Endocrinology: Adrenal Disease Flashcards

1
Q

State the effects of cortisol on glucose metabolism [3]

A

Increases glucose levels

Increased glucose through stimulation of hepatic and renal gluconeogenesis,
and glycogenolysis
Reduces sensitivity to insulin in peripheral tissues
Increased efficacy of glucagon / adrenaline

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2
Q

Which bone disease can Cushing’s syndrome / disease lead to? [1]

A

Osteoporosis (due to excess cortisol)

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3
Q

State the effect of cortisol on protein metabolism [2]

A

 Protein breakdown and muscle wasting
 Reduces bone formation leading to bone loss

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4
Q

Name 4 causes of hypoadrenalism [4]

A
  • Addison’s–autoimmuneadrenalitis
  • Infections: TB/fungal
  • Waterhouse-Friedrichson syndrome –adrenal haemorrhage due to meningococcal infection
  • Congenital adrenal hyperplasia
  • Drugs: long term steroids suppressing adrenals. Ketoconazole
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5
Q

What are signs of Addison’s disease? [5]

A
  • anorexia & weight loss
  • fatigue, generalised weakness,
  • increased pigmentation - particularly in mouth, scars and skin creases
  • dizziness on standing
  • nausea & vomiting
    (Remember Addison’s is due to decreased cortisol and aldosterone)
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6
Q

State 5 signs of Addison’s disease [5]

A

(Addison’s disease refers specifically to when the adrenal glands have been damaged, resulting in reduced cortisol and aldosterone secretion)

Postural hypotension (>10 mmHg)
Vitiligo (came up in CBL)
Depression & pyschosis
Abodominal pain (w/ n & v)
Flu like myalgias
Pigmentation – buccal, scars, skin crease

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7
Q

Addison’s should be considered in all patients who exhibit which symptom? [1]

A

Unexplained abdominal pain or vomiting

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8
Q

How may an Addisonian crisis present? [5]

A

Acute presentation of severe adrenal insufficiency, where the absence of steroid hormones (cortisol and aldosterone) leads to a life-threatening emergency. They may present with:

  • Reduced consciousness
  • Hypotension
  • Abdominal pain
  • Nausea and vomiting
  • Hypoglycaemia
  • Hyponatraemia and hyperkalaemia
  • Pigmentation – buccal, scars, skin crease
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9
Q

What does this picture indicate? [1]

A

Pigmentation in the mouth - Addisons

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10
Q

Which skin pathology is a sign of Addisons? [1]

A

Vitilgo

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11
Q

When taking blood tests, what would hypoadrenalism have? [6]

  • Na & K levels
  • Urea levels
  • Glucose levels
  • Type of anaemia
  • Ca levels
  • Effect on leukocytes
A

Low Na; High K
High urea (increased salt and water loss / dehydration)
Low glucose
Normocytic anaemia
Eoisinophilia
Mild hypercalcemia

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12
Q

Aside from running blood tests, what would you test for with a patient you suspect of having hypoadrenalism? [4]

A
  • Short synthetic ACTH [synacthen] test
  • If synacthen test not available: Random cortisol and ACTH: 9am ATCH raised
  • 21 hydroyxlase adrenal antibodies positive in 80% patients
  • Abdomen x-ray (if TB has caused calcification of adrenal glands)
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13
Q

What is the diagnostic test of choice for hypoadrenalism? [1]

A

Short synthetic ACTH [synacthen] test

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14
Q

Describe the method of conducting a short synthetic ACTH [synacthen] test

A
  • A dose of Synacthen, (synthetic ACTH).
  • The blood cortisol is checked before and 30 and 60 minutes after the dose.
  • The synthetic ACTH will stimulate healthy adrenal glands to produce cortisol.
  • The cortisol level should at least double.
  • A failure of cortisol to double indicates either:
  1. Primary adrenal insufficiency (Addison’s disease)
  2. Very significant adrenal atrophy after a prolonged absence of ACTH in secondary adrenal insufficiency
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15
Q

Autoantibodies directed at the adrenal cortex to the autoantigens [] and [] can be seen in 70% of patients with idiopathic or primary Addison’s disease

A

Autoantibodies directed at the adrenal cortex to the autoantigens 21-hydroxylase and 17 alpha hydroxylase can be seen in 70% of patients with idiopathic or primary Addison’s disease

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16
Q

Management of Addisonian crisis;

Acute treatment? [2]
Long term treatment? [2]

A

Acute treatment:
* 0.9% saline
* IV hydrocortisone 100mg bolus stat; then IM doses until can take tablets

Long term treatment:
* Oral hydrocortisone – usually 10mg/5mg/5m
* Oral fludrocortisone (mineralocorticoid)

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17
Q

Long term management of Addisonian crisis is:
Oral hydrocortisone
Oral fludrocortisone

What are the doses and dosing regimen like? [2]

A

 Oral hydrocortisone – usually 10mg/5mg/5mg(reduce dose during the day so can sleep at night (cortisol is lowest at midnight))

 Oral fludrocortisone - once daily; first thing at morning. Dose is titrated around BP; normally 100 - 200 mg dose

18
Q

What blood results would you expect to see a ptx with Cushings syndrome? [3]

A

Hypokalaemia: due to excess cortisol having a mineralocorticoid effect (acts on aldostorone receptors)
Hyperglycaemia
High white blood cell count: Polycythaemia, Neutrophilia, Lymphopenia

19
Q

What would you expect a midnight salivary or serum cortisol levels to be like in a Cushing’s syndrome patient? [1]

A

Elevated (normally these are lowest)

20
Q

Name and explain the diagnostic test of choice for Cushing’s syndrome

A

Normal: dexamethasone suppresses cortisol release from adrenal glands
Cushings: cortisol levels are high despite dexamethasone suppressing cortisol release

21
Q

State 4 reasons that can cause increase in cortisol, which would give false positive results in a dexamethasone suppression test [4]

A

depression
alcohol excess
obesity
acute illness

22
Q

What would differing ACTH levels indicate about the whether Cushings is ACTH dependent or independent?

A

ACTH elevated: more likely to be pituitary ectopic disease causing an increase in ACTH and therefore more cortisol - ACTH dependent

ACTH suppressed: more likely to be adrenal disease causing more cortisol - ACTH independent

23
Q

How would you differ imaging to determine whether Cushings was ACTH dependent or ACTH independent? [2]

A

If ACTH-dependent: Pituitary vs ectopic
- MRI image of the pituitary

If ACTH-independent:
- imaging of adrenals/chest

24
Q

Ectopic ACTH dependent Cushings is often caused by which type of cancer? [1]

A

ectopic ACTH: small cell lung cancer

25
Q

Adrenal Cortex:
Zona [] - adreno androgens. Eg. [].
Zona [] - glucocorticoid hormones eg. []
Zona [] - minerocorticoid hormones eg. []

A

Adrenal Cortex
Zona reticulars - adreno androgens. Eg. testosterone

Zona fasciculata - glucocorticoid hormones eg. cortisol

Zona glomerulosa - minerocorticoid hormones eg. aldosterone

26
Q

What are the 3 arteries that supply the adrenal glands? [3]
Which arteries do they come from? [3]

A

Superior adrenal artery – arises from the inferior phrenic artery
Middle adrenal artery – arises from the abdominal aorta.
Inferior adrenal artery – arises from the renal arteries.

27
Q

What is release of aldosterone stimulated by? [2]

A

rising K+ [1]
fall in blood volume/BP [1]

28
Q

Explain effect of aldosterone on RAAS system

A

Renin converts angiotensin -> ANG1

ANG1 converted to ANGII by ACE (from lungs) ANG II:

Causes direct vasoconstricton + binding to ANG II receptors in ZG

ZG cells produce aldosterone: causes vasoconstriction + remodelling - (ininflammation in heart + vasculature).

Second effect of aldosterone: ‘sodium savour’: Na reabsorption + water reabsorption : Have to exchange K+ at the ENAC channels on the distal tubule.

29
Q

mineralocorticoid receptor is activated by which two substrates? [2]
Why is that important? [1]

A

mineralocorticoid receptor: activated by cortisol AND aldosterone

So in cells where aldosterone is active, cortisol is deactivated otherwise receptor would be overwhelmed

30
Q

Effect of aldosterone on Na [1] and K [1]

A

Aldosterone increases Na reabsorption; increases K excretion

31
Q

Aldosterone XS causes which 3 physiological changes? [3]

A

Hypertension, hypokalaemia and metabolic alkalosis

32
Q

Which enzyme being suppressed / mutated causes syndrome of apparent mineralocorticoid excess? [1]

Why does that create symptoms of hyperaldosternism? [1]

A

When 11BHSD-2 enzyme is supressed/mutated - cortisol is NOT deactivated and will binds to MR.
symptoms of hyperaldosteronism

33
Q

Adrenal haemorrhage due to meningococcal infection can cause hypoadrenalism.

What is the name for this syndrome? [1]

A

Waterhouse-Friedrichson syndrome

34
Q

Patients with primary adrenal insufficiency are at risk of developing which autoimmune diseases? [3]

A

R.A.
Crohn’s Disease
Coealic Disease

35
Q

Describe the three types of adrenal insufficiency

A

Primary (adrenal):
* destruction or dysfunction of the adrenal gland resulting from intrinsic diseases of the adrenal cortex and leading to impairment in steroid hormone synthesis and secretion

Central: the term central adrenal insufficiency is often used to refer to hypocortisolaemia secondary to a deficiency in adrenocorticotrophic hormone (ACTH) secretion:

Secondary (pituitary):
* inadequate pituitary ACTH release and subsequent production of cortisol and dehydroepiandrosterone (DHEA)/ Intrinsic pituitary disease includes tumours, irradiation, and inflammation (hypophysitis).

Tertiary (hypothalamus):
* inadequate hypothalamic CRH and subsequent ACTH release. Diseases include inflammatory disease (e.g., tuberculosis, sarcoidosis), or tumours such as craniopharyngiomas. Hypothalamic suppression of ACTH secretion is caused by prolonged (more than 2 weeks) treatment with exogenous glucocorticoids.

36
Q

Name three causes of adrenal insufficiency caused infections [3]

A

Pseudomonas aeruginosa
Meningococcal infection
TB

37
Q

Women of childbearing potential should always have pregnancy excluded in the evaluation of []

A

Hypercortisolism

38
Q

What is the first line test used for suspected primary hyperaldosteronism? [1]

What result would suggest primary hyperaldosteronism? [1]

A

A plasma aldosterone/renin ratio is the first-line investigation in suspected primary hyperaldosteronism

Confirmation of the diagnosis is given by an elevated ratio, suggestive of aldosterone raised inappropriately in comparison to normal/low circulating renin.

39
Q

Describe how a patient with Addison’s disease should alternate their medication during periods of illness? [2]

A

Double the hydrocortisone dose
Keep the same fludrocortisone dose

In patients with Addison’s disease, it is important to adjust their glucocorticoid replacement therapy during times of stress or illness. This is because the body requires higher levels of cortisol to cope with such situations. Doubling the hydrocortisone dose helps ensure that the patient has enough cortisol to manage her current infection. Fludrocortisone, on the other hand, is a mineralocorticoid that regulates electrolyte balance and blood pressure; it does not need to be adjusted during acute illness.

40
Q

Label A-F [6]

A

Cushing syndrome
* Cortisol: Not suppressed
* ACTH: Suppressed

Cushing Disease
* Cortisol: Suppressed
* ACTH: Suppressed

Ectopic ACTH
* Cortisol: Not suppressed
* ACTH: Not suppressed

41
Q

Label A-C

A