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Endocrine Pathology > Clinical Aspects of the Adrenal Gland > Flashcards

Clinical Aspects of the Adrenal Gland Flashcards

1
Q

The common approach to assessing a clinical suspicison to the adrenal gland

A 
Testing for assessing functional status
- is it functioning?
- it is primary or secondary?
What is the cause?
If it is a tumour
- can it be removed?
- is additional chemo or radiotherapy required?
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2
Q

An abnormality of cortisol, aldosterone, insulin and vasopressin can cause what?

A

HTN

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3
Q

Endocrine causes of HTN

A 
Primary hyperaldosteronism (unilateral adenoma, bilateral hyperplasia)
Phaechromocytoma 
Cushings syndrome
Acromegaly
Hyperparathyroidism 
Hypothyroidism 
Congenital adrenal hyperplasia
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4
Q

Most common cause of endocrine cause of HTN

A

Primary hyperaldosteronism

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5
Q

Presentation of Cushing’s syndrome

A 
Central obesity
HTN
Glucose intolerance
Hirsutism 
Amenorrhea / impotence
Purple striae 
Plethoric facies
Easily bruise
Osteoporosis
Personality changes 
Acne
Oedema 
Headache 
Poor wound healing
Thin skin ulcers
Pendulous breasts and abdomen 
Moon face
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6
Q

Why do people put on weight in cushing’s disease?

A

Muscle atrophy is replaced by fat

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7
Q

Causes of cushing’s syndrome

A

Corticosteriod Tx for e.g. asthma, IBD
ACTH-dependent
- 75% pituitary tumour (disease)
- 5% ectopic ACTH secretion (e.g. lung carcinoid)
ACTH-independent
- 20% of cases; adrenal tumour (adeno or carcinoma)

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8
Q

What tests are done to screen for hypercortisolism?

A

Overnight Dex test

24 hour urine Free cortisol

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9
Q

What is a DEX test?

A

Dexamethasone Suppression test
Measures how cortisol levels change in response to an injection of dexamethasone.
Dexamethasone provides negative feedback to the pituitary gland to suppress ACTH

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10
Q

How is hypercortisolism confirmed?

A

24 urine free cortisol

Low dose dexamethasone suppression test

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11
Q

Low dose vs high dose Dex Tests

A

Low dose suppresses cortisol in individuals who have no pathology in endogenous cortisol production
A high dose exerts negative feedback on pituitary neoplastic ACTH producing cells (cushing’s disease) but not on ectopic ACTH producing cells or adrenal adenoma (cushing’s syndrome)

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12
Q

How would you test if the hypercortisolism is ACTH dependent or not?

A

Paired morn-midnight ACTH cortisol

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13
Q

How would you localise where the hypercorticolism was coming from?

A

MRI sella turnica
CT adrenal glands
BIPSS
CT chest

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14
Q

How would you know if the ACTH had to do with the pituitary or not in hypercorticolism?

A

High dose dex test

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15
Q

What is conn’s syndrome?

A

Primary hyperaldosteronism

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16
Q

What does conn’s syndrome result in?

A

Decreased renin

Retention of sodium and loss of potassium, leading to HTN

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17
Q

What tests are used to screen for Conn’s syndrome?

A

PAC

PA/PRA Ratio

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18
Q

If the PA/PRA ratio = > 20, what does this indicate?

A

Primary hyperaldosteronism (conns syndrome)

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19
Q

If the PA/PRA ratio = <20, what could this indicate?

A

(Less reliable)
Secondary hyperaldosteronism
Essential hypertension

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20
Q

What does PRA stand for?

A

Plasma renin activity

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21
Q

What does PAC stand for?

A

Plasma aldosterone concentration

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22
Q

Confirmatory tests for Conns syndrome

A

24 hour urine aldosterone > 12 ug/day

Urinary sodium > 200mEq/day during 4 days of salt loading

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23
Q

How do you establish the aldosterone source in conns syndrome?

A

CT scan of adrenal glands
Upright posture test
Plasma 18-hydroxycorticosterone
Adrenal venous sampling if CT scan inconclusive of discordant with posture test

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24
Q

Presentation of phaemochromocytoma

A 
Hypertension (persistent in 70%)
Headache
Sweating
Palpitations 
Tremor
Pallor
Anxiety/fear
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25
Q

How much of phaemochromocytoma is inherited and what genes are implicated?

A

30%
Genes - RET
Familial syndromes - MEN-2, VHL, NF1, PGL

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26
Q

How would you test if clinical suspicion of phaemochromocytoma?

A

24 hour urine

  • total metanephrines
  • catecholamines
  • plasma metanephrines
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27
Q

How would you localise a phaemochromocytoma?

A

Adrenal/abdominal MRI/CT scan

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28
Q

Causes of addisons disease

A 
Autoimmune destruction 
Invasion 
Infiltration 
Infection 
Infarction 
Iatrogenic
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29
Q

What is addisons disease?

A

Primary adrenal insufficiency - hypocortiolsim and hypoaldosteronism

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30
Q

Pathology of autoimmune Addison’s disease

A

+ve adrenal autoantibodies (to 21-OHase) in 70%

lymphocytic infiltrate of adrenal cortex

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31
Q

Assosiated diseases with autoimmune addison’s

A 
Thyroid disease (20%)
T1DM (15%)
Premature ovarian failure (15%)
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32
Q

Presentation of primary adrenal failures

A 
Weakness
Fatigue 
Anorexia
Weight loss 
Nausea and vomiting 
Hyperpigmentation/Skin pigmentation (especially palmar creases) or vitiligo 
Loss of pubic hair in women 
Hypotension 
Hypoglycaemia 
Hyponatraemia and hyperkalaemia may be seen 
Unexplained vomiting or diarrhoea
Salt craving 
Postural symptoms
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33
Q

Causes of primary adrenal insufficiency

A

Addison’s disease

Adrenal enzyme defects - congenital adrenal hyperplasia

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34
Q

What is vitiligo?

A

Pale white patches develop on the skin

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35
Q

Clues to the diagnosis of adrenal failure

A 
Disproportion between severity of illness and circulatory collapse/hypotension/dehydration 
Unexplained hypoglycaemia
Other endocrine features
- hypothyroidism 
- body hair loss
- amenorrhoea
Previous depression or weight loss
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36
Q

Investigations to diagnose adrenal insufficiency

A

U + Es, glucose, FBC
Random cortisol
Synacthen test and basal ACTH

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37
Q

What value of random cortisol shows that it is not addisons?

A

> 700 nmol/l

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38
Q

What is synacthen?

A

Synthetic ACTH

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39
Q

What would be ideal in a synacthen test If all is working?

A

A rise in cortisol level

> 500 = reassuring

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40
Q

What would happen in a synacthen test to diagnose primary adrenal failure?

A

If impaired cortisol response and ACTH > 200ng/l

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41
Q

If plasma ACTH is fine, what does this show?

A

Adrenal problem

Pituitary response is fine

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42
Q

If plasma ACTH is low, what does this show?

A

A problem with the pituitary response

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43
Q

Examples of glucocorticoid replacements

A

Hydrocortisone
Prednisolone
Dexamethasone

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44
Q

Doses of glucocorticoid replacements

A

Given in doses to mimic normal diurnal variation

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45
Q

What synthetic steroid is given in mineralocorticoid replacement?

A

Fludrocortisone

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46
Q

What circumstances should treatment be altered when on steroid treatment?

A

Minor short lived illness or stress (double glucocorticoid dose)
Major illness or operation (IV medications)

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47
Q

Self care rules for patients on steriods

A

Never miss steroid doses
Double the hydrocortisone dose in the event of intercurrent illness (e.g. flu, UTI)
If severe vomiting or diarrhoea call for help without delay (may need IM)

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48
Q

What are over 90% of the cases of congenital adrenal hyperplasia due to?

A

21-hydroxylase deficiency

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49
Q

Results of 21-hydroxylase deficiency

A 
Congenital adrenal hyperplasia
Neonatal salt losing crisis
Ambiguous genitalia 
Pseudo-precocious puberty (boys)
Hirsutism (women)
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50
Q

Investigations for conns syndrome

A

Random aldosterone:renin ratio
Saline suppression test
Scan the adrenals
Adrenal vein sampling

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51
Q

What is conns syndrome?

A

Hyperaldosteronism

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52
Q

What is a saline suppression test?

A

The patient is given saline IV, after which the measures of renin and aldosterone are measured

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53
Q

If have conns syndrome, what would be the result of the saline suppression test?

A

Aldosterone high

Renin is low

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54
Q

What is deficient in congenital adrenal hyperplasia?

A

21 hydroxylase

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55
Q

What type of inheritance is congenital adrenal hyperplasia?

A

Autosomal recessive

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56
Q

Symptoms of congenital adrenal hyperplasia

A

Virilising

Salt wasting

57
Q

How is congenital adrenal hyperplasia measured for?

A

Precursors can be measured from a heel prick test

58
Q

Treatment of congenital adrenal hyperplasia

A

Stop ACTH
Bring androgens down
- hydrocortisone
- sometimes fludrocortisone

59
Q

Why could congenital adrenal hyperplasia be late onset?

A

Autosomal recessive

Hirsituism - men wouldn’t be found or would just go unnoticed

60
Q

What medicine can be used in PCOS that is also used in DM?

A

Metformin

61
Q

What is spironolactone?

A

Aldosterone antagonist

Anti-androgen

62
Q

S/Es of spironolactone

A

Gynaecomastia

Erectile dysfunction

63
Q

What is hirsituism a result of?

A

Increased androgen production

64
Q

Examples of causes of hirsituism

A

PCOS

Adrenal carcinoma

65
Q

Causes of purple abdominal striae

A

Cushings syndrome
Pregnancy
Anyone putting on weight quickly

66
Q

When should cortisol be measured to get the most accurate reading?

A

At midnight to see when it should be lowest - sleeping midnight cortisol (serum)

67
Q

What can cortisol be measured from?

A

Urine
Serum
Saliva

68
Q

When would a dexamethasone suppression test be done?

A

When you suspect overproduction of ACTH from the pituitary

69
Q

What does a dexamethasone suppression test do?

A

Switches off pituitary ACTH

70
Q

When is dexamethasone given and when thereafter is the cortisol measured?

A

Given at night

Cortisol measured in morning

71
Q

What is the normal response to a dexamethasone suppression test and to what level?

A

Cortisol should drop

< 50

72
Q

If the dexamethasone test is higher than normal, what should be done next?

A

A higher dose

73
Q

Causes of Cushings syndrome

A

Steroids
Cushings disease
Ectopic ACTH production
Adrenal adenomas

74
Q

Effects of hypercortisolaemia

A

Impaired insulin tolerance
Hyperglycaemia
T2DM

75
Q

What are cortisol readings often?

A

Unhelpful

76
Q

What would you measure if you suspected the problem was coming from the pituitary?

A

ACTH

77
Q

Why can CRH still be tested even in Cushings disease?

A

Still has a slight sensitivity to CRH

78
Q

What size are the pituitary adenomas often in cushings disease?

A

Tiny

79
Q

What is BIPSS?

A

Gradient between venous drainage and the peripheral blood +/- CRH injection

80
Q

What ratio does BIPSS look at?

A

Central ACTH : Peripheral ACTH

81
Q

What is the cut off for BIPSS?

A

> 2.0

82
Q

Treatment of cushings disease

A

Metyrapone
Pituitary transphenoidal microadenomectomy
Hydrocortisone post op

83
Q

What does metyrapone do?

A

Reduces enzymes in the adrenal gland to decrease glucocorticoid production

84
Q

Why is hydrocortisone given post op?

A

In case there has been damage to surrounding tissue as could get adrenal crisis post op

85
Q

What is the initial remission rate of cushings disease?

A

70 - 80%

86
Q

What is the permanent cure rate of cushings disease?

A

60-70%

87
Q

What could be done if a pituitary adenoma causing cushings disease came back?

A

Bilateral adrenalectomy

88
Q

Causes of leg cramping at night

A

Calcium problems
Iron deficiency
Exercise
Circulatory problems

89
Q

Cause of conns syndrome

A

Adenoma of adrenal cortex (aldosterone producing unilateral adenoma)

90
Q

Who gets conns syndrome?

A

Younger women

91
Q

Causes of secondary hyperaldosteronism

A

Increased levels of renin
HF
Liver failure etc

92
Q

If serum bicarbonate is high, what does this indicate?

A

Alkalosis

93
Q

What is another name for the saline suppression test?

A

Salt loading test

94
Q

What should happen after the saline suppression test?

A

Aldosterone should decrease

95
Q

If after a saline suppression test aldosterone has failed to be suppressed, what is the diagnosis?

A

Primary hyperaldosteronism

96
Q

What test is used to exclude renal artery stenosis?

A

Renal USS

97
Q

What happens before a tumour develops in any gland?

A

Hyperplasia

Over production

98
Q

Causes of primary hyperaldosteronism

A

Acquired bilateral adrenal hyperplasia
Conns syndrome
Glucocorticoid suppressive hyperplasia

99
Q

Who gets acquired bilateral adrenal hyperplasia?

A

Older men and women

100
Q

What is the purpose of adrenal venous sampling?

A

To demonstrate the source of aldosterone

101
Q

How does adrenal venous sampling work?

A

Put catheter into adrenal veins and put in ACTH
Cortisol and adrenaline responses are looked at
Right versus left are looked at
Peripheral vs inside the gland are looked at
Tells us if bilateral or unilateral

102
Q

Treatment of conns syndrome

A

Spironolactone
or
Epllerelone

103
Q

Why is epperelone a good alternative to spironolactone?

A

Does not have anti androgen effects

104
Q

What is amiloride?

A

A K+ sparing diuretic `

105
Q

What does POMC stimulate?

A

MSH

ACTH

106
Q

What does excess MSH result in?

A

Scar pigmentation

107
Q

What is a decreased cortisol effect on POMC?

A

POMC decreases

108
Q

What treatment should be done immediately before diagnosis when suspect addisons crisis?

A

IV hydrocortisone

109
Q

Causes of primary hypoaldosteronism

A 
Autoimmune adrenalitis (addisons)
TB
Adrenal haemorrhage 
Adrenal metastases
Fungal infections 
Others e.g. CAH, iatrogenic
110
Q

What is the most common cause of primary hypoaldosteronism?

A

Addisons (autoimmune adrenalitis)

111
Q

What is the most common cause of primary hypoaldosteronism worldwide?

A

TB

112
Q

What gets pigmented in Addisons?

A

Gums
Scars
Hands
Skin (tanned)

113
Q

Treatment of addisons

A

Steroids; hydrocortisone, fludrocortisone

114
Q

What is hydrocortisone replacing?

A

Glucocorticoids

115
Q

What is fludrocortisone replacing?

A

Mineralcorticoids

116
Q

What must be done to the dose of steroids treating addisons if ill?

A

Dosage doubled 24 or 48 hours

Injection available if vomiting

117
Q

Why can short syncathen test be used in both primary and secondary hypoaldosteornism?

A

As adrenal atrophy occurs in 2ndry

118
Q

What happens in the long term for people with secondary hypoaldosteronism?

A

Adrenal atrophy

119
Q

What is the level of Na in secondary hypoaldosteronism? Why?

A

Decreased
Increased levels of vasopressin (due to increased CRH) - which is an ACTH releaser - causing H20 retention and dilutional hyponatraemia

120
Q

How to distinguish between primary and secondary?

A

ACTH levels

121
Q

Causes of hypercalcaemia

A 
Metastatic disease
Sarcoidosis
Primary hyperthyroidism 
Hyperparathyroidism 
Myeloma
Addisons
122
Q

What is the effect of decreased Ca on PTH?

A

Increased PTH

123
Q

Causes of decreased Ca

A

Vit D deficient

Malabsorption

124
Q

What can too much calcium in the kidneys lead to?

A

Kidney stones

125
Q

What can you check for calcium to monitor the kidneys?

A

Urine calcium

126
Q

What do gastrinomas lead to?

A

Gastric duodenal ulceration

127
Q

Features of Addisonian crisis

A

Collapse
Shock
Pyrexia

128
Q

Causes of hypoadrenalism

A 
Addisons (autoimmune)
TB
Metastases (e.g. bronchial carcinoma)
Meningococcal septicaemia (waterhouse friederichsen syndrome)
HIV
Antiphosopholipid syndrome 
Pituitary disorders 
- tumours
- irridation 
- infiltration 
Exogenous glucocorticoid therapy
129
Q

1ry vs 2ndry addisons hyperpigmentation

A

1ry yes

2ndry no

130
Q

3 features of conns syndrome

A
  1. HTN
  2. Alkalosis
  3. Hypokalaemia (muscle weakness)
131
Q

Features of Addisonian crisis

A

Hyponatraemia
Hypoglycaemia
Hyperkalaemia

132
Q

Treatment of phaeochromocytoma

A
  1. Phenoxybenzamine FIRST (non selective a blocker)

2. BBs

133
Q

What is NOT required in the treatment of Addisonian crisis?

A

IV fludrocortisone

134
Q

Treatment of Addisonian crisis

A

IV hydrocortisone

135
Q

What is nelsons syndrome?

A

Occurs due to rapid enlargement of pituitary corticotroph adenoma (ACTH producing adenoma) that occurs after the removal of both adrenal glands (bilateral adrenalectomy)

136
Q

Pathology of nelsons syndrome

A

Removal of both adrenals leads to the elimination of production of cortisol, and the lack of cortisols -ve feedback can allow any pre existing adenomas to grow unchecked.

137
Q

What can spironolactone cause?

A

Gynaecomastia

138
Q

How to treat an Addisonian patient if they are unwell

A

Double hydrocortisone dose

Fludrocortisone dose can stay the same

Endocrine Pathology (11 decks)

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