Endocrinology: Adrenal Disease Flashcards

(41 cards)

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
Adrenal Cortex: Zona [] - adreno androgens. Eg. []. Zona [] - glucocorticoid hormones eg. [] Zona [] - minerocorticoid hormones eg. []
Adrenal Cortex Zona **reticulars** - adreno androgens. Eg. **testosterone** Zona **fasciculata** - glucocorticoid hormones eg. **cortisol** Zona **glomerulosa** - minerocorticoid hormones eg. **aldosterone**
26
What are the 3 arteries that supply the adrenal glands? [3] Which arteries do they come from? [3]
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
What is release of aldosterone stimulated by? [2]
rising K+ [1] fall in blood volume/BP [1]
28
Explain effect of aldosterone on RAAS system
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
mineralocorticoid receptor is activated by which two substrates? [2] Why is that important? [1]
mineralocorticoid receptor: activated by **cortisol AND aldosterone** So in cells where aldosterone is active, cortisol is deactivated otherwise receptor would be overwhelmed
30
Effect of aldosterone on Na [1] and K [1]
Aldosterone increases Na reabsorption; increases K excretion
31
Aldosterone XS causes which 3 physiological changes? [3]
**Hypertension**, **hypokalaemia** and **metabolic alkalosis**
32
Which enzyme being suppressed / mutated causes syndrome of apparent mineralocorticoid excess? [1] Why does that create symptoms of hyperaldosternism? [1]
When **11BHSD-2 enzyme is supressed/mutated** - **cortisol is NOT** **deactivated** and will binds to MR. symptoms of hyperaldosteronism
33
Adrenal haemorrhage due to meningococcal infection can cause hypoadrenalism. What is the name for this syndrome? [1]
**Waterhouse-Friedrichson syndrome**
34
Patients with primary adrenal insufficiency are at risk of developing which autoimmune diseases? [3]
R.A. Crohn's Disease Coealic Disease
35
Describe the three types of adrenal insufficiency
**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
Name three causes of adrenal insufficiency caused infections [3]
Pseudomonas aeruginosa Meningococcal infection TB
37
Women of childbearing potential should always have pregnancy excluded in the evaluation of **[]**
Hypercortisolism
38
What is the first line test used for suspected primary hyperaldosteronism? [1] What result would suggest primary hyperaldosteronism? [1]
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
Describe how a patient with Addison's disease should alternate their medication during periods of illness? [2]
**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
Label A-F [6]
**Cushing syndrome** * Cortisol: **Not suppressed** * ACTH: **Suppressed** **Cushing Disease** * Cortisol: **Suppressed** * ACTH: **Suppressed** **Ectopic ACTH** * Cortisol: **Not** **suppressed** * ACTH: **Not suppressed**
41
Label A-C