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Endocrine > Pituitary Adrenal Disease > Flashcards

Pituitary Adrenal Disease Flashcards

1
Q

What are the causes of seller masses?

A 
Benign tumours: 
-pituitary adenoma
-craniopharyngioma
-meningioma
Malignant tumours:
-primary (vanishingly rare)
-metastatic tumours (lung, breast)
Cysts: Rathke's cleft, arachnoid, dermoid
Lymphocytic hypophysitis
Carotid aneurysm
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2
Q

What are the local effects of pituitary tumours?

A
    1. Headaches
  • ->a) stretching of dura by tumour
  • ->b) hydrocephalus (rare).
    1. Visual field defects (nasal retinal fibres compressed)
    1. Cranial nerve palsies and temporal lobe epilepsy (lateral extension of tumour)
    1. CSF rhinorrhea (downward extension of tumour)
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3
Q

What are the types of pituitary adenoma?

A

Prolactinoma - prolactin secreting
Acromegaly - GH secreting
Cushing’s - ACTH secreting

RARE: TSH secreting, Gonadotrophin secreting (FSH and LH).
Non funtioninig - just mass effect features but no hormone disruption.

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4
Q

What are the symptoms of prolactinoma in female?

A
  • Galactorrhoea

- Hypogonadism - infertility + amenorrhoea or oligomenorrhea

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5
Q

What are the symptoms of prolactinoma in males?

A
  • Hypogonadism - decreased libido, infertility, impotence, gynaecomastia.
  • Rarely galactorrhoea.
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6
Q

What is the treatment for prolactinoma?

A

Dopamine agonists usually reduce tumour size and prolactin secretion e.g. bromocriptine, carbergoline.

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7
Q

What are the causes of acromegaly?

A

> Common: GH secreting pituitary adenoma
Rare:
-GH secreting extra pituitary tumour.
-GHRH hormone secreting tumour.

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8
Q

What are the clinical features of acromegaly?

A
  • Insidious onset
  • Enlarged jaw, hands and feet (dental problems, tight rings, increased shoe size).
  • Coarsening facial features, enlarged frontal bones and nose.
  • Thickened skin
  • Enlargement of tongue, deepening of voice.
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9
Q

Investigations in suspected acromegaly?

A
  • GH biochem: Increased
  • OGTT: Failure to suppress GH w/ OGTT
  • Increased IGF1 / Somatomedin C
  • Diabetes or impaired OGTT
  • CT/MRI: pit tumour
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10
Q

What is the treatment for acromegaly?

A

1’: transphenoidal hypophysectomy to remove tumour

Surgical resection unsuccessful:

  • radiotherapy
  • octreotide: long acting prep every 1/12
  • bromocriptine
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11
Q

What is the size cut off for pituitary adenoma macro v micro?

A

10mm macro

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12
Q

What are the causes of Cushing’s syndrome?

A
    1. ACTH dependent Cushing’s syndrome:
  • Cushing’s
  • ectopic ACTH
  • ectopic CRF.
    1. ACTH-independent Cushing’s syndrome:
  • adrenal adenoma
  • adrenal carcinoma
  • micronodular hyperplasia
  • macronodular hyperplasia.
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13
Q

What are the clinical features of Cushingoid appearance??

A
  • Obesity: redistribution of weight centrally, moon face, buffalo hump, wasting of buttocks.
  • Skin: atrophy of epidermis; thin skin, plethoric face, easy bruising, striae.
  • Hirsutism
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14
Q

What are the major AEx of bromocriptine?

A

N/V, postural dizziness.

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15
Q

What are the neuropsychiatric clinical features of Cushing’s?

A
  • Depressed mood/ crying
  • decreased concentration and memory;
  • insomnia
  • decreased libido.
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16
Q

What are the MSK alterations of Cushing’s?

A
  • Proximal myopathy

- Osteopaenia: crush fractures of vertebrae.

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17
Q

What are the metabolic features of Cushing’s?

A
  • Diabetes 25%;

- glucose intolerance 75%

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18
Q

What are the investigations and expected results in Cushing’s syndrome?

A
  • FBE: Hb high normal; WCC slightly elevated, decreased neutrophils
  • Electroytes: hypokalemia and metabolic alkalosis in ectopic ACTH.
  • Hyperglycemia: due to insulin resistance
  • Increased Ca2+ absorption and hypercalciuria
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19
Q

How is Cushing’s diagnosed?

A
  • 24h urine free cortisol

- Overnight dexamethasone suppression test.

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20
Q

How is pathological cause of Cushing’s determined?

A

ACTH:

  • if suppressed, likely adrenal cause.
  • Normal or elevated: likely pituitary dependent.
  • Very high, likely ectopic ACTH.
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21
Q

Describe the 4 major forms of Cushing’s syndrome.

A
  • Pituitary Cushing Syndrome
  • Adrenal Cushing syndrome
  • Paraneoplastic Cushing Syndrome
  • Iatrogenic Cushing syndrome
22
Q

Pituitary dependent Cushing’s treated?

A

Transphenoidal hypophysectomy to remove tumour.

23
Q

How is adrenal adenoma or carcinoma Cushing’s treated?

A

Adrenal surgery

24
Q

How is ectopic ACTH or CRF treated?

A

Treat the tumour associated with the hormone production.

25
Q

What are the causes of adrenocortical insufficiency?

A
  1. Hypopituitarism: Insufficient section of ACTH by pituitary
  2. Addison’s Disease: Destruction of adrenal glands
26
Q

What are the clinical features of primary Addison’s disease?

A
  • Dark skin and mucosae
  • High potassium
  • Low sodium
  • Metabolic acidosis
  • Associated with primary hypothyroidism, DMI, vitiligo, near defects
27
Q

What are the associated symptoms of Addison’s disease?

A

-Weakness, fatigue, myalgia, arthralgia
-weight loss,
-hypotension, postural dizziness
-salt craving.
GI: N/V/D and GI pain.

28
Q

What is the aetiology of primary adrenocortical insufficiency?

A
  • AI: AI associated atrophy
  • Infection: TB, fungi (histoplasmosis, coccidiomycosis, HIV and AIDS)
  • Infiltration: metastatic carcinoma
  • Haemorrhage/infarction
  • Drugs: inhibit cortisol/increase cortisol metabolism
  • Adrenoleukodystrophy
29
Q

Which drugs can lead to primary adrenocortical insufficiency?

A
  • Inhibit cortisol: ketoconazole, megestrol acetate

- Increase cortisol metabolism: rifampin, phenytoin, barbituates, heparin, coumadin

30
Q

What are the expected electrolyte disturbances of Addison’s disease?

A
  • Hyponatremia
  • Hyperkalemia
  • Moderate acidosis
  • Increased urea

-Hypoglycaemia

31
Q

Ix for Addison’s disease?

A
  • Serum cortisol - low
  • ACTH - high
  • Synacthen test (ACTH infusion)
  • Adrenal antibodies (17hydroxylase enzyme Abs)
  • Adrenal imaging - calcification or enlargement of adrenals (TB or infiltration)
32
Q

What is the management of Addisonian Crisis?

A
  • Hydrocortisone 100mg IV 6hrly
  • Fluid replacement - IV normal saline
  • Glucose if hypoglycaemic
33
Q

What is long term Addison’s disease management?

A

GLUCOCORTICOIDS:

  • Cortisone acetate 25mg/12.5mg
  • Dexamethasone 0.25mg bd
  • Prednisolone 5mg daily

MINERALOCORTICOIDS
-Fludrocortisone 0.1mg daily

34
Q

What is Conn’s syndrme?

A

Excess aldosterone from adrenal cortex

35
Q

What is a phaechromocytoma?

A

Tumour of chromaffin cells located in adrenal medulla; derived from neural crest cells.
Results in catecholamine excess.

36
Q

What are the two major complications of acromegaly?

A
  • Bowel cancer: excess GH stimulates polyp growth - may become cancerous.
  • Cardiac: cardiac hypertrophy (ischaemic change, HOCM)
37
Q

Pituitary dependent Cushing’s treated?

A

Transphenoidal hypophysectomy to remove tumour.

38
Q

How is adrenal adenoma or carcinoma Cushing’s treated?

A

Adrenal surgery

39
Q

What are the two major complications of acromegaly?

A
  • Bowel cancer: excess GH stimulates polyp growth - may become cancerous.
  • Cardiac: cardiac hypertrophy (ischaemic change, HOCM)
40
Q

What is the role of inferior petrosal sinus sampling?

A

Sample central and peripheral cortisol level to confirm pituitary adenoma visualised on MRI is the same site from which excess cortisol is coming.

41
Q

What are the types of primary aldosteronism?

A

(1) - Aldosterone producing adenoma
(2) - Bilateral idiopathic hyperaldosteronism
(3) - Glucocorticoid suppressible hyperaldosteronism
(4) - aldosterone producing adrenal Ca

42
Q

What is the clinical triad of primary aldosteronism?

A
  • Hypertension
  • Hypokalemia
  • Metabolic alkalosis
43
Q

Symptoms of hypokalemia?

A
  • Headaches
  • palpitations
  • polydipsia
  • polyuria
  • nocturia
44
Q

Diagnostic approach to primary aldosteronism?

A
  • 24h urine: document inappropriate K+ loss in presence of hypokalemia
  • Plasma renin: suppressed
  • Plasma aldosteorne: increased
  • 2L N Sal –> Aldosterone fails to suppress
  • High aldosterone/renin ratio
45
Q

How can primary aldosteronism be localised radiologically?

A
  • CT or MRI

- 131-iodocholesterol scanning

46
Q

Treatment for primary aldosteronism?

A
  • Adrenal adenoma = surgical excision
  • Aldactone = competitive antagonist to aldosterone
  • Amiloride = decrease K+ excretion by blocking Na+ channels in proximal tubule.
47
Q

Phaeochromocytoma diagnosis?

A
  • Urine catecholamines (24h)

- Plasma catecholamines

48
Q

Localisation of phaeochromocytoma?

A
  • CT
  • Meta iodo benzyl guanidine scanning (MIBG)
  • Octreotide scanning
  • Venous sampling
49
Q

What is polyglandular autoimmune syndrome type 1?

A

Very rare AR disorder.

Caused by mutation in AIRE gene on Chr 21.

50
Q

What is MEN1?

A

AD condition due to defect in gene on Chr 11.

Tumours of Pituitary / Pancreas / Parathyroid

51
Q

What causes MEN2?

A

AD condition due to mutations on RET proto oncogene on Chr 10.

52
Q

Conditions associated with MEN2a?

A
  • Medullary carcinoma of thyroid
  • Phaeochromocytoma
  • Parathyroid hyperplasia

Endocrine (21 decks)

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