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Baz Y2 Semester 1 > Week 6 Endocrinology Adrenal Dissorders > Flashcards

Week 6 Endocrinology Adrenal Dissorders Flashcards

1
Q

What is the difference between 1st, 2nd and 3rd degree hormonal dissorders

A

1st - Problem is with the target gland
2nd - problem is with the pituitary
3rd - problem is with the hypothalamus

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2
Q

Fill in this

A
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3
Q

What are the names for 1st and 2nd degree hypercortisolism?

A

Cishing’s syndrome means high cortisol due to an HPA problem.

1st: Adrenal tumour (Adrenal Cushing’s)

2nd: Pituitary tumour (Cushing’s Disease)

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4
Q

Key prensentation of cushing’s and non cortisol biomarkers

A

Presentation:

weight gain, stretch marks, easy bruising, proximal muscle weakness
diabetes mellitus (high plasma glucose), menstrual irregularities, depression, osteoporosis

Phenotype:

hypertension, high Na+, low K+, low renin & low aldosterone

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5
Q

Why does cushing’s cause hypertension? What are the renin/aldosterone levels likely to look like?

A

Although primarily a glucocorticoid in high levels the kidneys get overun and fail to convert sortisol into inactive cortisone but the free cortisol can bind to mineralocorticoid receptors in the kidney’s causing sodium retention and high BP.

Due to hypertensive feedback this then results in low/normal renin and low/normal aldosterone.

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6
Q

How does cushing’s syndrome present differently from cushing’s disease?

A

Cushing’s disease - High ACTH & High cortisol

Cushing’s syndrome - Low ACTH & High Cortisol

Cushing’s disease with therefore also present with hyperpimentation of the skin due to high ACTH

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7
Q

If cortisol normally cause fat breakdown why does cushing’s result in weight gain?

A

It is more like weight re-distribution from the peripheries where it is broken down to the abdomen and chin.

While it get broken down you are not actually using the blood glucose because you aren’t stressed so instead it deposits again in the centre of the body

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8
Q

Draw out the RAAS

A
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9
Q

Presentation of hyperaldosteronism

A

Hypertension
Hypokalemia - Muscle weakness

Metabolic Alkalosis (due to exchange of H+ for Na+ with urine)

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9
Q

What is Cohn’s syndrome?

A

Definition: Cohn’s syndrome refers specifically to primary hyperaldosteronism caused by an aldosterone-producing adrenal adenoma. It is a subtype of primary hyperaldosteronism.

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10
Q

How does primary and secondary hyperaldosteronism present differently?

A

High aldosterone & Low Renin = Primary Hyperaldosteronism

High Aldosterone & High Renin = Secondary Hyperaldosteronism

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11
Q

Some examples of primary and secondary hyperaldosteronism?

A

Primary hyperaldosteronism

Different causes: aldosterone-producing adrenal adenoma (Conn’s syndrome), bilateral adrenal hyperplasia, Glucocorticoid-Remediable Aldosteronism (GRA)

Secondary hyperaldosteronism

Different causes: renin-secreting JG cell tumour; renal arterial stenosis

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12
Q

Most common causes of hyperaldosteronism?

A

Bilateral idiopathic adrenal hyperplasia (60-70%)
Adrenal Adenoma (20-30%)
Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal Carcinoma

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13
Q

Definition of addison’s disease?

A

Primary Adrenal Insufficiency (aquired)

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14
Q

What is the cause of addison’s disease?

A

Causes:
destruction of adrenal gland
by tuberculosis, cancer metastases, autoimmune disease

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15
Q

What is affected by addison’s disease?

A

Disease of all three adrenocortical zones
aldosterone, cortisol & adrenal androgens all affected

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16
Q

Likely blood tests from addison’s?

A

low plasma aldosterone = lack of MR activation
low Na+, high K+, reduced ECF, hypotension,
Low plasma cortisol, low glucose, high ACTH (lack of cortisol feedback)

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17
Q

Presentation of addison’s?

A

Lethargy, Weakness
Anorexia & Weight loss
Nausea & Vomiting
Salt-Craving
Hyperpigmentation due to high ACTH (especially skin creases)
Vitiligo
Loss of pubic hair in woman
Hypotension

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18
Q

What does high ACTH do to the skin?

A

Hyperpigmentation

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19
Q

How would secondary hypocortisolism present?

A

General Symptoms of Cortisol Deficiency:

Fatigue and Weakness, Hypoglycemia, Weight Loss

But with lack of Hyperpigmentation because ACTH levels are low or absent.

Lack of Hypotension and Hyperkalemia due to aldosterone being unaffected.

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20
Q

Treatment of addison’s?

A

Treatment:

Fluid & hormone replacement.

synthetic glucocorticoid (hydrocortisone, prednisone)

synthetic mineralocorticoid (fludrocortisone)

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21
Q

What is anti-21-hydroxylase?

A

The auto-immune anti-body responsible for destruction of the adrenal cortex

22
Q

If you found a low 9am cortisol what further test could you do to identify addison’s?

A

ACTH stimulation (synactin test), if cortisol doesn’t rise then addison’s.

If synactin test fails, likely to be a problem witht he adrenal gland and therefore 1st degree hypocortisolism.

However if secondary hypocortisolism it could still fail a synactin test the first time if ACTH has been chronically low for a while the adrenal gland will be small and alseep due to understimulation from lack of ACTH. But in this case it should pass a second time once the adrenal gland has woken up from the 1st test.

23
Q

Treatment for hypercortisolism

Primary,
Secondary

A

Secondary:

Transphenoidal removal of pituitary adenoma.
Surgical Removal of tumour producing Ectopic ACTH (e.g. small cell lung cancer)

Primary:

Surgical Removal of Adrenal Tumour
Surgical removal of both adrenal glands (Adrenalectomy) and give patient life-long steroid replacement therapy

24
Q

Describe what a dexamethasone suppression test does?

A

You give dexamethosone which is an exogenous glucocorticoid.

You then see how it affects cortisol and ACTH levels.

Types are:
Low-dose overnight test
High-dose

Low-dose used to diagnose cushing’s syndrome e.g. a problem with the HPA axis. If both are surpresssed this is a normal resonse (low dose won’t make much difference in cushing’s disease). If cortisol remains high this is a diagnosis of an HPA problem.

High dose used to distinguish between different causes of cushing’s.

25
Q

Fill in this table

A
26
Q

What are the medium term and then long term effects of exogenous corticosteroids

A

Medium: Presents as primary hypercortisolism

Long term: Can cause perminant pituaitary suppression resulting in secondary adrenal insufficiency when exogenous steroids removed

27
Q

What goes on in congential adrenal hyperplasia?

A

It is caused by an inherited deficiency in 21-hydroxylase which is involved in the synthesis of aldosterone and cortisol

This results in high ACTH causing growth (hyperplasia) of the adrenal cortex.

21-hydroxylase does not effect production of adrenal androgen therefore adrenal androgens are high due to high ACTH (and a build up of products) resulting in virilisation in boys and male traits in girls. At puberty LH and FSH will be low due to adrogen suppression.

28
Q

If both are hyperplasia why does Bilateral Idiopathic Adrenal Hyperplasia (BIAH) and Congenital Adrenal Hyperplasia (CAH) have such different effects?

A

Bilateral Idiopathic Adrenal Hyperplasia (BIAH) is aquired as an adult, the hyperplasia cause is unknown (idiopathic), the hyperplasia results in hyperaldosteronism.

In Congenital Adrenal Hyperplasia (CAH) the lack of aldosterone and cortisol comes first due to 21-hydroxylase deficiency. This then results in high ACTH causing hyperplasia but with low aldosterone.

29
Q

What is pheochromocytoma?

A

Catecholamine-secreting tumour of the adrenal medulla

High adrenaline and noradrenaline

30
Q

What is the tumour involved in pheochromocytoma

A

Chromaffin cell tumor

31
Q

When there is a chromaffin cell tumour what is the adrenal condition called?

A

Pheochromocytoma

32
Q

How ddoes pheochromocytoma present?

A

Palpitations
Heachache
Episodic Sweating
Anxiety
Hypertension
Diabetes Mellitus

33
Q

Pheochromocytoma investigations

A

Plasma free metanephrines
24 hour urine catecholamines
CT or MRI to look for tumour
Genetic Testing

34
Q

Pheocromocytoma treatment

A

Alpha blockers (e.g. phenoxybenzamine or doxazosin)
Beta blockers once established on alpha blocker
Surgical Removal of tumour

Must do medical treatment first to get dangerous symptoms under control before surgery

35
Q

How do the Na+ and K+ levels vary between primary and secondary adrenal insufficiency? Why?

A

Primary: Aldosterone low therefore low Na+ and high K+ (sodium potassium ying yang)

Secondary: Aldosterone normal so Na+ and K+ both balanced. However cortisol inhibits vasopressin therefore low cortisol results in high vasopressin which brings in water thus resulting in dillutional hyponatraemia (Low Na+ and low K+)

36
Q

What is the golden rule for pituitrary tumours and their functionality?

What is the exception?

A

Small microadenomas are functional

Large macroadenomas are non-functional

Exception is prolactin, where a microadenoma is functional but also a macroadenoma can be functional if it decreases dopamine which in turn surpresses vasopressin therefore more vasopressin is released

37
Q

Look at this, homemade so not perfect but I think it makes sense

A
38
Q

Where is vassopressin released?

A

From the posterior pituitary

39
Q

What is the cortisol - vassopressin relationship?

A

Vassopressin bind to V3 receptors in the anterior pituitary resulting in increased ACTH and hence cortisol.

Cortisol inhibits vassopressin therefore low cortisol can result in high vassopressin and dilutional hyponatremia (hyponatremia without hyperkalemia)

40
Q

Vassopressin main function?

A

To increase water retention

41
Q

Which protein is responsible for binding the majority of bound cortisol?

A

Transcortin - 80%
Albumin - 20%

42
Q

What is metanephrine a sign of?

A

It is a metabolite of catecholamines. High levels indicate pheochromacytoma

43
Q

Three ways that hypercortisolism can contribute to HBP?

A
  1. Innapropriate binding to the kidney mineralocorticoid receptor (MR)
  2. Inhibiting eNOS (nitric oxide synthase). Vascular nitric oxide is a vasodialator
  3. Increase the effect of catecholamines on the heart and vasculature
44
Q

What is glucocorticoid-remediable aldosteronism?

A

A form of primary aldosteronism where the ezyme normally responsible for conversion of cortisone into cortisol 11β-OHase is merged with aldo synthase making aldo synthase ACTH regulated.

This can therefore be remediated by giving a glucocorticoid to bring down ACTH thus bringing down aldosterone

45
Q

How does liqorice cause hypertension?

A

Increases the activity of glucocorticoids by inhibiting 11β-HSD2 (responsible for conversion of cortisol to cortisone) thus allowing cortisol to bind to the mineralocorticoid receptors

46
Q

What is the difference between 11β-HSD1 and 11β-HSD2

A

11β-HSD2 cortisol-cortisone (HS2 is still slow)

11β-HSD1 cortisone-cortisol

47
Q

What is Apparent mineralocorticoid excess

A

Apparent mineralocorticoid excess:
- Autosomal recessive ‘loss of
function’ mutation in 11β-HSD2
- ↓conversion of cortisol to cortisone

Therefore cortisol can bind to the mineralocorticoid receptors

48
Q

What enzmes are mutated in Congenital Adrenal Hyperplasia (rare form of addison’s). Different ones present as low cortisol and aldosterone and one is just low cortisol

A

Low aldosterone and low cortisol : 21-OHase

Just low cortisol: 11β-OHase

49
Q

How does an 11β-OHase mutation present?

A

high DOC, low RAS,

MR activation, high Na+, low K+ (activated by DOC)
ECF expansion, hypertension

High ACTH (ACTH not surpressed by DOC), adrenal androgens are increased due to build up

50
Q

If you suspected congenital adrenal hyperplasia with low aldosterone and low cortisol. However adrenal androgen was also low. What enzyme is going to be deficient?

A

3-hydroxysteroid dehydrogenase (3β-HSD)

The one at the top

51
Q

In terms of converison of cholesterol into all the adrenal hormones, what is the order from the top?

A

One that is used for all 3:
3β-HSD

One that is used for aldosterone and cortisol:
21-OHase

One that is used for aldosterone:
Aldo synthase

One that is used for cortisol:
11β-OHase

52
Q

An effect of congenital adrenal hyperplasia noticable from birth in females?

A

Ambigious genitalia due to increased androgen production

53
Q

How does cushing’s result in osteoporosis?

A

Cortisol directly reduces bone formation by interfering with osteoblast differentiation and function.

It also indirectly inhibits calcium absorption

Baz Y2 Semester 1 (17 decks)

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