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Endocrine > Adrenal Clinical > Flashcards

Adrenal Clinical Flashcards

1
Q

What causes primary adrenal insufficiency (life threatening as adrenal gland damaged)

A

Addison’s = 85%
Congenital adrenal hyperplasia
Destruction of gland

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2
Q

What is most common cause of congenital

A

AR 21 hydroxylase deficinecy

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3
Q

What does it lead too

A

Low cortiosol and aldosterone
AP secretes high ACTH to try stimulate

This stimulates adrenal androgens
= Neonatal salt loss / ambitious genitalia / female civilisation / precocious puberty

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4
Q

What destroys gland

A 
Meningococcal septicaemia (Waterhouse-Fridrichsen
Infection
- TB = most common in developing
- HIV 
- Fungal
Anti-phospholipid 
Mets
Atrophy from prolonged steroid use (can also cause tertiary if suppress CRH from hypothalamus)
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5
Q

What causes secondary adrenal insuffieicny (inadequate ACTH stimulating gland)

What causes tertiary (not enough CRH from hypothalamus)

A 
Iatrogenic due to long term (apparent on withdrawal of steroid) 
Pituitary tumour
Surgery 
Pituitary infiltration / infections 
Pituitary radiation
Sheehan = post partum haemorrhage
Loss of blood

Tertiary
- Usually long term steroid

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6
Q

What causes an adrenal / Addisonian crisis

A

1st presentation of adrenal insufficiency
If stop steroids too quickly
Don’t double hydrocortisone dose in acute illness

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7
Q

What does this result in

A 
Severe hypoglycaemia
Hypotension
Hyponatraemia
Hyperkalaemia
Pyrexia
Shock
Renal failure 
Circulatory collapse
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8
Q

How of you investigate

A

ABCDE
VBG show hypoNa, hyperK, hypoBg
Cortisol / ACTH / BG
Don’t wait to do investigate need to ask fast

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9
Q

How do you treat

A

Senior and ITU help
IV hydrocortisone and saline till BP improves
- Will act on cortisol and aldosterone in acute
Correct hypo with IV dextrose10-20%
Careful monitoring of electrolyte and fluid balance
Search for cause

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10
Q

What is Addison’s

A

Autoimmune destruction of adrenal cortex leading to cortisol and aldosterone deficiency

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11
Q

What Ab

A

+ve 21-OHase autoAb

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12
Q

What is associated

A

Thyroid
Type 1 DM
Premature ovarian failure

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13
Q

What are the features

Electrolyte features

A 
Can be undetected till stress precipitates a crisis 
Muscle weakness
Fatigue
Anoreixa
Weight loss
N+V
Hypotension - particularly postural leading to syncope / dizzy 
Skin pigmentation in primary as ACTH stimulates melanocytes
Buccal mucosa hyperpigment in primary as ACTH stimulates melanocytes 
Vitiligo
Loss of pubic hair
Reduced libido 
Depression
Salt craving 
Postural drop in BP 
Hypoglycaemia
Hyponatraemia due to high levels of ADH 
Hyperkalamia
Metabolic acidosis
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14
Q

What are clues to Dx

A

Disproportion between severity of illness and circulatory collapse

Hyponatraemia - can sometimes be only presentaiton

Unexplained hypo ??

+ other endocrine - hypothyroid/ hair loss / amenorrhoea

Previous depression or weight loss

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15
Q

How do you investigate in primary care

A

Bloods - FBC, glucose, U+E, urinanalyis, BP
Can do CXR / ECG
Random cortisol / early morning will give Dx

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16
Q

Random cortisol results

A

If >700 = NOT

If <700 = perform SYnacthen (ACTH stimulation test) = 1st line test

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17
Q

What is Synthacten and what other test in secondary care

A

Give synthetic ACTH IM or IV and take blood for cortisol and ACTH level before and after
Should double
If doesn’t = Addison’s as gland can’t make
Adrenal auto Ab - anti-21 hydroxyls if autoimmune
CT or MRI for haemorrhage / tumour esp if old
MRI pituitary

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18
Q

Results of Synthacten and what do you do after

Cortisol
ACTH

A

If normal = not
If abnormal = do ACTH to differentiate between primary and secondary

If suppressed = secondary as pituitary not producing
If elevated = primary as pituitary trying to stimulate gland

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19
Q

What do you do if high suspicion

A

Treat with steroid and do synacathen later

IV steroid + IV fluid

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20
Q

How do you Rx

A 
Glucocorticoid replacement
- Hydrocortisone
- Prednisolone
- Dexamethasone
Mineralocorticoid replacement
- Fludrocortisone
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21
Q

What do you adjust dose according too

A

BP
Oedema
U+E
Plasma renin

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22
Q

How do you follow up

A

ACTH levels monitored
Steroid education
Steroid card

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23
Q

What is steroid education

A 
Never miss a dose
Double dose of hydrocortisone in illness
Maintain fludrocortisone at same dose 
Use IM hydrocortisone when vomiting
If severe D+V = get help
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24
Q

What do you need to have special care when doing

A

Withdrawing chronic glucocorticoid Rx due to -ve feedback on exogenous
Become hypoadrenal due to atrophy

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25
Q

What causes primary hyperaldosterone

What causes secondary

A

Adrenal hyperplasia = 70%
Adrenal adenoma = Conn’s

Secondary
- High renin from decreased renal perfusion e.g. renal artery stenosis / diuretics / CCF o rheumatic failure

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26
Q

What are features of primary hyperaldosterone

A 
Hypertension 
HYpernatraemia 
Hypokalaemia
Alkalosis
Increased albumin
Muscle weakness, nocturne, polyuria, tetnay due to hypokalameia
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27
Q

What is 1st line investigation

A

Aldosterone / renin ratio = 1st line

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28
Q

What will results show if primary hyperaldosterone

A

High aldosterone
Low renin as high BP
If renin is high then renin is driving force of aldosterone e.g. secondary hyperaldosterone
If both low = other causes of hypertension

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29
Q

What other test

A 
BP = hypertension
U+E = hypokalaemia
ABG = alkalosis 
Adrenal vein sampling if imaging shows adenoma - if one side revels increased ratio compared to other suspect adenoma
Urinary catecholamines 
Renal USS to look for stenosis which would be 2nd cause 
Dex suppression to rule out Cushing's 
CT to look for adenoma
30
Q

How do you treat

A

Surgery if adenoma

Aldosterone antagonist if hyperplasia

31
Q

What is Cushing’s syndrome

A

S+S of hypercortisol after prolonged abnormal elevation

32
Q

What are primary causes of hypercortisol (ACTH independent due to -ve feedback)

A

Adrenal adenoma

Adrenal hyperplasia

33
Q

What are secondary causes (ACTH dependent)

A

Pituitary adenoma - Cushing’s disease = 2nd most common to corticosteroid
Ectopic ACTH- SCLC

34
Q

What is pseudo-cushings

A

Alcohol / severe depression
All the signs of Cushing’s
Normal but can have increased dex suppression or 24 hour urinary free cortisol

35
Q

How do you differentiate

A

Insulin stress test

36
Q

What do high levels of cortisol cause

A

Round in middle with thin limbs
High levels of stress hormone
Extra

37
Q

What does round in middle with thin limbs / tissue breakdown cause

A 
Round moon face
Facial plethora 
Central obesity
Abdominal striae
Oedema 
Proximal limb muscle wasting
Proximal myopathy 
Skin atrophy 
Easily bruised
Spontaneous purpura
38
Q

What are affects of stress hormone

A 
Hypertension
Cardiomyopathy
CCF due to Na retention 
Hyperglycaemia
Depression
Insomnia
Osteoporosis
39
Q

What are other features

A 
Hirsutism 
Poor wound healing 
Headache 
Growth arrest 
Hypokalaemia metabolic alkalosis
40
Q

How do you screen

A

Overnight low dose dex suppression test (1mg)

24 hour urinary free cortisol

41
Q

What is Dex suppression

A 
1mg dexamethasone
Test cortisol and ACTH next morning
Should be low as endogenous switched off
If high = Cushing's syndrome (hypercortisol) so do high dose dex suppression
If normal = excludes Cushing's
42
Q

What are Ddx

A

Cushing’s disease
PCOS
Congenital adrenal hyperplasia

43
Q

What tests can you do

A

FBC - raised WCC
U+E - high Na as reabsorbed and low K as secreted if aldosterone involved
Glucose
Testosterone to see if sex steroids involved
17a hydroxylase enzyme for congenital
BP

44
Q

What do you do if low dose dex abnormal

A

High dose

45
Q

If due to adrenal tumour (primary cause) what is the result

A

Low ACTH (differentiates from others) as adrenal tumour making cortisol with no stimulation from ACTH so ACTH suppressed by cortisol but cortisol will still be high as independent
Others will all have high ACTH
Cortisol not suppressed

46
Q

If due to Cushing’s disease (secondary from pituitary)

A

Not suppressed by low
Cortisol suppressed by high dose as still some -ve feedback
Both low

47
Q

If ectopic

A

ACTH and cortisol NOT suppressed by his or low dose as completely independent

48
Q

If not suppressed by low or high

A

Ectopic as completely independent

49
Q

If CRH

A

Pituitary - cortisol rises

Ectopic / adrenal = no change

50
Q

How do you localise lesion

A

Plasma ACTH - if low suggest adrenal
MRI brain for pituitary adenoma
CT chest for SCLC
Abdo CT for adrenal

51
Q

How can you give steroid

A

Systemic - oral or IV

Local - cream / inhaler / eye drop / intra-articular

52
Q

What type of activity fludrocrotsione (replace aldosterone)

A

High mineral

Low glucocorticoid

53
Q

What type of activity in hydrocortisone (replace cortisol)

A

High mineral and glucocorticoid

- Used in crisis as both

54
Q

What type of activity in prednisiolone

A

High glucocorticoid
Minimal mineral
Use long term

55
Q

What type of activity in dexamethasone

A

High glucocorticoid
No mineral - used to reduce swelling in brain as mineral would cause fluid retention
Use short term

56
Q

What are SE of glucocorticoid

Endocrine
MSK
Immune
Psych
GI
Eye 
Other
A 
Cushing's 
Endocrine
- DM
- Appetite / weight
- Hirsutism
- Hyperlipid
MSK
- AVN femoral
- Osteoporosis 
Infection 
Reactivation TB
Psych
- Insomina
- Mania / depression / psychosis
GGI 
- Ulcer
- Pancreaitits
Eye
- Glaucoma
- Cataract
Suppressed growth
Benign Intracranial hypertension / papilloedema 
Neutrophilila
57
Q

What are SE mineralocortioicd

A

Fluid retention

Hypertension

58
Q

When do you need to gradually withdrawal

A

If >40mg for >1 week

59
Q

What is a pheochromocytoma

A

Rare catecholamine secreting tumour of adrenal medulla

Release adrenaline

60
Q

What is associated with

A

MEN2A+B

Neurofibromatosis

61
Q

What are features

A 
Persistent hypertension
Episodic attacks due to sudden release
Hyperglycaemia
Headache
Palpitations
Tachycardia 
AF
Sweating
Anxiety 
DM
Weight loss
62
Q

How do you Dx

A

24 hour urine metanephrine

CT / MRI

63
Q

How do you treat

A

Surgery

64
Q

What do you give before surgery

A

A blocker + BB to control HTN as catelchoamines increase
BB
A blocker 1st = phenoxybenzamine
Labetalol = Rx of choice once controlled on A blocker
Must do A blocker first as if unopposed alpha will get hypertensive crisis
IV fluid
Surgery to remove tumour once established on medical to prevent hypertension in surgery

65
Q

What are other tumours of adrenal gland

A

Adenoma cortex

Carcinoma cortex - mets from lung or breast

66
Q

If functioning or malignant what do you do

A

Surgery

67
Q

If non-functioning

A

Surveillance

68
Q

What are endocrine causes of hypertension

A

Primary hyperaldosterone - adenoma/ hyperplasia = most common
Pheochromocytoma = 24 hour urine metanephrine
Cushing’s = dex suppression
Acromegaly
Hyperparathyroid
Hypothyroid
Renal USS for stenosis

69
Q

What are DDX of hypokalaemia alkalosis

A

Primary hyperaldosteronism
Cushing
Phaeochromocytoma

70
Q

How do you Rx Cushing’s syndrome

A

Surgery to remove cause

or remove adrenal gland and give replacement steroid

71
Q

What can occur after bilateral adrenelectomy

A

Nelon syndome
-ve feedback as no cortisol causing pituitary adenoma to enlarge
Monitor ACTH and MRI 3-6 months post surgery

72
Q

What is risk of taking anabolic steroid

A

Hypogonadism and low sperm count when stop

Endocrine (17 decks)

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