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Year 2 - T2 Theme 1 > L4 Endocrine/diabetes > Flashcards

L4 Endocrine/diabetes Flashcards

1
Q

What is each adrenal gland comprised of

A
  • Two distinct structures, the outer part of the adrenal glands called the adrenal cortex
  • The inner region is known as the adrenal medulla
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2
Q

Adrenal causes of hypertension

A 
• Primary Hyperaldosteronism
• Zona Glomerulosa
○ Adenoma
○ Hyperplasia
○ Rare genetic causes 
Phaeochromocytoma ( phaeo) 
• Tumour of the adrenal medulla
• Some forms of Congenital Adrenal Hyperplasia 
• Enzyme defect  - Uncommon
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3
Q

Layers of the adrenal gland

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
  • Medulla
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4
Q

Adrenal causes of hypertension

A
  • Primary hyperaldosteronism
  • Zone glomerulosa
    Adenoma
    Hyperplasia
    Rare genetic causes
    Phaeochromocytoma
  • Tumour of the adrenal medulla
  • Some forms of congenital adrenal hyperplasia
  • Enzyme defect - uncommon
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5
Q

What is aldosterone produced by

A
  • Zona glomerulosa of the adrenal cortex in the adrenal gland
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6
Q

Pathway for aldosterone secretion - RAAS

A

If the perfusion of the juxtaglomerular apparatus in the kidney’s macula densa decreases, then the juxtaglomerular cells (granular cells, modified pericytes in the glomerular capillary) release the enzyme renin.

Renin cleaves a decapeptide from angiotensinogen, a globular protein. The decapeptide is known as angiotensin I.

Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE) which is thought to be found mainly in endothelial cells of the capillaries throughout the body, within the lungs and the epithelial cells of the kidneys.

Angiotensin II causes tcells to contract along with the blood vessels surrounding them and causing the release of aldosterone

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7
Q

What does activation of AT II receptors cause

A
  • Vasodilation

- ADH secretion

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8
Q

What does activation of AT I receptors cause

A
  • Vasoconstriction

- Sympathetic activation

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9
Q

Overall effects of renin, angiotensin and aldosterone

A
  • Decrease K+ levels
  • Increase Na+ levels
  • Increase blood volume and pressure
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10
Q

What is primary hyperaldosteronism

A

Primary aldosteronism, also known as primary hyperaldosteronism or Conn’s syndrome, refers to the excess production of the hormone aldosterone from the adrenal glands, resulting in low renin levels.

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11
Q

Who do you screen for primary hyperaldosteronism

A
  • Hypokalaemia
  • Patients with resistant hypertension
  • Younger people
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12
Q

Comparison of vascular and renal pathology between individuals with primary aldosteronism and essential hypertension and similar blood pressure

A

Individuals with PA have more vascular and renal pathology than people with essential hypertension and similar blood pressure

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13
Q

What do initial screening tests investigate for

A
  • Suppressed renin

- Normal/high aldosterone

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14
Q

Confirmatory test for primary hyperaldosteronism

A
  • Oral or IV Na+ suppression test
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15
Q

Primary hyperaldosteronism tests for specific aetiology ie secreting adenoma or bilateral hyperplasia

A
  • Adrenal CT scan

- Adrenal venous sampling - Metomidate PET CT

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16
Q

What does primary hyperaldosteronism usually result from

A
  • Aldosterone secreting adenoma of the adrenal cortex
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17
Q

Unilateral adenoma vs bilateral hyperplasia

A

Unilateral disease is usually caused by an aldosterone producing adenoma (benign tumor) and less commonly by adrenal cancer or hyperplasia (when the whole gland is hyperactive).

Bilateral disease is usually caused by bilateral hyperplasia (when both glands are hyperactive).

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18
Q

Treatment for unilateral adenoma

A
  • Laparoscopic adrenalectomy

- Medical treatment (sometimes)

19
Q

Treatment for bilateral hyperplasia

A
  • Medical treatment (aldosterone antagonists)

- Spironolactone

20
Q

What is a phaeochromocytoma

A
  • Tumour of the adrenal medulla
21
Q

how do sympathetic neurones in the spinal cord cause release of adrenalin and noradrenalin in the adrenal medulla

A

Symp neurones in spinal cord –Ach–> adrenal medulla

Tyrosine –> L-dopa –> dopamine –> noradrenalin –> adrenalin

22
Q

Products of the adrenal medulla

A

· Catecholamines

  • Dopamine
  • Norepinephrine (noradrenalin) – cortisol–> epinephrine(adrenalin)
23
Q

Is the adrenal medulla essential for life ‘stress/flight/fight’ response

A

Nope

24
Q

Effects of noradrenalin (alpha 1 and 2)

A
  • Vasoconstriction –> increased BP, pallor

- Glycogenolysis

25
Q

Effects of adrenalin (alpha 1, beta 1 and 2)

A
  • Vasoconstriction
  • Vasodilatation in Muscle
  • Increased heart rate
  • Sweating
26
Q

What percentage of phaeos are diagnosed in the mortuary

A

20%

27
Q

How does a phaeochromocytoma present

A

· Spells

  • Headache, sweating
  • Pallor, palpitation
  • Anxiety

· Hypertension

  • Permanent
  • Intermittent
28
Q

Which genetic conditions are associated with phaeochromocytomas

A

· Neurofibromatosis Type 1 (NF1)
· Multiple endocrine neoplasia type 2 ( MEN 2 )
· Von hippel - lindau syndrome

29
Q

When are tumors under the skin likely to appear

A
  • May appear at any age but especially during adolescence
30
Q

What are neurofibromas

A
  • Tumors which grow on the nerves, are made up of cells that surround nerves and other cell types, are called neurofibromas
31
Q

What is crowe’s sign

A
  • The Crowe sign or Crowe’s sign is the presence of axillary (armpit) freckling in people with neurofibromatosis type I (von Recklinghausen’s disease). These freckles occur in up to 30% of people with the disease and their presence is one of six diagnostic criteria for neurofibromatosis.
32
Q

What is von-hippel lindau syndrome

A

Is an inherited disorder characterized by the formation of tumors and fluid-filled sacs (cysts) in many different parts of the body

33
Q

Which tumours are characteristic of von-hippel lindau syndrome

A
  • Hemangioblastomas
34
Q

What are hemangioblastomas

A
  • These growths are made of newly formed blood vessels. Although they are typically noncancerous, they can cause serious or life-threatening complications.
  • Hemangioblastomas that develop in the brain and spinal cord can cause headaches, vomiting, weakness, and a loss of muscle coordination (ataxia).
  • Hemangioblastomas can also occur in the light-sensitive tissue that lines the back of the eye (the retina).
35
Q

24 hour urine test for phaeochromocytomas

A
  • Normetanephrines and metanephrines

- 3 Methoxytyromine

36
Q

Plasma test for phaeochromocytomas

A
  • Noradrenalin and adrenalin

- Metanephrines

37
Q

What other things elevate the measured catecholamines

A
  • Obstructive Sleep Apnoea
  • Amphetamine like drugs
  • L-DOPA
  • Labetalol
38
Q

What does urine dopamine come from

A

Kidney & Nervous system
NOT the Adrenal Medulla
So measure urine Methoxytyramine

39
Q

What is an MIBG scan

A

An MIBG scan is a nuclear medicine scan that involves an injection of a radioactive medication (radiopharmaceutical) called iodine-123 meta-iodobenzylguanidine – MIBG for short

The radiopharmaceutical is injected into a vein usually on the inside of the elbow

40
Q

Alpha blockers used to manage phaeochromocytomas

A

□ Phenoxybenzamine

□ Doxazocin

41
Q

Beta blockers used to manage phaeochromocytomas

A
  • Propanolol
42
Q

What is laparoscopic adrenalectomy

A

Laparoscopic adrenalectomy is a minimally invasive technique used to remove a diseased or cancerous adrenal gland

43
Q

Post adrenalectomy care

A 
· Consider Genetic testing
	• 30% are genetic ( 13 mutations so far)
· Annual Metanephrines 
	• 24 hour urine
	• Plasma
· Additional treatment if Malignant 
	• 10%

Year 2 - T2 Theme 1 (20 decks)

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