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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
What is the long term treatment of an Addisons
 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
What should you tell a patient with Addisons
 What to do when ill–doubling dose, carrying steroid emergency pack  Management over surgery  Steroid card/medicalert bracelet
27
What is the definition of Cushing's syndrome
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
What are the two cases of Cushing's syndrome
- ACTH dependent causes | - ACTH independent causes
29
What are the ACTH dependent causes of Cushing's syndrome
- 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
What are the ACTH independent causes of Cushing's syndrome
- 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
What is the most common cause of Cushing's syndrome
iatrogenic - steroid therapy is the most common cause
32
What are the symptoms of Cushing disease
- 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
What are the signs of Cushing's syndrome
- 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
what are the first line tests done for Cushing's syndrome
- overnight dexamethasone suppression test | - 24 hour urinary free cortisol
35
What are the second line tests for Cushing's syndrome
Do if first line tests are abnormal - 48 hour dexamethasone suppression test - 48 high dose dexamethasone suppression test - midnight cortisol
36
How does an overnight dexamethasone suppression test work
- 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
what is the normal level of 24 hour urinary free cortisol
less than <280nmol/24hr
38
how do you do a 48h dexamethasone suppression test and a 48 hr high dose dexamethasone suppression test
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
How does midnight cortisol test work
- 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
How do you localise where the cause of Cushing's is
- 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
How does a plasma ACTH work
- 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
What is the management of iatrogenic Cushing's syndrome
- stop medications if possible
43
What is the management of Cushing's disease
- selective removal of pituitary | - bilateral adrenalectomy if source unlocatable or post-op recurrence
44
What are the complications of bilateral adernalectomy
- Nelson's syndrome | - skin pigmentations due to ACTH from enlarging pituitary tumour after adrenalectomy due to loss of negative feedback
45
What is the management of Cushing's syndrome caused by adrenal adenoma or carcinoma
- adrenalectomy and radiotherapy and adsrenolytic drugs if carcinoma
46
What is the management of Cushing's syndrome caused by ectopic ACTH
- Surgery if tumour is located and hast spread - to decrease cortisol - metyrapone, ketoconazole, fluconazole - Severe ACTH - association psychosis: intubation + mifepristone + etomidate
47
What is the prognosis of Cushing Syndrome
- Untreated - increase in vascular rmortality - Treated - good prognosis though issues may persist: myopathy, obesity, menstrual irregularity, hypertension, osteoporosis, mood changes, diabetes
48
What are the causes of Addisons disease
- 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
What is the pathology of Addisons disease
- destruction of the adrenal cortex leading to cortisol and aldosterone deficiency
50
What is secondary adrenal insufficiency
- aldosterone production remains intact and there is no hyperpigmentation - decrease ACTH
51
What are the causes of secondary adrenal insufficiency
= Iatrogenic - long-term steroid therapy leading to suppression of HPA axis - hypothalamic pituitary disease leading to a decrease in ACTH
52
what is the prognosis of Addisons disease
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
What are the precipitating factors for an Addisonian crisis
- infection - trauma - surgery - missed medication
54
What do the blood results show in Addisons disease
- 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
What is the interpretation of the following? - Cortisol following a low dose dexamethasone test = Decreased - Cortisol following a high dose dexamethasone = decreased - ACTH = same
- Normal
56
What is the interpretation of the following? - Cortisol following a low dose dexamethasone test = normal - Cortisol following a high dose dexamethasone = normal - ACTH = decreased
Cushing syndrome due to other causes such as an adrenal adenoma
57
What is the interpretation of the following? - Cortisol following a low dose dexamethasone test = normal - Cortisol following a high dose dexamethasone = decreased - ACTH = increased
Cushing's disease e.g. pituitary adenoma resulting in ACTH secretion
58
What is the interpretation of the following? - Cortisol following a low dose dexamethasone test = normal - Cortisol following a high dose dexamethasone = normal - ACTH = increased
Ectopic ACTH syndrome likely

Year 3 - Met3b (26 decks)

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