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2ND YEAR SYSTEMS: Diabetes and Endocrinology > The adrenal gland clinical > Flashcards

The adrenal gland clinical Flashcards

1
Q

Hypofunction of the adrenal gland can result in which 3 things?

A

Adrenal Dysgenesis
Adrenal destruction
Impaired steroidgenesis

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2
Q

Adrenal disorders: hyposecretion

A

Primary adrenal insufficiency - Addison’s disease - autoimmune destruction

Adrenal enzyme defects - congenital adrenal hyperplasia (most commonly 21-hydroxylase deficiency)

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3
Q

What is Autoimmune Addison’s disease?

A

lymphocytic infiltrate of adrenal cortex
+ve adrenal autoantibodies (to 21-OHase) in 70% cases

Associated autoimmune diseases are common
thyroid disease (20%)
Type 1 diabetes mellitus (15%)
premature ovarian failure (15%)
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4
Q

Common symptoms of primary adrenal failure

A

Weakness, fatigue, anorexia, weight loss

Skin pigmentation or vitiligo

Hypotension

Unexplained vomiting or diarrhoea

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5
Q

Possible clues to the diagnosis of adrenal failure

A

Disproportion between severity of illness & circulatory collapse / hypotension / dehydration

Unexplained hypoglycaemia

Other endocrine features (hypothyroidism, body hair loss, amenorrhoea)

Previous depression or weight loss

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6
Q

How might you diagnose adrenal insufficiency

A

Non-specific symptoms - so must think of the diagnosis in the first place!

Routine bloods: U&E, glucose, FBC

Early morning cortisol
>450 nmol/l (not Addison’s)
<350 nmol/l (adrenal status uncertain)

Synacthen test (and basal ACTH) 
- If suspicion high &amp; patient unwell, treat with steroids and do Synacthen test later
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7
Q

What is the Synacthen test/Rapid ACTH Stimulation test?

A

Test using a chemical called tetracosactrin that tests how well your adrenals are producing cortisol

Give tetracosactrin IM or IV

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8
Q

What is ACTH?

A

Adrenocorticotropic hormone (ACTH) is a hormone produced in the pituitary gland in the brain. The function of ACTH is to regulate levels of the steroid hormone cortisol

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9
Q

Explain the results of Synacthen test/Rapid ACTH Stimulation test: abnormal and normal

A

Abnormal => Adrenocortical
insufficiency => then test Plasma ACTH

Normal - Excludes primary adrenocortical insufficiency

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10
Q

An abnormal Synacthen test leads you to testing for plasma ACTH levels. What is the diagnosis if plasma ACTH is either suppressed or elevated?

A

Suppressed - secondary adrenocortical insufficiency

Elevated - Primary adrenocortical insufficiency

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11
Q

Glucocorticoid replacement drug names

A

Hydrocortisone
Prednisolone
Dexamethasone

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12
Q

Why are glucocorticoid replacement drugs given in divided doses?

A

To mimic normal diurnal variation

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13
Q

Name a mineralocorticoid

A

Aldosterone

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14
Q

Name a Corticocoticoids

A

Cortisol

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15
Q

Mineralocorticoid replacement: what is the drug of choice, dose etc

A

Synthetic steroid - Fludrocortisone (drug of choice)

Binds to mineralocorticoid (aldosterone) receptors

50-300 micrograms daily

Adjust dose according to:
clinical status (postural BP, oedema)
U&E
plasma renin level

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16
Q

Management of stressed patients

A

Minor short-lived illness or stress - double glucocorticoid dose

Major illness or operation
(especially if nil by mouth or GI upset)
100mg hydrocortisone iv stat

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17
Q

Who needs special care when on steroids?

A

Hypoadrenal patients on replacement steroids

Patients on steroids in doses sufficient to suppress the pituitary adrenal axis (>7.5mg prednisolone daily, or equivalent)

Patients who have received such treatment during the previous 18/12 (HPA axis may still be suppressed)

18
Q

What should be done in short lived illness or stress for patients who need special care (they are on steroidal treatment)?

A

Double glucocorticoid dose

19
Q

What should be done if there is major illness or surgery for patients who are on steroids?

A

(especially if nil by mouth or GI upset)

100mg hydrocortisone iv stat

50-100mg HC iv 8-hourly

as stress abates, reduce HC by 50% per day until back on usual replacement dose

20
Q

What are the 3 important ‘self care’ rules that patients on steroids should follow

A

Never miss steroid doses/stop steroids

Double the hydrocortisone dose in the event of intercurrent illness (eg flu, UTI)

If severe vomiting or diarrhoea call for help without delay (likely to need IM hydrocortisone)

21
Q

What are some endocrine causes of hypertension?

A

Primary hyperaldosteronism - unilateral adenoma
bilateral hyperplasia

Rarer causes - cushing’s syndrome, acromegaly

22
Q

What are the hypersecretion disorders involving the cortex and the medulla?

A

Cortex - cushings (cortisol, androgens)

-Conn’s syndrome (aldosterone)

Medulla -
phaechromocytoma (catecholamines)

23
Q

Side effects of glucocorticoid therapy

A

Muscle wastage

Loss of percutaneous fat stores gives appearance of “thinning skin” making it more fragile.

Increased severity and frequency of infection

24
Q

ACTH-dependent cushing’s syndrome

A

75% cases - pituitary tumour (cushing’s disease)

5% - ectopic ACTH secretion - lung carcinoid

25
Q

ACTH-independent cushing’s syndrome

A

20% - adrenal tumour - adenoma or carcinoma

26
Q

Screening test for Cushing’s syndrome (2)

A

24 hr Urinary free cortisol:
normal 14- 135 nmol/24h

Dexamethasone suppression test taken at midnight - 1mg tablet. Then take blood at 9am next morning. Normal response would show suppression of cortisol. Suppression in patients with Cushing’s syndrome is rare with this test.

27
Q

What is Conn’s syndrome?

A

The excess production of aldosterone from the adrenal glands causes increase in blood vol, BP and [K+]urine => resulting in low renin levels.

28
Q

How does aldosterone increase your BP/ blood vol?

A

increase in salt and water reabsorption into the bloodstream

29
Q

How do you tell the difference between primary hyperaldosteronism and secondary hyperaldosteronism?

A

PA/PRA ratio is above 20 in primary

PA/PRA ratio is less than 20 in secondary although this is less reliable

(plasma aldosterone vs plasma renin activity)

30
Q

What are the confirmatory tests after establishing that there is an abnormality with the aldosterone / plasma renin ratio?

A

24 hour urine aldosterone

Urinary sodium

During 4 days of salt loading

31
Q

How do you establish the source of the aldosterone?

A

CT scan of adrenal glands

Upright posture test

Plasma 18-hydroxycorticosterone

Adrenal venous sampling if CT is inconclusive or discordant with posture test

32
Q

What are the features of phaeochromocytoma?

A

Hypertension

Paroxysmal attacks (sudden):
Headache
Sweating
Palpitations
Tremor
Pallor
Anxiety/fear
33
Q

Why is phaeochromocytoma called the 10% tumour?

A

10% extra-adrenal

10% malignant

10% multiple

10% hyperglycaemia

34
Q

What percent of phaeochromocytoma has an inherited component?

A

30%

35
Q

What are the potential investigations for phaeochromocytoma?

A

24 hour urine: total metanephrines, catecholamines, plasma metanephrines

MRI

CT

PET

Genetic testing

36
Q

What is the treatment for a clinically inapparent adrenal mass?

A

Test for hypersecretion:

  • Free metanephrine in plasma or urine (phaeochromocytoma)
  • Dexamethasone suppression test (cushings)
  • If hypertension - PA / PRA ratio (Conn’s)

If no hypersecretion - CT and surgery

37
Q

What is the most common reason for congenital adrenal hyperplasia?

A

> 90% cases due to 21-hydroxylase deficiency

38
Q

What are the severe cases of congenital adrenal hyperplasia? (2)

A

Neonatal salt-losing crisis- too much sodium is lost in urine

Ambiguous genitalia (girls)

39
Q

What are the incomplete defects associated with adrenal hyperplasia? (2)

A

pseudo-precocious puberty (boys) high sex steroid levels

hirsutism (women) - excessive body hair

40
Q

What is the precursor for all the androgens?

A

DHEA

41
Q

Why does a deficit in 21-hydroxylase cause adrenal hyperplasia?

A

Lack of 21-hydroxylase inhibits synthesis of cortisol => this removes the negative feedback on ACTH and CRH release.

Increased ACTH secretion is responsible for enlargement of adrenal glands.

Negative feedback of ACTH on CRH synthesis (in hypothalamus) remains.

42
Q

Look

A

Hypothalamus produces CRH

which stimulates the pituitary to secrete ACTH which acts on the adrenal cortex to produce cortisol

2ND YEAR SYSTEMS: Diabetes and Endocrinology (21 decks)

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