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Endocrinology > Adrenal Diseases > Flashcards

Adrenal Diseases Flashcards

1
Q

What are the two parts of the adrenal gland?

A
  • cortex

- medulla

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2
Q

What does the cortex secrete?

A

glucocorticoids, mineralocorticoids and androgens

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3
Q

What does the medulla secrete?

A

catecholamine

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4
Q

Describe the main mineralcorticoid?

A

Aldosterone

Involved in the renin-angiotensin system and ADH in the maintenance of blood volume

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5
Q

Causes of adrenocortical hyperfunction?

A

Hyperplasia (includes cushings, pituitary disease, congenital issues), adenoma and carcinoma

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6
Q

Causes of primary adrenocortical hypofunction?

A

Chronic: Addison’s disease
Acute: Water-Friderichsen syndrome (bleeding in glands due to severe bacterial infection)

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7
Q

Describe location of the adrenal glands?

A

Bilateral and sit superior and medial to the upper pole of the kidneys

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8
Q

Weight of normal adrenal glands?

A

4-5g (so can be quite hard to find)

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9
Q

Describe pathology of adrencortical adenomas?

A

Well circumscribed, encapsulated yellow brown lesions, cells resemble adrenal cortical cells, well differentiated, more often non-functional so can be an incidental finding

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10
Q

Describe pathology of adrenocortical carcinomas?

A

Rare, more likely to be functional, can closely resemble adenoma. Can be difficult to distinguish between benign and malignant, and sometimes only definite is if it has metastasised. Other features: large size, haemorrhage, necrosis, frequent mitoses, atypical mitoses, lack of clear cells, capsular or vascular invasion (added together)

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11
Q

Cushing’s syndrome vs Conn syndrome?

A 
Cushings= corticosteroid excess
Conn= mineralocorticoid excess
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12
Q

What is Addison’s disease?

A

Chronic Adrenal Insufficiency

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13
Q

3 causes of addison’s disease?

A

Auto-immune adrenalitis- most common
Tuberculous destruction of adrenals
Metastatic neoplasms

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14
Q

What cells in the medulla secrete catecholamines?

A

Chromaffin cells

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15
Q

What are three adrenal medullary tumours?

A

Phaeochromocytoma
Ganglioneuroma
Neuroblastoma

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16
Q

What type of cells are phaeochromocytomas composed of? What do they therefore secrete?

A

Chromaffin cells

Catecholamines

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17
Q

What are neuroblastomas? Who do they arise in?

A

very malignant tumour of primitive nerve cells occurring in children

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18
Q

Describe phaeochromocytomas and if you know if they are malignant?

A

More of a spectrum. Difficult to tell if malignant from histology as like with most endocrine tumours it cells don’t predict how the tumour will act, only really know if it has metastasised. Malignant tumours tend to be larger.

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19
Q

Layers of cortex from outside to inside closest to medulla?

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

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20
Q

Zona glomerulosa secretes ___1____
Zona fasciculata secretes ____2____
Zona reticularis secretes ____3___

A

1) aldosterones/ mineralocorticoids
2) cortisol/ glucocorticoid
3) Androgens

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21
Q

Cortisol and androgen secretion is controlled by which axis? What axis is aldosterone controlled by? Clinical implications?

A

Cortisol and androgens by hypothalamic pituitary. Mineralocorticoids by the RAAS system, so if pituitary disease it shouldn’t be affected.

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22
Q

Major actions of cortisol?

A

Changes mood- euphoria and psychosis
Accelerates osteoporosis, decreases serum calcium, decreases collagen formation and wound healing
Decreases capillary dilation and permeability, decreases leucocyte migration, decreases macrophage activity and inflammatory cytokine production
Increases blood sugar, increases fat deposition, central redistribution, increases proteolysis
Increases CO, BP, renal blood flow and GFR

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23
Q

Does RAAS system increase or decrease blood pressure? What system counteracts it?

A

Increase

Natriuretic Peptides

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24
Q

3 main components of the RAAS system?

A

Renin
Angiotensin
Aldosterone

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25
Q

Describe activation of the RAAS system

A

Stimulated by renal artery hypotension, renal sympathetic nerves or decreased sodium in renal tubular fluid

  • Renin is released from the kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (produced by the liver)
  • Angiotensin I is converted to angiotensin II by Angiotensin converting enzyme - ACE (mainly produced by pulmonary vascular endothelium)
  • Angiotensin II (1) stimulates the release of Aldosterone from the adrenal cortex (2) Causes systemic vasoconstriction - increases SVR. It also stimulates thirst and ADH release - i.e. contributes to increasing plasma volume mainly brought about by aldosterone
  • Aldosterone (a steroid hormone) acts on the kidneys to increase sodium and water retention – increases plasma volume
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26
Q

Primary hypoadrenalism/ addisons causes?

A

Usually due to auto-immune destruction of adrenal gland- more than 90% destroyed before symptomatic
In developing countries may be TB related
Could be caused by metastatic neoplasms
(often Addisons just refers to auto-immune form)

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27
Q

Addisons is more common in male or females? What else is associated?

A

Females

Other autoimmune diseases and 21 hydroxylase antibodies

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28
Q

Most common antibody in addisons?

A

21 hydroxylase

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29
Q

Presentation of Addisons disease?

A 
Anorexia/ weight loss
Fatigue/ lethargy
Dizziness and low BP
Abdo pain, vomiting and diarrhoea
Skin hyperpigmentation and buccal pigmentation (due to excess ACTH reacting with melanocytes)
Amenorrhea
30
Q

Hyponaetremia with hyperkalaemia think…

A

Addisons disease

31
Q

Investigations for Addisons?

A

Hyponaetremia and hyperkalaemia and children may present with hypoglycaemia
Short synacthen test- normal adrenal glands should raise cortisol
Adrenal antibodies present in 90%
Plasma renin is high due to low aldosterone
A single cortisol reading is of little value but a high reading does make diagnosis unlikely
Imaging to check for TB or calcified adrenals

32
Q

Treatment for Addisons?

A

Glucocorticoid replacement: Hydrocortisone is usually used 15-30 mg in divided doses. Prednisolone or dexamethasone if struggle to take several doses
Fludrocortisone is used as mineralocorticoid replacement usually 50-300 mg
Patients need educated about steroids- increase dose in illness, carry a steroids car, medic alert bracelets.

33
Q

Signs of adrenal crisis?

A

Hypotension, hyponaetremia, hyperkalaemia, hypoglycaemia, dehydration, pigmentation often with precipitating infection, infarction, trauma or operation

34
Q

Major deficiencies in adrenal crisis?

A

Salt, steroid and glucose

35
Q

Treatment of adrenal crisis?

A

Urgent! don’t wait for results

Give person hydrocortisone IM or IV and stables with IV saline infusion

36
Q

2 causes of secondary hypoadrenalism? Which is most common? Treatment?

A

Most common cause is long term steroid therapy leading to hypothalamic pituitary adrenal suppression- weaning off steroid is difficult
Other cause is hypothalamic pituitary disease- often panhypopituitarism so needs hormone replacement.

37
Q

What can give cushionoid appearance?

A

Long term steroids

38
Q

What may you need to do before taking someone off long course of steroids?

A

Refer to endocrinology to have synacthen to see if have adrenal suppression, need to be weaned off the steroids gradually.

39
Q

Endocrine causes of hypertension?

A

Excessive renin and thus angiotensin 2 production (renal disease)
Excessive catecholamine production in pheochromocytoma
Excessive growth hormone- acromegaly
Excessive aldosterone production- Conn syndrome, adrenal hyperplasia
Cushing Syndrome
Congenital adrenal hyperplasia
Tumours producing other mineralocorticoids
Exogenous mineralocorticoids or enzyme inhibitors

40
Q

What is Primary hyperaldosteronism/ Conn syndrome?

A

Disorder of the adrenal cortex characterised by excess aldosterone production leading to sodium retention, potassium loss, hypokalaemia and hypertension

41
Q

Causes of primary hyperaldosteronism/ Conn syndrome?

A

Adrenal aldosterone secreting adenomas (Conn adenoma), bilateral adrenal hyperplasia
Rarely genetic mutations, unilateral hyperplasia as rare causes

42
Q

Clinical features of primary hyperaldosteronism/ Conn syndrome?

A

Mainly just hypertension

Sometimes with hypokalaemia

43
Q

What is the most common cause of primary hyperaldosteronism / Conn syndrome?

A

Bilateral adrenal hyperplasia

44
Q

What is the commonest cause of secondary hypertension?

A

Conn syndrome/ primary hyperaldosteronism

45
Q

Who with hypertension should you the suspicious of primary hyperaldosteronism?

A 
Under 35 yrs
Accelerated hypertension
Hypokalaemia
Resistant hypertension
Other symptoms e.g. sweating attacks or weakness
46
Q

Investigations for primary hyperaldosteronism?

A

Plasma aldosterone: Renin ratio as screening test. Increased ratio as increased aldosterone and decreased renin
If ARR positive then saline suppression- failure of plasma aldosterone to suppress by more than 50% with 2 litres of normal saline confirms
Adrenal CT to demonstrate adenoma or bilateral hyperplasia (NOTE: lots of incidentalomas need to prove the tumour found is causing symptoms)

47
Q

Screening test for primary hyperaldosteronism?

A

Plasma aldosterone: renin ratio as screening test

48
Q

Explain incidentalomas and significance?

A

Adrenal masses are common and may not be causing the problem- need to check if they are functional before removing

49
Q

Treatment for primary hyperaldosteronism?

A

Adenoma > unilateral adrenalectomy ( may not cure if been there a long time so may still need medical treatment)
Hyperplasia and uncured surgery > spironolactone

50
Q

Describe the pathophysiology of congenital adrenal hyperplasia?

A

Results from autosomal recessive deficiency of an enzyme in the cortisol synthetic pathway
Most common mutation is 21-hydroxylase deficiency
As a result cortisol secretion is reduced and feedback leads to increased ACTH to maintain adequate cortisol causing adrenal hyperplasia

51
Q

What is the most common mutation causing congenital adrenal hyperplasia?

A

21-hydroxylase deficiency

52
Q

Explain why you get certain symptoms with congenital adrenal hyperplasia?

A

You have decreased cortisol so get symptoms of Addisons. Diversion of steroid precursors into androgenic steroid pathway may occur so virilization will occur (women get men features) Aldosterone synthesis may also be impaired and then salt wasting (as low blood sodium and dehydration)

53
Q

What is salt wasting? Symptoms?

A

Results from impaired aldosterone synthesis which causes low blood sodium and dehydration so get salt wasting with excessive thirst and extreme salt cravings. High sodium content in urine.

54
Q

Presentation of congenital adrenal hyperplasia?

A

Sexual ambiguity in females
Adrenal failure
Non-classified disease will present later in life as precocious puberty, hirsutism (excessive body hair) and amenorrhea. Hirsutism before puberty is suggestive of CAH.

55
Q

Hirsutism before puberty is suggestive of…

A

CAH

56
Q

Define hirsutism and virilization and trichosis?

A 
Hirsutism= unwanted male growth pattern of hair in females
Virilization= women get men features 
Trichosis= any abnormal condition of hair
57
Q

Investigations for congenital adrenal hyperplasia?

A

Measure levels of 17-OH progesterone (should be raised)
Basal ACTH is raised
Levels of other steroid precursors and androgens is raised
Genetic testing

58
Q

Treatment of congenital adrenal hyperplasia?

A

Glucocorticoid activity must be replaced
May need to control androgen excess and restore fertility
Mineralocorticoid replacement in some

59
Q

What is a pheochromocytoma?

A

Adrenal medulla tumour composed of chromaffin cells.

60
Q

Pheochromocytoma vs paraganglioma?

A 
Phaeochromocytoma= in adrenal medulla
Paraganglioma= extra adrenal in sympathetic chain
61
Q

Risk factors for phaeochromocytoma?

A

It can occur in familial syndromes such as MEN2, VHL and neurofibromatosis, age 30-50 usually and equally prevalence in men and women

62
Q

Symptoms in pheochromocytoma are due to _____ and are usually but not always _____

A

catecholamine excess

intermittent

63
Q

Symptoms of phaeochromocytoma?

A

Catecholamine excess often intermittent
Classic triad= hypertension, headache and sweating
Also palpitations, breathlessness, constipation, anxiety and weight loss.

64
Q

Investigations for phaeochromocytoma?

A

Measurement of 24hr metanephrine
Plasma metanephrine ideally at time of symptoms
Identify source- MRI, MIBG (nuclear imaging test) and PET scan

65
Q

Treatment of phaeochromocytomas?

A

Tumours need removed where possible
Perioperative treatment: full alpha and beta blockade. A BEFORE B or could worsen hypertension. Phenoxybenzamine then propanolol. IV hydration. Need careful anaesthetic assessment.

66
Q

Are the adrenal glands retro or intra peritoneal?

A

Retroperitoneal

67
Q

Chromaffin cells secrete… which are stored…

A

catecholamines synthesised and stored in the cells

68
Q

Catecholamines have a long or short half life?

A

V short (that’s why urinary catecholamines in phaeochromocytoma can be normal)

69
Q

Conns disease has a low potassium because….

A

aldosterone causes sodium and water retention and to retain the sodium it pumps out the potassium in exchange

70
Q

What causes muscle wasting in Cushings?

A

Decreased protein synthesis

71
Q

What other endocrine condition can you get as a result of Cushings? Why?

A

Diabetes as your blood sugar is raised by cortisol

72
Q

Effect on phaeochromocytoma on bowel? Explain?

A

Constipation which could lead to paralytic ileum as adrenaline causes blood to be moved away from the bowel

Endocrinology (11 decks)

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