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Year 2 Endocrine > Adrenal Pathology > Flashcards

Adrenal Pathology Flashcards

1
Q

Common causes of hyper active adrenals?

A

Hyperplasia
Adenoma
Carcinoma

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2
Q

Common causes of hypo active adrenals?

A

Acute - Waterhouse friderichsen

Chronic - Addisons

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3
Q

What are the two types of adrenocortical hyperplasia?

A

Acquired

Congenital

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4
Q

What are the two causes of acquired adrenocortical hyperplasia ?

A 
Endogenous ACTH (Cushings disease)
Ectopic ACTH ( From small cell lung cancer)
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5
Q

If the hyperplasia is diffuse how is the growth driven?

A

ACTH driven

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6
Q

If the hyperplasia is nodular how is the growth driven?

A

ATCH independant (tumour sarcoid etc)

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7
Q

Why does an increase in ACTH cause hyperplasia?

A

ACTH is a stimulant and bind to receptors within the adrenal gland, increase in stimuli increases the drive for growth to keep up with demand.

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8
Q

What is the main cause of congenital adrenocortical hyperplasia?

A

Autosomal recessive metabolic disorder

-deficiency in enzyme required for steroid biosynthesis

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9
Q

What is likely to be seen in an autosomal recessive metabolic disorder resulting in adrenocortical hyperplasia?

A

Deficiency in target hormone

Increased ACTH and another hormone

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10
Q

If a child presents with an adrenal tumour what should be screened for?

A

Genetic syndrome p53 inhibition

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11
Q

How can adrenal tumours be found?

A

Hormonal affects
Mass lesion, incidental finding
Carcinomas can undergo necrosis resulting in a fever

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12
Q

Adrenal adenoma

A

Well circumscribed
Yellow cut surface
Well differentiated
N/C ratio is normal

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13
Q

Are most adrenal adenomas functional?

A

Most aren’t but some can be

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14
Q

Why are the cut surfaces of adrenal adenomas yellow?

A

Adrenal glands are the centre of lipid metabolism into steroids

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15
Q

Carcinomas are less likely to be functional that adenomas?

A

False - more likely to be

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16
Q

If a carcinoma is virilising what does this usually signify?

A

Malignant potential

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17
Q

Adrenal Carcinoma

A

Closely resembles and adenoma
Local invasion - retroperitoneal and kidney
Metastasis - Liver Lung Bone

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18
Q

What is the 5 year survival with an adrenal carcinoma?

A

20-35%

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19
Q

What is the main differentiating feature between a carcinoma and an adenoma?

A

Carcinomas undergoes metastasis

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20
Q

How else are carcinomas different to adenomas?

A

Can weigh over 50g or >20cm
Haemorrhage and Necrosis
Atypical frequent mitosis
Capsular invasions

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21
Q

Primary hyperaldosteronism

A

Conns

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22
Q

Primary Hypercortsisolism

A

Cushings

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23
Q

Causes of acute adrenal failure?

A

Rapid withdrawal of steroids

Massive adrenal haemorrhage

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24
Q

Causes of adrenal haemorrhage?

A

Newborn
Anticoagulation therapy
Septicaemic infection

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25
Q

What is Waterhouse- Friderichsen syndrome?

A

Acute adrenal failure due to severe adrenal haemorrhage as a result of a septicaemic infection

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26
Q

In ectopic ACTH production what else is notable ?

A

Hypokalaemia, due to high levels of ACTH and mineralocorticoids causing water retention.

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27
Q

What is the main chronic adrenal insufficiency?

A

Addisons disease

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28
Q

What is Addisons disease?

A

Inadequate adrenocorticoid levels due to bilateral autoimmune destruction of the adrenal glands.

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29
Q

Symptoms of Addison’s

A 
Anorexia
Weight loss
Dizziness and feinting
Non specific abdominal pain
D+V
Hyperpigmentation
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30
Q

In Addisons where is hyperpigmentation first noticed?

A

Palmar creases

Dentists may notice in Buccal cavity

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31
Q

Why does hyperpigmentation occur in addison’s?

A

ACTH can stimulate melanocytes to produce melanin

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32
Q

What is used to diagnose Addisons?

A 
Low Na+ High K+ Hypoglycaemia
ACTH levels
High Renin and Low Aldosterone
Adrenal autoantibodies 
CT MRI
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33
Q

What variation of the SynACTHen test is used and why?

A

Short synACTHen
-plasma cortisol levels 30 mins after IV ACTH
As this is a medical emergency patients die quickly

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34
Q

What results should be looked for in a short synACTHen test?

A

Normal - >250 pre and post ACTH of >550

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35
Q

What is the key point in treating suspected Addison’s disease?

A

Don’t wait for lab results

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36
Q

What is the treatment of Addisons and any acutely presenting adrenal failure?

A

IV 100mg Cortison and 1000ml of saline

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37
Q

What is the treatment for Addisons?

A

Oral 15-30 mg divided 3x daily

10mg morning 5mg lunch and 5mg at dinner

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38
Q

In regards to Addisons what should also be considered?

A

Aldosterone replacement- Fludrocortisones

-monitor BP and K+

39
Q

Much like diabetics what is important to tell the patient?

A

Don’t stop treatment if ill, in fact increase dose

If unable to digest orally due to D+V then admission for IV

40
Q

What is secondary adrenal insufficiency ?

A

Lack of CRH or ACTH

41
Q

What is the commonest cause of secondary adrenal insufficiency?

A

Exogenous long term steroid use

42
Q

Why does exogenous steroid use result in insufficiency ?

A

Negative feedback inhibits ACTH production, which is main stimulant for adrenal growth, as a result adrenal glands are atrophied - don’t react to ACTH anymore

43
Q

What test can still be used in secondary insufficiency?

A

SynACTHen test

44
Q

What are the key features that can distinguish secondary from primary adrenal insufficiency?

A

Pale skin as no ACTH

Aldosterone production is intact

45
Q

What is the management of secondary adrenal failure

A

Hydrocortisone but no mineralcorticoids

46
Q

As well as autoimmune list some other common causes of adrenal failure

A

TB

HIV

47
Q

How can an iatrogenic Cushing’s lead to Addisons?

A

Chronic ACTH suppression leads to adrenal Hypotrophy so unable to produce steroids endogenously

48
Q

If a patient with iatrogenic cushings falls ill what must be given?

A

Extra steroids whilst ill

49
Q

What should be done if withdrawing a patient of long term steroids?

A

Done slowly over 4/6 weeks,

If patient unable to tolerate continue with treatment.

50
Q

What is the physiology behind primary aldosteronism?

A

Autonomous production of aldosterone independent of the Renin-Angiotensin system.
Reabsorption on Na+ and excretion of K+

51
Q

What are some of the effects aldosterone has?

A

Increased Cardiac collagen, sympathetic outflow, altered endothelial pressor response, sodium retention.

52
Q

What are some clinical signs and symptoms in Primary aldosteronism?

A

Significant resistant hypertension
Increased Left Ventricular hypertrophy
Increased atheromas
Hypokalaemia

53
Q

What is Conns?

A

Aldosterone production from an Adrenal Adenoma

54
Q

What is the commonest cause of primary hyperaldosteronism?

A

Bilateral Adrenal Hyperplasia

55
Q

List a rare cause of Primary hyperaldosteronism

A

K+ Channel mutation

56
Q

What is main stay of diagnosis in hyperaldosteronism?

A

Aldosterone excess - Aldosterone higher than renin

Give 2L of saline - normal would lead to aldosterone suppression.

57
Q

What else can be used after aldosterone excess test in hyperaldosteronism?

A

Imaging CT and PET scan

Adrenal Vein sampling

58
Q

What is the medical treatment of hyperaldosteronism and when is it used?

A

Spironolactone

In bilateral adrenal hyperplasia

59
Q

What is spironolactone?

A

A Potassium sparing diuretic

Steriod which blocks the effect of aldosterone

60
Q

What is the surgical treatment of hyperaldosteronism and when is it used?

A

Unilateral laparoscopic adrenalectomy
Designed as curative treatment for adrenal adenoma
- 30-70% curative
- older is less curative

61
Q

Congenital adrenal hyperplasia

A

Rare conditions linked to defect enzyme in steroid synthesis

62
Q

What is the most common cause of congenital adrenal hyperplasia?

A

21α hydroxylase deficiency

- autosomal recessive

63
Q

In 21α hydroxylase deficiency what occurs?

A

No aldosterone or cortisol and excess androgens

64
Q

What happens as a result of excess aldosterone?

A

Salt Wasting

65
Q

What happens as a result of excess androgens?

A

Virilisation

66
Q

What is the diagnostic test of a 21α hydrolase deficiency?

A

17-OH progesterone levels will be high when tested

67
Q

In a Neonatal adrenal crisis what signs indicate a 21α hydroxylase deficiency ?

A

Male - excess testosterone

Female - Ambiguous genitalia

68
Q

What is a classic presentation of 21α hydroxylase deficiency ?

A

Presents 2/3 weeks old with biochemical Addisons

-hypoglycaemia and poor weight gain

69
Q

What is the non classical presentation of 21α hydroxylase deficiency ?

A

Presents generally in older female

-Hirsutism, Acne, Precocious puberty, infertility, oligomenorrhoea

70
Q

What is the treatment for a classic presentation of a 21α hydroxylase deficiency ?

A

Glucocorticoid and mineralocorticoid replacement

Surgical correction - to achieve maximum growth

71
Q

Why does excess androgens reduce maximum height?

A

As triggers early onset puberty so growth plates fuse early.

72
Q

What is the treatment aims for a non classic presentation of a 21α hydroxylase deficiency ?

A

Restore fertility

Suppress excess androgens

73
Q

What are some clues that could hint towards a Phaechromyocytoma

A

Labile hypertension - rapidly fluctuating BP
High Diastolic
Postural hypotension

74
Q

What is a Phaechromyocytoma?

A

Rare adrenal medullary tumour
1 in 100,000
Insidious onset

75
Q

Why is a Phaechromyocytoma called a tumour of 10’s?

A

10% malignant
10% Bilateral
10% Extra adrenal
10% children

76
Q

If the a Phaechromyocytoma occurs in the sympathetic chain what is it called?

A

Paraganglioma

77
Q

Why can the same tumour occur in the medula and sympathetic chain?

A

Because the medulla is made up of sympathetic splanchnic nerves.

78
Q

What is Phaechromyocytoma linked to?

A

MEN2

- Think Phaechromyocytoma and Neurofibromatosis

79
Q

What is Phaechromyocytoma often confused with?

A 
Angina
Anxiety
Menopause
Pregnancy
Hypoglycaemia
80
Q

What is the classic triad of a Phaechromyocytoma symptoms?

A

Hypertension
Headache
Sweating

81
Q

What others presenting complaints do people with a Phaechromyocytoma come in with?

A 
Palpitations
Panic attacks
Anxiety
Weight loss
Flushing
Constipation
82
Q

List some complications of a Phaechromyocytoma

A

LVF
Myocardial necrosis
Stroke
Paralytic ileum

83
Q

What are the biochemical signs of a Phaechromyocytoma?

A

Hyperglycaemia
Slightly low K+
High haematocrit
Mild hypercalcaemia

84
Q

When should investigations be under taken?

Phaechromomycytoma

A

Over 50 with marked resistant hypertension

Family members diagnosed with MEN2

85
Q

Which is more useful in the diagnosis of a Phaechromyocytoma?
Catelcolamines or Metanephrines

A

Metanephrines as they are more stable, so give a more accurate measurement.

86
Q

What is the diagnostic test for a Phaechromyocytoma?

A

24 hr metanephrine urine collection
MRI
Plasma at time of symptoms

87
Q

Why if possible should an MRI be done from pelvis to head?

A

As Phaechromyocytoma can occur anywhere in the sympathetic chain as preganglioma

88
Q

What is the first step in the treatment of a Phaechromyocytoma?

A

Alpha blocker followed by a Beta blocker

89
Q

Give an example of an alpha blocker used

A

Phenoxybenzamine

90
Q

What is the beta blockers used in Phaechromyocytoma’s?

A

Propanolol

91
Q

What should follow the Alpha and beta blockade in the treatment of Phaechromyocytoma?

A

Fluid and Blood replacement to control the hypotension as a result of vasodilation due to the blockade

92
Q

What are the final steps in the treatment of a Phaechromyocytoma?

A

Surgical excision is posible

Chemotherapy or radiotherapy if surgery isn’t an option

93
Q

If surgery is successful what will happen in the case of a Phaechromyocytoma?

A

Reversal of the hypertension to normal requiring no other treatment.

94
Q

Following treatment what should a patient who suffered with a Phaechromyocytoma undergo?

A

Long term follow up
Genetic testing
- if +ve check immediate family members

Year 2 Endocrine (21 decks)

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