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F1:CEP20/21 > Adrenal Gland and Adrenal Disorders > Flashcards

Adrenal Gland and Adrenal Disorders Flashcards

1
Q

What are the levels from most superficial of the adrenal gland what do they produce?

A

Outer fibrous connective tissue layer

Zona glomerulosa responsible for production of mineralocorticoids (aldosterone) SALT

Zona fasiculata responsible for the production of glucocorticoids (cortisol)
SUGAR

Zona reticularis responsible for the production of adrenal adrogens (SEX)

Gets sweeter as you go down!

And then Adrenal medulla
that contains neuroendocrine cells that produce and secrete
Adrenaline and noradrenaline

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2
Q

What is the major processor of all steroid hormone synthesis what is it converted into and how

A

Cholesterol converted to pregnenolone using CYP11A

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3
Q

What is the role of Glucocorticoids

A

Essential to life
Important in homeostasis and control the stress response

Increase glucose metabolism augmenting gluconeogenesis increase lipolysis and stimulate amino acid generation

Help to maintain vascular tone and salt water balance

Help with immunomodulation through anti-inflammatory properties and dampening immune response preventing hyperactivity

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4
Q

How do Glucocorticoids act?

A

By binding to intracellular nuclear receptors (bound to HSP)

Bind to receptor causes release of HSP

Travel to the nucleus where bind to glucocorticoid response element and along with other coactivators augments gene expression

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5
Q

How are glucocorticoids transported

A

Steroid horomones therefore need transport protein

Majority heavily bound to corticosteroid binding globulin

small amount bound to albumin

small amount free glucocorticoids that are bioavalible

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6
Q

What happens to cortisol in stress and unstressed states?

A

In unstressed state lots bound to CBG (corticosterioid binding globulin)

In stressed states CBG is cleaved leading to lots of bioavalible cortisol

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7
Q

What is the hypothamo-pituitary-adrenal axis

A

NT stimulates release of CRH from the hypothalamus

Stimulatory tropic factor (CRH)
stimulates anterior pituitary to produce ACTH

ACTH causes production of cortisol in the Zona fasiculata

Increased serum cortisol inhibits production of more CRH and ACTH via negative feedback

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8
Q

What is the circadian cycle of cortisol production

A

Pulsatile release of ACTH causes fluctuation in production of cortisol
Most ACTH produce in early morning causing peak cortisol levels at around 9am

Lowest at midnight

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9
Q

What is stress?

A 
sum of the body response to adverse stimuli including:
infection
trauma
medical illness
psychological

Regardless of source stressors all increase cortisol levels

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10
Q

What effect does surgery have on the circadian cycle of cortisol production

A

Surgery massive surge in cortisol (lots of stress)

levels remain elevated for several days post op

diurnal variation is lost

regained after a few days

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11
Q

What causes cortisol levels to remain elevated for a few days post surgery?

A

Stress cytokines destroy negative feedback cycle and repeatedly stimulate CRH release from the hypothalamus

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12
Q

Where are adrenal androgens produced? What is the main one produced and what is its function

A

Zona reticularis

Produce: Dehydroepinadrosterone (DHEA)

Major source of androgens in women produces oestrogen precursors in post-menopausal women

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13
Q

Where are mineralocorticoids

A

Aldosterone synthase present in Zona glomerulosa

Main one produced is Aldosterone

Responsible for salt regulation
critical for salt and water balance in the kidney (also the colon pancreas)

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14
Q

what is significant about aldosterone production

A

Not simulated by ACTH
produced mainly via:
Renin-angiotensin aldosterone system

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15
Q

What is the renin-angiotensin-aldosterone system?

A

Juxtaglomerular cells detect decrease in blood pressure in kidney

Kidney produces Renin that converts plasma angiotensiongen (produced in liver) to angiotensin I

Angiotensin I is converted to angiotensin II via Angiotensin converting enzyme in the lungs

Angiotensin II then binds to cells in the Zona glomerulosa stimulating aldosterone production

Causes more Na+ and CL- ions to be reabsorbed in the DCT of the kidney and more water to therefore also be reabsorbed increasing blood pressure

Increase in blood pressure negatively feedbacks on renin production

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16
Q

What are the non classical affects of mineralocorticoids?

A

Myocardial collagen production

cardiac fibrosis and remodelling

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17
Q

How do mineralocorticoids work in terms or receptors?

What is significant

A

Specific mineralocorticoid receptors

Aldosterone and cortisol can bind to mineralocorticoid receptors and both have the same affinity to it

Cortisol is present in much higher conc so would swamp receptor but cortisol at the MR is converted to cortisone (inactive) via 11B-HSD2 at the kidney

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18
Q

What results in the production of cortisone? What can stop this?

A

Cortisol converted to Cortisone via 11B-HSD2 enzyme

Inhibited by the liquorice can lead to hypertension

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19
Q

What is significant about the adrenal medulla?

A

receives direct preganglionic sympathetic innervation fibres synapse directly with neuroendocrine (chromaffin) cells that release mainly adrenaline (80%) and some noradrenaline into the blood

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20
Q

What is the action of catecholamines?

A

Not essential to life
Acts through many different adrenergic receptors:

Increase cardiac contractility
Results in vasodilation of blood vessels supplying the heart and SK muscles
Increase gluconeogenesis in liver and muscle tissues

21
Q

How are catecholamine produced? What is significant?

A

Relies on the permissive action of cortisol, SNS innervation and specific enzymes

High local cortisol levels are requires to induce :
conversion of tyrosine to DOPA (also triggered by SNS)

DOPA is then converted to dopamine (which can be released in very small quantities from medulla)

Dopamine converted to noradrenaline (requires SNS stimulation)

noradrenaline converted to adrenaline requires cortisol induction

22
Q

What are permissive action is relation to glucocorticoids?

A

Permissive actions do not directly initiate action but allow other action to occur due to there presence

23
Q

What is primary adrenal insufficiency?

A

occurs due to failure of adrenal cortex to produce sufficient amount of cortisol aldosterone and DHEA

Also known as Addisons disease

24
Q

What are the main causes of primary adrenal insufficiency/ Addisons disease?

A

Autoimmune adrenalitis most common cause –> cortex progressively destroyed by autoantibodies

Infections e.g. TB

Congenital adrenal hyperplasia

Bilateral adrenalectomy

25
Q

What are some of the symptoms and signs of Adrenal insufficiency?

A 
Symptoms:
Weakness and fatigue
Anorexia
Nausea, Vomiting Abdominal pain
Salt craving
loss of libido (women)
Signs:
Weight loss
Hypotension
hyonatraemria
Hyperkalaemia
Anemia
Hyperpigmentation (become tanned especially in areas where there is a lot of abrasion palmar crease in the roof of mouth 
Vitiligo (autoimmune conditions often occur together not rare to see diabetes I
26
Q

How do you test for primary adrenal insufficiency?

A

Total serum cortisol before and after adrenal stimulation known as the short Synacthen test

Raised ACTH levels

Screen for adrenal autoantibodies

Exclude TB

CT of adrenals gland after all testing has been done

27
Q

What is Short Synacthen test?

What are the normal and then abnormal results?

A

Stimulation of adrenal glands using ACTH1-24

In health individuals will result in raised cortisol

Primary AI there will be high ACTH but no raise in cortisol level

28
Q

What is secondary adrenal insufficiency?

A

Due to ACTH defence due to hypopituitarism

29
Q

What is significant about secondary adrenal insuffiency?

A

Not an autoimmune cause there will no no vitiligo etc

RAAS system remains intact therefore there is no mineralocorticoid deficiency

All symptoms of cortisol deficiency are the same as PAI

30
Q

What is the treatment for Primary adrenal insufficiency?

A

Hydrocortisone to replace glucocorticoids (does also have mineralocorticoid receptor activity is above 50mg fludrocortisone can be paused

Can also use Dexamethasone and Prednisolone more potent (higher affinity longer lasting) IMPORTANTLY have no mineralocorticoid receptor activity therefore fludrocortisone must not be stopped

Fludrocortisone to replace aldosterone acts on mineralocorticoid receptor
increases the amount of Na+ reabsorption in DCT

Replacement of adrenal androgens should there be symptoms

31
Q

How is secondary AI treated?

A

Hydrocortisone

No fludrocortisone is needed as there is no damage to RAAS pathway

32
Q

What is adrenal ciris?

A

Acute life threatening medical emergency causing by insufficient levels of cortisol

33
Q

What is adrenal ciris?

A

Acute life threatening medical emergency causing by insufficient levels of cortisol
Addisons crisis

34
Q

What do you do if you suspect Adrenal crisis?

A

Treat immediately with IV hydrocortisone and generous saline

DONT wait for bloods

35
Q

What are the sick-day rules

A

Aim to prevent adrenal crisis:

Sick day rule 1: moderate stress
fever infection requiring antibiotics, minor surgery under LA –> double glucocorticoid dose

Sick day rule 2: severe stress
Trauma, Major surgery, persistent vomiting, colonoscopy, labor
Give 100mg hydrocortisone bolous immediately via IV or IM followed by continuous infusion of hydrocortisone 24hrs

All of this information is found on a steroid card or indicated by a steroid bracelet to show steroid dependance

36
Q

What is glucocorticoid excess?

A

Cushing’s syndrome

a constellation of signs and symptoms that reflect high glucocorticoid levels

37
Q

What is the most common cause of Cushing’s

A

ACTH dependant cushings

Pirtuarty adenoma - ACTH secreting Cushings disease

Or Ectopic ACTH secreting tumor small cell lung carcinoma cushings syndrome

38
Q

What are the two endogenous causes of Cushing’s syndrome

A

ACTH dependant cushing’s syndrome

ACTH independent Cushing’s syndrome

39
Q

What are the endogenous causes of Cushing’s syndrome

A

ACTH dependant cushing’s syndrome

ACTH independent Cushing’s syndrome

Ectopic ACTH dependant Cushing’s syndrome due to small cell lung carcinomas

40
Q

What is ACTH dependant Cushing’s syndrome caused by ?

A

Most common

CUSHING’S DISEASE
Due to a pituitary adenoma causing excess ACTH secretion

41
Q

What is ACTH independat Cushing’s syndrome caused by

A

Due to adrenocortical adenomas or carcinomas

42
Q

What are the signs symptoms of Cushing’s syndrome?

A 
Thin skin
Easy bruising
Purple striae
Proxmial myopathy
decreased linerar growth in children
Central obestoy
Buffalo hump
Facial fullness (moon face)
osteoporosis
43
Q

How can Cushing’s syndrome be diagnosed?

A

Dexamethasone suppression test

24 hour urinary free cortisol test (below 130ug/24hr)

Late night salivary cortisol test (less than 5nmol/L)

44
Q

What is the dexamethasone suppression test?

A

Plasma cortisol measured before test

Then given 1mg Dexamethasone (huge amount)

Should result in ACTH and CRH inhibition in healthy individuals resulting in a massive reduction in cortisol levels

Take blood in morning 8-9am when cortisol should be highest

In a Cushing’s disease there will be no reduction in ACTH therefore cortisol remains high (above 50nmol/L)

If the levels are suppressed then the patient may well still have ACTH independent Cushings

45
Q

How can you find the cause of Cushing’s syndrome from the Dexamethasone suppression test?

A

ACTH dependant Cushing’s (Cushing’s Disease) there will be no reduction in ACTH even in presence of Dexamethasone therefore cortisol reading in morning remains high (above 50nmol/L)

ACTH Independent Cushing’s there will be suppression of cortisol levels

46
Q

When do you do scanning of adrenals or pituitary and why?

A

Following biochemical testing as many people have nodules in the adrenal gland and even in the pituitary that are not causing any harm

47
Q

What is the treatment for cushings syndrome?

A

Surgery:
trasspehnoidal surgery for ACTH dependant (Cushing’s disease)
Bilateral adrenalectomy
Laprascopic adrenalectomy for adrenal adenomas

Drugs:
block cortisol production
block glucocorticoid receptor
or destroy adrenal tissue
only used short term to prepare for surgery
48
Q

A patient with Cushing’s syndrome has another dexamethasone suppression test with high/normal cortisol and low ACTH. He takes no regular medications. What does this suggest about the cause of his Cushing’s syndrome?

What would it be if his ACTH was high?

A

Caused by an Adrenal tumour

If ACTH was high would be suggestive of a ectopic hypothalamic releasing or pituitary releasing hormone tumour

F1:CEP20/21 (12 decks)

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