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Gen med ends > HPA > Flashcards

HPA Flashcards

1
Q

Hormones released by anterior pituitary

A 
Thyroid Stimulating Hormone (TSH)
Adrenocorticotropic Hormone (ACTH)
Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH)
Growth Hormone (GH)
Prolactin
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2
Q

Hormones released by posterior pituitary

A

Oxytocin

ADH

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3
Q

How does the thyroid axis function

A

Hypothalamus releases thyrotropin-releasing hormone (TRH).

This stimulates the anterior pituitary to release thyroid stimulating hormone (TSH).

This in turn stimulates the thyroid gland to release triiodothyronine (T3) and thyroxine (T4).

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4
Q

What is cortisol released by

A

Secreted by the two adrenal glands, which sit above each kidney. The release of cortisol is controlled by the hypothalamus.

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5
Q

Pattern of cortisol release

A

Released in pulses and in response to a stressful stimulus

Diurnal variation

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6
Q

How does hypothalamus control cortisol release

A

Hypothalamus –> CRH –> Anterior pituitary –> ACTH –> Cortisol

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7
Q

Actions of cortisol within the body

A 
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
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8
Q

How does the hypothalamus control release of growth hormone

A

GHRH is released from hypothalamus which stimulates growth hormone release from anterior pituitary

Growth hormone stimulates release of insulin-like growth factor 1(IGF-1) from liver

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9
Q

Effects of growth hormone

A

Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs

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10
Q

What is parathyroid hormone released in response to

A

Low serum calcium

Also released in response to low magnesium and high serum phosphate

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11
Q

Action of PTH

A

Increases the activity and number of osteoclasts in bone, causing reabsorption of calcium from the bone into the blood thereby increasing serum calcium concentration.

PTH also stimulates an increase in calcium reabsorption in the kidneys meaning that less calcium is excreted in the urine.

Also stimulates the kidneys to convert vitamin D3 into calcitriol, which is the active form of vitamin D that promotes calcium absorption from food in the small intestine.

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12
Q

Where is renin secreted

A

Renin is a hormone secreted by the juxtaglomerular cells that sit in the afferent (and some in the efferent) arterioles in the kidney.

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13
Q

What causes secretion of renin

A

JG cells sense low blood pressure and secrete more renin

Renin is an enzyme that acts to convert angiotensinogen (released by the liver) into angiotensin I. Angiotensin I converts to angiotensin II in the lungs with the help of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II acts on blood vessels to cause vasoconstriction. This results in an increase in blood pressure. Angiotensin II also stimulates the release of aldosterone from the adrenal glands.

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14
Q

What is aldosterone

A

Mineralocorticoid steroid hormone

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15
Q

actions of aldosterone

A

Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts

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16
Q

What is cushing’s syndrome

A

Used to refer to signs and symptoms that develop after prolonged abnormal elevation of cortisol

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17
Q

What is cushing’s disease

A

Refers to the specific condition where a pituitary adenoma (tumour) secretes excessive ACTH. Cushing’s Disease causes a Cushing’s syndrome, but Cushing’s Syndrome is not always caused by Cushing’s Disease.

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18
Q

Physical features of Cushing’s syndrome

A 
Round “moon” face
Central Obesity
Abdominal striae
Buffalo Hump (fat pad on upper back)
Proximal limb muscle wasting
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19
Q

Effects of cushing’s syndrome due to high levels of stress hormone

A 
Hypertension
Cardiac hypertrophy
Hyperglycaemia (Type 2 Diabetes)
Depression
Insomnia

Osteoporosis
Easy bruising and poor skin healing

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20
Q

Causes of cushing’s syndrome

A

Exogenous steroids (in patients on long term high dose steroid medications)
Cushing’s Disease (a pituitary adenoma releasing excessive ACTH)
Adrenal Adenoma (a hormone secreting adrenal tumour)
Paraneoplastic Cushing’s

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21
Q

What is paraneoplastic cushing’s

A

Is when excess ACTH is released from a cancer (not of the pituitary) and stimulates excessive cortisol release. ACTH from somewhere other than the pituitary is called “ectopic ACTH”.

Small Cell Lung Cancer is the most common cause of paraneoplastic Cushing’s.

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22
Q

IX of choice for diagnosing Cushing’s syndrome

A

Dexamethasone suppression test

Involves initially giving the patient the “low dose” test. If the low dose test is normal, Cushing’s can be excluded. If the low dose test is abnormal, then a high dose test is performed to differentiate between the underlying causes.

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23
Q

How is the dexamethasone suppression test carried out

A

To perform the test the patient takes a dose of dexamethasone (a synthetic glucocorticoid steroid) at night (i.e. 10pm) and their cortisol and ACTH is measured in the morning (i.e. 9am). The intention is to find out whether the dexamethasone suppresses their normal morning spike of cortisol.

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24
Q

Cortisol and ACTH findings after DST in pituitary adenoma

A

Cortisol not suppressed by low doses but is suppressed by high doses

ACTH normal to elevated

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25
Q

Cortisol and ACTH findings after DST in adrenal adenoma

A

Cortisol not suppressed buy low or high doses

ACTH undetectable or low

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26
Q

Cortisol and ACTH findings after DST in ectopic ACTH

A

Cortisol not suppressed by high or low doses

ACTH elevated

27
Q

Alternative to DST for diagnosis of Cushing’s syndrome

A

24 hour urinary free cortisol

28
Q

Management of Cushing’s syndrome

A

Trans-sphenoidal (through the nose) removal of pituitary adenoma
Surgical removal of adrenal tumour
Surgical removal of tumour producing ectopic ACTH

29
Q

What does Addison’s disease refer to

A

Refers to the specific condition where the adrenal glands have been damaged, resulting in a reduction in the secretion of cortisol and aldosterone. This is also called Primary Adrenal Insufficiency.

30
Q

Most common cause of primary adrenal insufficiency

A

The most common cause is autoimmune.

31
Q

What is secondary adrenal insufficiency due to

A

inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release. This is the result of loss or damage to the pituitary gland.

32
Q

What can cause secondary adrenal insufficiency

A

Can be due to surgery to remove a pituitary tumour, infection, loss of blood flow or radiotherapy. There is also a condition called Sheehan’s syndrome where massive blood loss during childbirth leads to pituitary gland necrosis.

33
Q

What is tertiary adrenal insufficiency and what is usually due to

A

result of inadequate CRH release by the hypothalamus. This is usually the result of patients being on long term oral steroids (for more than 3 weeks) causing suppression of the hypothalamus.

When the exogenous steroids are suddenly withdrawn the hypothalamus does not “wake up” fast enough and endogenous steroids are not adequately produced. Therefore long term steroids should be tapered slowly to allow time for the adrenal axis to regain normal function.

34
Q

Symptoms of adrenal insufficiency

A 
Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido
35
Q

Signs of adrenal insufficiency

A

Bronze hyper pigmentation to skin
(ACTH stimulates melanocytes to produce melanin)

Hypotension (particularly postural hypotension)

36
Q

IX for adrenal insufficiency

A 
Short synacthen test 
Hyponatraemia 
Hyperkalaemia 
Early morning cortisol 
ACTH 
Adrenal autoantibodies 
CT/MRI
37
Q

ACTH in primary adrenal failure

A

In primary adrenal failure the ACTH level is high as the pituitary is trying very hard to stimulate the adrenal glands without any negative feedback in the absence of cortisol.

38
Q

ACTH in secondary adrenal failure

A

ACTH level is low as the reason the adrenal glands are not producing cortisol is that they are not being stimulated by ACTH.

39
Q

Which antibodies may be present in autoimmune adrenal insufficiency

A

adrenal cortex antibodies and 21-hydroxylase antibodies

40
Q

Purpose of long synacthen test

A

used to distinguish between primary adrenal insufficiency and adrenal atrophy secondary to prolonged under stimulation in secondary adrenal insufficiency

In primary adrenal failure there is no cortisol response as the adrenals no longer function.
In adrenal atrophy (secondary adrenal insufficiency), the prolonged ACTH eventually gets the adrenals going again and cortisol rises.
Now we can simply measure ACTH and this indicates the underlying cause.

41
Q

Treatment of adrenal insufficiency

A

Hydrocortisone to replace cortisol as it is a glucocorticoid hormone

Fludrocortisone is a mineralocorticoid used to replace aldosterone if insufficient

Patients given steroid card and emergency ID tag

42
Q

What does addisonian crisis refer to

A

acute presentation of severe Addisons, where the absence of steroid hormones leads to a life threatening presentation.

43
Q

Features of addisonian crisis

A

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkaemia

44
Q

What can trigger addisonian crisis

A

Triggered by infection, trauma or other acute illness in someone with established Addisons.

It can present in someone on long term steroids suddenly withdrawing those steroids.

45
Q

Management of addisonian crisis

A

Intensive monitoring if unwell

Parenteral steroids (i.e. IV hydrocortisone 100mg stat then 100mg every 6 hours)

IV fluid resuscitation

Correct hypoglycaemia

Careful monitoring of electrolytes and fluid balance

46
Q

VBG abnormality seen in cushion’s

A

Hypokalaemic metabolic alkalosis - due to excess aldosterone which increases acid and potassium excretion in the kidney

Also impaired glucose tolerance

Ectopic ACTH secretion is characteristically associated with very low potassium levels

47
Q

How can pituitary and ectopic ACTH secretion be differentiated

A

Petrosal sinus sampling of ACTH

48
Q

How can true cushing’s and pseudo-cushing’s be differentiated

A

Insulin stress test

49
Q

Which cells produce adrenaline

A

Chromaffin cells in the adrenal medulla

50
Q

What is a phaechromocytoma

A

phaeochromocytoma is a tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline.

In patients with a phaeochromocytoma the adrenaline tends to be secreted in bursts giving periods of worse symptoms followed by more settled periods.

51
Q

Aetiology of phaechromocytoma

A

25% are familial and associated with multiple endocrine neoplasia type 2 (MEN 2).

There is a 10% rule to describe the patterns of tumour:

10% bilateral
10% cancerous
10% outside the adrenal gland

52
Q

Diagnosis of phaeochromocytoma

A

24 hour urine catecholamines

Plasma free metanephrines

53
Q

Presentation of pheochromocytoma

A 
Anxiety
Sweating
Headache
Hypertension
Palpitations, tachycardia and paroxysmal atrial fibrillation
54
Q

Mx of pheochromocytoma

A 
Alpha blockers (i.e. phenoxybenzamine)
Beta blockers once established on alpha blockers
Adrenalectomy to remove tumour is the definitive management

Patients should have symptoms controlled medically prior to surgery to reduce the risk of the anaesthetic and surgery.

55
Q

Classification of pituitary adenomas

A

size (a microadenoma is <1cm and a macroadenoma is >1cm)

hormonal status (a secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess)

56
Q

Most common type of pituitary adenomas

A

Prolactinomas

57
Q

Symptoms of pituitary adenomas

A

Dependent on excess/depletion of hormone
Stretching of the dura within/around pituitary fossa(causing headaches)
Compression of the optic chasm(bitemporal hemianopia)

58
Q

Mx of pituitary tumours

A

hormonal therapy (e.g. bromocriptine is the first line treatment for prolactinomas)
surgery (e.g. transsphenoidal transnasal hypophysectomy)
e.g. if progression in size
radiotherapy

59
Q

What is nelson’s syndrome

A

Nelson’s syndrome occurs due to rapid enlargement of a pituitary corticotroph adenoma (ACTH producing adenoma) that occurs after the removal of both adrenal glands (bilateral adrenalectomy) which is an operation used for Cushing’s syndrome

60
Q

What is conn’s syndrome

A

Primary hyperaldosteronism - bilateral idiopathic adrenal hyperplasia or adrenal adenoma

61
Q

Features of conn’s syndrome

A 
hypertension
hypokalaemia
e.g. muscle weakness
this is a classical feature in exams
alkalosis
62
Q

IX for conn’s syndrome

A

plasma aldosterone/renin ratio is the first-line investigation in suspected primary hyperaldosteronism

HRCT abdo and adrenal vein sampling to differentiate between unilateral and a bilateral sources

63
Q

Mx of conn’s syndrome

A

adrenal adenoma: surgery

bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

64
Q

Mx of hirsutism

A

Weight loss
Cosmetic techniques
COCP

Eflornithine for facial hirsutism

Gen med ends (9 decks)

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