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Chemical Pathology Wits > Adrenals > Flashcards

Adrenals Flashcards

1
Q

Discuss the anatomy of the adrenal glands

A

Suprarenal
Triangular
Consists of
- outer cortex (80-90%)
- inner medulla (10-20%)

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2
Q

What are the 3 layers of the adrenal cortex?

A

Zona glomerulosa (15%)
Zona fasciculata (75%)
Zona reticularis (10%)

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3
Q

Which hormones does the zona glomerulosa release?

A

Mineralocorticoid (aldosterone)

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4
Q

Which hormone does the zona fasciculata release?

A

Glucocorticoid (cortisol)

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5
Q

Which hormone does the zona reticularis release?

A

Androgens (DHEA)

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6
Q

Which hormones does the adrenal medulla release?

A

Catecholamines (adrenaline, noradrenaline)

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7
Q

What regulates the zona glomerulosa?

A

Angiotensin 2

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8
Q

What regulates the zona fasciculata?

A

ACTH

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9
Q

What regulates the zona reticular?

A

ACTH

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10
Q

Discuss the mineralocorticoid pathway

A
  1. **Cholesterol **
    -> cholesterol desmolase
  2. Pregnenolone
    -> 3 beta hydroxydehydrogenase
  3. **Progesterone **
    -> 21-hydroxylase
  4. 11-deoyxycorticosterone
    -> 11 beta hydroxylase
  5. **Corticosterone **
    -> corticosterone methyloxidase I
  6. **18-hydroxy-corticosterone **
    -> corticosterone methyloxidase 2
  7. Aldosterone
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11
Q

Discuss the main cortisol pathway

A
  1. **17 alpha hydroxypregnenolone **
    3 beta hydroxydehydrogenase
  2. 17 alpha hydroxyprogesterone
    21 hydroxylase
  3. **11-deoxycortisol **
    11 beta hydroxylase
  4. **Cortisol **
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12
Q

Which substrate from the mineralocorticoid pathway can become 17 alpha hydroxypregnenolone and via which enzyme?

A

Pregnenolone
17 alpha hydroxylase

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13
Q

Which substrate from the mineralocorticoid pathway can become 17 alpha hydoxyprogesterone and via which enzyme?

A

Progesterone
17 alpha hydroxylase

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14
Q

Which substrate from the mineralocorticoid pathway can become 11-deoxycortisol and via which enzyme?

A

11-deoxycorticosterone
11 beta hydroxylase

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15
Q

Discuss the androgen pathway

A
  1. Dehydroepiandosterone
    3 beta hydroxy dehydrogenase
  2. Androstenedione
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16
Q

Which substrate from the cortisol pathway can become dehydroepiandrosterone and via which enzyme?

A

17 alpha hydroxypregnenolone
Desmolase

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17
Q

Which substrate from the cortisol pathway can become androstenedione and via which enzyme?

A

17 alpha hydroxyprogesterone
Desmolase

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18
Q

Which enzyme allows androstenedione to become testosterone?

A

17 beta hydroxyl steroid dehydrogenase

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19
Q

Which enzyme allows androstenedione to become oestrone?

A

Aromatase

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20
Q

Which enzyme allows cortisol to become cortisone?

A

11-beta hydroxyl steroid dehydrogenase

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21
Q

What is the function of cortisol?

A
  1. Immune system
    - function suppressed
  2. Liver
    - gluconeogenesis
  3. Muscle
    - protein catabolism
  4. Adipose tissue
    - lipolysis
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22
Q

Which cells produce ACTH?

A

Corticotroph cells in anterior pituitary gland

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23
Q

ACTH is co-secreted with which hormones?

A

Vasopressin
Oxytocin

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24
Q

What is the pattern of cortisol secretion? When are levels highest and lowest?

A

Diurnal pattern
Highest in morning (8am)
Lowest at midnight

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25
Q

What can affect the diurnal pattern of cortisol?

A
  1. Alternate work shifts
  2. Changing sleep patterns
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26
Q

How is cortisol involved in the metabolic control of carbohydrates?

A
  1. Decreases uptake of circulating glucose by muscle and adipose tissue
  2. Stimulates liver gluconeogenesis from FFA and amino acids produced by actions in muscle and adipose tissue
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27
Q

How is cortisol involved in the metabolic control of fats?

A
  1. Lipolysis
  2. Fatty acid mobilisation from adipose tissue
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28
Q

How is cortisol involved in the metabolic control of proteins?

A
  1. Proteolysis
  2. Amino acid mobilisation from muscle tissue
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29
Q

How does cortisol affect bone?

A

Inhibits bone formation via inhibition of type 1 collagen synthesis and decreased osteoblast function

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30
Q

How does cortisol affect calcium?

A

Decreased gut calcium absorption
Decreased renal calcium reabsorption

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31
Q

Name other effects of cortisol

A
  1. Water excretion
  2. Epinephrine synthesis
  3. Vasoconstriction
  4. GFR
  5. Mild mineralocorticoid activity
  6. Inhibits ACTH secretion
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32
Q

How does aldosterone affect fluid and electrolyte balance?

A

Na retention
Water retention
K excretion
H excretion

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33
Q

What is the short-term stress response of the adrenal gland?

A

Mediated by catecholamines

  1. Incr HR
  2. Incr BP
  3. Liver converts glycogen to glucose -> released to blood
  4. Bronchiole dilation
  5. Blood flow pattern changes
    - incr alterness
    - decr GI activity
    - decr urine output
  6. Incr metabolic rate
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34
Q

What is the long term stress response of the adrenal gland?

A

Mediated by mineralocorticoids
1. Sodium and water retention by kidneys
2. Increased blood volume -> BP

Mediated by glucocorticoids
1. Protein and fat -> glucose
2. Incr blood sugar
3. Immune system suppression

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35
Q

What is the function of DHEA, DHEAS and androstenedione?

A

Libido stimulation
Pubic and axillary hair development in females

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36
Q

What is the measurement of androgens important for?

A

CAH diagnosis and management
Virilization investigation

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37
Q

Give examples of adrenal cortex disorders

A
  1. Cushing’s syndrome
  2. Adrenal insufficiency
  3. Conn’s syndrome
  4. Congenital adrenal hyperplasia (CAH)
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38
Q

What is Cushing’s syndrome?

A

Clinical syndrome due to chronic exposure of body tissues to excess cortisol

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39
Q

What is the epidemiology of Cushing’s syndrome?

A

Relatively rare
20-50yo
M:F = 1:5

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40
Q

Discuss the etiological classification of Cushing’s syndrome

A
  1. Exogenous
    - glucocorticoid therapy
  2. Endogenous
    a) ACTH dependant
    b) ACTH independent
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41
Q

Name ACTH dependent causes of Cushing’s syndrome

A

Pituitary adenoma
Ectopic ACTH production
Ectopic CRH releasing syndrome

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42
Q

Name examples of ectopic ACTH production

A

Small lung cell carcinoma
Carcinoid tumours
Pancreatic islet cell tumours
Medullary carcinoma

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43
Q

Name ACTH independent causes of Cushing’s syndrome

A

Adrenal adenoma
Adrenal carcinoma
Adrenal hyperplasia

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44
Q

Name causes of pseudo-Cushing’s states (PCS)

A

Severe stress
Psychiatric disorders
Alcoholism
Obesity

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45
Q

Explain pseudo-Cushing’s state (PCS)

A

Hypercortisolism with no pathology in the HPA axis (no autonomous secretion)
Reversible with cause removal

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46
Q

Name signs and symptoms of Cushing’s syndrome

A

General
- central obesity, moon face, buffalo hump, hypertension
Skin
- thin, easily bruised, heals slowly
- striae
- hirsutism
- acne
- red cheeks
MSK
- mm weakness
- fatigue
- osteoporosis
Gonadal
- amenorrhoea, impotence
Metabolic
- DM
- hyperlipidemia
Neuropsychiatric
- depression
- anxiety
- psychosis
- poor memory
Immune system
- recurrent infections

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47
Q

What is the aim of diagnostic evaluation of Cushing’s syndrome?

A
  1. Confirm presence of hypercortisolism
  2. Determine the cause
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48
Q

What are the baseline tests for Cushing’s syndrome?

A

Midnight serum cortisol
Late night salivary cortisol
24hr urinary free cortisol

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49
Q

What are dynamic function tests for Cushing’s syndrome?

A
  1. Dexamethasone suppression test (DST)
  2. Combined DST-CRH test
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50
Q

What are the 2 types of DST?

A
  1. Overnight low dose
  2. Prolonged low dose
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51
Q

Which tests can be done to confirm the cause of Cushing’s syndrome?

A
  1. Biochemical
  2. Imaging studies
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52
Q

Which biochemical tests can be done to determine the cause of Cushing’s syndrome?

A

Plasma ACTH
High dose DST
CRH stimulation test
BIPSS

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53
Q

What is BIPSS?

A

Bilateral inferior petrosal sinus sampling

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54
Q

What are limitations of the midnight serum cortisol test?

A
  1. Expectation of blood test may release cortisol
  2. Majority of total serum cortisol is bound to CBG (influenced by OCPs, pregnancy, etc)
  3. Not reflective of bioactive cortisol
  4. False positives
  5. Patient must be admitted for >48h to avoid stress
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55
Q

Which conditions can cause false positive for midnight serum cortisol test?

A

Critical illness
Acute infection
Pseudocushing’s states

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56
Q

What is the rational of late night salivary cortisol?

A

Salivary cortisol in equilibrium with serum free cortisol (independent of saliva production)
Used to demonstrate loss of circadian rhythm

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57
Q

What are advantages of late night salivary cortisol?

A

Easy
Convenient
Can be collected at home
Useful if cyclical Cushing’s suspected

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58
Q

What are the limitations of late night salivary cortisol?

A

Not suitable for patient’s with variable sleep patterns
False positive

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59
Q

Which conditions can cause false positive late night salivary cortisol?

A

Liquorice
Tobacco use

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60
Q

What are the advantages of 24h urine free cortisol?

A

Non-invasive
Not influenced by diurnal rhythm

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61
Q

What is the sleeping vs non sleeping cut off for midnight serum cortisol?

A

Sleeping >50
Non-sleeping >229

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62
Q

What influences the diagnostic ranges of late night salivary cortisol?

A

Analytical method

63
Q

What influences the diagnostic ranges of 24h urine free cortisol?

A

Method specific
>3-4x upper RR = diagnostic
<250nmol/24h = exclude

64
Q

What are the limitations of the 24h urine free cortisol test?

A

Correct urine collection
Normal renal function
May be normal in cyclical or mild CS
Assay interferences (cross reactivity with other steroid metabolites)

65
Q

Which conditions can cause a false positive 24h urine free cortisol?

A

Pseudocushing’s states

66
Q

How does renal CrCl <60 affect 24h urine free cortisol?

A

Result will be falsely low

67
Q

What is the rational of the low dose DST?

A

Dexamethasone (DMT) is a synthetic cortisol analogue -> inhibits CRH and ACTH -> decr cortisol production -> decr serum and urine cortisol in normal people

68
Q

How is low dose DST performed?

A
  1. Baseline serum cortisol sample at 8am
  2. Give 1mg po DMT at 12pm
  3. Repeat blood collection the following morning at 8am
69
Q

How do you interpret the results of low dose DST?

A

<50nmol/L = normal
Inadequate suppression = Cushing’s

70
Q

Name causes of false positive LDDST

A

Decr DMT absorption
Incr hepatic metabolism
Incr CBG
Pseudocushing’s
Non-compliance

71
Q

Which medications can increase hepatic metabolism?

A

Phenytoin
Phenobarbitone
Rifampicin
Carbamazepine

72
Q

Which conditions can increase CBG?

A

Pregnancy
Oestrogen treatment

73
Q

Name causes of false negative LDDST

A

Liver and renal failure (decreased DMT clearance)

74
Q

How is the prolonged LDDST performed?

A
  1. Day 1 collect cortisol sample at 8am
  2. Administer 0.5mg po DMT every 6h for 2 days
  3. Day 3 repeat cortisol blood collection at 8am
75
Q

Which test has more false positives: low dose or prolonged DST?

A

Low dose DST

76
Q

How do you perform the combined DMT-CRH test?

A
  1. Do standard LDDST
  2. Inject 1uk/kg of CRH 2hrs after last DMT dose
  3. Collect blood cortisol 15min after CRH injection
77
Q

What DMT-CRH test level is in keeping with Cushing’s syndrome?

A

> 38

78
Q

Which tests helps to classify Cushing’s syndrome and determine further work up?

A

Plasma ACTH

79
Q

Which test helps to differentiate between Cushing’s disease and an ectopic source of ACTH production?

A

High doe DST

80
Q

What is the rationale of the high dose DST?

A

Corticotroph tumour cells in Cushing’s disease retain some responsiveness to negative feedback of glucocorticoids while ectopic ACTH tumours do not

81
Q

How is the overnight HDDST performed?

A

Same as LDDST, with 8mg DMT instead

82
Q

How is the 2 day HDDST performed?

A

Same as LDDST, with 2mg DMT instead

83
Q

How do you interpret the 2 day HDDST result?

A

Suppression <50% of baseline = Cushing’s disease
No suppression = ectopic ACTH

84
Q

What is the rationale of the CRH stimulation test?

A

Exogenous CRH -> incr ACTH (pituitary) -> incr serum cortisol

85
Q

Discuss the procedure of CRH stimulation test

A
  1. Collect blood for cortisol and ACTH 15min prior to first CRH dose
  2. Give 1uk/kg CRH iv at 8am
  3. Continue to repeat blood collections at 5, 10, 15, 30, 45, 60 and 120min after dose
86
Q

How do you interpret the result of a CRH stimulation test?

A

Peak in ACTH followed by peak in cortisol at 30min and 60min =1 hr normal
Incr ACTH >50% and CRH >20% of baseline = Cushing’s disease

87
Q

Which patients with Cushing’s disease do not respond to CRH?

A

Ectopic ACTH tumours
Adrenal sources

88
Q

How is the BIPSS performed?

A

ACTH levels sampled from veins draining pituitary gland and peripheral veins then compared
Greater ratio variation indicates the source of elevated ACTH

89
Q

What are the typical results of adrenal function tests in Cushing’s disease?

A

Basal cortisol ++
LDDST no suppression
HDDST suppression
CRH response
Plasma ACTH +

90
Q

What are the typical results of adrenal function tests in adrenal tumours?

A

Basal cortisol +
LDDST no suppression
HDDST no suppression
CRH no response
Plasma ACTH -

91
Q

What are the typical results of adrenal function tests in

A

Basal cortisol +
LDDST no suppression
HDDST no suppression
CRH no response
Plasma ACTH ++

92
Q

What are the diagnostic challenges in evaluation of Cushing’s syndrome?

A

Clinical
- non-specific signs and symptoms
Laboratory
- test sensitivity and specificity
- interfering substances
- test procedure
- result interpretation

93
Q

What is the epidemiology of adrenal insufficiency?

A

All ages
Males = females

94
Q

Name chronic causes of primary adrenal insufficiency

A

Autoimmune adrenalitis
Granulomatous disease
AIDS
Neoplastic infiltration
Metabolic (amyloidosis, haemochromatosis)
Abdominal irradiation
Post bilateral adrenalectomy
Drugs

95
Q

Name acute causes of primary adrenal insufficiency

A

Adrenal haemorrhage
- meningococcal infection
- pseudomonas
- anticoagulant
- adrenal artery embolism
- adrenal vein thrombosis
Post bilateral adrenalectomy

96
Q

Which drug can cause primary adrenal insufficiency?

A

Ketoconazole

97
Q

Name causes of secondary/tertiary adrenal insufficiency

A
  1. Glucocorticoid therapy
  2. Pituitary/hypothalamic failure -> decr ACTH production
98
Q

Name common features of adrenal insufficiency

A

Weakness
Weight loss
Postural hypotension
Pigmentation
Anorexia, N+V
Decr libido
Body hair loss
Hyponatremia
Hyperkalemia
Pre-renal uremia

99
Q

Name uncommon features of adrenal insufficiency

A

Salt craving
Hypoglycemia
Depression

100
Q

How often is adrenal insufficiency diagnosed during adrenal crisis?

A

25% of cases

101
Q

What screening tests can be done to diagnose adrenal insufficiency?

A
  1. Serum cortisol
  2. Plasma ACTH
  3. Electrolytes
  4. Glucose
102
Q

How do you interpret serum cortisol in diagnosis of adrenal insufficiency?

A

<50nmol/L = diagnostic
>550nmol/L = exclude

103
Q

How do you interpret plasma ACTH in diagnosis of adrenal insufficiency?

A

Incr - primary AI
Decr/normal - secondary/tertiary AI

104
Q

How will electrolytes and glucose be affected in adrenal insufficiency?

A

Decr sodium
Incr potassium
Decr glucose

105
Q

What dynamic tests can be done to diagnose adrenal insufficiency?

A

Rapid ACTH stimulation test

106
Q

What is rapid ACTH stimulation test also known as?

A

Short synacthen test

107
Q

What are limitations of the rapid ACTH stimulation test in diagnosing adrenal insufficiency?

A
  1. Peak value is more NB than incremental value
  2. False negatives in stressed patients
  3. Test does not differentiate primary from secondary
  4. Test not reliable to detect pituitary AI
108
Q

How is the short ACTH stimulation test performed?

A
  1. Take blood cortisol sample at 9am
  2. Inject 250ug ACTH
  3. Repeat blood samples after 30 and 60min
109
Q

How do you interpret the results of a short ACTH stimulation test

A

Plasma cortisol incr by 200nmol/L with peak >55nmol/L = normal

110
Q

How is the long ACTH stimulation test performed?

A
  1. Take blood cortisol at 9am
  2. Inject 1mg ACTH IM
  3. Repeat blood samples at 15:00 and 09:00
111
Q

How do you interpret the results of the long ACTH stimulation test

A

No cortisol increase = primary AI
Incr at 6h with incr at 24h total >200nmol/L = secondary AI

112
Q

What other tests can be used to distinguish between primary and secondary AI?

A

Insulin tolerance test
CRH stimulation test
Metyrapone test

113
Q

Which tests can be done to determine the underlying cause of adrenal insufficiency?

A
  1. Anti-adrenal antibodies
  2. Imaging (XR, CT, MRI)
  3. HIV
  4. TB
114
Q

What should you suspect in adrenal insufficiency with enlarged adrenal glands on imaging?

A

Infections
Cancers

115
Q

What should you suspect in adrenal insufficiency with small or normal adrenal glands on imaging?

A

Autoimmune
Secondary AI

116
Q

Name causes of Addisonian crisis

A
  1. Sudden stop of steroid therapy without tapering
  2. Stress (trauma, surgery, severe infection) without increasing dose
  3. Uncontrolled Addison’s
  4. Undiagnosed Addison’s
117
Q

Discuss clinical features of Addisonian crisis

A
  1. General
    - N+V, diarrhoea
    - dehydration
    - hypotension
    - hypoglycaemia
    - tachycardia
    - tachypnea
  2. CNS
    - weakness
    - confusion
    - headache
118
Q

Discuss management of Addisonian crisis

A
  1. Rapid IV fluid infusion 0.9% NaCl
  2. Monitor fluid and urine input and output
  3. ECG monitoring
  4. Solucortef IV 6hrly until signs and symptoms resolve
119
Q

What is primary hyperaldosteronism also called?

A

Conn’s syndrome

120
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism characterised by excessive aldosterone secretion from the adrenal glands

121
Q

What is the epidemiology of Conn’s syndrome?

A

30-50yo
F>M

122
Q

Name causes of Conn’s syndrome

A
  1. Adrenal adenoma
  2. Bilateral hypertrophy of zona glomerulosa cells

Other:
Adrenal carcinoma
Glucocorticoid remediable hyperaldosteronism
Idiopathic

123
Q

What is “glucocorticoid remediable aldosteronism”?

A

Autosomal dominant disorder caused by hybrid gene mutation composed of regulatory and coding sequences

124
Q

From which gene are the regulatory sequences in FH-1 derived?

A

11-beta-hydroxylase CYP11B1

125
Q

From which gene are the coding sequences in FH-1 derived?

A

Aldosterone synthase CYP11B2

126
Q

What is glucocorticoid-remediable aldosteronism also known as?

A

FH-1 (familial hyperaldosteronism type 1)

127
Q

Discuss features of Conn’s syndrome

A

Often asymptomatic
Hypertension
Hypokalemia
No edema

128
Q

Name symptoms of hypokalemia

A

Fatigue
Muscle weakness
Parasthesia
Occasional paralysis
Latent tetany
Polydipsia
Polyuria
Nocturne

129
Q

How will a patient with Conn’s syndrome biochemical results appear?

A

Incr sodium
Decr potassium
Kaliuria
Alkalosis

130
Q

How do you screen for Conn’s syndrome?

A
  1. Electrolytes
  2. Urine
  3. Plasma aldosterone renin activity (ARR) ratio
131
Q

Which factors can affect the plasma ARR ratio?

A
  1. Posture
  2. Hypokalemia
  3. Dietary salt restriction
  4. Drugs
  5. Renal dysfunction
132
Q

What is PRA?

A

Plasma renin activity

133
Q

What is the physiological effect of ACE-I that impacts on Conn’s syndrome and how long is required to remove the interference?

A

Increase PRA
Reduced aldosterone

2w

134
Q

What is the physiological effect of beta blockers that impacts on Conn’s syndrome and how long is required to remove the interference?

A

Reduced PRA > aldosterone

2w

135
Q

What is the physiological effect of CCBs that impacts on Conn’s syndrome and how long is required to remove the interference?

A

Reduce aldosterone
Stimulate renin production

2w

136
Q

What is the physiological effect of diuretics that impacts on Conn’s syndrome and how long is required to remove the interference?

A

Incr PRA
Incr aldosterone

2w

137
Q

What is the physiological effect of hypokalemia that impacts on Conn’s syndrome and how long is required to remove the interference?

A

Inhibits aldosterone secretion

2w

138
Q

What is the physiological effect of NSAIDs that impacts on Conn’s syndrome and how long is required to remove the interference?

A

Retain sodium
Reduce PRA
2w

139
Q

What is the physiological effect of oestradiol that impacts on Conn’s syndrome and how long is required to remove the interference?

A

Incr renin substrate

6w

140
Q

What is the physiological effect of spironolactone that impacts on Conn’s syndrome and how long is required to remove the interference?

A

Incr PRA
Variable effect on aldosterone

6w

141
Q

Which drugs require 6 weeks removal to not interfere with Conn’s diagnosis?

A
  1. Oestradiol
  2. Spirinolactone
142
Q

How is a patient prepared prior to an ARR?

A
  1. Adequate sodium (100-150mmol/d) and potassium (50-100mmol/d) prior to test
  2. Stop potassium supplement 24h before test
  3. Stop medications that influence the test
143
Q

How is the ARR performed?

A
  1. Patient seated for 10min prior to blood collection
  2. Collect sample at 8am for PRA, aldosterone and potassium
  3. Send sample to lab within 30min
144
Q

Why should the ARR sample be taken at 8am?

A

8am is when aldosterone is physiologically high

145
Q

How do you interpret the ARR result in screening for Conn’s syndrome?

A

<800 = excluded
800-2000 =-1,200 confirmatory tests required
>2000 = diagnosis likely

146
Q

Name diagnostic tests for Conn’s syndrome

A
  1. Saline suppression test
  2. Fludrocortisone suppression test
  3. Furosemide stimulation test
147
Q

What is the rationale of the saline suppression test?

A

IV saline infection -> rapid incr in plasma volume -> decr aldosterone in normal patient’s

148
Q

How do you prepare the patient for a saline suppression test?

A
  1. Correct any hypokalemia
  2. Remove interfering drugs
149
Q

How is the saline suppression test performed?

A
  1. Wake patient at 6am
  2. Keep upright posture for 2h
  3. Plasma aldosterone collected at 8am
  4. Patient assumes supine position and 1.25L of isotonic saline infused over 2h
  5. Plasma aldosterone collected at 12:00
150
Q

How is the saline suppression test interpreted?

A

Aldosterone >240pmol/L = Conn’s syndrome

151
Q

What is the rationale of the fludrocortisone suppression test?

A

Fludrocortisone = potent mineralocorticoid -> decr aldosterone production in normal patients

152
Q

How is the fludrocortisone suppression test performed?

A
  1. Patient upright for 30min prior to venipuncture
  2. Collect midmorning plasma aldosterone
  3. Administer fludrocortisone 0.1mg po and slow Na 2x10mmol tabs 8hrly for 4 days
  4. Measure plasma potassium twice daily and maintain potassium levels
  5. Collect plasma aldosterone after 30min upright prior to venipuncture
153
Q

How do you interpret the fludrocortisone suppression test?

A

Plasma aldosterone >140pmol/L = Conn’s

154
Q
A

Chemical Pathology Wits (4 decks)

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