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Gastrointestinal pathophysiology > Adrenal structure and function > Flashcards

Adrenal structure and function Flashcards

1
Q

Where are the adrenal glands found?

A

Above the kidneys on the posteromedial surface

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2
Q

Mneumonic to remember the different zones of the adrenal cortex

A

GFR (outer to inner)

Salt, sweet and sex (for their functions respectively)

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3
Q

What do mineralocorticoids (aldosterone) do and what controls their release?

A

Their function is salt retention

Their release is controlled by renin

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4
Q

What do glucocorticoids (cortisol) do and what controls their release?

A

They are involved in controlling how our cells use sugar, fat and curbing inflammation

Their release is controlled by ACTH

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5
Q

What do sex steroids do and what controls their release?

A
  • They are involved in increasing bone density, decreasing body fat, improve sexual function and correct some hormonal problems
  • Their release is controlled by ACTH
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6
Q

What do adrenaline and noradrenaline do and what controls their release?

A
  • They are involved in the fight or flight response

- Their release is controlled by the sympathetic nervous system

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7
Q

What is the common structure of all steroid hormones?

A

Three cyclohexane rings and a single cyclopentane ring

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8
Q

The increased pigmentation seen in Addison’s disease is due to what?

A

Activation of the melanocortin receptor by ACTH

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9
Q

What is the main precursor for all steroid hormones?

A

CHOLESTEROL

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10
Q

The production of glucocorticoids and adrenal androgens is under the control of what?

A

The hypothalamic-pituitary axis (HPA)

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11
Q

The production of mineralocorticoids is under the control of what?

A

RAAS

- Specifically angiotensin 2

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12
Q

Explain the HPA axis

A
  1. The hypothalamus releases CRH
  2. CRH acts on the ACTH cells in the pituitary gland (anterior), causing them to release ACTH
  3. ACTH acts on the adrenal cortex, releasing cortisol into the circulation which inhibits (NEG FEEDBACK LOOP) the ACTH and CRH
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13
Q

Give an example of a factor which causes activation of the HPA axis by activating CRH in the hypothalamus?

A

Stress

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14
Q

ACTH and cortisol follow which pattern of secretion?

A

A diurnal pattern!

  • Highest in the morning, fall throughout the day but spike after your meals. Lowest levels are seen around midnight
  • A diurnal cycle is any pattern that recurs every 24 hours as a result of one full rotation of the planet Earth around its axis
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15
Q

Why is it important to recognise the circadian pattern of ACTH and cortisol secretion in practice?

A

When treating those with adrenal insufficiency:
1) replacement dose you give tries to mimic the normal circadian pattern

2) In Cushing’s syndrome (xs cortisol secretion), the diurnal pattern is disrupted (this is why we use midnight salivary cortisol reading to diagnose Cushing’s syndrome)

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16
Q

Glucocorticoids vs mineralocorticoids vs adrenal androgens, which ones are secreted in the highest amounts per day?

A
  1. Glucocorticoids = HIGH amounts
  2. Mineralocorticoids = LOW amounts
  3. Adrenal androgens = Most abundant
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17
Q

What is the consequence of the structural similarities between the glucocorticoids/corticosteroids, cortisol and cortisone, and the mineralocorticoid aldosterone?

A

The glucocorticoids can bind to the mineralocorticoid receptor and have mineralocorticoid activity which is Na & H2O retention and K+ excretion

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18
Q

Since glucocorticoids are secreted in HIGH amounts every day, what mechanism does the body put in place to stop them from activating the mineralocorticoid receptors?

A

The body deactivates the active steroids (cortisol, corticosterone, prednisolone) by the enzyme 11-betahydroxysteroid-dehydrogenase type 2 which converts them into inert steroids

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18
Q

What is adrenal insufficiency?

A

Adrenal insufficiency is a condition where there is deficiency or impairment in cortisol secretion

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19
Q

What can adrenal insufficiency be divided into?

A

Primary, secondary and tertiary adrenal insufficiency

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20
Q

What is primary adrenal insufficiency also known as?

A

Addison’s disease

21
Q

What is Addison’s disease?

A

A condition in which there is destruction of the adrenal glands
- Most commonly autoimmune but it can have other causes

22
Q

What is secondary adrenal insufficiency?

A

Adrenal glands are intact but there is a lack of cortisol secretion due to lack of ACTH (pit) or CRH (hypothalamus)

23
Q

What is the most common cause of Addison’s disease in developed countries vs worldwide?

A

Auto-immune adenalitis (80% cases)

  • Up to 75% have positive antibodies (so the remaining 25% can have the disease without the antibodies)
  • 50% or more may have other auto-immune conditions
  • WORLDWIDE = Tuberculosis-induced adrenocortical deficiency
24
Q

Clinical features of Addison’s disease

A
  • Skin hyperpigmentation
  • Low blood pressure
  • Weakness
  • Weight loss
  • Nausea
  • Diarrhoea
  • Vomiting
  • Constipation
  • Abdominal pain
  • Vitiligo
  • Buccal pigmentation
25
Q

Clinical features of Addison’s disease (adrenal) crisis

A
  1. Fever
  2. Syncope
  3. Convulsions
  4. Hypoglycaemia
  5. Hyponatraemia
  6. Severe vomiting and diarrhoea
26
Q

Causes for Addison’s disease

A
  • Auto-immune
  • Infection: TB, fungal, CMV
  • Infiltration: metastases, lymphoma, amyloidosis
  • Infarction: thrombophilia
  • Haemorrhage: meningococcal septicaemia, anticoagulants
  • Adrenoleukodystrophy: condition which is inherited and seen in younger children
27
Q

Diagnosis for Addison’s disease

A
  1. Random cortisol: check cortisol at any point of the day
  2. 9am cortisol: this is when cortisol level is supposed to be greatest (<100nmol confirms adrenal insufficiency)
  3. Short synacthen/ACTH stimulation test (definitive test)
28
Q

What is the short synacthen test?

A
  1. We take a basic cortisol sample from patient
  2. Inject synthetic ACTH (intramuscular or intravenous)
  3. Check cortisol levels 30 mins later
    - Normal response is 30 min cortisol > 540 nmol/L
29
Q

What is primary adrenal insufficiency and its effect on CRH and ACTH?

A

Addison’s disease

  • Main pathology is at the adrenal gland level, destruction of glands
  • In an effort to increase cortisol levels, there is an increase in CRH and ACTH levels
30
Q

What is secondary adrenal insufficiency and its effect on CRH and ACTH?

A
  • The defect is at the pituitary level
  • ACTH is either normal or low because the defect is at the pituitary level
  • CRH is high
31
Q

What is tertiary adrenal insufficiency and its effect on CRH and ACTH?

A
  • The defect is at the hypothalamus level

- CRH is low and ACTH is low or normal

32
Q

Causes for secondary adrenal insufficiency

A
  • Structural lesions

- Radiotherapy-related damage to the pituitary or hypothalamus

33
Q

What is the major hormonal factor precipitating adrenal crisis?

A

Mineralocorticoid

- NOT glucocorticoid deficiency

34
Q

What is the predominant manifestation of adrenal crisis?

A

Hypotensive shock

- Rarely hypoglycaemia is seen

35
Q

Total loss of adrenocortical function causes death within what time period?

A

3 days to 2 weeks

36
Q

How do you manage an Addisonian crisis?

A
  • Fluid replacement: 1-3L of saline in first 12-24hrs
  • Hypoglycaemia: IV dextrose
  • Prompt IV hydrocortisone replacement
  • Precipitating cause should be treated
37
Q

Long term treatment for Addisonian patient no longer in crisis

A
  1. Hydrocortisone
    - 10mg morning
    - 5mg lunch
    - 5mg evening
  2. Fludrocortisone (aldosterone agonist)
  3. Androgen replacement: DHEA daily
  4. HPA axis suppression: reduce dose gradually to prevent crisis
38
Q

What are the sick day rules?

A
  1. Never stop steroids
  2. Double dose during illness/infection
  3. If unable to take PO hydrocortisone, need IM/IV hydrocortisone
  4. Carry steroid card / MedicAlert bracelet
39
Q

What is the most common cause of secondary adrenal insufficiency?

A
  • HPA axis suppression due long term steroid use
  • Pituitary/hypothalamic disease
  • Structural lesions of pituitary or hypothalamus (less common)
40
Q

Clinical presentation of secondary adrenal insufficiency

A

Similar to primary insufficiency except:

  1. No hyperpigmentation: since ACTH levels are normal or low
  2. No dehydration or hyperkalaemia: because aldosterone secretion is intact, which is mediated by RAAS
  3. Hypoglycaemia more common
  4. Clinical manifestations of pituitary or hypothalamic tumour if this is the underlying cause (visual disturbances, headaches, cranial nerve palsies)
41
Q

What is Cushing’s syndrome?

A

Associated with prolonged exposure to elevated levels of glucocorticoids

42
Q

What is the most common cause of Cushing’s syndrome?

A

Exogenous corticosteroid use (IATROGENIC)

- Causes suppression of the HPA axis which can last as long as a year

43
Q

Clinical features of Cushing’s syndrome

A
  1. Thinning and bruising of the skin
  2. Skin ulcers (poor wound healing)
  3. Central obesity
  4. Buffalo hump: deposition of fat at the back of the neck
  5. Moon face
  6. Osteoporosis: due to high cortisol level
  7. Cardiac hypertrophy
  8. Hirsutism/Dark facial hair (in women)
  9. Muscle wasting in extremities
  10. Abdominal striae (purple)
  11. Amenorrhea (in women)
  12. Erectile dysfunction (men)
44
Q

Difference between Cushing’s disease and Cushing’s syndrome

A

Cushing’s disease = condition due to an ACTH-producing pituitary adenoma causing hypercortisolaemia

Cushing’s syndrome = resulting from ANY cause of hypercortisolism

45
Q

How can Cushing’s syndrome be sub-classed?

A
  1. ACTH dependent
    - This is where the Cushing’s syndrome is driven by >ACTH levels (most common cause of Cushing’s)
    - Pituitary adenoma = 60-70% of these cases
    - Ectopic ACTH production = less common cause of ACTH-dependent Cushing’s
  2. ACTH independent
    - Due to Xs cortisol secretion at the level of the adrenal glands
    - Majority caused by exogenous steroids = 80-90%. Distinguishing feature is that ACTH levels are suppressed
    - Adrenal adenomas/carcinomas = 10-20%
46
Q

Differential diagnoses for Cushing’s syndrome

A
  • Alcoholism
  • Depression
  • Obesity
  • Anorexia
  • Bulimia
47
Q

Screening tests for Cushing’s syndrome

A
  1. 24 hour urine free cortisol
  2. 1mg overnight dexamethasone suppression test
  3. Midnight serum cortisol
  4. Late night salivary cortisol
48
Q

Associated laboratory abnormalities with Cushing’s syndrome

A
  1. Raised WBC
  2. Hyperglycaemia
  3. Hypokalaemic metabolic alkalosis
49
Q

How is the overnight dexamethasone suppression test carried out?

A
  1. Take 1mg dexamethasone at 11pm
  2. Check 9am cortisol
  3. Timing is crucial
  4. In normal individuals, 9am cortisol is <50nmol/L
    - Sensitivity 98% for Cushing’s
    - False positive results, due to: decreased absorption, increased dex clearance (anti-convulsants), increase in CBG (oestrogen), pseudo-cushing’s states
50
Q

What is the treatment for ACTH-dependent Cushing’s?

A
  • The primary treatment for ACTH-dependent Cushing’s is removal of the cortisol producing adenoma
  • Other treatment includes: Adrenalectomy
51
Q

Gold standard treatment for Cushing’s

A

Transsphenoidal surgery, with either:

  1. Microadenomectomy: where an identifiable adenoma is found this can be resected leaving residual tissue of the anterior pituitary
  2. Subtotal resection of the anterior pituitary: used where no identifiable adenoma and no desire for fertility after counselling the patient. There is a risk of hypopituitarism.

Gastrointestinal pathophysiology (22 decks)

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