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year 2 > adrenal gland > Flashcards

adrenal gland Flashcards

1
Q

what are the 3 zones of the adrenal cortex

A

glomerulosa
fasiculata
reticularis

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2
Q

what is made in the zona glomerulosa

A

mineralocorticoids

aldosterone

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3
Q

what is made in the zona fasiculata

A

glucocorticoids

cortisol

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4
Q

what is made in the zona reticularis

A

sex steroids

glucocortioids

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5
Q

what is the medulla of the adrenal gland innervated by

A

presynaptic fibres from sympathetic system (splanchnic nerves)

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6
Q

what are the neuroendocrine cells in the medulla of the adrenal gland called and what do they secrete

A

chromaffin cells

secrete catecholamines - adrenaline and noradrenaline

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7
Q

how is the release of cortisol and androgen from the adrenal gland controlled

A

HPA axis

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8
Q

how is the release of aldosterone from the adrenal gland regulated

A

RAAS and plasma potassium

activated in response to fall in BP

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9
Q

where are mineralocorticoid receptors for aldosterone found

A

kidneys
salivary glands
sweat glands
gut

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10
Q

what are the effects of aldosterone via mineralocorticoid receptors

A

sodium reabsorption
K+/H+ excretion
–> BP regulation, ECFV regulation and sodium/potassium balance

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11
Q

what is the cause of CAH

A

deficiency of enzymes required for steroid biosynthesis

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12
Q

what is the enzyme most commonly deficient in CAH

A

alpha-21-hydroxylase

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13
Q

what is the inheritance pattern of CAH

A

autosomal recessive

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14
Q

how does a lack of alpha-21-hydroxylase cause cortical hyperplasia

A

lack of cortisol causes release of ACTH from hypothalamus causing hyperplasia of the adrenal gland

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15
Q

what are the 2 main presentations of CAH

A

classical - simple virilising/salt wasting

non-classical - hyperandrogenaemia

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16
Q

how does classical CAH present

A

salt wasting crisis at 2-3 weeks age
female genital ambiguity
poor weight gain
high potassium low sodium

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17
Q

how does non-classical CAH present

A 
hirsute
acne
oligomenorrhoea
precocious puberty
masculinisation
infertility/subfertility
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18
Q

does non-classical or classical present earlier

A

classical

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19
Q

how can CAH be diagnosed

A

basal or stimulated 17-OH progesterone
genetic mutation analysis
synacthen

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20
Q

what is the treatment for CAH

A

replace glucocorticoid
replace aldosterone (in some)
surgical correction
in older - correct androgen excess

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21
Q

true/false

adrenocortical tumours are more common in females

A

false - equal men and women

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22
Q

what are the 2 main types of adrenocortical tumours

A

adrenocortical adenoma

adrenocortical carcinoma

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23
Q

how would you describe an adrenocortical adenoma

A

well circumscribed encapsulated lesion buried within gland

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24
Q

what colour are adrenocortical adenomas

A

yellow/yellow-brown surface (lipid)

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25
Q

what size are adrenocortical adenomas?

do they cause a mass lesion?

A

usually small 2-3cm

no

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26
Q

do adrenocortical adenomas usually occur alone or multiple

A

solitary

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27
Q

adrenocortical adenomas are composed of cells resembling —-

A

adrenocortical cells

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28
Q

what may been seen in adrenocortical adenomas

A

spironolactone bodies

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29
Q

what are the nuclei like in adrenocortical adenomas

A

small

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30
Q

are mitoses rare or common in adrenocortical adenomas

A

rare

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31
Q

are adrenocortical adenomas usually functional or non-functional

A

can be functional but usually not

Can cause Conn’s syndrome

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32
Q

is the adjacent and contralateral tissue in adrenocortical adenomas atrophic

A

no - ACTH not suppressed so adjacent and contralateral tissue not atrophic

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33
Q

are adrenocortical carcinomas functional

A

more likely to be

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34
Q

although adrenocortical carcinomas can resemble adrenocortical adenomas, what are some features suggestive of a carcinoma

A 
large size
haemorrhage and necrosis
frequent, atypical mitoses
lack of clear cells
capsular or vascular invasion
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35
Q

what is the 5 year survival rate of adrenocortical carcinomas

A

20-30%

50% dead in 2 years

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36
Q

what is an example of a functional adrenocortical carcinoma

A

androgen secreting tumour

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37
Q

how would an androgen secreting adrenocortical carcinoma be diagnosed

A

MRI of adrenals and ovaries

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38
Q

what would happen with an androgen secreting adrenocortical carcinoma

A

rapid onset symptoms
virilisation
high levels testosterone

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39
Q

where would an adrenocortical carcinoma spread locally

A

retroperitoneum

kidney

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40
Q

where would mets of an adrenocortical carcinoma tend to go/spread

A

haem spread

liver, lung, bone

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41
Q

where else might an adrenocortical carcinoma spread

A

peritoneum

pleura

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42
Q

what is primary hyperaldosteronism

A

autonomous production of aldosterone independent of its regulation

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43
Q

primary hyperaldosteronism is the commonest secondary cause of what

A

hypertension

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44
Q

what is the most common cause of primary hyperaldosteronism

A

adrenal adenoma (Conn’s syndrome)

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45
Q

what is the second commonest cause of primary hyperaldosteronism

A

bilateral adrenal hyperplasia

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46
Q

what is a genetic mutation that can cause Conn’s syndrome

A

mutation in the KCNJ5 channel

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47
Q

what is the KCNJ5 channel

A

rectifying selective channel that maintains membrane hyperpolarisation - mutations lead to loss of selectivity and Na+ entry and depolarisation

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48
Q

give 2 other rare causes of primary hyperaldosteronism

A

adrenal carcinoma

unilateral hyperplasia

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49
Q

what is the main s/s of primary hyperaldosteronism

A

significant hypertension

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50
Q

what happens to potassium levels in primary hyperaldosteronism

A

hypokalaemia

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51
Q

do you get acidosis or alkalosis with primary hyperaldosteronism

A

alkalosis

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52
Q

what causes hypertension in primary hyperaldosteronism

A

Na reabsorption - water retention

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53
Q

what would the renin levels be like in primary hyperaldosteronism

A

decreased renin

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54
Q

what are the 2 stages in diagnosing primary hyperaldosteronism

A

confirm aldosterone excess

confirm subtype

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55
Q

how do you confirm aldosterone excess in primary hyperaldosteronism

A

measure of aldosterone to renin plasma ratio

if raised, further investigate with a saline suppression test

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56
Q

what would happen in a saline suppression test with primary hyperaldosteronism

A

failure of plasma aldosterone to suppress by >50% with 2L normal saline - primary hyperaldosteronism

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57
Q

how do you confirm the subtype of primary hyperaldosteronism

A

adrenal CT/adrenal vein sampling for adenoma

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58
Q

what is the treatment of Conn’s

A

unilateral laparoscopic adrenalectomy

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59
Q

what is the treatment of bilateral adrenal hyperplasia

A

MR antagonists

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60
Q

give 2 examples of MR antagonists

A

spironolactone

eplerenone

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61
Q

what can cause secondary hyperaldosteronism

A

high renin from decreased renal perfusion

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62
Q

what are some causes of acute primary adrenocortical hypofunction

A

Waterhouse-friderichsen (bilateral adrenal cortex haemorrhage) - commonly after infection
rapid withdrawal of steroid treatment
adrenal crisis in patient with chronic adrenocortical insufficiency due to stress

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63
Q

what is the most common cause of primary adrenal insufficiency

A

addisons

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64
Q

what is a cause of secondary adrenocortical hypofunction

A

lack of ACTH stimulation

  • hypopituitarism
  • suppression of adrenal cortex (exogenous steroids)
65
Q

what is addisons disease

A

autoimmune destruction of the adrenal cortex leading to glucocorticoid and mineralocorticoid deficiency

66
Q

what percentage of people with addisons are antibody positive

A

70%

67
Q

what are some s/s of addisons

A 
weakness
fatigue
anorexia
N+V
weight loss
craving salty food
tearful/depression
vitiligo
diarrhoea
constipation
skin pigmentation
dizzy/faint
low BP
abdominal pain
myalgia
arthralgia
postural hypotension
68
Q

what causes the skin pigmentation in addisons

A

ACTH cross reacts with melanin receptors

69
Q

what would the Na and K levels be like in addisons

A

low Na

high K

70
Q

would someone with addisons by hypo or hypertensive

A

hypotensive

71
Q

would someone with addisons by hypo or hyper glycaemia

A

hypogylcaemia

72
Q

what other biochemistry might be seen in someone with addisons

A

uraemia
increased calcium
eosinophilia
anaemia

73
Q

how is addisons diagnosed

A

biochemistry
short synacthen test
adrenal autoantibodies

74
Q

describe a short synacthen test and what results would be normal as baseline cortisol and after the test

A

measure plasma cortisol before and 30 mins after IV/IM ACTH injection
normal:
cortisol baseline > 250 nmol/L
cortisol after ACTH > 550nmol/L

75
Q

what would the levels of ACTH and renin be like in addisons

A

raised

76
Q

what is the treatment for addisons

A

hydrocortisone + fludrocortisone

77
Q

how should dosage be changed in a person with addisons if they are ill/injured/stressed

A

double dose

78
Q

should you wait until a diagnosis before starting treatment?

A

no - start treatment before disgnosis

79
Q

what is the treatment for an adrenal crisis

A

hydrocortisone 100mg IV
IV fluid bolus
monitor blood glucose - risk of hypo
if high K - calcium gluconate

80
Q

would someone with secondary adrenal insufficiency have tinted skin

A

no - no increased ACTH

81
Q

what are the 2 main tumours of the adrenal medulla

A

neuroblastoma

phaeochromocytoma

82
Q

when are neuroblastomas usually diagnosed

A

around 18 months

83
Q

40% of neuroblastomas arise in the adrenal medulla - where do the rest arise?

A

along sympathetic chain

84
Q

how do the cells in a neuroblastoma appear

A

primitive but can show maturation/differentiation towards ganglion cells

85
Q

what 2 genetic features predict a poor outcome of neuroblastoma

A

amplification of n-myc

expression of telomerase

86
Q

what is a phaechromocytoma

A

neoplasm derived from chromaffin cells of adrenal medulla that secretes catecholamines

87
Q

where do phaeochromocytoma mets go

A

skeletal, regional lymph nodes, liver, lung

88
Q

what is the appearance of a phaeochromocytoma

A

necrotic tumour mass and may see adrenal remnants on surface
yellow/red-brown
necrotic
haemorrhagic

89
Q

why will potassium chromate turn tumour dark brown

A

oxidation of catecholamines in tumour cells

90
Q

tumour cells in phaeochromocytoma form nests what are these called

A

zellballen

91
Q

what are the 6 10% rules of phaeochromocytoma

A 
10% extra adrenal
10% bilateral
10% malignant
10% not assoc. hypertension
10% familial
10% assoc. hyperglycaemia
92
Q

where do extra-adrenal phaeochromocytoma occur

A

along sympathetic chain

93
Q

when phaeochromocytomas occur extra adrenally what are they called

A

paraganglioma

94
Q

where exactly do paragangliomas occur

A

organs of Zuckerkandl (aortic bifurcation)

carotid body

95
Q

what is the only definitive evidence of malignancy with phaeochromocytoma

A

mets

96
Q

if a phaeochromocytoma is familial, is it more or less likely to occur in someone who is younger and is it more or less likely to be bilateral

A

more likely to be younger and bilateral

97
Q

phaeochromocytoma is more often malignant if assoc. with what germline mutation

A

germline mutation of beta subunit of succinate dehydrogenase

98
Q

what is the classic presenting triad of phaeochromocytoma

A

hypertension (50% paroxysmal)/tachycardia/palpitations
headache
sweating

99
Q

what other s/s may be seen in phaeochromocytoma

A 
palpitations
breathlessness
constipation
anxiety
weight loss
flushing
pallor
pyrexia
100
Q

what are some complications of phaeochromocytoma

A 
paralytic ileus of bowel
LV failure
myocardial necrosis
stroke
shock
101
Q

what would K and Ca levels look like in phaeochromocytoma

A

low K

mild hypercalcaemia

102
Q

what would to the WCC in phaeochromocytoma

A

increased

103
Q

what would happen to the haematocrit in phaeochromocytoma

A

high

104
Q

would people with phaeochromocytoma be more likely to be acidotic or alkalotic

A

lactic acidosis

105
Q

who should be investigated for phaeochromocytoma

A 
family members with syndromes
resistant HT
HT < 50
classical symptoms
HT with hyperglycaemia
106
Q

what is an investigation for phaeochromocytoma

A

urine analysis of vanillymandelic acid (VMA) - may be false +ves

107
Q

what are the 2 stages in diagnosing phaechromocytoma

A

confirm catecholamine excess

identify source of catecholamine excess

108
Q

how can you confirm catecholamine excess

A

urine - 2 x 24 hr catecholamines or metanephrines

plasma - ideally at time of symptoms

109
Q

how can you confirm the source of catecolamines

A

MRI/CT
MIBG scan
PET scan

110
Q

what is an MIBG scan

A

meta-iodobenzylguanidine scan - looks for extra adrenal tumours

111
Q

what is the treatment of phaeochromocytoma

A

full alpha and beta blockade
laparoscopic total excision if possible/tumour debulking
chemo if malignant - radio labelled MIBG

112
Q

what comes first alpha or beta blockade in phaeochromocytoma

A

alpha before beta

113
Q

what is an example of an alpha blocker

A

phenoxybenzamine

114
Q

what is an example of a beta blocker used in phaeochromocytoma

A

propranolol, atenolol, metoprolol

115
Q

if someone has borderline catecholamine excess what test can be done

A

clonidine suppression test

116
Q

give 5 syndromes where phaeochromocytoma may be seen

A 
MEN2A/2B
VHL syndrome
succinate dehydrogenase mutations
neurofibromatosis
tuberose sclerosis
117
Q

what else might cause catecholamines to be raised

A

heart failure

118
Q

why might someone with phaeochromocytoma have normal catecholamine levels

A

episodic secretion

119
Q

what is cushings syndrome

A

excess cortisol

120
Q

what is cushings disease

A

cushings syndrome caused by pituitary adenoma

121
Q

are men or women more likely to get cushings

A

women

122
Q

what is the most common cause of cushings

A

pituitary adenoma

123
Q

what is a pituitary adenoma and how does it cause cushings

A

tumour arising from corticotroph cells of anterior pituitary - secretes ACTH

124
Q

is a pituitary adenoma an ACTH dependent or indepentent cause of cushings

A

ACTH dependent

125
Q

is adrenal adenoma/carcinoma an ACTH dependent or indepentent cause of cushings

A

ACTH independent

126
Q

is ectopic CRH from medullary thyroid cancer/prostate cancer an ACTH dependent or indepentent cause of cushings

A

ACTH dependent

127
Q

is an adrenal nodular hyperplasia an ACTH dependent or indepentent cause of cushings

A

ACTH independent

128
Q

is ectopic ACTH from a paraneoplastic syndrome an ACTH dependent or indepentent cause of cushings

A

ACTH dependent

129
Q

what paraneoplastic syndrome causes ectopic ACTH release

A

small cell lung carcinoma

130
Q

what 3 things can cause pseudocushings

A

alcohol
depression
prolonged steroid medication

131
Q

what 2 genetic syndromes can cause cushings

A

Carney complex
Mccune Albright
both ACTH independent

132
Q

what is the first step in diagnosing cushings

A

confirm raised plasma cortisol - overnight dexamethasone suppression test

133
Q

describe the overnight dexamethasone suppression test

A

1mg PO at midnight and measure serum cortisol at 8am

normal: cortisol suppressed to < 50
cushings: no suppression

134
Q

what is a normal level for 24hr urinary free cortisol

A

< 250

135
Q

what is a normal value for cortisol/creatinine ratio

A

< 25

136
Q

what is another easy test to do to measure serum cortisol

A

late night salivary cortisol

137
Q

describe a 48hr low dose dexamethasone suppression test and the findings

A

0.5mg/6hr PO for 2 days
normal: cortisol suppressed to < 50 (6hrs after last dose)
cushings syndrome: no suppression

138
Q

how would you find out if the cause of cushings was pituitary after discovering that the person does have cushings using 48hr low dose dexamethasone suppression test

A

48 hour high dose dexamethasone suppression test
- 2mg/6hr
pituitary cause - suppression
other cause - no/part suppression

139
Q

what are 2 other localising tests

A

plasma ACTH

CRH test

140
Q

if plasma ACTH is undetectable what is likely

A

adrenal tumour

141
Q

if you suspected an adrenal tumour what tests would you carry out

A

CT adrenals

or adrenal vein sampling or adrenal scintigraphy (if no mass found)

142
Q

would plasma ACTH be higher in ectopic ACTH or a pituitary adenoma

A

ectopic ACTH

143
Q

describe a CRH test

A

100 ug CRH IV and measure cortisol at 120 mins

144
Q

what would the results of a CRH test show if cushings was caused by pituitary disease

A

cortisol rises

145
Q

what would you do if you suspected pituitary disease

A

MRI pituitary

146
Q

in ectopic ACTH production what would the CRH test show

A

cortisol doesnt rise

147
Q

if you suspected ectopic production of ACTH what tests would you carry out

A

IV CT contrast of chest,abdo,pelvis

+/- MRI neck, thorax, abdomen

148
Q

pituitary cause LDDT

A

no suppression

149
Q

pituitary cause ACTH

A

< 300

150
Q

pituitary cause HDDT

A

suppression

151
Q

pituitary cause CRH

A

cortisol rises

152
Q

adrenal cause LDDT

A

no suppression

153
Q

adrenal cause ACTH

A

<1

154
Q

adrenal cause HDDT

A

no suppression

155
Q

ectopic LDDT

A

no suppression

156
Q

ectopic ACTH

A

> 300

157
Q

ectopic HDDT

A

no suppression

158
Q

ectopic CRH

A

cortisol doesnt rise

year 2 (19 decks)

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