Adrenals Flashcards

(42 cards)

1
Q

What does the adrenal cortex do

A

Produced steroids -
Glucocorticoids e.g. cortisol, which affect carbohydrate, lipid, and protein metabolism
Mineralocorticoids - aldosterone, which control sodium and potassium balance
Androgens - sex hormones which have a weak effect until peripheral conversion to testosterone and dihydrotestosterone

Layers of the adrenal cortex
G - glomerulosa - mineralocorticoids
F - fasiculata - glucocorticoids
R - reticularis - androgens

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2
Q

How does the adrenal cortex become stimulated

A

Corticotropin releasing factor - from hypothalamus stimulates ACTH release from ant pit
That stimulates cortisol and androgen production

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3
Q

How is cortisol excreted

A

Urinary free cortisol various 17-oxogenic steroids

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4
Q

What is Cushing’s syndrome

A

Clinical state produced by chronic glucocorticoid excess and loss of normal feedback mechanisms of the HPA axis And loss of the circadian rhythm of cortisol release - inc release on waking

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5
Q

What are the main causes of Cushing’s syndrome

A

Exogenous steroids - iatrogenic and used by patient for other purposes
The other main type is ACTH producing pituitary adenoma -
Cushings disease
Rarer: adrenal adenoma, carcinoma producing cortisol
Cancers such as small cell lung ca and carcinoid tumours producing ACTH which acts on the adrenals inc cortisol

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6
Q

What are the symptoms of Cushing’s syndrome

A

Weight gain, mood change (depression, lethargy, irritability, psychosis), proximal weakness, gonadal dysfunction (irregular menses, hirsutism, erectile dysfunction), acne, recurrent Achilles’ tendon rupture, occasionally virilisation if female - become more masculine looking

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7
Q

Signs of cushings

A

Central obestity, plethoric, moon face, buffalo hump, supraclavicular fat distribution, skin and muscle atrophy, bruises, purple abdominal striae, osteoporosis, inc glucose, infection prone , poor healing,

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8
Q

Tests not done in cushings

A

Random cortisol as it affected by many things
Such as time of day, illness, stress
Also imaging cannot be relied upon and adrenal incidentalomas do not cause any problems in many but many have them and same with some pituitary adenomas and some ACTH producing micro adenomas are too small to be seen on scans

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9
Q

Tests done in investigating suspected Cushing’s syndrome

A

1) find a raised cortisol
Then you do tests that localise where the cortisol is coming from
1st line tests
-Overnight dexamethasone suppression test
1mg dexamethasone PO midnight do serum cortisol at 8 am
Normally cortisol would be suppressed below 50 but in Cushing’s syndrome it is not
- 24 hr urinary free cortisol alternative
2nd line tests
-48hr dexamethasone suppression test
Give measure cortisol at 0 and 48 hr- no suppression seen so still high
-48hr high dose dexamethasone suppression test
Pituitary (there would be suppression) from other ectopic (no suppression)
-midnight cortisol - blood or saliva at midnight cortisol should be lowest but in cushings the circadian rhythm is lost therefore may still be high
Localisation tests
If 1st and 2nd line +ve then do plasma ACTH- if undetectable = adrenal adenoma - CT/MRI adrenals
If ACTH detectable distinguish pituitary from ectopic - high dose suppression or CRH test - cortisol rises with pit disease not ectopic

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10
Q

What to do if cushings disease found as the pituitary is implicated

A

MRI/CT of the pituitary and consider bilateral inferior petrosal blood sampling

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11
Q

What to do if an ectopic cause is indicated as the reason for the Cushing’s syndrome

A

Hunt for the source
CT chest abdo pelvis
MRI neck thoracand abdo
Hunting small cell lung and small carcinoid tumours

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12
Q

What is Addison’s disease

A

Primary adrenocortical insufficiency
Rare can be fatal
There is destruction of the adrenal cortex leading to glucocorticoid and mineralocorticoid deficiency

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13
Q

Causes of Addison’s disease

A
In the Uk autoimmune 
Other causes TB - commonest worldwide
Adrenal mets
Lymphoma
Opportunity infections in HIV
Adrenal haemorrhage 
Anti-phospholipid syndrome
Congenital - late onset CAH
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14
Q

What is the cause of secondary adrenal insufficiency

A

Commonest cause is iatrogenic due to long term steroid use
Which suppresses the HPA
Only becomes apparent on steroid withdrawal
Rare - HP disease leading to dec ACTH

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15
Q

Symptoms of Addisons disease

A
Lean 
Tanned
Tired 
Tearful 
\+/-weakness, anorexia, dizzy, faint, flu-like, myalgia, arthralgia
Mood depressed
GI N/V abdo pain diarrhoea, constipation
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16
Q

Signs of Addison’s disease

A

Hyperpigmented palmar creases and bucks mucosa
Inc ACTH, cross reacts with melanin receptors postural hypotension
Vitilogo

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17
Q

Biochemistry of Addison’s disease

A
Low Na+
High K+ - due to low mineralocorticoid - aldosterone 
Low glucose - due to cortisol
Uraemia
Inc Ca2+
Eosinophilia
Anaemia
18
Q

What test doe you do for Addison’s disease

A

Short synacthen test
Do plasma cortisol half hour before synacthen given if 30 min cortisol over 550 Addison’s can be excluded
9am ACTH inappropriately high >300

19
Q

How to assess mineralocorticoid status

A

Plasma renin and aldosterone

20
Q

Tx Addison’s

A

Replace the steroids
15-25mg daily
Fludrocortisone to correct the mineralocorticoid
Adjust on clinical grounds

21
Q

What should steroid users wear

A

Bracelet declaring steroids use

22
Q

Advice when sick in Addison’s disease

23
Q

What is hyperaldosteronism

A

Excess production of aldosterone, independent of the renin-angiotensin system

24
Q

What does hyperaldosteronism cause

A

Inc sodium and water retention and dec renin release

25
When to consider hyperaldosteronism
High BP, hypokalaemia, or alkalosis in someone who is not on diuretics
26
Symptoms of hyperaldosteronism
Often asymptomatic o signs of hypokalaemia | Weaknesss cramps, parasthesia, polyuria, polydipsia, inc BP but not always
27
Causes of hyperaldosteronism
Solitary aldosterone producing adenoma linked to mutations in K+ channels this is conns syndrome Bilateral adrenocortical hyperplasia Rare- carcinoma, GRA hereditary where aldosterone gene becomes under the control of ACTH
28
Syndrome associated with hyperaldosteronism
Conns syndrome
29
Tests in hyperaldosteronism
``` U&E Renin aldosterone Adrenal vein sampling Genetic - GRA ```
30
Tx conn’s
Laparoscopic adrenalectomy | Spironolactone for 4 weeks pre-op controls BP and K+
31
Tx of hyperplasia
Treated medically spironolactone or amiloride
32
Tx of GRA
Dexamethasone normalises biochemistry but not alway BP if high use spironolactone as an alternative.
33
Tx adrenal carcinoma
Surgery +/- post-op adrenolytic therapy with mitotane - prognosis is poor
34
What is secondary hyperaldosteronism
Due to high renin from dec renal perfusion e.g. renal artery stenosis, accelerated hypertension, diuretics, CCF or hepatic renal failure
35
What is Bartters syndrome
This is a major cause of congenital (autosomal recessive) salt wasting - via sodium and chloride leak into the loop of henle via mutations in channels and transporters. Presents in childhood with failure to thrive, polyuria, polydipsia Sodium loss leads to volume depletion, causing inc renin and inc aldosterone production. Leading to hypokalaemia, and metabolic acidosis Tx - k+ replacement, NSAIDS (to inhibit prostaglandins) and ACEi
36
What is a phaeochromocytoma
Rare catecholamine producing tumour arise from sympathetic para ganglia cells Which are collections of chromaffin cells Usually found in the adrenal medulla
37
Are phaeochromocytoma not found in the adrenals
``` No Xtra adrenal They are rare Often found in the formation of the aorta the organs of zuckerkandl 10% extra adrenal ```
38
Can phaeochromocytoma metastasise
Yes 10% do
39
Are phaeochromocytoma familial
10% are | FHx crucial can be offered genetic testing as some gene mutations have been shown to inc risk
40
What is the classic triad iof phaeochromocytoma
Episodic headache, sweating,and tachycardia | +/- deranged up down or normal BP
41
Tests for phaeochromocytoma
24hr urine metanephrines Plasma metanephrines Inc WCC Imaging MRI/CT abdo pelvis
42
Tx of phaeochromocytoma
Surgery Remove Need to prep with an alpha blockade and then beta blockade This is to prevent crisis from unopposed alpha adrenergic stimulation