons that project to neurohypophysis, neurons that regulate ACTH and TSH secretion, gastric reflexes, maternal behaviour, blood pressure, feeding, immune responses, temperature

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36
Q

what hypothalamic hormones control anterior pituitary secretions?

A

CRH, TRH, GnRH, GHRH, SMS, dopamine

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37
Q

what is CRH?

A

corticotrophin releasing hormone

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38
Q

structure of CRH?

A

41 amino acid peptide hormone

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39
Q

function of CRH?

A

stimulates release of ACTH

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40
Q

what is TRH?

A

thyrotropin releasing hormone

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41
Q

structure of TRH?

A

3 aa peptide hormone

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42
Q

function of TRH?

A

stimulates release of TSH and prolactin

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43
Q

structure of GnRH?

A

10 aa peptide hormone

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44
Q

function of GnRH?

A

stimulates release of LH and FSH

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45
Q

what is GHRH?

A

growth hormone releasing hormone

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46
Q

structure of GHRH?

A

44 aa peptide

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47
Q

function of GHRH?

A

stimulates release of GH

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48
Q

what is SMS?

A

somatostatin (growth hormone inhibiting hormone)

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49
Q

structure of SMS?

A

14 aa peptide

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50
Q

function of SMS?

A

inhibits release of GH, gastrin VIP, glucagon, insulin, TSH, prolactin

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51
Q

structure of dopamine?

A

monoamine

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52
Q

function of dopamine?

A

inhibits release of PRL

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53
Q

what is the hypophysis?

A

the pituitary gland

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54
Q

what is the neurohypophysis?

A

the posterior pituitary

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55
Q

what is the adenohypophysis?

A

the anterior pituitary

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56
Q

what is the posterior pituitary?

A

down-growth of brain

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57
Q

what nerves does the posterior pituitary contain?

A

nerves from the paraventricular and supraoptic regions of the hypothalamus

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58
Q

where are the cell bodies of the paraventricular and supraoptic nerves, and where are the nerve endings?

A

cell bodies in hypothalamus, nerve endings in posterior pituitary

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59
Q

where are the hormones stored in the posterior pituitary made?

A

cell bodies of nerves which are in the hypothalamus

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60
Q

what hormones are released by the posterior pituitary?

A

ADH (vasopressin) and oxytosin

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61
Q

which pituitary is part of the brain, posterior or anterior?

A

posterior

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62
Q

how is the anterior pituitary connected to the brain?

A

hypophyseal portal vessels from the hypothalamus, no nervous connection

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63
Q

how are hormones from the hypothalamus delivered to the anterior pituitary?

A

secreted into the primary capillary plexus, delivered from there in hypophyseal portal vessels to anterior pituitary

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64
Q

what are the 6 main hormones secreted by the anterior pituitary?

A

ACTH, TSH, GH, prolactin, FSH, LH

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65
Q

what pattern of hormone release does the anterior pituitary use?

A

pulsatile

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66
Q

what does ACTH stand for?

A

adrenocorticotropic hormone

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67
Q

structure of ACTH?

A

39 aa hormone

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68
Q

what does TSH stand for?

A

thyroid stimulating hormone

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69
Q

structure of TSH?

A

glycoprotein with 2 subunits

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70
Q

target organ of ACTH?

A

adrenal gland

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71
Q

target organ of TSH?

A

thyroid gland

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72
Q

what is GH?

A

growth hormone

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73
Q

structure of GH?

A

191 amino acids

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74
Q

target organ of GH?

A

various

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75
Q

structure of prolactin?

A

199 amino acids

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76
Q

target organ of prolactin?

A

breast and other tissues

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77
Q

structure of FSH?

A

glycoprotein with 2 subunits

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78
Q

target organ of FSH and LH?

A

gonads

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79
Q

structure of LH?

A

glycoprotein with 2 subunits

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80
Q

what do lesions in the hypothalamus produce?

A

atrophy of some endocrine glands- similar to observed effect of removal of anterior pituitary

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81
Q

what does electrical stimulation of hypothalamus lead to in the adenohypophysis?

A

secretion of anterior pituitary hormones

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82
Q

what is the result of transection of the pituitary stalk?

A

atrophy of some endocrine glands

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83
Q

what happens when anterior pituitary transplanted to another site with and without a blood supply connection with hypothalamus established?

A

without doesn’t restore endocrine gland function, with will maintain endocrine gland function

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84
Q

what is the effect of adding purified hypothalamic releasing hormones to pituitary explants in cultures?

A

secretion of anterior pituitary hormones

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85
Q

how long is the approximate cycle of circadian rhythms?

A

24 hours

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86
Q

how long is the periodicity of pulsatile rhythms?

A

less than 24 hours (usually every 30 mins-2 hours)

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87
Q

what causes pulsatile rhythms of endocrine secretions?

A

pulsatile secretion of hypothalamic releasing hormones

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88
Q

what do pulsatile rhythms ensure?

A

no down-regulation of pituitary receptors

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89
Q

what is the eventual effect of continuous hypothalamic hormone secretion?

A

decreased hormone production from the anterior pituitary

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90
Q

what additional changes in release patterns do sex hormones show?

A

changes according to breeding season or oestrous cycle

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91
Q

what happens in negative feedback?

A

hormone produces response in the target cells that feeds back on the endocrine tissue to decrease hormone production

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92
Q

what happens in positive feedback? (hormones)

A

hormone produces response in target cells that feeds back on the endocrine tissue to increase hormone production. hormone production continues until hormone is depleted or feedback from target tissue is removed

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93
Q

how are hormones usually measured?

A

by immunoassays

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94
Q

what type of enzyme reaction is needed for an ELISA?

A

one that catalyses a colour change

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95
Q

what type of isotope is needed for an RIRIA (radio-immunoassay RIA)?

A

a radioisotope

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96
Q

what happens in a general ELISA?

A

sample with unknown amount of hormone immobilised in wells of microtiter plate (often via an antibody), detection antibody covalently linked to an enzyme added forming a complex with the hormone, between each step plate washed to remove antibodies that aren’t specifically bound. the antibody/hormone complex is detected by adding enzyme and substrate that catalyses reaction with colour change, higher hormone concentration in original sample= greater visual signal

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97
Q

what happens in a competitive ELISA?

A

the sample containing the hormone to be measured is mixed with fixed amount of the same hormone labelled with the enzyme. greater amount of hormone in sample= greater competition with labelled hormone for binding to the well. the higher the hormone conc. in original sample = the lower the visual signal

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98
Q

what characteristics are shared between both ELISA assays?

A

standard curve generated using pure hormone at known concentrations, comparison with unknown samples must be in linear range of standard curve

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99
Q

where are the adrenal glands located?

A

above each kidney

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100
Q

what does the outer cortex of the adrenal gland secrete?

A

glucocorticoids, mineralocorticoids and small amount of sex steroids

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101
Q

what does the zona glomerulosa secrete?

A

aldosterone (principal mineralocorticoid)

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102
Q

what is aldosterone responsible for?

A

homeostasis of blood pressure, sodium and potassium levels

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103
Q

what does the zona fasciculata secrete?

A

cortisol (principal glucocorticoid)

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104
Q

what is cortisol responsible for?

A

glucose homeostasis and stress responses

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105
Q

what does the zona reticularis secrete?

A

weak androgens (DHEA)

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106
Q

what does the inner medulla secrete?

A

adrenaline and noradrenaline - catecholamines

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107
Q

what are adrenal steroid hormones derivatives of?

A

cholesterol

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108
Q

what neurones release CRH, where are they found?

A

hypothalamic neurones, in paraventricular nucleus of hypothalamus

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109
Q

what does ACTH regulate and what doesn’t it regulate in the adrenal glands?

A

stimulates glucocorticoid and sex hormone production from adrenal cortex, doesn’t regulate mineralocorticoid or catecholamine secretion

110
Q

what is ACTH derived from?

A

proteolytic processing of POMC

111
Q

what regulates mineralocorticoid secretion?

A

renin-angiotensin system and plasma levels of Na+ and K+

112
Q

what are mineralocorticoids responsible for?

A

conservation of body sodium by stimulating resorption of sodium in the kidney in exchange for potassium

113
Q

what are glucocorticoids responsible for?

A

changes in carbohydrate, fat and protein metabolism. cortisol has weak binding to mineralocorticoid receptor- at high levels can act like aldosterone

114
Q

when are cortisol levels highest? why?

A

first thing in the morning, decline during the day. probably reflects the body’s response to low blood glucose after overnight fasting

115
Q

what are most of the actions of cortisol aimed at?

A

dealing with stressful events such as trauma

116
Q

effects of cortisol relating to starvation?

A

promotes FFA release from adipose tissue, promotes breakdown of muscle and plasma proteins to provide amino acids, promotes gluconeogenesis, increases appetite

117
Q

effects of cortisol relating to inflammation?

A

inhibits synthesis of substances that cause inflammation

118
Q

effects of cortisol relating to the immune system?

A

inhibits secretion of interleukins, increases apoptosis of lymphocytes, decreased antibody production

119
Q

what do interleukins do?

A

released by macrophages, attract lymphocytes to point of infection. promote secretion of CRH, ACTH and cortisol

120
Q

effects of cortisol relating to the fetus?

A

causes surfactant production, deposition of glycogen in liver, causes intestinal tract to secrete and absorb, acid secretion by stomach, increased filtration rate in kidney, causes T4 -> T3 conversion, in some species causes placenta to change steroid secretions into mother initiating birth

121
Q

effects of cortisol relating to the CNS?

A

can cross blood-brain barrier, can alter mood (cause euphoria), causes jet-lag

122
Q

effects of cortisol relating to the cardiovascular system?

A

allows vasoconstrictive actions of catecholamines, adrenaline causes smooth muscle contraction so blood vessel constriction, important in maintaining blood pressure, stimulates erythropoietin synthesis to increase RBC production

123
Q

% of adrenaline vs noradrenaline secreted by the adrenal medulla?

A

80% adrenaline, 20% noradrenaline

124
Q

actions of catecholamines?

A

stimulate heart rate, increase heart contractility, CO and systolic pressure, reduce diastolic pressure, piloerection, dilation of pupils, reduced gut motility, increased breakdown of glycogen to glucose in liver, increase glycogen breakdown in liver, reduce gut motility

125
Q

what causes release of catecholamines from the adrenal medulla?

A

sympathetic nervous stimulation of chromaffin cells

126
Q

what causes hyperadrenocorticism (Cushing’s syndrome)?

A

excessive glucocorticoids

127
Q

what causes Cushing’s syndrome?

A

adrenal gland tumour, increased ACTH, increased CRH, exogenous corticosteroid treatment

128
Q

typical symptoms of Cushing’s syndrome?

A

weight gain, rosy cheeks, skin pigmentation, skeletal muscle wasting, purple abdominal striations, capillary fragility, suppression of immune system, glucose intolerance, hyperglycaemia, insulin resistance

129
Q

how many cases of canine Cushing’s are caused by pituitary tumours?

A

80%

130
Q

signs of canine Cushing’s?

A

pot bellied abdomen- enlarged liver and abdominal muscle weakness, polyuria/polydipsia, muscle wasting over head shoulders, thighs and pelvis, polyphagia

131
Q

symptoms of equine Cushing’s syndrome?

A

excessive hairy coat, polyuria/polydipsia, muscle wasting, sweating

132
Q

what is Addison’s disease?

A

primary hypoadrenocorticism

133
Q

what does primary hypoadrenocorticism result in?

A

deficiency of both glucocorticoids and mineralocorticoids

134
Q

what causes Addison’s disease (primary hypoadrenocorticism)?

A

destruction of adrenals, autoimmune reaction/inflammatory disease, haemorrhage

135
Q

what does secondary hypoadrenocorticism result in?

A

deficiency of glucocorticoids

136
Q

what causes secondary hypoadrenocorticism?

A

lack of ACTH

137
Q

typical symptoms in absence of aldosterone and cortisol?

A

tiredness, weakness, vomiting, skin pigmentation, eventually hypotension and death

138
Q

symptoms of ACTH production impairment (so cortisol and sex hormone production impairment)?

A

loss of body hair in females, males get sex hormones from their testes

139
Q

what causes congenital adrenal hyperplasia?

A

lack of enzyme involved in cortisol production, increases in CRH-ACTH levels to compensate

140
Q

what does congenital adrenal hyperplasia cause?

A

excessive production of sex steroids, masculinisation of female fetus in utero, precocious puberty caused by excess adrenal androgen, decreased production of mineralocorticoids

141
Q

where is the thyroid gland located?

A

attached to the trachea just below the larynx, has rich blood and autonomic nerve supply

142
Q

what nerve supply does the thyroid gland receive?

A

sympathetic and parasympathetic (vagus) nerves

143
Q

what 3 hormones does the thyroid gland secrete?

A

thyroxine (T4), tri-iodothyronine (T3) and calcitonin

144
Q

what is the histological structure of the thyroid gland?

A

contain 1000s of follicles- each consists of central colloid filled cavity surrounded by epithelial cells, nerves control blood supply, c cells scattered between follicles

145
Q

where are T3 and T4 in the thyroid gland?

A

the 2 iodine containing hormones (T3 and T4) are attached to thyroglobulin and stored in the colloid material.

146
Q

what cells secrete calcitonin?

A

the C cells (parafollicular cells) secrete calcitonin which is involved in regulation of plasma Ca2+ levels.

147
Q

what is the most potent thyroid hormone?

A

tri-iodothyronine (T3)

148
Q

what enzyme in target tissues and the pituitary converts T4 to T3?

A

deiodinase enzyme

149
Q

how are the iodine containing thyroid hormones synthesised from tyrosine?

A

iodine is attached to tyrosine to produce mono-iodotyrosine (MIT) and di-iodotyrosine (DIT). MIT and DIT are coupled to produce T3, DIT and DIT are coupled to produce T4

150
Q

how can thyroxine be converted into T3 and rT3?

A

removal of an iodine atom

151
Q

what is rT3?

A

inactive tri-iodothyronine

152
Q

what are the principal steps in synthesis of thyroid hormones?

A

uptake of iodide from blood by sodium-iodide symporter (SLC5A5) and addition of iodine to exposed tyrosine residues of thyroglobulin protein in the follicles. thyroglobulin internalised into follicular cells by endocytosis and broken down in lysosomes to release T3 and T4 into the circulation

153
Q

what does TSH stimulate in the thyroid gland?

A

iodide uptake and oxidation to iodine, endocytosis of thyroglobulin and secretion of T3 and T4 into the blood

154
Q

how do thyroid hormones enter cells?

A

lipophilic so passive entry, also transport mediated entry

155
Q

cellular effects of thyroid hormones?

A

increase BMR so increase heat production, heat generation by stimulating Na+/K+ ATPase pump, increased cellular respiration, increase number of mitochondria per cell

156
Q

what is the overall effect of thyroid hormones?

A

increases the substrates for oxidative respiration in the cell

157
Q

what do thyroid hormones effect?

A

whole body growth, basal metabolic rate and CO

158
Q

effect of calcitonin?

A

reduces plasma CA2+ levels, inhibits osteoclast activity in bone, inhibits Ca2+ resorption in kidney.

159
Q

effect of parathyroid hormone on calcium regulation?

A

increases plasma Ca2+ levels

160
Q

effects of thyroid hormones on metabolism?

A

increase glucose uptake by muscle and adipose, and by GI tract, increase release of FFAs from adipose, increase gluconeogenesis, increase substrates for oxidative respiration, increase CO, T3 enhances effects of catecholamines, GH secretion, CNS development

161
Q

what does T3 do in peripheral thermogenesis?

A

acts on muscle to stimulate Na+/K+-ATPase, glycerol phosphate dehydrogenase (GPDH), uncoupling protein 2 and SERCA to generate heat

162
Q

what does T3 do in general thermogenesis?

A

acts at the ventromedial hypothalamus (VMH) to inhibit AMP kinase and increase sympathetic nerve action on brown adipose to generate heat via uncoupling protein 1 (UCP1)

163
Q

what causes hypothyroidism?

A

iodine deficiency, disease of thyroid, lack of TSH, congenital absence of thyroid

164
Q

symptoms of hypothyroidism?

A

weight gain, possible goitre, cold extremities, lethargy, muscle weakness, reduced CO and slow pulse

165
Q

long term effects of hypothyroidism?

A

short stature, lack of thyroid hormone during late fetal life and early post-natal development results in severe mental retardation

166
Q

treatment of hypothyroidism?

A

oral administration of thyroxine

167
Q

what causes hyperthyroidism?

A

overactivity of thyroid gland (hyperplasia and thyroid adenomas), autoimmune response (Graves’ Disease, causes 50%)

168
Q

symptoms of hyperthyroidism?

A

weight loss, sweating, tremor, possible goitres, agitation and nervousness, fast heart rate, atrial fibrillation, muscle weakness, rapid growth rate and bone maturation in children, staring eyes, infertility and lack of periods

169
Q

symptoms of feline hyperthyroidism?

A

weight loss, rapid heart rate, vomiting/diarrhoea, increased water consumption

170
Q

common cause of feline hyperthyroidism?

A

benign thyroid adenoma

171
Q

treatment for hyperthyroidism?

A

anti-thyroid drugs to block hormone production, oral thyroxine, surgery, destruction of thyroid by radioiodine treatment

172
Q

what does TRH from the hypothalamus stimulate?

A

thyrotrophs in anterior pituitary to release TSH

173
Q

when is human fetal growth greatest, what is the survival % after this point?

A

16-20 weeks gestation, greater than 50% after this point

174
Q

what does an earlier growth spurt mean for final height?

A

shorter

175
Q

when is the incidence of childhood lymphomas highest?

A

10 years old

176
Q

3 factors involved in growth?

A

genetic, environmental (nutrition), physiological (GH)

177
Q

structure of human GH?

A

191 amino-acid polypeptide with 2 internal di-sulphide bridges (tertiary structure critical for receptor binding)

178
Q

what secretes GH?

A

somatotrophs in anterior pituitary

179
Q

factors increasing GH release?

A

GHRH, arginine, lysine, ornithine, ghrelin, gonadal steroids, hypoglycaemia, sleep, exercise, thyroid hormones

180
Q

what releases GHRH?

A

arcuate neurons in hypothalamus

181
Q

what is used clinically to diagnose GH deficiency?

A

arginine (should be low in deficiency), hyperglycaemia

182
Q

what is involved in the GH surge at puberty?

A

gonadal steroids

183
Q

what decreases GH release?

A

GHIH (somatostatin), GH + IGF1 (negative feedback), lipids, age, thyroid deficiency, hyperglycaemia, dopamine

184
Q

structure of GHIH (somatostatin) and where is it released from?

A

14 a.a. peptide from periventricular neurons in hypothalamus

185
Q

what is used to treat excess GH?

A

dopamine agonists

186
Q

effect of GH on bone growth?

A

stimulates chondrocyte mitosis at the epiphyseal growth plate, stimulates osteoblasts to deposit new bone on surface

187
Q

what hormone limits long bone growth and how?

A

sex steroids by triggering epiphyseal fusion

188
Q

effect of GHRH?

A

stimulates somatotrophs in anterior pituitary to produce GH

189
Q

structure of the GHRH receptor?

A

G-protein coupled receptor that signals via Gs to increase cAMP in somatotrophs

190
Q

what opposes action of GHRH?

A

somatostatin (GHIH)

191
Q

how can GH exert indirect effects?

A

via production of somatomedins (e.g. IGF1) by the liver

192
Q

what sort of molecule is IGF1?

A

somatomedin

193
Q

metabolic effects of GH?

A

inhibition of glucose uptake by muscle and fat cells, increased lipolysis, increased sodium and fluid retention, increased BMR, hepatic gluconeogenesis, reduced insulin sensitivity, synergistic with cortisol, antagonistic with insulin, increase glomerular filtration rate in kidney and Na+/fluid retention

194
Q

why is GH diabetogenic?

A

synergistic with cortisol and antagonistic with insulin

195
Q

types of growth factors?

A

nerve GF, epidermal GF, transforming GF, fibroblast GF, platelet-derived GF, erythropoietin, interleukins

196
Q

what are growth factors usually?

A

small secreted peptides that act locally to promote growth of specific cell types

197
Q

systemic high gonadal hormone effects?

A

stimulates GH release- bring about pubertal growth spurt, increased rate of long bone growth

198
Q

local high gonadal hormone effects?

A

loss of chondrocytes, epiphysial fusion, sex steroids eventually trigger epiphyseal fusion to limit long bone growth

199
Q

effect of excess glucocorticoids on growth?

A

inhibit growth

200
Q

relationship of insulin and IGFs with growth?

A

essential for normal growth, especially in utero

201
Q

cause of gigantism?

A

hypersecretion of GH before puberty

202
Q

cause of acromegaly?

A

hypersecretion of GH in adulthood

203
Q

most common cause of acromegaly?

A

pituitary tumour

204
Q

is acromegaly more common in dogs or cats?

A

cats

205
Q

clinical appearance of acromegaly?

A

increased cartilaginous growth- so enlarged ears and nose, growth of jaw, enlarged hands, feet and tongue

206
Q

effect of GH deficiency during childhood?

A

pituitary dwarfs- reduced growth but normal body proportions

207
Q

GH deficiency in childhood treatment?

A

GH injection

208
Q

difference between pituitary dwarfism and achondroplasia?

A

in achondroplasia normal body proportions aren’t found

209
Q

common cause of achondroplasia?

A

mutation in FGFR3

210
Q

what is a (kilo)calorie?

A

energy needed to warm 1 (k)g of water by 1 degree

211
Q

what is basal metabolic rate?

A

energy required to keep a resting, awake individual alive in a thermoneutral environment

212
Q

what is indirect calorimetry?

A

measurement of the amount of heat generated in an oxidation reaction by determining the intake or consumption of oxygen or measuring the amount of CO2 released and translating these quantities into a heat equivalent

213
Q

factors that increase BMR?

A

infection/high temp, high growth rate, pregnancy, lactation, menstruation, large size, high stress, male gender

213
Q

factors that decrease BMR?

A

low temp, old age, starvation, female gender

214
Q

effect of insulin on energy storage?

A

promotes it

215
Q

effect of glucagon on energy storage?

A

decreases it

216
Q

which hormones improve the response of the endocrine pancreas to absorbed nutrients?

A

GLP-1, GIP and potentially OX

217
Q

what is GLP-1?

A

glucagon like peptide 1

218
Q

what is GIP?

A

gastric inhibitory peptide

219
Q

how do GLP-1, GIP and maybe OXM improve the response of the endocrine pancreas to absorbed nutrients?

A

act on pancreatic islets of Langerhans to stimulate insulin and inhibit glucagon production

220
Q

what cells produce GLP-1?

A

L cells in GI tract

221
Q

what cells produce GIP?

A

K cells in duodenum

222
Q

which areas of the hypothalamus regulate food intake?

A

satiety centre in ventromedial hypothalamus and feeding centre in lateral hypothalamus

223
Q

effect of destruction of the lateral hypothalamus in rats

A

reduces food intake

224
Q

effect of destruction of the ventromedial nucleus in rats?

A

induces hyperphagia and obesity

225
Q

what does anoretic mean?

A

causes appetite suppression

226
Q

what does oretic mean?

A

causes appetite stimulation

227
Q

what experiment was performed to identify a blood borne satiety factor?

A

parabiosis experiments in rats- connect obese rat with VMN lesion and normal rat- normal rat stopped eating and died

228
Q

structure of leptin?

A

16 KDa protein

229
Q

what produces leptin?

A

white and brown adipose tissue

230
Q

what is the level of leptin in the blood directly proportional to?

A

amount of adipose tissue in the body

231
Q

effect of mutation in leptin/leptin receptor gene in mice?

A

hyperphagic, obese, increased risk of developing type 2 diabetes

232
Q

effect of leptin injection in ob/ob and db/db mice?

A

induces weight loss in ob/ob mice, not in db/db mice

233
Q

structure of ghrelin?

A

28 a.a. peptide hormone

234
Q

what cells produce ghrelin?

A

P/D1 cells in fundus of stomach, ε-cells in islets of Langerhans

235
Q

how does ghrelin signal hunger?

A

stimulates NPY/AgRP neurons in hypothalamus

236
Q

effect of ghrelin on pituitary?

A

increases GH secretion

237
Q

relationship between ghrelin and insulin levels after each meal?

A

inverse

238
Q

change in GH secretion when stomach is pretty full (after full meal)

A

decreases

239
Q

what do anoretic produce?

A

POMC peptides: MSH, CART

240
Q

what does POMC stand for?

A

pro-opiomelanocortin

241
Q

what does MSH stand for?

A

melanocyte stimulating hormone

242
Q

what does CART stand for?

A

cocaine and amphetamine stimulated transcript peptide

243
Q

what receptors does MSH act on?

A

melanocortin receptors MC3 and MC4

244
Q

what is the effect of alpha MSH?

A

suppresses feeding

245
Q

effect of defective MC4R in humans?

A

leads to obesity

246
Q

what do oretic neurons contain?

A

NPY and AgRP

247
Q

what is NPY?

A

neuropeptide Y

248
Q

what is AgRP?

A

agouti related peptide

249
Q

what is the effect of NPY?

A

acts on Y receptors to stimulate feeding

250
Q

what is the effect of AgRP?

A

antagonist of MC3/4 R activity

251
Q

how does leptin cause anoretic effects?

A

inhibits the activity of NPY/AgRP neurons and increases activity of POMC/CART neurons

252
Q

what signals regulate food intake?

A

signals from leptin, neuronal pathways, gut peptides, ghrelin

253
Q

how do neuronal pathways provide information about food digestion and stomach distension to the DVC?

A

via the vagus nerve

254
Q

what is the DVC?

A

the dorsal vagus complex

255
Q

what gut hormones released from the lower GI tract stimulate satiety?

A

cholecystokinin (CCK), oxyntomodulin (OXM), PYY, GLP-1

256
Q

what does pancreatic polypeptide do and where is it released from?

A

stimulates satiety, released from islets of Langerhans

257
Q

what are the medical/pharmalogical treatments for obesity?

A

eat less, exercise, liposuction (cosmetic), restrict food absorption

258
Q

what does bariatric surgery involve?

A

reduction of stomach volume using gastric band or gastric bypass surgery- limits amount patient can eat at one time and slows passage of food

259
Q

what is bariatric surgery most effective when combined with?

A

a malabsorptive technique to bypass part of the digestive tract to reduce absorption

260
Q

effect of bariatric surgery on ghrelin, PYY and GLP1?

A

reduces ghrelin, increases PYY and GLP1

261
Q

what is Xenecal?

A

a lipase inhibitor that prevents digestion of lipids

262
Q

side effect of xenecal?

A

steatorrhea

263
Q

difference in solubility of peptide/protein and steroid/iodine containing thyroid hormones?

A

peptide and protein are water soluble, steroid/iodine containing thyroid hormones are fat soluble

264
Q

difference in storage of peptide/protein and steroid/iodine containing thyroid hormones?

A

peptide/protein often substantial in secreting cell in secretory granules, in steroid/iodine containing storage is minimal

265
Q

difference in half life of peptide/protein and steroid/iodine containing thyroid hormones?

A

short (minutes) and long (hours) respectively

266
Q

target cell-binding site of peptide/protein and steroid/iodine containing thyroid hormones?

A

p/p target cell-surface receptor to start G protein pathway, s/i target cytoplasmic/nuclear receptor

267
Q

site of action of peptide/protein and steroid/iodine containing thyroid hormones?

A

plasma membrane and nucleus respectively

268
Q

process of catabolism in peptide/protein and steroid/iodine containing thyroid hormones?

A

proteases in lysosomes and modification in liver respectively

269
Q

time course of action of peptide/protein and steroid/iodine containing thyroid hormones?

A

rapid onset and short duration vs long latency and duration respectively

270
Q

difference in transport of peptide/protein and steroid/iodine containing thyroid hormones?

A

p/p not usually associated with binding proteins, s/i associated with specific binding proteins

HOM (9 decks)

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