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03- Endocrine > Principles > Flashcards

Principles Flashcards

1
Q

what is meant by endocrine glands?

A

ductless glands that secrete into the bloodstream

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2
Q

the anterior pituitary releases what hormone?

A

adrenocorticotropic hormone ACTH

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3
Q

what does the release of ACTH cause?

A

adrenal cortex synthesises and releases cortisol

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4
Q

specificity of signalling is achieved by what three things?

A

chemically distinct hormones

specific receptors for each hormone

distinct distibution of receptors across target cells

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5
Q

list the major endocrine organs

A

hypothalmus

pituitary

thyroid (and parathyroid)

adrenal

pancreas

ovary/testes

pineal and hypothalmus also

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6
Q

what are the four chemical natures of hormones?

A

Modified amino acids

Steroids

Peptides

Proteins

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7
Q

give examples of modified aminoo acid hormones

A

adrenaline

thyroid hormones

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8
Q

give examples of steroid hormones

A

cortisol

progesterone

testosterone

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9
Q

give examples of peptide hormones?

A

adrenocorticotropic hormone ATCH

antidiuretic hormone ADH

oxytocin

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10
Q

give example of protein hormone

A

insulin

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11
Q

what are the three types of chemical signalling

A

autocrine

paracrine

endocrine

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12
Q

describe autocrine signalling

A

cell releases signaling molecules that stimulate an effect on the same cell itself

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13
Q

describe paracrine signalling

A

cell releases signalling molecules that diffuse over a short distance in the interstitial fluid

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14
Q

describe endocrine signalling

A

cell synthesises signalling molecule then releases it into bloodstream

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15
Q

which chemical signalling works over ong distance?

A

endocrine signalling

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16
Q

how do hormones in endocrine signalling affect organs?

A

integrates organ function with hormones at very low concentration

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17
Q

in endocrine signalling hormones bind to what to initiate a biological response?

A

cognate receptors- (specific)

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18
Q

what triggers a biological response in endocrine signalling?

A

activated receptor engaging a signal transduction cascade

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19
Q

what is the purpose of the signal transduction cascade?

A

amplification of the original signal

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20
Q

hormone action is slower/faster than neurotransmitters?

A

slower

(seconds to days)

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21
Q

how is hormone action terminated?

A

enzyme mediated metabolic inactivation in the liver, or at sites of action

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22
Q

which hormones contribute to the response of the body to short term intense exercise?

A

adrenaline

cortisol

glucagon

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23
Q

adrenaline, cortisol and glucagon prevent what?

A

hypoglycaemia

hypokalaemia

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24
Q

which hormones are essential for normal growth?

A

growth hormone (GH)

insulin

IGF-1

sex steroids

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25
Q

give an example of hormones that have an antagonistic action?

A

insulin v glucagon

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26
Q

how are amines synthesised and stored?

A

they are pre-synthesised and stored in vesicles

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27
Q

what triggers the release of amines?

A

Ca2+ dependant exocytosis

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28
Q

how are amines transported?

A

mainly ‘free’ in the plasma

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29
Q

are amines hydrophilic/phobic?

A

hydrophilic

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30
Q

how are peptides and proteins synthesised and stored?

A

pre-synthesised usually from longer chain and stored in vesicles

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31
Q

where in the cell are the precursor proteins for peptide hormones synthesised?

A

ribosomes of the rough ER

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32
Q

what triggers the release of proteins and peptides?

A

Ca2+ dependant exocytosis

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33
Q

how are protiens and petides transported?

A

mainly ‘free’ in the plasma

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34
Q

peptides are hydrophilic/phobic

A

hydrophilic

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35
Q

how are steroids synthesised and stored?

A

they are synthesised and secreted upon demand

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36
Q

what affects the rate of synthesis of steroids?

A

1) Cellular uptake and availabiloty of cholesterol
2) Rate of conversion of cholesterol to pregnenolone

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37
Q

what is the rate limiting step in the synthesis of steroids?

A

conversion of cholesterol to pregnenolone

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38
Q

steroids are hyrdrophilic/phobic

A

hydrophobic

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39
Q

how are steroids transported?

A

90%- bound to plasma proteins

10%- free

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40
Q

which three hormones are relatively insoluble in plasma?

A

Steroids

thyroxine (T4)

triiodothyronine (T3)

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41
Q

what are the three main functions of carrier proteins?

A
  1. inc amount transported in blood
  2. provide reservoir of hormone
  3. extend half-life of hormone in circulation
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42
Q

what are the three specific carrier proteins?

A

cortisol-bindign globulin (CBG)

thyroxine-binding globulin (TBG)

sex steroid-binding globulin (SSBG)

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43
Q

what are the two general carrier proteins?

A

albumin- binds many steroids and thyroxine

tranthyretin- binds thyroxine and some steroids

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44
Q

which hormones are souluble in plasma and do not require carrier proteins?

A

proteins and peptides

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45
Q

which molecules act as a buffer and reservoir in the blood?

A

carrier proteins

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46
Q

free and bound hormone are in equilibrium in the blood true/false

A

true- carrier proteins maintain relatively constant conc of free lipophilic hormone in the blood

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47
Q

only ____ hormone can cross the capillary wall

A

free

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48
Q

free hormones activate receptors where?

A

target tissues

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49
Q

how are surges in hormone secretion controlled?

A

buffered by binding to carriers

note: free conc doesnt rise abruptly

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50
Q

how is free hormone removed from plasma?

A

elimination

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51
Q

what happens when free hormone is removed from the plasma?

A

replaced by bound hormone dissociating from carrier protein

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52
Q

what mechanism controls the synthesis and concentraon of cortisol?

A

negatiev feedback

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53
Q

what is short range negative feedback of cortisol?

A

cortisol carried back to the pituitary where it supresses release of ACTH

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54
Q

what is long range negative feedback control of cortisol?

A

cortisol carried back to hypothalmus to prevent further synthesis of cortisol

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55
Q

what does the hypothalmus release in the cortisol synthesis pathway?

A

secretes corticotropin releasing hormone

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56
Q

what does corticotropin releasing hormone from the hypothalmus act on?

A

anterior pituitary

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57
Q

what does the anterior pituitary secrete in the cortisol synthesis pathway?

A

adrenocorticotropic hormone

58
Q

what does adrenocorticotropic hormone act on in the cortisol synthesis pathway?

A

adrenal cortex

59
Q

what structure secretes cortisol

A

adrenal cortex

60
Q

what is the name given to the fluctuation of cortisol secretion rate over time?

A

diurnal (circadian) rhythm

61
Q

when is the plasma concentration greatest during hte day?

A

12.00pm before decreasign until 24.00am and then increasing again

62
Q

how does elimination of cortisol occur?

A

metabolism by the liver

excretion by the kidneys

63
Q

plasma conc of hormone= ?

A

rate of secretion- rate of elimination

64
Q

what is the half life of amines e.g adrenaline?

A

seconds

65
Q

what is the half life of proteisn and peptides?

A

minutes

66
Q

what is the half life of steroids and thyroid hormones?

A

hours- days

67
Q

what are the two groups of hormone receptors?

A

cell surface receptors

intracellular receptors

68
Q

which hormone receptor is hydrophilic and which is lipophilic?

A

cell surface- ligand is hydrophilic

intracellular receptor- ligand is lipophilic

69
Q

what are the two kinds of cell surface hormone receptor?

A

G-protein coupled

Receptor kinases

70
Q

what activates G-protein coupled receptors?

A

amines

some proteins/peptides

71
Q

what activates receptor kinases?

A

some proteins/peptides

72
Q

intracellular receptors are what kind of receptors?

A

nuclear receptors

73
Q

nuclear receptors can be subdivede into what?

A

class 1

class 2

hybrid class

74
Q

what activates class 1 nuclear receptors?

A

many steroid hormones

75
Q

what activates class 2 receptors?

A

mostly by lipids

76
Q

what activates hybrid class nuclear recpetors?

A

thyroid hormone (T3)

77
Q

where are nuclear receptors found?

A

in the nucleus or in the cytoplasm

78
Q

which type of hormone receptors are ligand-gated transcription factors?

A

nuclear receptors

79
Q

steroid hormones are lipophilic and enter cells by _____ across teh plasma membrane

A

diffusion

80
Q

what do steroid hormones combine with in the cell producing dissociation of inhibitory HSP proteins?

A

intracellular receptor

81
Q

in nuclear reeptor signalling the receptor steroid complex forms a dimer and binds to what?

A

hormone response elements in DNA

82
Q

what is the final step in nuclear receptor signalling?

A

transcription of specific genes is either ‘swithced-on’ or ‘swithced-off’ to alter the rate of synthesis of mediator proteins

83
Q

what are the cells of pancreatic islets?

A

beta cells

alpha cells

s cells

PP cells

84
Q

what do islet beta cells secrete?

A

insulin

85
Q

what do alpha islet cells secrete?

A

glucagon

86
Q

what do s islet cells secrete?

A

somatostatin

87
Q

what do PP islet cells secrete?

A

pancreatic polypepetide

88
Q

glucose homeostasis controls what?

A

blood sugar concentration

89
Q

what is the normal blood gluocse concentration?

A

5mmol

90
Q

where is insulin originally formed before being cleaved?

A

rough ER of B cells as a large chain

91
Q

what is the byproduct of cleavage of insulin

A

Connecting (C) peptide- no physiological function

92
Q

what is the name given to the insulin preparation given to diabetcis at nightitme to control their blood sugar while they sleep?

A

glargine

93
Q

how does glucose enter B cells?

A

enters through GLUT2 glucose transporter

94
Q

what is the name of the enzyme that phosphorylates glucise once in the B cells?

A

phosphorylated by glucokinase

95
Q

a change in glucose conc leads to dramatic change in glucokinase activity true/false

A

True

96
Q

increased metabolism of glucose leads to an increase/decrease in intraclellular ATP concentraion

A

increase

97
Q

how many ATP are produced per glucose in glycolysis?

A

36ATP

98
Q

ATP inhibits what within the secretion of insulin?

A

ATP sensitive K+ channel (KATP)

99
Q

what does the inhibition of KATP lead to within the secretion of insulin?

A

depolaristion of the cell membrane

100
Q

in the secretion of insulin depolaristion of he cell membrane results in what?

A

opeing of voltage gated Ca2+ channels

101
Q

in insulin secretion an increase in internal Ca2+ conc results inthe release of what?

A

insulin

102
Q

what is the only cell in the body capable of synthesisng and releasign insulin?

A

B cells

103
Q

when will B cells release insulin?

A

when blood glucose rises above 5mmol

104
Q

what happens ot the B cells in T1DM

A

they are mostly lost

105
Q

what happens to the B cells in other types of diabetes than T1DM?

A

B cells lose the abiloity to sense changes in glucose

106
Q

describe the pattern of release of insulin?

A

release of insulin is biphasic

107
Q

what % of insulin granules are availale for immediate release?

A

5%

108
Q

what does RRP stand for in insulin secretion?

A

Readily Releasable Pool

109
Q

what is used in the second phase of insulin release?

A

reservoir pool

110
Q

in poorly controlled T2DM what happens to insulin secretion?

A

it weakens and flattens

111
Q

Which drugs mimic the action of ATP to depolarise B cells in T2DM?

A

sulphonylurea drugs

112
Q

KATP channels consist of which two proteins?

A

Kir6

SUR1

113
Q

KATP channels exist as an _______ structure?

A

octomeric structure

114
Q

the sulphonylurea class of drugs directly inhibits what?

A

KATP

115
Q

KATP is stimulated by _______ which inhibtis insulin secretion?

A

diazoxide

116
Q

what is the second line therapy for T2DM

A

sulphonylurea drugs

117
Q

which type of mutation can lead to neonatal diabetes

A

mutation in the potassium channels of B cells

118
Q

some Kir6 or SUR1 mutations can lead to what?

A

congenital hyperinsulinism

119
Q

what does MODY stand for?

A

Maturity-onset diabetes of the young

120
Q

what is the treatment for MODY1 rather than type 1

A

SUlphonylurea rather than insulin

121
Q

describe the defect in MODY

A

defective glucose sensing in the pancreas and/or loss of insulin secretion

122
Q

describe the insulin signalling pathway

A
  1. reception- signal molecule acts on receptor
  2. transduction
  3. response
123
Q

binding of insulin to the alpha subunits causes the beta subunits ot do what?

A

dimerise and phosphorylatr themselves

124
Q

what activates the catalytic activity of the insulin receptor?

A

phosphorylation of the beta subunits

125
Q

describe insulin resistance?

A

reduced ability to respond to physiological insulin levels

126
Q

insuin is the key hormone in preventing what?

A

hyperglycemia

127
Q

Developmental abnormalities, growth retardation and the absence of subcutaneous fat with decreased muscle mass is seen in which severe insulin resistance syndrome?

A

donohue syndrome

128
Q

developmentl abnormalities, acanthosis nigricans (hyperpigmentation) and diabetic ketoacidosis is seen in which severe insulin resistance syndrome?

A

Rabson Mendenhall syndrome

129
Q

what are the symptoms of diabetic ketoacidosis (DKA)?

A

vomiting

dehydration

inc heart rate

distinctive smell on breath

130
Q

where are ketone bodies formed?

A

liver mitochondria

131
Q

what are ketone bodies derived from?

A

acetyl-CoA from the B oxidation of fats

132
Q

ketone bodies are important molecules of energy metabolism for what?

A

heart muscle

renal cortex

133
Q

what happens to ketone bodies once they have been used for enrgy metabolism?

A

converted back to acetyl-CoA which then enters the TCA cycle

134
Q

low levels of insulin inhibit _______ preventing ketone body overload

A

lipolysis

135
Q

in the TCA cycle low levels of which molecule will result in acetyl-CoA being converted to ketones?

A

oxaloacetate

136
Q

oxaloacetate is consumed for which process?

A

gluconeogenesis

137
Q

how would you treat DKA?

A

insulin and rehydration

138
Q

what are the greek meanings for mellitus and insulin?

A

mellitus- sweet (urine was sweet smelling due to high sugar content)

insulin- island (islet cells looked liek islands under microscope)

139
Q

which of the insulin hexamer and the insulin monomer is the active form?

A

insulin hexamer- inactive

insulin monomer- active

140
Q

T1DM is not diagnosable before what age?

A

1 yr- neonatal can be transient

141
Q
A

03- Endocrine (9 decks)

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