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phase 2 endo > Adrenal > Flashcards

Adrenal Flashcards

1
Q

What are the layers of adrenal cortex and what do they produce?

A
  • Zone glomerulosa →aldosterone (mineralocorticoids)
  • Zona fasciculata → cortisol (glucocorticoid)
  • Zona reticularis → androgens e.g. adrenosterone (converted to testosterone) and dihydrotestosterone
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2
Q

What are the principle cells of medulla of adrenal gland

A

chromaffin cells

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3
Q

What processes are suppressed by glucocorticoids

A
  • Amino acid uptake
  • Protein synthesis
  • Peripheral uptake of glucose Increase proteolysis in most tissue (not liver
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4
Q

What processes are stimulated by glucocorticoids

A
  • Hepatic gluconeogenesis and glycogenolysis

* Lipolysis in adipose tissue but really high levels of cortisol increases lipogenesis

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5
Q

What are the two types of addison’s disease

A
  • Primary: inability of adrenal to produce enough steroids

* Secondary: insufficient stimulation from pituitary or hypothalamus

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6
Q

What is the incidence of primary addison’s

A

o 0.1/1000/year
o Age: 30-50
o ↑↑F

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7
Q

What is the most common underlying cause of Addison’s in children

A

congenital adrenal hyperplasia

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8
Q

What are the causes of Primary AD

A

Surgical removal
Trauma
Infections: TB, histoplasmosis, cryptococcosis, syphilis, HIV
Haemorrhage e.g. anticoagulation
Infarction i.e. antiphospholipid syndrome
Invasion i.e. neoplasia, amyloidosis

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9
Q

How can HIV predispose to primary AD

A

medications and opportunistic infections

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10
Q

What infections can cause primary AD

A

TB, syphilis, HIV (drugs + other infections), Cryptococcosis

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11
Q

What are the principle causes of secondary AD

A
  • Iatrogenic →long term steroid use

* Skull fractures, neoplasia, congenital, CRH deficiency, infection (TB), infiltration (sarcoidosis)

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12
Q

What are the symptoms of AD i.e CVS, GI, neuri, others

A
  • Fatigue and weakness
  • GI symptoms: Anorexia, Nausea and vomiting, Weight loss, Abdominal pain, Diarrhoea or constipation
  • CVS symptoms: Dizziness and syncope, Confusion
  • Neurological: Personality change and irritability
  • Amenorrhoea
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13
Q

What are the signs of AD

A

hyperpigmentation, hypotension/postural

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14
Q

What sort of blood tests are useful in AD and what might they show (autoimmune)

A

 21-Hydroxylase adrenal autoantibodies

• Adrenal autoantibodies i.e. 21-Hydroxylase adrenal autoantibodies

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15
Q

What tests can be run to exclude secondary caused of AD

A
  • ECG → tented T; prolonged PR and QT
  • CXR: ?lung neoplasia, TB
  • AXR: ?TB
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16
Q

What specialist tests can be used in diagnosis of AD

A

Short Synacthen test and

Synacthen test

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17
Q

What are the test in Synacthen test

A
  1. 250 micrograms ACTH per day for 3-5 days IV

2. Daily urine check for 17-hydroxysteroid levels

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18
Q

What are the steps in short Synacthen test

A
  1. Baseline cortisol
  2. 250 micrograms of Synacthen IM
  3. 30 min cortisol check
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19
Q

What does Synacthen test demonstrates

A

a. Normal in primary

b. 3-5 x increase in secondary

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20
Q

What does short Synacthen test demonstrates

A

Exclude if 30 min level >550nmol/L (↑ by >200 nmol/l)

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21
Q

what are the problems with short Synacthen test

A
  • May be affected by steroids, pregnancy COCP

* Less useful for secondary causes

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22
Q

What is multi gland failure

A

Autoimmune condition presenting with multi-gland failure including T1DM, chronic hypoparathyroidism, autoimmune thyroid disease etc.

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23
Q

what is the genetics and presentation of multi gland failure

A
  • Autosomal recessive (T1) OR polygenic (T2)
  • Often seen in children
  • Range of symptoms depending on glands affected
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24
Q

What do patients with AD should be educated about

A
  • Info. About disease + not missing steroids
  • Medical alert bracelet
  • Steroid card
  • Actions with activities/exercise → add 5-10mg hydrocortisone
  • Double steroid dose with illness
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25
Q

What is the hormone replacement regime in AD?

A
  • Glucocorticoid: Hydrocortisone →10mg/5mg morning/lunch

* Mineralocorticoid: Fludrocortisone 50 – 200 micrograms

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26
Q

What is the follow up in primary AD

A
  • Yearly (BP, U&E)

* Screening for other autoimmune diseases

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27
Q

What are the principles of management of secondary AD

A
  • Try to stop/↓ steroids if iatrogenic
  • Hormone replacement
  • Manage secondary cause
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28
Q

What are the complications of AD

A
  • Addisonian crises: 8% annual admission
  • ↓ quality of life → ongoing symptoms i.e. fatigue, loss of libido, recurrent admissions
  • Osteoporosis
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29
Q

What is the prognosis in AD

A

management dependent i.e. addisonian crises or infection can cause death

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30
Q

What are the causes of addisonian crises (AC)

A
  • Addison’s disease → poor compliance
  • Long-term steroid use
  • Haemorrhage into adrenals
  • Drugs i.e. phenytoin
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31
Q

What factors may precipitate AC

A

Infection, trauma, surgery, missed medications

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32
Q

What is the presentation of AC

A
  • Sudden, severe back and abdominal pain
  • D&V
  • Shock: ↑HR, vasoconstriction, postural hypotension, oligoria, weakness, confusion, coma
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33
Q

What is the immediate management of AC

A
  • Suspected →treat before biochemical results
  • Urgent bloods→ ACTH, U&Es
  • Hydrocortisone 100mg IV/IM stat (children 50-100/50/25 mg in >6/1-6/
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34
Q

What is later management of AC

A
  • Glucose IV for hypoglycaemia
  • IV fluids →U+Es guided
  • Hydrocortisone 200mg/8h IV/IM
  • Oral steroids after 72h
  • Treat underlying cause
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35
Q

What is the difference between cushion’s disease and syndrome

A
  • Disease increased circulating ACTH from pituitary

* Syndrome symptoms related to prolonged exposure to glucocorticoids and loss of normal mechanism of HPA axis

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36
Q

what is the prevalence of Cushion’s

A

10-15/million

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37
Q

what is the previlence of cushion’s in IDDM with HTN and poor glucose control

A

2-5%

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38
Q

what are the RF for cushion’s

A
  • Female →adrenal/pituitary tumours 5:1

* Small lung cancer →smoking etc

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39
Q

What are the ACTH dependent causes of cushions and how previlent are they

A 
80% of cushion's 
Pituitary adenoma or cancer i.e. ectopic secretion o	Small cell lung cancer and bronchial carcinoid tumour
o	Pancreatic neuroendocrine tumour 
o	Medullary thyroid cancer 
o	GI carcinoids
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40
Q

What sort of symptoms may point towards ectopic ACTH secretion

A

↓weight, ↑↑pigmentation, hypokalemic metabolic ankylosis and hyperglycaemia

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41
Q

What sort of test can be used if pituitary adenoma is suspected and what are the results

A

(low dose dexamethasone ↓↓ cortisol as in normal)

42
Q

What are the ACTH independent causes of cushion’s

A
  • Iatrogenic i.e. medications

* Unilateral adrenal tumour (adenoma/carcinoma →60/40%)

43
Q

What are the symptoms of cushions related to adipost tissue

A

truncal, supraclavicular facial (moon face) fat, buffalo hum

44
Q

What are the symptoms of cushions related to skin

A

atrophy, purple striae, bruising, hirsutism, acne, ↑pigmentation

45
Q

What are the symptoms of cushions related to glucose

A

DM/Impaired glucose tolerance • Glycosuria - Thirst, polydipsia, polyuria
• diabetes

46
Q

What are the symptoms of cushions related to gonads

A

• Gonadal dysfunction/ ↓ libido

47
Q

What are the symptoms of cushions related to psychiatry

A

depression, cognitive dysfunction emotional lability

48
Q

What are the symptoms of cushions related to bones

A

• Osteoporosis, osteopenia

49
Q

What are the symptoms of cushions related to pituitary tumour

A

headaches, visual problems, and galactorrhoea

50
Q

What are the symptoms of cushions related to menstruation

A

irregular menses/amenorrhoea due to hypothyroidism

51
Q

What are the symptoms of cushions

A
  • Adipost tissue redistribution: truncal, supraclavicular facial (moon face) fat, buffalo hum
  • Proximal muscle wastage
  • DM/Impaired glucose tolerance Glycosuria - Thirst, polydipsia, polyuria
  • Gonadal dysfunction/ ↓ libido
  • HTN, kidney stones
  • Skin: atrophy, purple striae, bruising, hirsutism, acne, ↑pigmentation
  • Psychological: depression, cognitive dysfunction emotional lability
  • Osteoporosis, osteopenia
  • Oedema
  • F: irregular menses/amenorrhoea due to hypothyroidism
  • Cataracts
  • Impaired immune function: increased infections, difficulty with wound healing
  • Child: growth restriction
  • Pituitary tumour: headaches, visual problems, and galactorrhoea
52
Q

what are the DD for cushion’s

A
  • Prolonged+ excessive alcohol use
  • Obesity
  • Poorly controlled DM
  • HIV
  • Anxiety and depression
53
Q

When is the cortisol high and low

A

high morning

low midnight

54
Q

What are the possible tests for CS

A

Overnight dexamethasone suppression test
24h urine free cortisol
48 hour dexamethasone suppression tests
48 hour high-dose dexamethasone suppression tests
Midnight cortisol
ACTH level
CRH + cortisol level

55
Q

what are the principles of 48 hour dexamethasone suppression tests

A
  • Give dexamethasone 0.5mg/6h PO for 2 days
  • Measure cortisol at 0 hours and 6 hours after final dose
  • In CS → failure to suppress cortisol
56
Q

what are the principles of Overnight dexamethasone suppression test

A
  1. PO dexamethasone at midnight
  2. Serum cortisol at 8am
    • Normal → suppression to
57
Q

what are the principles of 24h urine free cortisol

A

• Normal →

58
Q

what are the principles of 48 hour high-dose dexamethasone suppression test

A
  • 2mg/6h
  • Pituitary suppression vs other causes
  • Pituitary adenoma (Cushing’s disease) suppression of more than 50%
  • Other causes no suppression
59
Q

what are the principles of Midnight cortisol

A

CS high cortisol at night

60
Q

what are the principles of CRH administration

A

100 micrograms of CRH ↑ cortisol at 2h in pituitary not ectopic

61
Q

What are the results of overnight dexomethasone supression test and what are the causes for false positives

A

Normal → suppression to

62
Q

What are the ACTH levels indicative of

A

• Undetectable → adrenal tumour (CT or venous sampling)

63
Q

what investigations can be used with ectopic ACTH release

A

• ? ectopic ACTH → CT chest, abdo, pelvis/MRI

64
Q

What is Nelson’s syndrome

A

Complication of bilateral adrenectomy due to pituitary tumour
Nelson’s syndrome rapid enlargement of pituitary adenoma post bilateral adenectomy→ bitemporal hemianopia

65
Q

What is the treatment for CD

A

removal of pituitary adenoma (transphenoidal) OR bilateral adrenectomy

66
Q

What is the treatment for Iatrogenic causes of CS

A

stop medication if possible

67
Q

what is the management of adrenal adenoma and carcinoma

A

Adrenal adenoma: adrenalectomy

Adrenal carcinoma: adrenalectomy + radiotherapy + adrenolytic drugs mitotane

68
Q

what is the management of CS in ectopic causes

A
  • Surgery for non-metastatic tumours
  • Metyrapone, ketoconazole and fluconazole → ↓ cortisol secretion pre-surgery
  • Etomidate →blocks cortisol synthesis (i.e. if cortisol induced psychosis)
69
Q

what is the prognosis for CS

A
  • ↑ vascular mortality if untreated

* Symptoms i.e. HTN, ↑BMI, mood changes etc.

70
Q

What is Pheochromocytoma

A

Rare catecholamine-producing tumours → from chromaffin cells OR rare extraadrenal

71
Q

What are the parameters of role of role of 10% in pheoochromocytoma

A
  • 10% are malignant
  • 10% are extra-adrenal
  • 10% are bilateral
  • 10% are familial/hereditary
72
Q

What is the parentage of sporadic cases of pheoochromocytoma

A

10%

73
Q

What is the triad of symptoms in pheoochromocytoma

A

Episodic headache, sweating, and tachycardia (± BP↑,↓ or ↔)

74
Q

What investigations can be used for diagnosis of pheochromocytoma

A

• ↑WCC
• Plasma + 3 x 24h urines for free metadrenaline and normetadrenaline
• Clonidine suppression test → measure catecholamines at 0 and 3h post 0.3mg dose
o +ve if normal levels
• Imaging → CT/MRI OR isotope for extraadrenal (MIBG)

75
Q

What is the suppression test pheochromocytoma

A

• Clonidine suppression test → measure catecholamines at 0 and 3h post 0.3mg dose
o +ve if normal levels

76
Q

What are the management steps in pheochromocytoma

A
  1. Short acting α IV phentolamine→ control BP
  2. When stable BP → long-acting α i.e. phenoxybenzamine 10mg/24h PO
    a. ↑by 10 mg/day as needed up to 30mg/12h PO
    b. SE: postural hypotension, tachycardia, tiredness, nasal congestion
  3. BP controlled + no postural hypotension → start β1-blocker
  4. Surgery after 4-6 weeks
77
Q

what is the post-op management of pheochromocytoma

A

• 24h urine metadrenalines 2wks post-op, monitor BP (risk of ↓↓BP)

78
Q

What is the follow-up fro pheochromocytoma and why

A
  • Lifelong: malignant recurrence may present late

* Genetic screening

79
Q

what are the triggers for pheochromocytoma crises

A

stress i.e. surgery, GA, contrast

80
Q

What is the presentation of pheochromocytoma crises

A 
•	Pallor, Pulsating headache, Hypertension
•	Feels ‘about to die’
•	Pyrexial
•	ECG: 
o	Signs of LVF,
o	↑ ST segment
o	VT and cardiogenic shock
81
Q

define Primary Hyperaldosteronism and primary findings

A

Excess production of aldosterone independent of RAAS
• Sodium and water retention
• ↓ renin relase
• HTN, hypokalaemia +alkalosis (without diuretics)

82
Q

what are the symptoms of Primary Hyperaldosteronism

A

Asymptomatic or signs of hypokalaemia i.e. weakness, cramps, paraesthesia polydipsia, polyuria, ↑BP

83
Q

what are the causes of Primary Hyperaldosteronism + proportions

A

2/3 conn’s
1/3 bilateral adrenocortical hyperplasia
• Rare genetic i.e. GRA

84
Q

define Conn’s syndrome

A

solitary aldosterone producing adenoma

85
Q

what are the investigations in Primary Hyperaldosteronism

A
  • U+Es: ?hypokalaemia (may be normal)

* Renin and aldosterone

86
Q

what is Secondary Hyperaldosteronism

A

Due to a high renin from ↓renal perfusion, e.g. in renal artery stenosis, accelerated hypertension, diuretics, CCF or hepatic failure.

87
Q

What is Bartter’s syndrome

A

Major cause of congenital (autosomal recessive) salt wasting—via a sodium and chloride leak in the loop of Henle via a defective channel

88
Q

How does Bartter’s syndrome present

A
  • Presents in childhood with failure to thrive, polyuria and polydipsia. BP is normal
  • Sodium loss leads to volume depletion, causing ↑ renin and aldosterone production → hypokalaemia and metabolic alkalosis + ↑ urinary K+ and Cl–
89
Q

what is the management of Bartter’s syndrome

A
  • K+ replacement

* NSAIDS (to inhibit prostaglandins), and ACE-i

90
Q

Define congenital adrenal hyperplasia (CAH)

A
  • Group of autosomal recessive disorders of cortisol synthesis e.g. 21-hydroxyl deficiency (95% of causes)
  • Salt lousing or non-salt lousing
91
Q

What is the epidemiology of CAH

A

1/18000

boys wors i.e. salt lousing

92
Q

What are the findings in CAH

A

↓Cortisol ± ↓aldosterone (salt lousing) and ↑androgen

93
Q

what are the change sin females with CAH

A

ambiguous genitalia and urogenital sinus instead of normal separation

94
Q

What are the changes in males with CAH

A

hyperpigmentation and penile enlargement

95
Q

What is non classical presentation of CAH

A

• Non-classic CAH can present with early pubarche, infertility, oligomonorrhoea

96
Q

What are the possible symptoms in adults with CAH

A

o Hyperandrogenism
o Iatrogenic Cushing’s syndrome
o Infertility
o Metabolic syndrome

97
Q

What are the investigations in CAH

A
  • U&Es
  • Serum 17-hydroxyprogesterone (high diagnostic of 21-hydroxylase deficiency)
  • Bone age
  • USS
  • Karyotype
98
Q

What is the management of CAH

A 
•	Glucocorticosteroids 
o	Children → hydrocortisone 
o	Adults → dexamethasone or prednisolone i.e. long-acting 
•	Mineralocorticoids 
o	Fludrocortisone 
o	Sodium chloride supplements in infancy with salt-lousing presentation 
•	↑ stress → trauma, illness, surgery 
o	Double the dose of hydrocortisone
99
Q

What are the complications of CAH

A
  • ↓ height
  • ↑ weight
  • Precocious puberty
  • Polycystic overies
  • Infertility
100
Q

What are the causes of endocrine hypertension

A 
•	Neurogenic hypertension → pheochromocytoma 
o	Resistant as due to ↑adrenalin and noradrenalin 
•	Conn’s syndrome ↑ aldosterone
•	Idiopathic hyperaldosteronism 
•	Cushion’s syndrome→ ↑glucocorticoids
•	Hyperparathyroidism 
•	 Acromegaly 
•	Hyper and hypothyroidism
101
Q

What is the adrenal incidentaloma and how can it be tested

A

Asymptomatic adrenal tumour from imaging i.e. lesion of >1cm
• ?primary/ metastatic/ benign
• Overnight dexamethasone test? Cushin’s or hyperaldosteronism
• 85% benign/non-functional

phase 2 endo (4 decks)

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