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Endocrine > Adrenal Gland Pathology > Flashcards

Adrenal Gland Pathology Flashcards

1
Q

What is Addison’s disease?

A

Hyposecretion of all adrenal steroid hormones due to autoimmune destruction of the adrenal cortex

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2
Q

Name the 3 layers of the adrenal cortex and what they produce

A

Zona Glomerulosa: Aldosterone

Zona Fasciculata: Cortisol

Zona Reticulum: Androgens

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3
Q

What are the functions of aldosterone?

A

Decreased K+

Increased Na+ and H2O as water follows salt

Increased blood volume and pressure

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4
Q

What are the causes of Addisons?

A

Autoimmune adrenalitis

Metastases

Infarction

Infiltration

  • Waterhouse-Friderichsen Syndrome

Infection

  • TB
  • HIV

Iatrogenic

  • Adrenalectomy
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5
Q

How does Addisons present?

A

Depression

Weakness/Fatigue

Hypotension

Amenorrhoea

Salt craving

Weight loss

Abdominal pain

Vitiligo

Unexplained vomiting and diarrhoea: Aldosterone loss

Dizziness: Worse standing, due to aldosterone loss

Areas of darkened skin, lips and gums

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6
Q

Why is hyperpigmentation seen in Addisons?

A

Low cortisol means no negative feedback and so causes overactive pituitary

This leads to production of pro-opiomelanocortin, a precursor for ACTH

This also leads to production of melanocyte stimulating hormone, as has the same precursor

Resulting in hyperpigmentation

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7
Q

When are symptoms of Addisons seen?

A

Adrenal cortex has high functional reserve, so when symptoms are present, up to 90% of the cortex has been destroyed

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8
Q

What investigations are used in Addisons diagnosis?

A

Random Cortisol Test

Short Synacthen Test

  • Measures adrenal response to ACTH

Adrenal Autoantibodies

  • 21-OHASE

< Na

> K

< Glucose

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9
Q

Describe the Short Synacthen Test?

A

Measures adrenal response to ACTH

Give ACTH

If cortisol rises, it is an issue at the pituitary, and Addisons

If cortisol stays the same, it is an issue at the adrenal gland

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10
Q

What level of cortisol suggests Addisons?

A

>550mol/l not Addisons

<500mol/l adrenal status is uncertain

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11
Q

How is Addisons managed?

A

Glucocorticoid (cortisol)

  • Hydrocortisone

Mineralocorticoid (aldosterone)

  • Fludrocortisone
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12
Q

What is Addisonian crisis?

A

Major stressor, such as injury or infection, meaning there is an increased need for cortisol. As body is failing to deliver, symptoms increase

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13
Q

How does Addisonian crisis present?

A

Loss of consciousness

Hypotension

Severe vomiting and diarrhoea

Sudden pain in back, abdomen or legs

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14
Q

What conditions are associated with Addisons?

A

Hypothyroidism

Type 1 DM

Premature Ovarian Failure

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15
Q

What is Waterhouse-Friderichsen Syndrome?

A

Sudden increase in BP causes vessels to rupture, filling adrenal glands with blood and causing ischaemia

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16
Q

What is Phaeochromocytoma?

A

Tumour of the adrenal medulla, secreting noradrenaline and adrenalin

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17
Q

What % of phaemochromocytomas are benign and unilateral?

A

90%

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18
Q

What % of phaemochromocytomas are malignant and multiple?

A

10%

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19
Q

What causes phaemochromocytoma?

A

Associated with MEN 2A/B

20
Q

How does phaemochromocytoma present?

A

Episodic flushing

Palpitations

Sweating

Headache

HTN

Pallor

21
Q

What investigations are used in phaemochromocytoma?

A

increased 24 hour urinary collection of metanephrines

MRI adrenal nuclear medicine scan

  • Exclude MEN 2
22
Q

How is phaemochromocytoma managed?

A

Phenoxybenzamine/Alpha blocker

  • Has to be given before B blocker therapy to prevent hypertensive crisis/cardiac arrest during surgery

B Blocker

  • HTN control once alpha blocker has had time to work

Laparoscopic adrenalectomy

  • Done when patient has stabilised, around 10 days after treatment has started
23
Q

What is congenital adrenal hyperplasia?

A

Autosomal recessive condition resulting in partial to complete deficiency of an enzyme necessary for the synthesis of aldosterone or cortisol production in the adrenal gland

24
Q

What are the causes of congenital adrenal hyperplasia?

A

21-Hydroxylase Deficiency

11-B-Hydroxylase Deficiency

17a-Hydroxylase Deficiency

25
Q

What is the most common cause of congenital adrenal hyperplasia?

A

21-Hydroxylase Deficiency

26
Q

How does 21-Hydroxylase Deficiency present?

A

Can present with either salt losing crisis or female virilization

27
Q

How does 11-B-Hydroxylase Deficiency present?

A

Presents with female virilization and HTN

28
Q

How does 17a-Hydroxylase Deficiency present?

A

Presents with male undervirilization, hypokalaemia and HTN

29
Q

How is congenital adrenal hyperplasia managed?

A

Long term replacement with glucocorticoid or aldosterone or both

30
Q

What is Conn’s syndrome?

A

Hypersecretion of Aldosterone

31
Q

How does Conn’s effect K+ and Na+?

A

>Na absorption

>K excretion

32
Q

What are the causes of Conns?

A

Unilateral Adrenocortical adenoma, producing aldosterone

Bilateral adrenal hyperplasia

33
Q

How does Conn’s present?

A

Asymptomatic

>HR

  • Due to >Na as RAAS is activated

HTN

Hypokalaemia

  • Fatigue
  • Muscle weakness
  • Myalgia
  • Muscle cramps
  • Hyporeflexia
  • Paralysis rarely
34
Q

What investigations are used in Conn’s diagnosis?

A

Plasma aldosterone to plasma renin ration

  • > Aldosterone (>20)

CT

  • Identify tumour

Adrenal Venous Sampling

  • Identify which gland is secreting excess hormone

> Na+

< K+

ABG

  • Metabolic alkalosis
35
Q

What is the first line investigation in Conn’s diagnosis and why is this tested?

A

Plasma aldosterone to plasma renin ration

Shows high aldosterone alongside low renin levels, as negative feedback due to sodium retention

36
Q

How is Conn’s managed if the cause is adrenal ademona?

A

Resection

37
Q

How is Conns managed if the cause is bilateral adrenocortical hyperplasia?

A

Aldosterone antagonist

38
Q

Give an example of an aldosterone antagonist

A

Spironolactone

39
Q

What organisms cause Waterhouse-Friderichsen Syndrome?

A

Neisseria Meningitidis

Escherichia coli

Streptococcus Pneumoniae

Haemophilus Influenzae

40
Q

How does Waterhouse-Friderichsen Syndrome present?

A

Purpuric rash across body, predominantly on lower limbs and abdomen

Hypoadrenalism symptoms

41
Q

How is Addison’s management adjusted during intercurrent illness?

A

Double glucocorticoid and keep the mineralocorticoid dose the same

42
Q

How is Addisonian crisis managed?

A

IV 100mg hydrocortisone, continue 6 hourly if patient is stable

Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

1l saline over 30-60mins or with dextrose if hypoglycaemic

43
Q

Give an example of an alpha blocker

A

Phenoxybenzamine

44
Q

What blood abnormality can gluccocorticoid treatment cause?

A

Neutrophilia

45
Q

What clinical sign can distinguish between primary adrenal failure and secondary adrenal insufficiency?

A

Skin hyperpigmentation

46
Q

How is hydrocortisone dose split throughout the day?

A

Majority is given the first half of the day

47
Q

What is the most common cause of Conn syndrome?

A

Bilateral adrenal hyperplasia

Endocrine (7 decks)

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