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Endocrine > Adrenocorticotropic hormone > Flashcards

Adrenocorticotropic hormone Flashcards

1
Q

How is ACTH hormone released? (5)

A
  1. Hypothalamus - releases Corticotropic releasing hormone
  2. Anterior pituitary gland - ACTH release into blood stream
  3. Adrenal cortex (zone fasciculata) - ACTH bind to adrencortical cells stimulates increase in cortisol level
  4. High cortisol level inhibits hypothalamic release of CRH
  5. Reduced CRH decreases ACTH
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2
Q

Which other cells have ACTH receptors?

A

Melanocytes - also have ACTH receptors and cause hyperpigmentation

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3
Q

What is cushing’s syndrome vs cushing’s disease?

A

Cushing’s syndrome : disease caused by excess secretion of glucocorticoids from the adrenal cortex

Cushing’s disease : Excess cortisol secondary to pituitary adenoma releasing ACTH which stimulates adrenal cortisol release

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4
Q

Which hormones are released by the Adrenal Cortex? (2)

A
  • Mineralcorticosteroids : Aldosterone
  • Glucocorticoids : Cortisol
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5
Q

What is the function of Aldosterone hormone? (3)

A
  • acts on kidneys to provide active reabsorption of sodium
  • active secretion of potassium
  • in the principle cell of the collecting tubules
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6
Q

What are the primary causes of Cushing’s syndrome? (2)

A
  1. Endogenous
    - Tumor/adenocarcinoma in adrenal gland secretes cortisol
  2. Exogenous -
    - Primary - Glucocorticoid steroid medication to treat inflammatory, autoimmune disorder
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7
Q

What are the secondary causes of Cushing’s syndrome? (3)

A
  1. Cushing’s disease - Pituitary adenoma - excess ACTH
  2. Ectopic ACTH - released from bronchial/lung paraneoplatic cancers
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8
Q

What are the 5 main clinical features of Cushing’s syndrome?

A
  1. Hyperglycaemia - Diabetes
    cortisol stimulate gluconeogenesis which triggers beta cells
  2. Central obesity, Buffalo hump, moon face, skin straie
    * high glucose triggers beta cells of the pancreas to release insulin which triggers increase adipose tissue to accumulate
  3. Sexual dysfunction - Amenorrhea
    high cortisol inhibits gonadotropin release hormone which
  4. Hypertension - high levels of corticosteroids reacting with mineralocorticoid receptors
  5. Immunosupression - Ulcers, infection
    cortisol dampens inflammatory and immune response by inhibits cytokine and T cell activity
  6. Osteoporosis
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9
Q

What are the common blood test results seen in Cushing’s syndrome? (3)

A
  1. Hypokalaemia
  2. Metabolic acidosis
    AKA ‘Hypokalaemic metabolic alkalosis’
  3. Raised blood glucose
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10
Q

What is the first line test to confirm the diagnosis of Cushing’s syndrome?

A

Overnight (low-dose) dexamethasone suppression test

  1. Low dose dexamethsone given before bed
  2. Cortisol levels checked in the morning
  • Low : normal
    cortisol levels should be supressed in response to Dex.
  • High : Abnormal
    Lack of Cortisol supression - Adrenal glands continue to produce cortisol
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11
Q

What is the first line localisation test for Cushing’s syndrome
- What is used for?

A
  1. 9am and midnight plasma ACTH (and cortisol) levels
    * Assess function of the hypothalamic-pituitary-adrenal (HPA) axis.
  2. 9 a.m. Plasma ACTH and Cortisol Test:
    * Cortisol levels expected to be at their highest in the morning
    * If ACTH is supressed - then non ACTH dependant cause such as adrenal adenoma
  3. Midnight Plasma ACTH and Cortisol
    * Cortisol expected to be at its lowest
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12
Q

What is the test used to localise pathology of Cushing’s syndrome?

A

high-dose dexamethasone suppression
used to identify whether excessive cortisol production is due to
* an adrenal tumor (ACTH-independent)
* overactive pituitary gland producing excess ACTH (ACTH-dependent).

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13
Q

Describe and explain the steps in the ‘High dose - dexamethasone test’

A
  1. Dexamethosone is administered to suppress ACTH production in the pituitary gland - normally this should decrease in serum cortisol levels
  2. Cortisol and ACTH levels are checked
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14
Q

Interpret results of Dexamethasone supression test;
Cortisol : not supression
ACTH : Supression

A

Adrenal adenomas producing Cortisol

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15
Q

Interpret results of Dexamethasone supression test;
Cortisol : Supression
ACTH : Supression

A

Cushing’s disease (i.e. pituitary adenoma → ACTH secretion)

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16
Q

Interpret results of Dexamethasone supression test;
Cortisol : Raised
ACTH : Raised

A

Ectopic ACTH syndrome

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17
Q

What are the different causes of ‘Cushing’s syndrome’?

A
  1. iatrogenic: corticosteroid therapy
  2. ACTH-dependent causes
    * Cushing’s disease (a pituitary adenoma → ACTH secretion)
    * ectopic ACTH secretion secondary to a malignancy
  3. ACTH-independent causes
    adrenal adenoma
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18
Q

What is the definition of ‘Adrenal insufficiency’

A
  1. Endocrine disorder characterised by primary adrenal insufficiency due to bilateral adrenal cortex destruction
  2. Reduced production of glucocorticoids, mineralcorrticoids, androgen deficiency - adrenals are the only source of androgens in female

Addision’sdisease : Autoimmune destruction of the adrenal glands is the most common cause of primary hypoadrenalism
reduced cortisol and aldosterone being produced.

Other causes of adrenal insufficiency
Primary causes
tuberculosis
metastases (e.g. bronchial carcinoma)
meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
HIV
antiphospholipid syndrome

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19
Q

Where is aldosterone produced?

A

A mineralcorticoid hormone produced in the zona glomerulosa of the adrenal cortex

20
Q

What is the function of the Adrenal cortex?

A
  1. Zona Glomerulosa:
    * Produces mineralocorticoids, primarily aldosterone,
    * MOA : regulates electrolyte balance, sodium retention, and potassium excretion in the kidneys.

2 . Zona Fasciculata:
* Produces glucocorticoids, primarily cortisol.
MOA : Cortisol is involved in the regulation of metabolism, immune response, and the body’s response to stress.

3 . Zona Reticularis:
* Produces androgens, including dehydroepiandrosterone (DHEA) and androstenedione.

Contributing to the development of secondary sexual characteristics and influencing sexual function.

21
Q

What are the causes of Adrenal Insufficiency?

A
  • Autoimmune destruction - Addison’s disease
  • Infection - tuberculosis
  • Adrenal haemorrhage - WFS
22
Q

What are the clinical features of Adrenal Insufficiency? (4)

A

Fatigue, weakness, weightloss

  1. Low cortisol levels -
    Hypotension - low vascular responsiveness to angiotensin II and norepinephrine
    Hypoglycaemia - reduced gluconeogenesis
  2. Low aldosterone levels -
    Hyponatremia and excess thirst - due to increased excretion of sodium, excess water loss
    Hyperkalaemia
  3. Low androgen levels - low libido, low pubic/axillary hair in females
  4. High ACTH levels
    Hyperpigmentation - due to ACTH stimulation of melanocyte activity
23
Q

What are the investigations of adrenal insufficiency? (2)

A
  • Short syacthen test(ACTH stimulation test) - plasma cortisol is measured before and 30 mins after giving synacthen 250ug IM

9 am serum cortisol can be useful:
> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l s

24
Q

What are the blood test results for Adrenal insufficiency? (2)

A
  1. Lab results -
    * low serum cortisol (100-500 - consider short synacthen test)
    * raised serum ACTH
    * raise plasma renin due to low aldosterone,
    * Low Na+, raised K+
25
Q

What is the management of Adrenal insufficiency?

A
  • IV hydrocortisone and IV dextrose - no fludrocortisone required because high cortisol exerts weak mineralocorticoid action, carry on with oral replacement over 3-4 days

Longterm
1. Hydrocrotisone and Fludrocortisone PO - during illness double hydrocortisone dose

26
Q

What is the definition of hyperaldosteronism?

A

Excess aldosterone - increased sodium and water retention - raised blood voume - raised BP

27
Q

What are the causes of Hyperaldosteronism? (2)

A

Primary
* Con’s syndrome - Adrenal adenoma - excess aldosterone production- unilaterally
* Bilateral idiopathic adrenal hyperplasia - most common cause - bilaterally
Secondary
* Hypotension - activates RAAS - leading to hyperaldosteronisms

28
Q

What are the clinical features of ‘Hyperaldosteronism’ (2)

A
  • Hypertension (increases water retention) often treatment resistant - headaches, facial flushing
  • Hypokalaemia - constipation, muscle weakness, arrhythmia
  • Metabolic alkalosis
29
Q

What is the first line investigation of Hyperaldosteronism?

A

First line
1. Plasma aldosterone/renin ratio - indicates primary hyperaldosteronism
* High aldosterone levels : low renin levels due to negative feedback due to sodium retention from aldosterone

30
Q

What is the second investigation of Hyperaldosteronism?

A

Second line.
High resolution CT abdomen

31
Q

What is the third line investigation of Hyperaldosteronism?

A

Adrenal venous sampling - used to distinguish between unilateral adenoma and bilateral hyperplasia.

32
Q

What is the management of hyperaldosteronism?

A

Conn’s tumor - Adrenectomy
Bilateral adrenal hyperplasia - Spirnolactone

33
Q

What is the mechanism of action of aldosterone?

A
  1. Aldosterone acts late distal tubule and collecting duct
  2. Acts on channels to favour;
    - Sodium and thus water reasborption
    - Potassium excretion
34
Q

Which channels does Aldosterone influence in the kidneys?

A

Within the late distal tubule and collecting duct, Aldosterone acts upon
- Sodium channels
- N+/K+ exchange pumps
- H+ ion atpases
- Bicarbonate-Chloride transporters

35
Q

State the ways in which Aldosterone impacts electrolyte balance in the body?

A
  1. Increases sodium reabsorption
  2. Increases water retention
  3. K+ and H+ ion excretion
  4. HCO3- excretion and Cl- reabsorption
36
Q

Describe the steps which lead to Aldosterone release?
(4)

A
  1. Low BP
  2. Renin is released from the juxtaglomerular cells of the kidneys
  3. Angiotensin cleaving enzyme
    - Converts Angiotensinogen into Angiotensin I
  4. Angiotensin converting enzyme from the lungs;
    - Converts Angiotensin 1 into Angiotensin 2

—> Triggers Aldosterone release

37
Q

What is the management of Hyperaldosteronism?

A
  • Laparoscopic adrenalectomy of adrenal ademona
  • Spirnalactone - aldosterone antagonist
38
Q

What is the steroid activity of : Fludrocortisone

A

mineralocorticoid activity

39
Q

What is the steroid activity of : Hydrocortisone

A

glucocorticoid and high mineralocorticoid activity

40
Q

What is the steroid activity of : Prednisolone

A

predominant glucocorticoid activity, low mineralocorticoid activity

41
Q

What is the steroid activity of : Dexamethasone

A

very high glucocorticoid activity

42
Q

What are the main side effects of long term steroid use? (4)

A
  • Endocrine - impaired glucose regulation, increased appetite, hypertipidaemia, hirsuitisim
  • MSK - osteoporosis, avascular necrosis of the femoral head
  • Immunosupression
  • Psychiatric - isomnia, mania, depression
    GI - peptic ulceration, acute pancreatitis
43
Q

Adrenal medulla : Function

A

Anatomy : Chromaffin Cells:
* The adrenal medulla contains chromaffin cells, which are modified sympathetic nervous system neurons.

Function
1. Release of Catecholamines:
The adrenal medulla releases catecholamines, primarily epinephrine (adrenaline) and norepinephrine (noradrenaline), into the bloodstream in response to stress or the “fight or flight” response.

44
Q

Phaeochromocytoma : Associations

A

Phaeochromocytoma is a rare catecholamine secreting tumour
develops in the adrenal glands, which are located on top of each kidney. These tumors arise from chromaffin cells and produce excess catecholamines, such as adrenaline and noradrenaline

MEN type II, neurofibromatosis and von Hippel-Lindau syndrome.

45
Q

Phaeochromocytoma : Clinical features

A

Features are typically episodic
* hypertension (around 90% of cases, may be sustained)
* headaches
* palpitations
* sweating
* anxiety

46
Q

Phaeochromocytoma : Investigations

A

24 hr urinary collection of metanephrines

47
Q

Phaeochromocytoma : Mx

A
  1. Initial medical mx
  2. alpha-blocker (e.g. phenoxybenzamine), given before a
    beta-blocker (e.g. propranolol)
  3. Surgery is definitive mx

Endocrine (11 decks)

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