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Year 3 - Met3b > Adrenal Disease > Flashcards

Adrenal Disease Flashcards

1
Q

Where are the adrenals

A

Triangular structures on top of the kidneys

- 3-4g of weight

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2
Q

What are the two parts that make up the adrenals

A
  • cortex and medulla
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3
Q

What are the three zones of the adrenals

A
  • Glomerulosa
  • Fasciculata
  • Reticularis
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4
Q

What do the three zones of the adrenals secrete and control

A

▪ Glomerulosa – mineralocorticoids e.g. aldosterone - controls sodium and potassium balance
▪ Fasciculata – glucocorticoids e.g. cortisol - affects carbohydrate, lipid and protein metabolism
▪ Reticularis – precursor androgens (DHEAS, androstenedione) - sex steroids

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5
Q

What does the medulla of the adrenals make

A

catecholamines

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6
Q

describe the release of cortisol in the hypothalamo-pituitary adrenal axis

A

Hypothalamaus

  • releases CRH
  • also responds to stress and releases other factors

Pituitary

  • ACTH
  • stimulates cortisol release from the adrenal gland (Z.fasciculata)
  • cortisol is then excreted as urinary free cortisol and various 17-oxogenic steroids
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7
Q

What cycle is cortisol released in

A

Dirunal cycle

  • lowest at night
  • highest in the morning
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8
Q

What is the function of cortisol

A

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

 Protein metabolism

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

 Modulation of inflammation
- Inhibits production of IL-2, TNF-a, IFN-a

 Salt and water balance
- Modest effect on salt and water retention - outweighed by mineralocorticoids

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9
Q

What factors can also cause cortisol release

A

Stress

Hypoglycaemia

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10
Q

What is the main releasing factor for aldosterone

A
  • angiotensin II
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11
Q

Where is angiotensinogen produced

A

liver

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12
Q

describe the RAAS

A
  • Angiotensinogen is produced in the liver
  • rennin produced by the kidneys causes it to be converted in to angiotensin I
  • Angiotensin I is converted by ACE in the lungs to angiotensin II
  • Angiotensin II produces aldosterone
  • adlsoterone increases reabsorption of sodium, and chloride - causes water to be retained
  • increases blood pressure
  • can lead to potassium loss
  • in someone who has excess aldosterone - leads to hypokalemia
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13
Q

What are the causes of hypoadrenalism

A

▪ Addison’s–autoimmuneadrenalitis
▪ Infections-TB/fungal
▪ Waterhouse-Friedrichson syndrome–adrenal haemorrhage due to meningococcal infection
▪ Congenital adrenal hyperplasia
▪ Drugs–long term
steroids suppressing adrenal, ketoconazole

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14
Q

What is Waterhouse-Friedrichson syndrome

A

adrenal haemorrhage due to meningococcal infection

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15
Q

What is hypopituitarism due to

A

due to lack of ACTH

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16
Q

What are the chronic symptoms of Addison

A

▪ anorexia & weight loss,
▪ fatigue, generalised weakness, dizzy
▪ increased pigmentation,
▪ postural hypotension
- depression, psychosis, low self-esteem
- nausea/vomiting, abdominal pain, diarrhoea and constipation

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17
Q

What are the chronic signs of Addisons

A

▪ Postural hypotension (>10 mmHg)
▪ Vitiligo
▪ Pigmentation – buccal, scars, skin crease

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18
Q

Name the symptoms of an addisonian criss

A
  • postural hypotension
  • tachycardia
  • nausea & vomiting
  • abdo pain
  • collapse due to postural hypotension
  • hypoglycaemic symptoms
  • weak
  • confused
  • comatose
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19
Q

Name the signs of an addisonian crisis

A

▪ Severe hypotension, often fluid resistant
▪ Hypoglycaemia
▪ Pigmentation – buccal, scars, skin crease

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20
Q

How do you investigate hypoadrenalism

A

Bloods:
 Low Na, High K - aldosterone deficiency
 Elevated urea/creat – salt and water loss
 Low glucose – due to low cortisol levels
 Normochromic/cytic anaemia
 Eosinophilia
 Mild hypercalcaemia

 Random cortisol and ACTH

 Consider abdo x-ray (TB calcification)

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21
Q

What is the diagnsotic test of hypoadrenalism

A

Short synthetic ACTH [synacthen] test
 Cortisol at 9.00am
 Administer synacthen injection
 Cortisol at 30 and 60 mins
Result
 Suboptimal response (cortisol not rising above lab reference range (usually ~ 480 nmol/l) = this suggests hypoadrenalism
- What you want to see is the cortsiol rise above 480nmol/L

 Adrenal antibodies +ve in most Addisons patients

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22
Q

How does a short synthetic ACTH (synacthen test) work

A

 Cortisol at 9.00am
 Administer synacthen injection
 Cortisol at 30 and 60 mins
Result
 Suboptimal response (cortisol not rising above lab reference range (usually ~ 480 nmol/l) suggests hypoadrenalism
- What you want to see is the cortsiol rise above 480nmol/L

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23
Q

what antibodies do patients have in Addisions

A

Adrenal antibodies +ve

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24
Q

How do you manage an addisonian crisis

A

Treat before biochemical results if suspected

  • IV fluid bolus 500ml 0.9% saline – often large volumes. 5-10%
  • monitor blood glucose for hypoglycaemia
  • IV hydrocortisone 100mg bolus stat
  • Then IM doses until patient able to take tablets (longer half life as IM dose)

Continuing Treatment

  • if hypoglycaemia IV glucose
  • IV fluids to correct U%E imbalance
  • continue hydrocortisone e.g. 100mg/8hr IV or IM
  • change to oral steroids after 72 hours if the patients condition is good
  • fludrocortisone may be needed if cause is adrenal disease
25
Q

What is the long term treatment of an Addisons

A

 Oral hydrocortisone – usually 10mg/5mg/5mg (morning, lunch, evening)
 Oral fludrocortisone (mineralocorticoid) 50-200ug- give that once a day in the morning, titre according to blood pressure

26
Q

What should you tell a patient with Addisons

A

 What to do when ill–doubling dose, carrying
steroid emergency pack
 Management over surgery
 Steroid card/medicalert bracelet

27
Q

What is the definition of Cushing’s syndrome

A

The clinical state produced by chronic cortisol excess + loss of the normal feedback mechanisms of the HPA axis and loss of circadian rhythm of cortisol secretion

28
Q

What are the two cases of Cushing’s syndrome

A
  • ACTH dependent causes

- ACTH independent causes

29
Q

What are the ACTH dependent causes of Cushing’s syndrome

A
  • pituitary tumour secreting ACTH producing bilateral adrenal hyperplasia
  • Peak age is 30-50
  • low does dexamethasone test doesn’t change plasma cortisol but 8mg may be enough to halve morning cortisol
30
Q

What are the ACTH independent causes of Cushing’s syndrome

A
  • Iatrogenic - steroid therapy ( most common)

Adrenal adenoma/cancer

  • may cause abdominal pain and virlisation in women
  • because the tumour is autonomous the dexamethasone will not suppress cortisol production

Adrenal nodular hyperplasia
- no dexamethasone suppression

Carney complex

McCune-Albright Syndrome

31
Q

What is the most common cause of Cushing’s syndrome

A

iatrogenic - steroid therapy is the most common cause

32
Q

What are the symptoms of Cushing disease

A
  • weight gain
  • mood change - depression, lethargy and irritability, psychosis
  • proximal weakness
  • gonadal dysfunction - irregular meses, hirsutism
  • acne
  • recurrent achilles tendon rupture
  • virilisation if female
33
Q

What are the signs of Cushing’s syndrome

A
  • central obesity
  • plethoric
  • moon face
  • buffalo hump
  • supraclavicular fat distribution
  • skin and muscle atrophy
  • bruises
  • purple abdominal striae
  • osteoporosis
  • hypertension
  • hyperglycaemia
  • infection prone
  • poor healing
34
Q

what are the first line tests done for Cushing’s syndrome

A
  • overnight dexamethasone suppression test

- 24 hour urinary free cortisol

35
Q

What are the second line tests for Cushing’s syndrome

A

Do if first line tests are abnormal

  • 48 hour dexamethasone suppression test
  • 48 high dose dexamethasone suppression test
  • midnight cortisol
36
Q

How does an overnight dexamethasone suppression test work

A
  • outpatient test
  • 1mg dexamethasone PO at midnight and measure serum cortisol at 8am
  • normal: cortisol suppresses to <50nmol/L
  • in Cushing’s syndrome there is no suppression
37
Q

what is the normal level of 24 hour urinary free cortisol

A

less than <280nmol/24hr

38
Q

how do you do a 48h dexamethasone suppression test and a 48 hr high dose dexamethasone suppression test

A

48h dexamethasone suppression test

  • 0.5mg/6h dexamethasone PO for 2 days and measure cortisol at 0 and 48 hr
  • there would be no suppression in Cushing’s syndrome

48 hr high dose dexamethasone suppression test

  • 2mg/6h dexamethasone PO for 2d + measure cortisol at 0 and 48 hr
  • may distinguish pituitary (suppression) from other causes (no/part suppression)
39
Q

How does midnight cortisol test work

A
  • Admit to hospital
  • Normal circadian rhythm (lowest at night highest in morning) lost in Cushing’s disease
  • Midnight blood via a cannula during sleep shows ↑cortisol in Cushing’s
  • Often inaccurate due to measurement issues
40
Q

How do you localise where the cause of Cushing’s is

A
  • Plasma ACTH
  • Adrenal tumour likely - CT/MRI adrenals or adrenal vein sampling if no mass is seen on CT/MRI adrenals
  • Pituitary tumour likely - MRI pituitary, bilateral inferior petrosal sinus blood sampling
  • Ectopic ACTH production - contrast CT chest, abdomen, and pelvis or MRI of neck, thorax and abdomen
41
Q

How does a plasma ACTH work

A
  • if ACTH is undetectable, adrenal tumour is likely
  • if ACTH detectable, distinguish pituitary cause from ectopic ACTH production: High-dose suppression test or CRH test
  • if cortisol is suppressed pituitary tumour likely
  • if no cortisol suppression ectopic ACTH production more likely
42
Q

What is the management of iatrogenic Cushing’s syndrome

A
  • stop medications if possible
43
Q

What is the management of Cushing’s disease

A
  • selective removal of pituitary

- bilateral adrenalectomy if source unlocatable or post-op recurrence

44
Q

What are the complications of bilateral adernalectomy

A
  • Nelson’s syndrome

- skin pigmentations due to ACTH from enlarging pituitary tumour after adrenalectomy due to loss of negative feedback

45
Q

What is the management of Cushing’s syndrome caused by adrenal adenoma or carcinoma

A
  • adrenalectomy and radiotherapy and adsrenolytic drugs if carcinoma
46
Q

What is the management of Cushing’s syndrome caused by ectopic ACTH

A
  • Surgery if tumour is located and hast spread
  • to decrease cortisol - metyrapone, ketoconazole, fluconazole
  • Severe ACTH - association psychosis: intubation + mifepristone + etomidate
47
Q

What is the prognosis of Cushing Syndrome

A
  • Untreated - increase in vascular rmortality
  • Treated - good prognosis though issues may persist: myopathy, obesity, menstrual irregularity, hypertension, osteoporosis, mood changes, diabetes
48
Q

What are the causes of Addisons disease

A
  • autoimmune (80% in UK)
  • TB - most common worldwide
  • adrenal metastases - from lung, breast and renal cancer
  • lymphoma
  • opportunistic infection in HIV, CMV
  • Adrenal haemorrhage - waterhouse-friederichsen syndrome, SLE
  • congenital
49
Q

What is the pathology of Addisons disease

A
  • destruction of the adrenal cortex leading to cortisol and aldosterone deficiency
50
Q

What is secondary adrenal insufficiency

A
  • aldosterone production remains intact and there is no hyperpigmentation
  • decrease ACTH
51
Q

What are the causes of secondary adrenal insufficiency

A

= Iatrogenic - long-term steroid therapy leading to suppression of HPA axis
- hypothalamic pituitary disease leading to a decrease in ACTH

52
Q

what is the prognosis of Addisons disease

A

Adrenal crises and infections cause excess deaths

  • Men - mean age at death - 65 years (decrease 11 year In LE)
  • Women - a decrease in 3 years of LE
53
Q

What are the precipitating factors for an Addisonian crisis

A
  • infection
  • trauma
  • surgery
  • missed medication
54
Q

What do the blood results show in Addisons disease

A
  • cortisol, ACTH U&Es should be done
  • if rise in potassium - check ECG and give calcium gluconate if needed
  • If decrease in sodium - resolve with rehydration and steroids
55
Q

What is the interpretation of the following?

  • Cortisol following a low dose dexamethasone test = Decreased
  • Cortisol following a high dose dexamethasone = decreased
  • ACTH = same
A
  • Normal
56
Q

What is the interpretation of the following?

  • Cortisol following a low dose dexamethasone test = normal
  • Cortisol following a high dose dexamethasone = normal
  • ACTH = decreased
A

Cushing syndrome due to other causes such as an adrenal adenoma

57
Q

What is the interpretation of the following?
- Cortisol following a low dose dexamethasone test = normal

  • Cortisol following a high dose dexamethasone = decreased
  • ACTH = increased
A

Cushing’s disease e.g. pituitary adenoma resulting in ACTH secretion

58
Q

What is the interpretation of the following?
- Cortisol following a low dose dexamethasone test = normal

  • Cortisol following a high dose dexamethasone = normal
  • ACTH = increased
A

Ectopic ACTH syndrome likely

Year 3 - Met3b (26 decks)

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