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year 2 > endocrine basic principles > Flashcards

endocrine basic principles Flashcards

1
Q

what makes up the diencephalon

A

thalamus and hypothalamus

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2
Q

what makes up the rhombencephalon (hindbrain)

A

medulla oblongata
pons
cerebellum

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3
Q

how is the action of a hormone terminated

A

enzymes

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4
Q

what are the 3 categories of hormones

A

modified amino acids (amines)
steroid hormones
protein and peptide hormones

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5
Q

adrenaline is an example of what kind of hormone

A

amine

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6
Q

cortisol is an example of what kind of hormone

A

steroid

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7
Q

progesterone is an example of what kind of hormone

A

steroid

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8
Q

melatonin is an example of what kind of hormone

A

amine

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9
Q

insulin is an example of what kind of hormone

A

protein/peptide

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10
Q

ACTH is an example of what kind of hormone

A

protein/peptide

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11
Q

testosterone is an example of what kind of hormone

A

steroid

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12
Q

ADH is an example of what kind of hormone

A

protein/peptide

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13
Q

oxytocin is an example of what kind of hormone

A

protein/peptide

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14
Q

thyroid hormones are an example of what kind of hormone

A

amine

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15
Q

GH is an example of what kind of hormone

A

protein/peptide

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16
Q

prolactin is an example of what kind of hormone

A

protein/peptide

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17
Q

what are amine hormones derived from

A

tyrosine and tyramine

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18
Q

how/when are amine hormones synthesised

A

pre-synthesised within cells

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19
Q

how are amine hormones stored?

A

in vesicles

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20
Q

what causes amine hormones to be released

A

Ca2+-dependent exocytosis

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21
Q

how are amine hormones transported

A

free in plasma as they are hydrophilic

except thyroid hormones - they are free and bound

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22
Q

where are the receptors for amine synthesis

A

on cell membrane

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23
Q

what is the half life of amine hormones

A

seconds

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24
Q

what are steroid hormones derived from

A

cholesterol

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25
Q

when are steroid hormones synthesised

A

synthesised and secreted on demand

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26
Q

how are steroid hormones synthesised

A

stimuli increases cellular uptake and availability of cholesterol and rate of conversion of cholesterol to pregnenolone

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27
Q

what is the rate limiting step in the synthesis of steroid hormones

A

rate of conversion of cholesterol to pregnenolone

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28
Q

how are steroid hormones transported

A

in plasma mainly bound to plasma proteins

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29
Q

are steroid hormones active when bound or free

A

free

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30
Q

where are the receptors for activating steroid synthesis

A

within cells

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31
Q

what is the half life of steroid hormones

A

hours/days

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32
Q

why is the half life of steroid hormones long?

A

due to extensive binding to proteins that suppress elimination

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33
Q

what are protein/peptide hormones made from

A

proteins

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34
Q

how are protein/peptide hormones made

A

pre-synthesised usually from a longer precursor - proteolytic steps by convertases during intracellular transport

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35
Q

how are protein/peptide hormones stored

A

in vesicles

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36
Q

how are protein/peptide hormones released

A

in response to stimuli by Ca2+ dependent exocytosis

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37
Q

are protein/peptide hormones hydrophobic or hydrophilic

A

hydrophilic

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38
Q

how are protein/peptide hormones transported in the blood

A

free

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39
Q

where are the receptors for peptide synthesis found

A

on cell membrane

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40
Q

what is the half life of peptide hormones

A

minutes

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41
Q

in what state can hormones cross the capillary wall to activate receptors in target tissues (biophase)

A

free

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42
Q

give 3 functions of carrier proteins

A

increase amount of hormone transported in blood
provide a reservoir/buffer of hormone
extend half life of hormone in circulation

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43
Q

what does albumin bind

A

many steroids and thyroxine

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44
Q

what does transthyretin bind

A

some steroids and thyroxine

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45
Q

what does cortisol binding globulin bind

A

cortisol (and aldosterone) selectively

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46
Q

what does thyroxine binding globulin bind

A

T4 (and some T3) selectively

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47
Q

what does sex steroid binding globulin bind

A

mainly testosterone and oestradiol

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48
Q

what happens if free hormones diffuses out of the blood into cells

A

bound and free hormones in blood are in equilibrium - bound hormone will be freed to replace it

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49
Q

what happens if lots of hormone is suddenly secreted

A

free carrier proteins are available to bind them

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50
Q

what is the primary determinant of plasma concentration of a hormone

A

rate of secretion

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51
Q

what is the equation of plasma concentration of a hormone

A

plasma concentration of hormone = rate of secretion - rate of elimination

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52
Q

what are the 2 broad types of hormone receptors

are the ligands hydrophilic or lipophilic for each?

A

cell surface receptors - ligand is hydrophilic

intracellular receptors - ligand is lipophilic

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53
Q

what are the 2 types of cell surface receptors

A

GPCRs

receptor kinases

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54
Q

what hormones activate GPCRs

A

amines and some peptide/proteins

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55
Q

what hormones activate receptor kinases

A

some proteins/peptides

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56
Q

what are the 3 types of nuclear receptor (intracellular receptors)

A 
class 1
class 2
hybrid class
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57
Q

what hormones activate class 1 nuclear receptors

A

many steroid hormones

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58
Q

where are class 1 nuclear receptors located in the absence of an activating ligand and what are they bound to

A

mainly located in the cytoplasm

bound to inhibitory heat shock proteins

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59
Q

where to class 1 nuclear receptors move when they are activated

A

to nucleus

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60
Q

what hormones activate class 2 nuclear receptors

A

lipids

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61
Q

where are class 2 nuclear receptors located

A

nucleus

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62
Q

what hormones activate the hybrid class

A

T3 (and others) - similar function to class 1

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63
Q

how does insulin signal

A

receptor kinases

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64
Q

where does insulin bind to receptor kinases

A

alpha subunit

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65
Q

what does binding of insulin to the alpha subunit of receptor kinases cause

A

beta subunits to dimerise and phosphorylate themselves (autophosphorylation)
(autophosphorylation of intracellular tyrosine residues)

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66
Q

what does autophosphorylation of intracellular tyrosine residues cause

A

recruitment of multiple adapter proteins e.g. IRS1 (insulin receptor substrate 1) that are also tyrosine phosphorylated —> protein kinase B –> metabolic effects/catalytic activity of the receptor

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67
Q

what channels cause glucose entry into cells upon insulin binding

A

GLUT4

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68
Q

true/false

GLUT4 channels remain in the cell membrane at all times

A

false - stimulated to move to cell membrane when insulin binds

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69
Q

how do steroid hormones enter cells

A

diffusion across plasma membrane

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70
Q

what does binding of a steroid hormone to an intracellular nuclear receptor cause

A

dissociation of inhibitory heat shock proteins (HSP)

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71
Q

in the case of steroid hormones, where is the inactive receptor located

A

in the cytoplasm

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72
Q

where does the receptor-steroid complex move and what does it do there

A

moves to the nucleus
forms a dimer
binds to hormone response elements in DNA

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73
Q

what does binding to the hormone response elements cause

A

transactivation or transrepression

- alter mRNA levels and rate of synthesis of mediator proteins

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74
Q

what is transactivation

A

transcription of specific genes is switched on

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75
Q

what is transrepression

A

transcription of specific genes is switched off

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76
Q

how do glucocorticoids cause transactivation

A

binding of the activated glucocorticoid receptor homodimer to a GRE in a promoter region of steroid sensitive genes

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77
Q

what does binding of the activated glucocorticoid receptor homodimer to a GRE in a promotor region of steroid sensitive genes cause

A

transcription of genes encoding anti-inflammatory mediators

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78
Q

what does the glucocorticoid-receptor-corticosteroid complex interact with to cause transrepression

A

large co-activator moleules with intrinsic HAT (histone acetyltransferase) activity which is activated by proinflammatory transcription factors
thus, switching off inflammatory gene expression that are activated by these transcription factors

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79
Q

where is ADH released from

A

posterior pituitary

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80
Q

what does ADH cause and how

A

water reabsorption from renal tubules by counter current multiplication

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81
Q

what steroid controls sodium balance

A 
aldosterone mainly 
(also others e.g. cortisol)
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82
Q

what does aldosterone do to Na conc

A

Na reabsorption in renal tubules in exchange for K+/H+

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83
Q 
increased pulse
dry mucous membranes
soft/sunken eyeballs
decreased skin turgor
decreased consciousness
decreased urine output
postural decrease in BP
- all indicate what?
A

decreased {Na+} / decreased ECF

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84
Q

what can cause decreased Na

A

increased Na loss
decreased Na intake
decreased water excretion e.g. SIADH
increased water intake

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85
Q 
coughing 
tiredness
SOB
pulmonary oedema
weak heart
peripheral oedema
ascites
pleural effusion
- all indicate what?
A

increased [Na+] - increased ECF

86
Q

what can cause increased Na

A

increased Na intake e.g. IV meds, near drowning, malicious
decreased Na loss
increased water loss e.g. diabetes insipidus
decreased water intake

87
Q

what qualifies as life threatening levels of sodium

A

< 120 nmol
> 160 nmol
if Na rises or falls rapidly even if to a point in normal range

88
Q

where would 5% dextrose go

A

plasma
interstitial fluid
intracellular fluid

89
Q

where would 0.9% saline go

A

plasma

interstitial fluid

90
Q

where would plasma/blood go

A

plasma

91
Q

what are some s/s of life threatening hypo/hypernatraemia

A

altered consciousness
confusion
nausea/vomiting
fitting

92
Q

what does [Na] reflect

A

Na loss

93
Q

what does [K] reflect

A

K retention

94
Q

what are some physiological causes of raised prolactin

A

breast feeding
pregnancy
stress
sleep

95
Q

what are 5 drugs that cause raised prolactin

A 
dopamine antagonists e.g. metoclopramide
antipsychotics e.g. phenthiazines
antidepressants e.g. TLA, SSRIs
oestrogens
cocaine
96
Q

would hypothyroidism cause raised or lowered prolactin

A

raised

97
Q

would a prolactinoma cause raised or lowered prolactin

A

raised

98
Q

would a stalk lesion (iatrogenic, RTA) cause raised or lowered prolactin

A

raised

99
Q

what does aldosterone do to the blood pressure

A

raised BP

100
Q

does aldosterone increase parasympathetic or sympathetic outflow

A

sympathetic

101
Q

what effect does aldosterone have on the heart/BVs

A

increased cardiac collagen
LVH
atheroma
altered endothelial function/increased pressure response

102
Q

what GPCR do adrenaline, glucagon and CRH signal via

A

Gs

103
Q

what does Gs do to the production of cAMP from ATP by adenylyl cyclase

A

increases it

104
Q

what does increased cAMP do

A

stimulates protein kinase A leading to phosphorylation of Ser/Thr residues in target proteins

105
Q

what GPCR does melatonin signal via

A

Gi

106
Q

what does Gi do to the production of cAMP from ATP by adenylyl cyclase

A

decreases it

107
Q

what GPCR do angiotensin II, GnRH and TRH signal via

A

Gq

108
Q

what does Gq do to the activity of PLC (phosolipase C)

A

increases it

109
Q

what is the role of PLC in the Gs pathway

A

converts PIP2 to DAG and IP3

110
Q

what does IP3 do

A

binds to IP3 receptor on the endoplasmic reticulum causing calcium release to cause cellular effects

111
Q

what does DAG do

A

stimulates protein kinase C causing phosphorylation of Ser/Thr residues in target proteins leading to cellular effects

112
Q

what does the kidney release when BP falls

A

Renin

113
Q

what does renin do

A

converts angiotensinogen to angiotensin I

114
Q

how does angiotensin I get to angiotensin II

A

ACE

115
Q

what does angiotensin II do

A

causes BP to rise

stimulates adrenal gland to produce aldosterone

116
Q

what does aldosterone do to increase the BP

A

salt retention

117
Q

what is released from the hypothalamus to stimulate the anterior pituitary to produce ACTH

A

CRH

118
Q

what causes the hypothalamus to release CRH

A

time of day
stress
illness

119
Q

where does ACTH act and what does it cause

A

stimulates adrenal cortex to produce cortisol

120
Q

what effect does increased cortisol have on CRH and ACTH levels

A

negative feedback - cortisol goes up, CRH and ACTH go down

121
Q

how is adrenaline and noradrenaline released from the adrenal gland

A

direct control by nervous system

122
Q

where is MSH released and where does it act

A

anterior pituitary

melanocytes

123
Q

where are LH and FSH released from and where do they act

A

anterior pituitary

ovaries and testes

124
Q

where is ADH released from

A

posterior pituitary

125
Q

where is oxytocin released from

A

posterior pituitary

126
Q

where does oxytocin act

A

uterine smooth muscle and mammary glands

smooth muscle in vas deferens and prostate gland

127
Q

where is PRL released from

A

anterior pituitary

128
Q

where does PRL act

A

mammary glands

129
Q

where is GH released from

A

anterior pituitary

130
Q

where does GH act

A

liver

also adipose tissue and target tissues

131
Q

what does GH cause the liver to produce

A

somatomedins

132
Q

where do somatomedins work

A

bone, muscle etc

133
Q

where is TSH released from

A

anterior pituitary

134
Q

what does TSH cause the thyroid to produce

A

T3 and T4

135
Q

what does ACTH cause the adrenal gland to produce

A

glucocorticoids

136
Q

what gland is under direct control by the nervous system

A

adrenal gland

137
Q

what gland is under indirect control through release of regulatory hormones

A

anterior pituitary

138
Q

where are oxytocin produced and stored

A

produced in hypothalamus

stored in posterior pituitary

139
Q

where is ADH produced and stored

A

produced in the hypothalamus

stored in posterior pituitary

140
Q

what hormone from the hypothalamus causes ACTH to be released

A

CRH

141
Q

what hormone from the hypothalamus causes TSH to be released

A

TRH

142
Q

what hormone from the hypothalamus causes LH/FSH to be released

A

GnRH

143
Q

what hormone from the hypothalamus causes GH to be released

A

GHRH

144
Q

what hormone from the hypothalamus inhibits prolactin

A

dopamine (DA)

145
Q

what hormone from the hypothalamus inhibits GH secretion

A

somatostatin (SS)

146
Q

what does GH cause the liver to produce

A

IGF-1

147
Q

where does IGF-1 act

A

target tissues

148
Q

what does GH cause adipose tissue to produce

A

leptin and free fatty acids

149
Q

what effect do free fatty acids have on hypothalamus

A

negative feedback

150
Q

what effect does leptin have on the hypothalamus

A

positive feedback

151
Q

what kinds of things stimulate the hypothalamus to produce GHRH

A 
ghrelin
sleep
exercise
stress
amino acids
sex hormones
152
Q

what effect does IGF1 have on the anterior pituitary and hypothalamus

A

negative feedback

153
Q

what effect does GH have on the hypothalamus

A

negative feedback

154
Q

what feedback does PRL have on the hypothalamus

A

positive feedback

155
Q

what feedback does PRL have on the anterior pituitary

A

negative feedback

156
Q

what kind of signalling does PRL show at the breast tissue

A

paracrine/autocrine

157
Q

what stimulates the hypothalamus to cause ADH release from the posterior pituitary

A

fall in BP

158
Q

what does V1 do

A

constricts blood vessels to increase systemic vascular resistance and increase blood pressure

159
Q

what does V2 do

A

causes fluid reabsorption in the kidneys to increase blood volume and increase blood pressure

160
Q

how is glucose taken up into pancreatic beta cells

A

GLUT2 transporter

161
Q

what happens after the uptake of glucose into pancreatic beta cells

A

glucose is phosphorylated by glucokinase

162
Q

how are the Katp channels inhibited in the pancreatic Beta cells and how does this eventually lead to insulin release

A

phosphorylation of glucose by glucokinase increases intracellular ATP which inhibits Katp channels. This causes depolarisation of the cell membrane which leads to opening of voltage gated Ca2+ channels
increase in Ca2+ conc. leads to fusion of secretory vesicles with the cell membrane and release of insulin

163
Q

what is released by pancreatic alpha cells

A

glucagon

164
Q

what is released by pancreatic delta cells

A

somatostatin

165
Q

what is released by pancreatic PP cells

A

pancreatic polypeptide

166
Q

how and where is insulin synthesised

A

in the RER of pancreatic beta cells as a larger single chain preprohormone - preproinsulin which is cleaved to form insulin

167
Q

what is the structure of insulin

A

2 polypeptide chains linked by disulfide bones

168
Q

what is a biproduct of insulin formation

A

C-protein

169
Q

how is the release of insulin described

A

biphasic

170
Q

what % of insulin is from a readily releasable pool

A

5%

171
Q

what happens to the curve of insulin secretion in poorly controlled type 2 diabetes

A

curve flattens and weakens

172
Q

at what blood glucose should B cells produce insulin

A

over 5mM

173
Q

what happens in type 1 diabetes

A

destruction of beta cells

174
Q

what is glucokinases Km for glucose

A

within the physiological range of concentration - change in glucose conc leads to a dramatic change in glucokinase activity

175
Q

how do beta cells lose ability to sense changes in glucose in other types of diabetes

A

hyperglycaemia takes glucose conc. outwith the Km of glucokinase, mitochondrial exhaustion

176
Q

the Katp channel is a ____ complex and consists of 2 proteins - pore subunit and regulatory subunit

A

octomeric complex

consists of 2 proteins

177
Q

what makes up the pore subunit

A

4 potassium inward rectifier 6.2 subunits

Kir6.2

178
Q

what makes up the regulatory subunit

A

4 sulphonylurea receptor 1 subunits

SUR1

179
Q

what does the tetramer of Kir6.2 subunits form

A

K selective ion channel

180
Q

what happens to the Katp channel when extracellular glucose is high

A

ATP binding to each of the Kir6.2 subunits closes the channel causing depolarisation of the beta cell and insulin release

181
Q

what happens to the Katp channel when extracellular glucose is low

A

ADP-Mg2+ binding to the SUR1 subunits opens the channel maintaining the resting potential of the beta cell and inhibiting the secretion of insulin

182
Q

what does diazoxide do to the Katp channel

A

stimulates the Katp channel inhibiting insulin release

183
Q

what can some mutations in Kir6.2 lead to and how

A

neonatal diabetes

constitutively activated Katp channels or increase in Katp numbers

184
Q

what may some cases of neonatal diabetes respond to

A

sulfonylureas e.g. tolbutamide

185
Q

what else could a Kir6.2 mutation lead to

A

congenital hyperinsulinism

trafficking or inhibiting mutations

186
Q

what could be used to treat congenital hyperinsulinism

A

diazoxide

187
Q

what does insulin do to amino acid uptake in muscle

A

increases

188
Q

what does insulin do to DNA synthesis

A

increases

189
Q

what does insulin do to protein synthesis

A

increases

190
Q

what does insulin do to lipolysis

A

inhibits

191
Q

what does insulin do to gluconeogenesis in liver

A

inhibits

192
Q

what does insulin do to glycogen synthesis in liver and muscle

A

increases

193
Q

what does insulin do to glucose uptake in muscle and adipose tissue

A

increases

194
Q

what does insulin do to lipogenesis in adipose tissue and liver

A

increases

195
Q

what is another name for donotive syndrome

A

leprechaunism

196
Q

what is the inheritance pattern of leprechaunism

A

autosomal recessive

197
Q

where is the mutation in donotive syndrome and what does it cause

A

mutation in gene for insulin receptor
defects in insulin binding/insulin receptor signalling
—> severe insulin resistance

198
Q

what are some features of leprechaunism

A

elfin facial appearance
growth retardation
absence of SC fat
decreased muscle mass

199
Q

what is the inheritance pattern of Rabson Mendenhall syndrome

A

autosomal recessive

200
Q

what is the issue in rabson mendenhall syndrome

A

severe insulin resistance, hyperglycaemia and compensatory hyperinsulinaemia

201
Q

what are some features of RMS

A

developmental abnormalities
acanthosis nigricans
DKA

202
Q

severe cases of RMS are linked to mutations in what

A

insulin receptor that reduces sensitivity

203
Q

where are ketone bodies formed and where do they go

A

liver mitochondria

diffuse into blood stream and into peripheral tissues

204
Q

what are ketone bodies derived from

A

acetyl-coA

205
Q

where is acetyl-coA from

A

beta oxidation of fats / fatty acid oxidation

206
Q

how are ketones used for energy metabolism

A

converted back to acetyl co-A which enters the TCA cycle

207
Q

how does insulin prevent ketone body overload

A

prevents lipolysis

208
Q

how does DKA occur in T1DM

A

if insulin is missed –> break down of fats

209
Q

when might acetyl coA be converted to ketones

A

if supply of oxaloacetate is limited e.g. no glycolysis

210
Q

why are ketones formed in glucose limiting conditions e.g. DMT1, starvation

A

increased lipolysis
oxaloacetate used for gluconeogenesis so crebs cycle inhibited
acetyl coA goes to ketones

year 2 (19 decks)

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