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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
What is the treatment for Addison's disease?
Hydrocortisone replacement
26
Define primary aldosteronism
Autonomous production of aldosterone, independent of its regulators (angiotensin II & potassium)
27
What is the result of excess mineralocorticoid on sodium & potassium?
Sodium retention & potassium wasting
28
What is the effect of aldosterone on the heart?
Increased BP, LVH, Atheroma
29
State three clinical features of primary aldosteronism
- hypertension - hypokalaemia - alkalosis
30
Name three causes of primary aldosteronism
- Adrenal adenoma (Conn's syndrome) - Bilateral adrenal hyperplasia - Genetic disorders
31
What is the first line diagnostic test of primary aldosteronism? What do you do if it is abnormal?
Aldosterone:Renin ratio, if raised 2L of saline should suppress aldosterone unless there is pathology
32
If A:R ratio and saline suppression is abnormal what is the next line diagnostic test?
Adrenal CT
33
Describe the treatment for Primary Aldosteronism
Surgical - unilateral laparoscopic adrenalectomy | Medical - mineralocorticoid antagonists
34
What two mineralocorticoid antagonists can be used in Primary aldosteronism?
- spironolactone | - eplerenone
35
What is congenital adrenal hyperplasia a broad term for?
Rare conditions associated with enzyme defects in the steroid pathway
36
What is the commonest enzyme defect in CAH?
21 alpha hydroxylase deficiency (classical & non-classical)
37
Describe the difference between classical and non-classical 21 alpha hydroxylase deficiency
classical - salt-wasting & viriling | non-classical - hyperandrogenaemia
38
How is CAH diagnosed?
Basal/stimulated 17-OH progesterone | Genetic mutation analysis
39
Describe the pathology of CAH
Progesterone & 17-OH progesterone cannot be converted into aldosterone/cortisol intermediates and instead much be converted into androstenedione & testosterone
40
How does CAH present?
males - adrenal insufficiency, poor weight gain, excess testosterone females - genital ambiguity Late presentation - hirsute, acne, oligo/amenorrhoea, infertility, precocious puberty
41
What happens to the cortex as a result of reduced cortisol?
Stimulates ACTH release & cortical hyperplasia
42
How is CAH treated?
Paeds - glucocorticoid/mineralocorticoid replacement | Adults - control androgen excess, restore fertility & avoid steroid over-replacement
43
What is a phaemochromocytoma?
Neoplasma derived from chromaffin cells of the adrenal medulla which secretes catecholamines
44
How does the phaemochromocytoma appear brown?
Oxidation of catecholamines from adrenal remnants on the surface
45
What other rare syndromes are associated with phaemochromocytoma?
- MEN 2 - Von -hippel Lindau - Neurofibromatosis
46
What is the classic triad of symptoms for phaemochromocytoma?
- hypertension - headache - sweating
47
Name some other clinical features of phaemochromocytoma
- palpitations - SOB - anxiety - weight loss
48
Name four biochemical signs of phaemochromocytoma
Hyperglycaemia High haematocrit Lactic acidosis Low potassium
49
Why is phaemochromocytoma known as the 10% tumour?
10 % are; extra- adrenal malignant not associated with hypertension
50
What are extra adrenal phaemochromocytoma called?
Paragangliomas
51
What percentage of phaemochromocytoma are familial?
25%
52
How is phaemochromocytoma diagnosed?
- Urine/plasma metinepherine | - MRI, MIBG, PET scans
53
How are phaemochromocytomas managed?
Full alpha and beta blockade to block catecholamine receptors Fluid & Blood replacement Surgery to remove Chemotherapy if malignant
54
What type of cells are found in a neuroblastoma?
Primitive cells that show differentiation towards ganglion cells - arise in the medulla or along the sympathetic chain
55
When are the majority of neuroblastomas diagnosed?
Childhood
56
What predictors of neuroblastoma indicate a poor outcome?
Amplification of N-myc | Expression of telomerase
57
How do adrenocortical tumours present?
Incidental finding, hormonal effects, mass lesion or carcinoma with necrosis can cause a fever
58
Describe an adrenocortical adenoma
Well circumscribed, encapsulated usually small & yellow/brown due to lipids. well differentiated, can be functional
59
Describe an adrenocortical carcinoma
More likely to be a functional, virilsing tumour that is malignant. Often difficult to distinguish from adenoma.
60
What factors can help distinguish adenoma from carcinoma?
- local invasion - metastases - peritoneum/pleura spread - regional lymph nodes
61
What percentage of patients with adrenocortical adenoma will be dead in 2 years?
50%
62
What is adrenal crisis?
Life threatening medical condition due to sever adrenal insufficiency can occur due to stopping steroid therapy
63
How is an adrenal crisis managed?
Isotonic saline | Hydrocortisone

Endocrine (17 decks)

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