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Endocrine > Basic Principles > Flashcards

Basic Principles Flashcards

1
Q

what is ACTH?

A

adrenocorticotrophic hormone

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2
Q

what gland produces adrenocorticotrophic hormone (ACTH)?

A

anterior pituitary

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3
Q

what is the function of adrenocorticotrophic hormone (ACTH)?

A

stimulates the adrenal cortex to synthesise and release cortisol

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4
Q

what does anti-diuretic hormone (ADH) do to the concentration of urine?

A

increases the concentration

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5
Q

what type of target cells are involved in endocrine signalling?

A

distant target cell

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6
Q

what type of target cells are involved in autocrine signalling?

A

acting on itself

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7
Q

what type of target cells are involved in paracrine signalling?

A

surrounding (local) cells

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8
Q

what are the 3 main classes of hormones?

A
  1. (glyco)proteins and peptides
  2. steroids
  3. tyrosine and tryptophan derivatives
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9
Q

what molecule are steroids derived from?

A

cholesterol

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10
Q

what type of hormone is oxytocin?

A

protein/peptide

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11
Q

what type of hormone is cortisol?

A

steroid

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12
Q

what type of hormone is aldosterone?

A

steroid

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13
Q

what type of hormone is adrenaline or epinephrine?

A

tyrosine/tryptophan derivatives

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14
Q

what type of hormones are the thyroid hormones?

A

tyrosine derivatives

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15
Q

what type of hormone is insulin?

A

protein/peptide

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16
Q

what type of hormone is testosterone?

A

steroid

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17
Q

are amines pre-synthesised and stored or synthesised on demand?

A

pre-synthesised and stored

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18
Q

where are amines stored?

A

intracellular vesicles

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19
Q

what is the exocytosis of vesicles concentrated with amine hormones dependent on?

A

Ca2+ influx caused by a stimuli

calcium dependent exocytosis

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20
Q

are peptide/protein hormones pre-synthesised and stored or synthesised on demand?

A

pre-synthesised and stored

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21
Q

where are proteinpeptide hormones stored?

A

intracellular vesicles

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22
Q

what is the exocytosis of vesicles concentrated with protein/peptide hormones dependent on?

A

Ca2+ influx caused by a stimuli

calcium dependent exocytosis

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23
Q

are peptide hormones hydrophilic or hydrophobic?

A

hydrophilic

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24
Q

are amine hormones hydrophilic or hydrophobic?

A

hydrophilic

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25
Q

how are amine hormones transported in the plasma?

A

free

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26
Q

how are protein/peptide hormones transported in the plasma?

A

free

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27
Q

in the first stage of production of a steroid hormone, what is cholesterol converted into?

A

pregnenolone

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28
Q

what is the rate limiting step in the production of a steroid hormone from cholesterol?

A

conversion of cholesterol to pregnenolone

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29
Q

where does the conversion of cholesterol to pregnenolone occur?

A

mitochondrial membrane

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30
Q

where are steroid hormones stored?

A

they aren’t stored within the cell, as soon as they are made they are released directly into the blood stream

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31
Q

why is there a slow time frame of steroid hormone action?

A

because it depends on synthesis and release of a new hormone and not just release of a pre-existing hormone

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32
Q

how are steroid hormones transported in the plasma?

A

bound to a carrier protein

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33
Q

what are the 2 functions of a carrier protein in the transportation of hormone?

A
  1. increase amount transported in blood

2. prevent rapid excretion by preventing filtration at the kidney

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34
Q

what amine hormones needs to be transported in the bloodstream bound to a carrier protein because it is relatively insoluble in plasma?

A

thyroid hormones

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35
Q

what is the important carrier protein specific to cortisol?

A

cortisol-binding globulin

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36
Q

apart from cortisol, what hormone does cortisol-binding globulin also transport?

A

some aldosterone

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37
Q

what is the important carrier protein specific to thyroxine (T4)?

A

thyroxine-binding globuline

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38
Q

apart from thyroxine, what hormone does thyroxine-binding globulin also transport?

A

some triiodothyronine (T3)

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39
Q

what is the important carrier protein specific to testosterone and estradiol?

A

sex steroid-binding globulin

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40
Q

when are the levels of cortisol in the body highest and when are they lowest?

A

highest- 9/10am
lowest- 12am
(diurnal rhythm)

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41
Q

when are the levels of testosterone in the body highest?

A

first thing in the morning

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42
Q

what are the 3 main types of hormone receptor?

A
  1. g-protein coupled
  2. receptor kinases
  3. nuclear receptors
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43
Q

what type of hormones activate g-protein coupled receptors?

A

amines and some proteins/peptides

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44
Q

what type of hormones activate receptor kinases?

A

proteins/peptides

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45
Q

what are the 3 subclasses of nuclear receptors?

A 
class 1
class 2
hybrid class
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46
Q

what is the difference between class 1 and class 2 nuclear receptor?

A 
class 1- in the absence of hormone, located within the cytoplasm, move to nucleus once activated by hormone
class 2- always present in the nucleus, hormone has to diffuse into nucleus to have it's effect
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47
Q

what are class 1 nuclear receptors bound to when in the cytoplasm?

A

inhibitory heat shock proteins

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48
Q

what type of hormones activate class 1 nuclear receptors?

A

mainly steroids

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49
Q

what type of substance activate class 2 nuclear receptors?

A

lipids

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50
Q

what type of receptor does insulin signal via?

A

tyrosine kinase receptor

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51
Q

once the receptor steroid complex (class 1 nuclear receptor) moves to the nucleus, it forms a dimer. what does this dimer bind to within the DNA?

A

hormone response elements

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52
Q

what endogenous substance might make urine red or red/brown?

A

haemoglobin

myoglobin

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53
Q

what endogenous substance might make urine smokey red?

A

intact RBC

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54
Q

what endogenous substance might make urine yellow and frothy when shaken?

A

bilirubin

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55
Q

what inborn error of metabolism makes urine brown-black on standing?

A

alkaptonuria

due to homogentisic acid

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56
Q

what does leucocyte presence in urine indicate?

A

UTI

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57
Q

what does urobilinogen presence in urine indicate?

A

a normal finding

increased urobilinogen might indicate liver abnormalities or excessive destruction of RBCs (eg haemolytic anaemia)

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58
Q

what is the normal pH of urine?

A

5-6

5.5 average

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59
Q

when are pH values for urine at their lowest?

A

after overnight fast

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60
Q

when are pH values of urine at their highest?

A

after meals

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61
Q

what may a strongly acidic urine pH indicate?

A

uncontrolled diabetes
starvation
dehydration

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62
Q

what may an alkaline urine pH of >8 indicate?

A

stale sample

UTI

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63
Q

what does specific gravity of urine assess?

A

the concentration and diluting power of the kidneys

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64
Q

what does the presence of bilirubin in urine indicate?

A

hepatic or biliary disease

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65
Q

what does the presence of nitrites in urine suggest?

A

UTI

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66
Q

what type of bacteria causing UTIs cause the presence of nitrites in urine and why?

A

gram negatives

convert dietary nitrates into nitries

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67
Q

what main 5 diagnoses does the persistent presence of protein in urine suggest?

A 
renal disease
UTI
hypertension
pre-eclampsia
congestive heart failure
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68
Q

what does the presence of blood in urine suggest?

A

serious renal or urological disease

UTI

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69
Q

what does the presence of ketones in urine suggest?

A

starvation

uncontrolled diabetes

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70
Q

what are the 5 main causes of glucose in urine?

A 
uncontrolled diabetes
stress
cushings syndrome
post-general anaesthetic 
acute pancreatitis

(because of either increased blood glucose levels or reduced renal glucose absorption)

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71
Q

if not tested within one hour of collection, where should urine be stored?

A

refrigerator

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72
Q

where should the urine reagent strips be stored?

A

a cool, dry place

do not put in refrigerator

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73
Q

are acinar cells the exocrine or endocrine part of the pancreas?

A

exocrine

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74
Q

what cells secrete insulin?

A

pancreatic beta cells

found in pancreatic islets

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75
Q

what cells secrete glucagon?

A

pancreatic alpha cells

found in pancreatic islets

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76
Q

compare glucagon and insulin in terms of effect on hepatic glucose output? (gluconeogenesis)

A

insulin decreases gluconeogenesis

glucagon increases gluconeogenesis

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77
Q

what secretes somatostatin?

A

pancreatic delta cells

found in pancreatic islets

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78
Q

what organelle synthesise preproinsulin? (the larger single chain preprohormone of insulin)

A

rough endoplasmic reticulum

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79
Q

what type of insulin was used before human insulin?

A

bovine insuline

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80
Q

what transporter does glucose enter pancreatic B cells via?

A

GLUT 2

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81
Q

once inside a pancreatic B cell, what enzyme phosphorylates the glucose?

A

glucokinase

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82
Q

once inside a pancreatic B cell, what does glucokinase convert glucose into?

A

glucose-6-phosphate

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83
Q

what happens to the pancreatic beta cell intracellular ATP concetration as the metabolism of glucose increases?

A

ATP concentration increases

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84
Q

how many molecules of ATP are produced after oxidative phosphorylation of one glucose molecule?

A

36

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85
Q

what does ATP within the pancreatic beta cell do to the ATP-sensitive K+ channels? and what does this cause?

A

ATP inhibits the ATP-sensitive K+ channels

prevents K+ efflux

therefore cause depolarisation of the beta cell membrane

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86
Q

inhibition of K+ efflux within the pancreatic beta cell cause depolarisation of the beta cell membrane, what does this result in?

A

opening of voltage-gated Ca2+ channels

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87
Q

what does an increase of intracellular calcium within the pancreatic beta cell cause?

A

fusion of the secretory vesicles with the cell membrane (exocytosis)
–> release of insulin into the bloodstream

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88
Q

how many stages of insulin release are there after glucose is administered orally?

A

2 stages

biphasic

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89
Q

compare the 2 stages of insulin release?

A

1st stage: insulin granules immediately available for release from readily releasable pool
2nd stage: reserve pool must undergo preparation reactions to become mobilised and then release

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90
Q

what is the target for sulphonylurea drugs? (in diabetes)

and how does it work?

A

the sulphonylurea subunit of the ATP-sensitive K channel

inhibits the ATP-sensitive K channel to cause depolarisation

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91
Q

how many proteins make up the ATP-sensitive K channel?

A

2

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92
Q

what cells must be functioning in order for sulphonylureas to be useful in the treatment of diabetes?

A

pancreatic B cells

working beta cells, but defective ATP-sensitive K channels

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93
Q

what is the function of diazoxide on ATP-sensitive K channels within pancreatic B cells?

A

stimulates the ATP-sensitive K channels causing repolarisation and inhibits insulin secretion

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94
Q

what is MODY?

A

maturity-onset diabetes of the young

familial form of early-onset type 2 diabetes

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95
Q

what enzyme do mutations causing MODY affect?

A

glucokinase

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96
Q

what do MODY mutations do to the blood glucose threshold for insulin secretion?

A

increase the blood glucose threshold for insulin secretion

glucose sensing defect

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97
Q

why can MODYs be treated with sulphonylurea?

A

because they have working beta cells

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98
Q

what is the primary problem in type 2 diabetes?

A

reduced insulin sensitivity in tissues

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99
Q

what are the 3 amino acids that can be phosphorylated and why?

A

serine
threonine
tyrosine

because they have an OH group

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100
Q

what charge is introduce into the protein structure when serine, threonine or tyrosine are phosphorylated?

A

a large negative charge

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101
Q

what are the subunits of an insulin receptor?

A

2 extracellular alpha subunits

2 transmembrane beta subunits

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102
Q

what are the insulin-binding domains on the insulin receptor?

A

the 2 extracellular alpha subunits

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103
Q

what are the subunits of the insulin receptor linked by?

A

disulfide bonds

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104
Q

what does binding of insulin to the alpha subunits cause?

A

autophosphorylation of the beta subunits thus activating the catalytic activity of the receptor

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105
Q

glucose enters cells via what transporter?

A

GLUT 4

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106
Q

in which type of diabetes can ketoacidosis occur?

A

type 1 diabetes

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107
Q

where are ketone bodies formed?

A

liver mitochondria

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108
Q

what type of oxidation converts acetyl Co-A into ketone bodies?

A

beta-oxidation

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109
Q

when is acetyl coA converted to ketone bodies?

A

when there is no oxaolacetate to allow acetyl CoA to enter the TCA

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110
Q

why might oxaloacetate be unavailable for the TCA cycle?

A

during times of starving oxaloacetate is used for gluconeogenesis and is not generated through glycolysis

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111
Q

what is broken down into acetyl CoA?

A

fatty acids

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112
Q

why does ketoacidosis occur in type 1 diabetes?

A

when insulin isn’t injected, cells fail to receive enough glucose and therefore switch to fat breakdown.
fatty acids are broken down into acetyl CoA which can’t go through the TCA cycle so form ketone bodies
–> ketoacidosis

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113
Q

why is there no ketoacidosis normally in type 2 diabetes?

A

the high concentrations of insulin in inhibit lipase (the enzyme which breaks down triglycerides into glycerol and free fatty acids)

–> no excessive breakdown of fat resources

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114
Q

what does insulin do to the activity of hexokinase?

A

increases the activity of hexokinase

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115
Q

what does glucagon do to the activity of phosphofructokinase?

A

decreases the activity of phosphofructokinase

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116
Q

what are the 3 ketone bodies?

A

acetone
acetoacetic acid
beta-hydroxybutyric acid

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117
Q

compare the half lives of steroid hormones to tyrosine derivative hormones?

A

steroid hormones have a longer half life

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118
Q

how many transmembrane domains are there in a G-protein coupled receptor?

A

7 transmembrane domains

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119
Q

what are the 5 hormones secreted from the anterior pituitary?

A
  • growth hormone (GH)
  • luteninsing hormone/follicle stimulating hormone (LH/FSH)
  • adrenocorticotrophic hormone (ACTH)
  • thyroid stimulating hormone (TSH)
  • prolactin (PRL)
120
Q

what are the 2 hormones secreted from the posterior pituitary gland?

A
  • ADH

- oxytocin

121
Q

what does normal TSH usually indicate about thyroid function?

A

normal thyroid function

122
Q

what does raised TSH usually indicate about thyroid function?

A

hypothyroid

123
Q

what does low TSH usually indicate about thyroid function?

A

hyperthyroid

124
Q

when might TSH not be a reliable marker of thyroid status?

A 
when there is pituitary dysfunction
eg
secondary hypothyroidism
(low TSH causing hypothyroid)
or 
TSHoma
(high TSH causing hyperthyroid)
125
Q

what is released by the hypothalamus to stimulate the anterior pituitary to secrete ACTH?

A

CRH

corticotrophin-releasing hormone

126
Q

what 2 hormones does cortisol have negative feedback upon?

A

CRH
(corticotrophin-releasing hormone)
ACTH
(adrenocorticotrophic hormone)

127
Q

when is the best time to measure cortisol?

128
Q

why are cortisol levels highest in the morning?

A

prepares body for physiological demands of the day

129
Q

what hormone released by the hypothalamus acts as a positive stimulatory hormone on the pituitary gland, causing it to release growth hormone?

A

-GHRH

growth hormone releasing hormone

130
Q

growth hormone acts on the liver to produce what hormone?

A

insulin-like growth factor 1

IGF-1

131
Q

what is a surrogate marker used to estimate GH activity?

A

IGF-1

insulin-like growth factor 1

132
Q

when GH is at high concentrations, what will the surrogate marker IGF-1 be?

133
Q

when GH is at low concentrations, what will the surrogate marker IGF-1 be?

A

might be normal

other things cause the production of IGF-1

134
Q

can IGF-1 measurement indicate GH hypersecretion or hyposecretion?

A

hypersecretion

when IGF-1 is high, GF is high; when IGF-1 is normal, GF might be normal or low- unable to tell

135
Q

when should you measure testosterone?

136
Q

dopamine (produced by the hypothalamus) has what effect on the anterior pituitary gland in terms of prolactin secretion?

A

dopamine inhibits prolactin secretion

137
Q

what autocrine/paracrine effect does prolactin have on target breast tissue?

A

positive feedback

138
Q

what receptor mediates the effects or prolactin?

A

prolacin receptor (PRLR)

139
Q

what effect does vasopressin have on blood vessels?

A

constriction

140
Q

what effect does vasopressin have on the kidneys?

A

increases fluid reabsorption

141
Q

what overall effect does vasopressin have on the blood pressure?

A

increases arterial pressure

142
Q

what is cortisol deficiency caused by?

A

adrenal insufficiency due to
-primary adrenal failure
or
-pituitary disease (secondary hypoadrenalism)

143
Q

in UK what is the most common cause of primary adrenal failure?

A

autoimmune (addison’s disease)

144
Q

what is addison’s disease caused by?

A

primary adrenal failure caused by autoimmune destruction of the adrenal cortex

145
Q

what is cushings syndrome?

A

cortisol excess for any reason

146
Q

what is cushings disease?

A

cortisol excess due to pituitary problem

147
Q

what are the 4 main causes of cortisol excess? (cushings syndrome)

A
  • pituitary origin
  • adrenal origin
  • ectopic ACTH
  • exogenous steoirds
148
Q

if there is a hormone excess, should you do a suppression or stimulation test?

A

suppression test

149
Q

if there is a hormone deficiency should you do a suppression or stimulation test?

A

stimulation test

150
Q

how do you undertake dynamic testing of a deficiency in cortisol production?

A

stimulation test
-synacthen test
(synthetic ACTH)

151
Q

how do you undertake dynamic testing of an excess in cortisol production?

A

suppression test

-using dexamethasone

152
Q

are the 4 causes of cushings syndrome ATCH- dependent or independent?

A
  • pituitary cause: ATCH- dependent
  • adrenal cause: ATCH-independent
  • ectopic cause: ATCH- dependent
  • exogenous steroids:@ ATCH- independent
153
Q

if there is a failure of cortisol suppression on low dose dexamethasone suppression testing, what does this indicate?

A

cushings syndrome

154
Q

if there is a failure of cortisol suppression on low dose dexamethasone suppression testing, and the ATCH is low, what is the likely origin of cushings syndrome?

A

adrenal cause

155
Q

if there is a failure of cortisol suppression on low dose dexamethasone suppression testing, and the ATCH is high, what is the likely origin of cushings syndrome?

A

pituitary, or ectopic aCTH

156
Q

compare hormones released from posterior and anterior pituitary in terms of where they are synthesiseed?

A

hormones released from anterior pituitary are synthesised in the anterior pituitary gland

hormones released from the posterior pituitary are synthesised in the hypothalamus

157
Q

what hormone produced from the hormone causes the release of LH/FSH within the pituitary?

A

GnRH

gonadotrophin releasing hormone

158
Q

what does an insulin stress test measure?

A

the increase in growth hormone and cortisol

159
Q

what do stress hormones do to the blood sugar?

160
Q

what is a synacthen test?

A

when you inject ACTH to measure cortisol response

stimulation test

161
Q

is an insulin stress test a suppression or stimulation test?

A

stimulation test

162
Q

what is a water deprivation test?

A

deprive patient of water for 8 hours and the measure concentration of urine
(it should have doubled by 2)

163
Q

what hormone is a water deprivation test testing?

164
Q

is a water deprivation test a stimulation or suppression test?

A

stimulation

165
Q

what are the 5 physiological causes of raised prolactin?

A 
breast feeding
pregnancy
stress
sleep
nipple stimulation
166
Q

what are the 3 pathological causes of raised prolactin?

A

hypothyroidism (low DA)
stalk lesions
prolactinoma

167
Q

what is the first line treatment for raised prolactin?

A

dopamine agonists

168
Q

what do dopamine agonists do to prolactinomas?

A

make them shrink

169
Q

is a glucose tolerance test for testing GH a stimulation or suppression test?

A

suppression test

170
Q

compare the GH response in a patient with acromegaly to a normal response after a glucose tolerance test?

A

normal GH should decrease

acromegaly: GH will not be suppressed

171
Q

what medications can be used in the treatment of acromegaly?

A

somatostatin analogues
(dopamine analogues,
GH antagonist)

172
Q

what are the 3 short term side effects of somatostatin analogues?

A

flactulence
diarrhoea
abdo pain

173
Q

what are the 2 long term side effects of somatostatin analogues?

A

gastritis

gallstones

174
Q

how do you do a suppression test for cushings?

A

dexamethasone

exogenous steroid

175
Q

compare normal response to exogenous dexamethasone to a cushings response?

A

normal: cortisol levels decrease
cushings: cortisol levels remain high

176
Q

what is mineralocorticoid activity?

A

the retention of sodium in exchange for potassium or hydrogen ions

177
Q

what is the main steroid with mineralocorticoid activity?

A

aldosterone

178
Q

what organ makes renin?

179
Q

what is the function of renin?

A

converts angiotensinogen to angiotensin I

180
Q

what happens to the rate of renin secretion if there is low blood pressure?

A

low blood pressure within the kidney causes increased rate of renin secretion

181
Q

what happens to the concentration of the urine when there is increased ADH secretion?

A

increased concentration of urine

182
Q

what happens to the concentration of the urine when there is decreased ADH secretion?

A

decreased concentration of urine (dilute)

183
Q

does concentrated urine have a low or high osmolality?

A

high osmolality

184
Q

does dilute urine have a low or high osmolality?

A

low osmolality

185
Q

what are the 2 possible causes of low serum sodium? (ie in terms of water or sodium)

A

too much water

too little sodium

186
Q

what are the 2 possible causes of high serum sodium? (ie in terms of water or sodium)

A

too much sodium

too little water

187
Q

what are the 2 main reasons for too much water? (in terms of excretion and intake)

A

decreased excretion

increased intake

188
Q

what condition causes increased intake of water which could cause decreased serum sodium?

A

compulsive water drinking

189
Q

what does syndrome of inappropriate anti-diuresis (SIAD) do to the rate of water excretion?

A

decreases the rate of water excretion

190
Q

what are the 2 main reasons for too little sodium? (in terms of excretion and intake)

A 
decreased intake (rare)
increased excretion
191
Q

what 3 organs are the main areas within the body wear sodium is lost?

A

kidneys
gut
skin

192
Q

what is addison’s disease?

A

adrenal insufficiency

193
Q

why might there be increased sodium loss from the kidneys in addison’s disease?

A

insufficient aldosterone is produced and so not enough sodium can be retained

194
Q

what are the 2 major reasons for sodium loss from the skin?

A

sweating

burns

195
Q

what are the 2 main causes for too little water? (in terms of excretion and intake)

A

decreased water intake

increased water excretion

196
Q

what is the name for disruption of water balance axis causing inappropriately increased water excretion?

A

diabetes insipidus

197
Q

what goes wrong in diabetes insipidus?

A
  • problem with ADH secretion (central diabetes insipidus)

- problem with ADH action on the kidneys (nephrogenic diabetes insipidus)

198
Q

what is the main cause of too much sodium? (in terms of excretion or intake)

A

increased intake

199
Q

what are the 3 main causes of increased sodium intake which can lead to increased serum sodium?

A

IV medications given as sodium salts

near-drowning in sea

high-salt infant feeds

200
Q

a low BP which falls on standing points to the likelihood that what salt is low?

201
Q

why might a patient with addison’s disease get symptoms of dizziness?

A

due to hypotension from too little water

202
Q

why might a patient with addison’s disease have excess pigmentation?

A

the adrenal glands are insufficient and so the lack of aldosterone/cortisol negative feedback causes the ACTH levels to greatly increase.
ACTH is degraded by proteases causing a release of melanocyte stimulating hormone which causes pigmentation

203
Q

when there is too much water due to inappropriate ADH secretion (SAID) what are the serum sodium levels and the volume status?

A

low serum sodium level

unremarkable volume status

204
Q

what investigation is used to look for Addison’s disease?

A

serum cortisol

205
Q

what does non-osmotic stimuli for ADH release do to the serum sodium?

A

decreases serum sodium

206
Q

what is the problem (sodium or water) when there is hypovolaemia and hyponatraemia?

A

too little sodium

207
Q

when is hypervolaemia most often seen?

208
Q

what is pseudohyponatraemia?

A

when total sodium is low but serum osmolality is normal

209
Q

what are trophic hormones?

A

hormones which act on other endocrine glands

210
Q

what are non-trophic hormones?

A

hormones which act on target cells directly

211
Q

what are the 4 trophic hormones produced by the anterior pituitary?

A

ACTH
TSH
FSH
LH

212
Q

what are the 2 non-trophic hormones produced by the anterior pituitary?

A

GH

prolactin

213
Q

what are the 3 main cell type within the anterior pituitary gland?

A

acidophils
basophils
chromophobes

214
Q

what cells within the anterior pituitary gland produce growth hormone? and what type of cell is this?

A

somatotrophs

a type of acidophil

215
Q

what cells within the anterior pituitary gland produce prolactin? and what type of cell is this?

A

mammotrophs

a type of acidophil

216
Q

what cells within the anterior pituitary gland produce adrenocorticotrophic hormone? and what type of cell is this?

A

corticotrophs

a type of basophil

217
Q

what cells within the anterior pituitary gland produce thyroid stimulating hormone? and what type of cell is this?

A

thyrotrophs

a type of basophil

218
Q

what cells within the anterior pituitary gland produce FSH/LH? and what type of cell is this?

A

gonadotrophs

a type of basophil

219
Q

what are the 2 main reasons for hyperfunction of the anterior pituitary gland?

A

adenoma

carcinoma

220
Q

what are the 5 main reasons for hypofunction of the anterior pituitary gland?

A
  • surgery/radiation
  • sudden haemorrhage into gland
  • ischaemic necrosis
  • tumours extending into sella
  • inflammatory conditions
221
Q

what is the most common functional pituitary adenoma?

A

prolactinoma

222
Q

what is panhypopituitarism?

A

pituitary hypofunction of all the anterior pituitary hormones
(not just individual ones)

223
Q

what are craniopharyngiomas derived from?

A

remnants of rathke’s pouch

the pouch from which the anteiror pituitary was derived

224
Q

craniopharyngiomas have a bimodal incidence, when are they prevalent?

A
  • 5-15 years

- 60- 75 to years

225
Q

what is the rare but serious complication of craniopharyngioma?

A

squamous cell carcinoma

esp following radiation

226
Q

what are the 2 main causes for central diabetes insipidus?

A

ADH deficiency

trauma/surgery

227
Q

what is the main cause of nephrogenic diabetes insipidus?

A

renal resistance to ADH

228
Q

what type of hormones are produced from the adrenal cortex?

A

steroid hormones

229
Q

what type of hormones are produced from the adrenal medulla?

A

catecholamine hormones

230
Q

what are the 3 zones of the cortex?

A

zona glomerulosa
zona fasciculata
zona reticularis

231
Q

what are the main hormones secreted by the zona glomerulosa of the adrenal cortex?

A

mineralocorticoids

eg aldosterone

232
Q

what are the main hormones secreted by the zona fasciculata of the adrenal cortex?

A

glucocorticoids

eg cortisol

233
Q

what are the main hormones secreted by the zona reticularis of the adrenal cortex?

234
Q

what is the adrenal medulla innervated by?

A

pre-synaptic fibres from the sympathetic nervous system

235
Q

what cells within the medulla secrete catecholamines?

A

chromaffin cells

236
Q

what are the 3 main reasons for hyperfunction of the adrenal gland? (primary)

A

hyperplasia
adenoma
carcinoma

237
Q

what are the 3 main causes of acute hypofunction of the adrenal gland? (primary)

A
  • waterhouse-friderichsen
  • rapid withdrawal of steroid treatment
  • adrenal haemorrhage
238
Q

what is the main cause of chronic hypofunction of adrenal gland? (primary)

A

addison’s disease

239
Q

acquired adrenocortical hyperplasia can be ACTH driven or independent. Is diffuse hyperplasia ACTH driven or independent?

A

ACTH driven

240
Q

acquired adrenocortical hyperplasia can be ACTH driven or independent. Is nodular hyperplasia usually ACTH driven or independent?

A

ACTH independent

241
Q

what syndrome describes the effects of primary hyperaldosteronism?

A

conn’s syndrome

242
Q

what are the 2 main causes of secondary hyperaldosteronism?

A
  • increased renin

- decreased renal perfusion (ie hypovolaemia)

243
Q

what are the 2 adrenal medullary tumours?

A

phaeochromocytoma

neuroblastoma

244
Q

when are neuroblastomas diagnosed?

A

within 18 months usually

otherwise diagnosed in infancy

245
Q

where do neuroblastomas arise?

A

adrenal medulla

sympathetic chain

246
Q

what are phaeochromocytoma cells derived from?

A

chromaffin cells of the adrenal medulla

247
Q

what hormones do phaeochromocytomas secrete?

A

carecholamines

248
Q

what do phaeochromocytomas do to blood pressure?

A

cause it to drastically increase

249
Q

what is the 10% phaeochromocytoma rule? (7)

A 
10% are extra-adrenal
10% are bilateral
10% malignant
10% are not associated with hypertension
10% are associated with hyperglycaemia
10% in children
10% familial (more like 25% now)
250
Q

are phaeochromocytomas part of MEN 1 or MEN 2?

251
Q

what are the 7 main contents of the cavernous system?

A
  • carotid artery
  • cavernous sinus
  • oculomotor nerve
  • trochlear nerve
  • opthalmic branch of trigeminal nerve
  • maxillary branch of trigeminal nerve
  • abducens nerve
252
Q

what system regulates the aldosterone levels within the body?

A

the renin-angiotensin system

253
Q

what doses of corticosteroids are use in the suppression of inflammation? (physiological, supraphysiological or subphysiological)

A

supraphysiological

254
Q

what doses of corticosteroid are used in the suppression of immune system? (physiological, supraphysiological or subphysiological)

A

supraphysiological

255
Q

what doses of corticosteroids are used in steroid replacement treatment? (physiological, supraphysiological or subphysiological)

A

physiological

256
Q

what are the 4 main causes of primary adrenal insufficiency?

A

Addison’s (autoimmune)
congenital adrenal hyperplasia
adrenal malignancy
adrenal TB

257
Q

compare Na and K levels in a patient with Addison’s disease to normal levels?

A

Na reduced

K increased

258
Q

what stimulation test can be used in the diagnosis of primary adrenal insufficiency?

A

short synacthen test

ACTH IV/IM and measure plasma cortisol

259
Q

when treating primary adrenal insufficiency what drugs are used as cortisol and aldosterone replacement?

A

hydrocortison to replace cortisol

fludrocortisone to replace aldosterone

260
Q

why do you not need to give fludrocortisone to a patient with secondary adrenal insufficiency?

A

because aldosterone production will be preserved due to renin-angiotensin system

261
Q

what is the most common cause of secondary adrenal insufficiency?

A

exogenous steroid use

262
Q

compare the clinical features of secondary adrenal insufficiency to Addison’s?

A

similar except in secondary adrenal insufficiency the aldosterone production is intact, and the skin remains pale (no excessive ACTH)

263
Q

what are the 3 main causes of ACTH dependent cushing’s syndrome?

A

pituitary adenoma (cushings disease)
ectopic ACTH
ectopic CRH

264
Q

what are the 3 main causes of ACTH independent cushing’s syndrome?

A

adrenal adenoma
adrenal carcinoma
nodular hyperplasia

265
Q

what are the 3 main screening tests used in cushings syndrome?

A
  • overnight dexamethasone suppression test
  • 24 hour urinary free-cortisol
  • late night salivary cortisol
266
Q

what is the definitive test for cushing’s syndrome?

A

low dose dexamethasone suppression test over 2 days

and repeat to confirm

267
Q

why can prolonged high dose steroid therapy cause secondary adrenal deficiency?

A

chronic suppression of pituitary ACTH production and adrenal atrophy

268
Q

what is the most common cause of cushing’s syndrome?

A

iatrogenic (due to high dose steroid therapy)

269
Q

what is the most common cause of primary aldosteronism?

A

bilateral adrenal hyperplasia

270
Q

what causes conn’s syndrome?

A

an adrenal adenoma

unilateral

271
Q

what suppression test can be used for the diagnosis of primary aldosteronism?

A

saline suppression test

272
Q

what is the treatment of a conn’s adenoma causing aldosteronism?

273
Q

what is the treatment of bilateral adrenal hyperplasia?

A

use mineralocorticoid receptor antagonists eg spironolactone or eplerenone

274
Q

what is the most common cause of congenital adrenal hyperplasia?

A

21a hydroxylase deficiency

an enzyme defect within the steroid pathway

275
Q

what type of inheritence is 21a hydroxylase deficiency? (which leads to congenital adrenal hyperplasia)

A

autosomal recessive

276
Q

what are the 2 variants of 21a hydroxylase deficiency?

A

classical

non-classical

277
Q

compare classical and non-classical variants of 21a hydroxylase deficiency in terms of the extent of deficiency?

A

classical: complete deficiency

non-classical

278
Q

how do you diagnose 21a hydroxylase deficiency?

A

basal or stimulated 17-OH progesterone level

279
Q

in 17 hydroxylase deficiency, what is the only cortex hormone which can still be made?

A

aldosterone

280
Q

in 21a hydroxylase deficiency, what is the only cortex hormone which can still be made?

A

testosterone (through DHEA)

281
Q

what is the name for a extra-adrenal phaeochromocytoma?

A

paraganglioma

within the sympathetic chain

282
Q

blocking sympathetic system is how some phaeochromocytomas are managed, which should be blocked first alpha or beta receptors?

A

alpha before beta

283
Q

compare MEN 1 and MEN 2 in terms of type of genes affected?

A

MEN1: tumour suppressor gene is inactivated
MEN2: ongogene is activated into proto-oncogene

284
Q

what type of inheritance is von hippel lindau syndrome?

A

autosomal dominant

285
Q

what gene is mutated in von hippel lindau syndrome?

A

von hippel lindau tumour suppressor gene

286
Q

what type of receptor does growth hormone signal via?

A

cytokine receptor

287
Q

what type of receptor does calcium signal via?

A

g-protein coupled receptor

288
Q

which facial nerve (trochlear or abducens) is involved in lateral gaze?

289
Q

which facial nerve (trochlear or abducens) is involved in medial gaze?

290
Q

what receptor do TZDs work on?

291
Q

what is the iodine uptake of acute thyroiditis on scan?

A

reduced/no uptake

292
Q

compare macroprolacitinomas and microprolactinomas in terms of size?

A

macro over 1cm

micro under 1cm

293
Q

what syndrome is usually present if there is metastatic disease to the pituitary gland/.

A

diabetes insipidus

294
Q

why must you always give hydrocortisone before thyroxine in panhypopituitarism? (ie in a non-functioning tumour)

A

to prevent an addisonian crisis

295
Q

what is the classic symptom triad of a phaeochromocytoma?

A

headaches
sweating
palpitations

Endocrine (5 decks)

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