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Week 128 - Gen Endocrine Flashcards

1
Q

Which two hormones are secreted by the hypothalamus to stimulate the release of ACTH from the anterior pituitary gland?

A

CRH and ADH

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2
Q

Hypothalamic-pituitary-adrenal axis: What is CRH?

A
  • Corticotropin-releasing hormone.

* It is secreted by the hypothalamus and causes stimulation to release ACTH from the anterior pituitary gland.

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3
Q

Hypothalamic-pituitary-adrenal axis: What is ADH?

A
  • Anti-diuretic hormone.

* It is secreted by the hypothalamus and causes stimulation of the anterior pituitary gland to release ACTH.

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4
Q

Hypothalamic-pituitary-adrenal axis: What is ACTH?

A
  • Adrenocorticotropic hormone.

* Secreted by the anterior pituitary gland in response to CRH and ADH.

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5
Q

What occurs when Adrenocorticotropic hormone binds to a adrenocortical cell? (Briefly).

A
  • It causes adenylate cyclase to convert ATP into cAMP, which in turn starts a protein cascade that results in the production of pregnenolone from cholesterol.
  • Pregnenolone is a prehormone for mineralcorticoids, glucocorticoids, androgens, estrogens and neuroactive steroids.
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6
Q

What is Cushing’s Syndrome?

A

A clinical state of increased free circulating cortisol.

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7
Q

Cushing’s syndrome is normally classified into two groups, what are they?

A

1) ACTH-dependant Cushing’s.

2) ACTH-independant Cushing’s.

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8
Q

What is the most common cause of Cushing’s syndrome?

A

Iatrogenic causes, injections of synthetic ACTH.

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9
Q

Give some examples of ACTH-dependant Cushing’s.

A

1) Cushing’s Disease (The most common cause of spontaneous Cushing’s disease) increased ACTH from the pituitary.
2) Ectopic ACTH-producing tumour.

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10
Q

Give some examples of ACTH-independant Cushing’s.

A

1) Adrenal tumour.

2) Nodular hyperplasia.

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11
Q

What are the major clinical features of Cushing’s Syndrome?

A
  • Plethora, Proximal neuropathy, Purple Striae, Skin thinning, bruising.
  • Central weight gain, moon face, backache, malaise, hirsutism, nocturia/polyuria, oligomenorrhoea/amenorrhoea, hypertension, glycosuria.
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12
Q

What are the three main investigations to confirm the diagnosis of Cushing’s syndrome?

A

1) 48hr low-dose dexamethasone test.
2) 24hr urinary free cortisol measurements.
3) Circadian rhythm.

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13
Q

Cushing’s Syndrome: What is the 48hr low-dose dexamethasone test?

A

• In normal individuals administration of dexamethasone would result in suppression of cortisol levels to s will show a decrease in cortisol levels after a period and a higher dose.

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14
Q

Cushing’s Syndrome: What is the circadian rhythm test?

A
  • After 48 hours in hospital, cortisol samples are taken at 9am and midnight.
  • Normal patients show a pronounced variation whilst those with Cushing’s Syndrome may have a normal 9am value but a high midnight value.
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15
Q

Once diagnosis of Cushing’s Syndrome has been confirmed what investigations can be undertaken to determine the cause?

A
  • Plasma ACTH - Low levels are a strong indicator of non-ACTH-dependant disease.
  • CT,MRI, X-ray - In order to find a tumour.
  • Plasma potassium levels - Hypokalaemia is common with ectopic ACTH secretions.
  • High-dose dexamethasone test - Failure to suppress cortisol levels suggests ectopic sources of ACTH or adrenal tumour.
  • CRH test - Exogenous CRH is given, an exaggerated ACTH and cortisol response suggests pituitary-dependant Cushing’s Disease.
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16
Q

What is the drug of choice for treating Cushing’s Disease and what is its mode of action?

A

Metyrapone, blocks the conversion of 11-deoxycortisol into cortisol thus reducing circulating levels of cortisol.

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17
Q

What is Congenital adrenal hyperplasia?

A
  • This is an autosomal recessive disorder where there is a deficiency of one of the enzymes in the cortisol synthetic pathways.
  • This results in reduced cortisol secretion, feedback causes increased ACTH secretion which leads to adrenal hyperplasia.
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18
Q

What is the most common type of congenital adrenal hyperplasia? What is the incidence?

A

21-hydroxylase deficiency, 1 in 15000 births.

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19
Q

21-hydroxylase deficiency is the leading cause of congenital adrenal hyperplasia, it causes disruption of the cortisol synthesis pathway. Down which pathway do the precursors get diverted?

A
  • The androgenic steroid pathway.

* Resulting in increased levels of 17-hydroxyprogesterone, androstenedione and testosterone which leads to virilization.

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20
Q

What is salt-wasting and how is it caused in congenital adrenal hyperplasia?

A
  • Loss of excessive amounts of sodium in urine, which can lead to potentially fatal electrolyte and water imbalance.
  • This is due to a deficiency in aldosterone production.
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21
Q

What are the three primary manifestations of 21-hydroxylase deficiency?

A

1) Simple Virilizing Form
2) Salt-wasting Form
3) Non-classical Form

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22
Q

What are the clinical presentations of the simple virilizing form of 21-hyroxylase deficiency? (congenital adrenal hyperplasia)

A
  • In females, sexual ambiguity.

* Both sexes, normal rate of growth as a child but epiphyseal plates fuse early resulting in short stature.

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23
Q

What are the clinical presentations of the non-classical form of 21-hydrocylase deficiency? (Congenital adrenal hyperplasia)

A

• Usually mild, with presentations of androgen excess. (Hirsutism, amenorrhoea, precocious puberty).

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24
Q

What investigations should be performed during the diagnosis of Congenital adrenal hyperplasia?

A

A profile of adrenocorticoid hormones should be measured before and one hour after synacthen administration.

  • Increased levels of 17-hydroxyprogesterone.
  • Increased pregnanetriol excretion.
  • Raised levels of Androstenedione
  • Raised basal levels of ACTH
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25
Q

What is the treatment for Congenital adrenal hyperplasia?

A
  • Glucocorticoid replacement therapy and mineralcorticoids (if there is a aldosterone deficiency).
  • Dexamethasone at night - To suppress ACTH secretion.
  • Corrective surgery
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26
Q

What is synacthen?

A

Tetracosactide, it is the first 24 amino acids of ACTH, and is used in diagnosis.

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27
Q

What is Addison’s Disease?

A

• Primary hypoadrenalism, destruction of the entire adrenal cortex. Glucocorticoid, mineralcorticoid and sex hormone are therefore all reduced.

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28
Q

What is the incidence of Addison’s disease?

A

3-4 per million per year.

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29
Q

What are the main causes of Addison’s Disease?

A
  • Autoimmune disease
  • T.B.
  • Adrenalectomy
  • Adrenal infarction
  • Metastatic tumour
  • AIDs
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30
Q

What are the main signs of Addison’s Disease?

A
  • Pigmentation, especially around new scars, palmar creases.
  • Postural hypotension - Due to hypovolaemia.
  • Loss of weight, General wasting, Dehydration, Fatigue, Malaise, Weakness, Fever.
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31
Q

What investigations are performed for suspected Addison’s Disease?

A
  • Single cortisol measurement - 80ng/L) with a low cortisol confirms primary hypoadrenalism.
  • Adrenal antibodies - present in many cases of autoimmune hypoadrenalism.
  • Electrolytes, Urea, glucose
  • Chest X-ray
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32
Q

What is the treatment for Addison’s Disease?

A

• Dexamethasone whilst waiting for results.

  • Replacement of Glucocorticoids (Hydrocortisone) and mineralcorticoids (Fludrocortisone).
  • ‘Steroid Card’
  • ‘Medic-alert’ bracelet.
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33
Q

What is Dexamethasone?

A

It is a glucocorticoid that is 25 times more potent than cortisol, it is used in the treatment of some endocrine pathologies in order to suppress ACTH production.

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34
Q

What is Conn’s Syndrome?

A

Endocrine Hypertension caused by excess production of Aldosterone from the zona glomerulosa. This is due to 65% bilateral hyperplasia or adrenal adenoma.

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35
Q

What are the signs/symptoms of Conn’s Disease?

A

Hypertension, (Hypokalaemia, metabolic alkalosis).

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36
Q

What are the three investigations for Conn’s Disease?

A
  • 9am Aldosterone:Renin ratio (Low renin, high aldosterone)
  • Adrenal venous sampling.
  • CT scan Adrenals.
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37
Q

What are the treatment options for Conn’s Disease?

A
  • Adrenalectomy
  • Low sodium diet
  • Spironolactone (Competitive antagonist of Aldosterone)
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38
Q

What is Phaeochromacytoma?

A
  • Excess production of catecholamines.

* Caused by adrenal or extra adrenal tumour.

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39
Q

What are the signs and symptoms of Phaeochromacytoma?

A
  • Intermittent or sustained hypertension.
  • Hypertension
  • Sweating
  • Tachycardia
  • Headaches
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40
Q

What are the two main investigations for Phaeochromacytoma?

A
  • 24hr catecholamine levels.

* CT/MRI to localise tumour.

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41
Q

What are the treatment options for Phaeochromacytoma?

A
  • Alpha and Beta blockers (Phenoxybenzamine and Propanolol)
  • High salt diet
  • Surgery
42
Q

What effect does PTH have on the regulation of calcium homeostasis? And what stimulates it’s secretion?

A
  • Increased calcium
  • Decreased phosphate

• It is stimulated by a decrease in serum Ca2+ levels.

43
Q

What effect does Calcitonin have on the regulation of calcium homeostasis? And what stimulates it’s secretion?

A
  • Decreased calcium
  • Decreased phosphate

• Secreted in response to increased serum Ca2+ levels and gastrin.

44
Q

What effect do Vitamin D metabolites have on the regulation of calcium homeostasis? And what stimulates it’s secretion?

A
  • Increased Calcium
  • Increased phosphate

• Secreted in response to increased PTH and decreased phosphate.

45
Q

What cell is PTH secreted from?

A

Chief cells of the parathyroid gland.

46
Q

How does PTH increase Calcium concentrations in the blood?

A
  • Renal tubular calcium reabsorption.

* Osteoclast mediated bone calcium resorption.

47
Q

What is primary hyperparathyroidism?

A

• Adenoma or hyperplasia of the parathyroid gland causing an excess of PTH and elevated calcium.

48
Q

What is secondary hyperparathyroidism?

A

• This is parathyroid hyperplasia resulting from hypocalcaemia leading to an increased PTH.

49
Q

What is tertiary hyperparathyroidism?

A

• This is an autonomous secretion of ATH resulting from long-term hypocalcaemia.

50
Q

What is malignant hypercalcaemia?

A

• This is where malignancy results in increased osteoclast bone resorption. The most common malignancies with hypercalcaemia are lung followed by breast.

51
Q

Hyperparathyroidism causes hypercalcaemia, what are the symptoms and signs of hypercalcaemia?

A
  • Generally asymptomatic.
  • But it can cause; tiredness, muscle weakness, dehydration, anorexia, nausea, polyuria, mental confusion, peptic ulcers, bone pain, cardiac arrhythmia’s, kidney stones.
52
Q

What is the prevalence of primary hyperparathyroidism? Which demographic is it most associated with?

A
  • 1-4/1000

* Women, Over 50 years, post menopausal.

53
Q

When investigating hyperparathyroidism?

A
  • Serum PTH
  • Serum phosphate
  • Serum calcium
  • Hyperchloraemic acidosis - often mild
  • Renal function
  • 24hr urinary calcium
  • Elevated serum alkaline phosphatase
54
Q

What would you expect to find in investigation of primary hyperparathyroidism?

A
  • High PTH
  • High Ca
  • Low PO4
  • High urinary calcium
55
Q

What would you expect to find in investigation of secondary hyperparathyroidism?

A
  • High PTH
  • Normal Ca (as they already have hypocalcaemia)
  • High PO4
56
Q

What would you expect to find in investigation of tertiary hyperparathyroidism?

A
  • High PTH
  • High Ca
  • Low PO4
57
Q

What would you expect to find in investigation of malignant hypercalcaemia?

A
  • Normal PTH
  • High Ca
  • Low PO4
58
Q

What are the three broad aspects of treatment for primary hyperparathyroidism?

A
  • Conservative
  • Medical
  • Surgical
59
Q

What is the conservative treatment of primary hyperparathyroidism?

A
  • Adequate hydration
  • Ambulation
  • Avoid diuretics
  • Diet
60
Q

What is the medical treatment of primary hyperparathyroidism?

A

There are some medicines, that require further clinical trials, that inhibit the effect of PTH on bones.

61
Q

What are the indications for surgical treatment of primary hyperparathyroidism?

A
  • If there are specific symptoms
  • Where observation is not desirable.
  • Age 0.25 above normal range
  • Bone mineral density <2.5 at any site
62
Q

What are the symptoms of severe hypercalcaemia?

A
  • Serum calcium >3.5mmol/L
  • Impaired tubular reabsorption
  • Extracellular volume depletion
  • dehydration, nocturia, polyuria, drowsiness, altered consciousness.
63
Q

What is the immediate treatment required for severe hypercalcaemia?

A
  • Rehydrate
  • Intravenous Biphosphonates
  • Prednisolone
  • Calcitonin
  • Oral phosphates
64
Q

What are the main causes of hypocalcaemia?

A
  • Hypoparathyroidism
  • Reduced PTH secretion
  • PTH resistance in target organs
  • Vitamin D-related disorders
65
Q

What are the signs/symptoms of hypocalcaemia?

A
  • Chvosteks sign
  • Trousseaus sign
  • Increased neuromuscular sensitivity
  • Tingling of extremities
  • Tetany
  • epileptic convulsions
  • ECG abnormalities
  • Cataracts
66
Q

What is the treatment for hypocalcaemia?

A
  • I.V. Calcium
  • I.V. Magnesium (If cause is hypomagnesaemia)
  • Oral calcium
  • Oral Magnesium
  • Oral or parenteral phosphate
67
Q

What is Chvosteks sign?

A

The facial nerve is tapped on the angle of the jaw causing contraction of the face on that side. This is due to nerve hyper excitability (tetany).

68
Q

What is Trousseaus sign?

A

A blood pressure cuff is placed around the arm and inflated to a pressure above systolic pressure and held for three minutes.
In the presence of hypocalcaemia the muscles of the hand and forearm go into spasm.

69
Q

What are some of the causes of hypoparathyroidism?

A
  • Surgical, transient or permanent.
  • Postradioactive iodine
  • Polyendocrine deficiency syndromes
  • Idiopathic
70
Q

What would you expect to find in investigation of hypoparathyroidism?

A
  • Low PTH
  • Low Ca
  • Low PO4
71
Q

What is pseudohypoparathyroidism?

A

This is resistance to PTH rather than a lack of it, it is associated to deficient G unit activity.

72
Q

What is the presentation of pseudohypoparathyroidism?

A

Type 1a presents with a phenotypic appearance (Albright’s Hereditary Dystrophy).

73
Q

What is Albrights Hereditary Dystrophy?

A
  • Short
  • Round face
  • Short Metacarpals
74
Q

What is Aldosterone? What stimulates it’s secretion? What are it’s effects?

A
  • Mineralcorticoid, secreted by the Zona Glomerulosa of the adrenal cortex.
  • Secreted in response to Angiotensin and ACTH.
  • Increases Na+ retention and increases K+ excretion.
75
Q

What is Conn’s Syndrome?

A
  • Primary Hyperaldosteronism

* Due to Adrenal hyperplasia or adrenal tumour.

76
Q

What are the symptoms of Conn’s Syndrome?

A
  • Usually asymptomatic other than hypertension.

* Hypertension, Retinopathy, Hypokalaemia, Hypernatraemia.

77
Q

What investigations should be performed for Conn’s Syndrome and what would you expect to find?

A
  • Bloods - Decreased Renin and Decreased K+.

* CT

78
Q

What is Cushing’s Syndrome?

A

This is a clinical state of increased serum cortisol.

79
Q

What is cortisol? What is it secreted in response to? What are it’s effects?

A
  • A glucocorticoid produced by Zona fasiculata of the adrenal cortex.
  • It is Stimulated by ACTH and normally has a circadian rhythm.
  • It increases blood glucose and inhibits the immune system.
80
Q

What are the main causes of Cushing’s Syndrome?

A

• Iatrogenic
• 1˚ causes - Excess production, i.e. adrenal tumour.
2˚ causes - Cushing’s Disease - A pituitary tumour that causes an excess of ACTH and therefore an excess of cortisol.

81
Q

What are the symptoms of Cushing’s Syndrome?

A
  • Central obesity and thin peripheries.
  • Purple Striae
  • Hirsutism
  • Increased Blood glucose
  • Appearance - Moon face and buffalo hump.
82
Q

How do you confirm a diagnosis of Cushing’s Syndrome?

A

24hr Urinary - Cortisol will be high.

83
Q

What tests can you perform to distinguish between 1˚ and 2˚ causes of Cushing’s Syndrome?

A

• Dexamethasone test- mimics cortisol but doesn’t show up on assays.

  • Normal response suppression of cortisol
  • High dose response in pituitary based Cushing’s.
  • No response in adrenal origin of Cushing’s.
84
Q

What would you expect the ACTH levels to be in 1˚ and 2˚ Cushing’s syndrome?

A

1˚ - Low levels

2˚ - High levels

85
Q

What is Addison’s disease?

A

It is the most common source of adrenal cortex insufficiency.

86
Q

What are the symptoms of adrenal insufficiency?

A
  • Postural hypotension
  • Malaise, N&V
  • Addisonian crisis - Hypotension, Hypoglycaemia, collapse, sudden onset of leg/back/abdo pain.
87
Q

What are the additional symptoms of Addison’s disease (in addition to those associated with adrenal insufficiency).

A

• Hyperpigmentation, Associated autoimmune disease.

88
Q

What is phaochromocytoma?

A

• Tumour of the adrenal medulla that results in an increased production of catecholamines.

89
Q

What are the symptoms of phaochromoctoma?

A
  • Sweating, Hypertension, Tachycardia

* Weight loss, increased blood glucose.

90
Q

Week 128 - Gen Endocrine: What effect does PTH have on levels of Calcium and Phosphate? What stimulates it’s release?

A
  • Increases calcium.
  • Decreases phosphate.

• Released in response to low serum Ca2+.

91
Q

Week 128 - Gen Endocrine: What effect does calcitonin have on levels of Calcium and Phosphate? What stimulates it’s release?

A
  • Decreases calcium.
  • Decreases phosphate.

• Released in response to high serum Ca2+.

92
Q

Week 128 - Gen Endocrine: What effect do Vitamin D metabolites have on levels of Calcium and Phosphate? What stimulates the release?

A
  • Increases calcium.
  • Increases phosphate.

• Released in response to low levels of phosphate and high levels of PTH.

93
Q

Week 128 - Gen Endocrine: What are the three physiological functions of PTH?

A
  • Enhances renal tubular reabsorption.
  • Enhances osteoclast mediated bone resorption.
  • Conversion of 25(OH) Vit D into 1,25(OH) Vit D3.
94
Q

Week 128 - Gen Endocrine: PTH converts which form of Vit D into which other form?

A

• 25(OH) Vit D into 1,25(OH) Vit D3.

95
Q

Week 128 - Gen Endocrine: PTH is produced from where?

A

• Chief cells of the parathyroid.

96
Q

Week 128 - Gen Endocrine: What are the main causes of hypercalcaemia?

A
  • Hyperparathyoidism

* Malignancy

97
Q

Week 128 - Gen Endocrine: What are the causes of primary hyperparathyroidism?

A
  • Adenoma
  • Carcinoma
  • Hyperplasia
98
Q

Week 128 - Gen Endocrine: What are the causes of secondary hyperparathyroidism?

A
  • Compensatory

* Elevated PTH secondary to hypocalcaemia with parathyroid gland hyperplasia.

99
Q

Week 128 - Gen Endocrine: What are the causes of tertiary hyperparathyroidism?

A

• Autonomous secretion of PTH following long term hypocalcaemia.

100
Q

Week 128 - Gen Endocrine: Hyperparathyoidism is generally asymptomatic, but what are some of the possible symptoms?

A
  • Renal - Stones, polyuria.
  • Musculoskeletal - Bone pain, osteopenia, fractures.
  • Gastrointestinal - Nausea, Vomitting, Constipation
  • Neurological - Tiredness, Lethargy, Depression, Confusion
  • Cardiac - Bradycardia, Heartblock

Revision Cards (61 decks)

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