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Endocrine > Adrenal Physiology & Pathology > Flashcards

Adrenal Physiology & Pathology Flashcards

1
Q

What are the two parts of the adrenal gland?

A
  • outer cortex

- inner medulla

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2
Q

Name the three zones of the adrenal cortex

A
  • zone glomerulosa
  • zone fasciculata
  • zone reticularis
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3
Q

What does the zone glomerulosa produce and what is it regulated by?

A

Produces mineralocorticoids e.g. aldosterone

Regulated by potassium & angiotensin II

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4
Q

What does the zone fasciculata produce and what is it regulated by?

A

Produces glucocorticoids e.g. cortisol

Regulated by ACTH

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5
Q

What does the zone reticularis produce and what is it regulated by?

A

Produces adrenal androgens

Regulated by ACTH

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6
Q

What stimulates the medulla?

A

Sympathetic stimulation

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7
Q

What does the medulla produce?

A

Catecholamines

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8
Q

Describe the mechanism of action of corticosteroids

A

Bind to intracellular receptors which subsequently bind to DNA to impact transcription

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9
Q

Name six systems that cortisol affects

A
  • Circulatory
  • Metabolic
  • CNS
  • Bones
  • Immune
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10
Q

Name three functions of aldosterone

A
  • sodium/potassium balance
  • blood pressure regulation
  • extracellular volume regulation
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11
Q

Define adrenal insufficiency

A

inadequate adrenocortical function

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12
Q

State four causes of primary adrenal insufficiency

A
  • Addison’s
  • Congenital adrenal hyperplasia
  • TB
  • Malignancy
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13
Q

State four causes of secondary adrenal insufficiency

A
  • Lack of ACTH stimulation
  • Iatrogenic
  • Pituitary disease
  • Hypothalamic disease
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14
Q

How does acute adrenal insufficiency occur?

A

Due to rapid withdrawal of steroid treatment
Complication of septicaemia (waterhouse friderichsen) which can occur in massive haemorrhage with extensive cortical necrosis

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15
Q

How much of the adrenal gland needs to be destroyed before symptoms present?

A

> 90%

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16
Q

Describe Addison’s disease

A

Autoimmune destruction of the adrenal cortex (21-OH antibody)

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17
Q

What cells infiltrate in Addison’s disease?

A

Lymphocyte & plasma

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18
Q

Name some clinical features of Addison’s disease

A
  • anorexia/weight loss
  • fatigue/lethargy
  • dizziness, hypotension
  • abdominal pain, vomitting, diarrhoea
  • pigmentation
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19
Q

How does Addison’s result in pigmentation?

A

ACTH cross reacts with melanocyte stimulating hormone leading to skin pigmentation

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20
Q

How is Addison’s diagnosed?

A

Serum/saliva cortisol - should be 0 at midnight, high serum ACTH, short synacthen test

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21
Q

Describe the treatment for Addison’s

A

Hydrocortisone

Fludrocortisone

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22
Q

Why is education vital for Addison’s patients?

A

They must not stop treatment suddenly & should wear an ID band in case of emergency

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23
Q

What is the difference between primary and secondary adrenal insufficiency in terms of clinical features?

A

There is no pigmentation as ACTH is low

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24
Q

How do exogenous steroids cause secondary adrenal insufficiency?

A

Act to decrease CRH & ACTH leading to decreased

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25
Q

What is the treatment for Addison’s disease?

A

Hydrocortisone replacement

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26
Q

Define primary aldosteronism

A

Autonomous production of aldosterone, independent of its regulators (angiotensin II & potassium)

27
Q

What is the result of excess mineralocorticoid on sodium & potassium?

A

Sodium retention & potassium wasting

28
Q

What is the effect of aldosterone on the heart?

A

Increased BP, LVH, Atheroma

29
Q

State three clinical features of primary aldosteronism

A
  • hypertension
  • hypokalaemia
  • alkalosis
30
Q

Name three causes of primary aldosteronism

A
  • Adrenal adenoma (Conn’s syndrome)
  • Bilateral adrenal hyperplasia
  • Genetic disorders
31
Q

What is the first line diagnostic test of primary aldosteronism? What do you do if it is abnormal?

A

Aldosterone:Renin ratio, if raised 2L of saline should suppress aldosterone unless there is pathology

32
Q

If A:R ratio and saline suppression is abnormal what is the next line diagnostic test?

A

Adrenal CT

33
Q

Describe the treatment for Primary Aldosteronism

A

Surgical - unilateral laparoscopic adrenalectomy

Medical - mineralocorticoid antagonists

34
Q

What two mineralocorticoid antagonists can be used in Primary aldosteronism?

A
  • spironolactone

- eplerenone

35
Q

What is congenital adrenal hyperplasia a broad term for?

A

Rare conditions associated with enzyme defects in the steroid pathway

36
Q

What is the commonest enzyme defect in CAH?

A

21 alpha hydroxylase deficiency (classical & non-classical)

37
Q

Describe the difference between classical and non-classical 21 alpha hydroxylase deficiency

A

classical - salt-wasting & viriling

non-classical - hyperandrogenaemia

38
Q

How is CAH diagnosed?

A

Basal/stimulated 17-OH progesterone

Genetic mutation analysis

39
Q

Describe the pathology of CAH

A

Progesterone & 17-OH progesterone cannot be converted into aldosterone/cortisol intermediates and instead much be converted into androstenedione & testosterone

40
Q

How does CAH present?

A

males - adrenal insufficiency, poor weight gain, excess testosterone
females - genital ambiguity
Late presentation - hirsute, acne, oligo/amenorrhoea, infertility, precocious puberty

41
Q

What happens to the cortex as a result of reduced cortisol?

A

Stimulates ACTH release & cortical hyperplasia

42
Q

How is CAH treated?

A

Paeds - glucocorticoid/mineralocorticoid replacement

Adults - control androgen excess, restore fertility & avoid steroid over-replacement

43
Q

What is a phaemochromocytoma?

A

Neoplasma derived from chromaffin cells of the adrenal medulla which secretes catecholamines

44
Q

How does the phaemochromocytoma appear brown?

A

Oxidation of catecholamines from adrenal remnants on the surface

45
Q

What other rare syndromes are associated with phaemochromocytoma?

A
  • MEN 2
  • Von -hippel Lindau
  • Neurofibromatosis
46
Q

What is the classic triad of symptoms for phaemochromocytoma?

A
  • hypertension
  • headache
  • sweating
47
Q

Name some other clinical features of phaemochromocytoma

A
  • palpitations
  • SOB
  • anxiety
  • weight loss
48
Q

Name four biochemical signs of phaemochromocytoma

A

Hyperglycaemia
High haematocrit
Lactic acidosis
Low potassium

49
Q

Why is phaemochromocytoma known as the 10% tumour?

A

10 % are;
extra- adrenal
malignant
not associated with hypertension

50
Q

What are extra adrenal phaemochromocytoma called?

A

Paragangliomas

51
Q

What percentage of phaemochromocytoma are familial?

A

25%

52
Q

How is phaemochromocytoma diagnosed?

A
  • Urine/plasma metinepherine

- MRI, MIBG, PET scans

53
Q

How are phaemochromocytomas managed?

A

Full alpha and beta blockade to block catecholamine receptors
Fluid & Blood replacement
Surgery to remove
Chemotherapy if malignant

54
Q

What type of cells are found in a neuroblastoma?

A

Primitive cells that show differentiation towards ganglion cells - arise in the medulla or along the sympathetic chain

55
Q

When are the majority of neuroblastomas diagnosed?

A

Childhood

56
Q

What predictors of neuroblastoma indicate a poor outcome?

A

Amplification of N-myc

Expression of telomerase

57
Q

How do adrenocortical tumours present?

A

Incidental finding, hormonal effects, mass lesion or carcinoma with necrosis can cause a fever

58
Q

Describe an adrenocortical adenoma

A

Well circumscribed, encapsulated usually small & yellow/brown due to lipids. well differentiated, can be functional

59
Q

Describe an adrenocortical carcinoma

A

More likely to be a functional, virilsing tumour that is malignant. Often difficult to distinguish from adenoma.

60
Q

What factors can help distinguish adenoma from carcinoma?

A
  • local invasion
  • metastases
  • peritoneum/pleura spread
  • regional lymph nodes
61
Q

What percentage of patients with adrenocortical adenoma will be dead in 2 years?

A

50%

62
Q

What is adrenal crisis?

A

Life threatening medical condition due to sever adrenal insufficiency can occur due to stopping steroid therapy

63
Q

How is an adrenal crisis managed?

A

Isotonic saline

Hydrocortisone

Endocrine (17 decks)

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