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Adrenal Glands Flashcards

1
Q

Left adrenal gland

A

Crescent shaped

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2
Q

Arterial supply to adrenal glands

A

Superior adrenal –> inferior phrenic artery –> Abdominal aorta
Middle Adrenal –> abdominal aorta
Inferior adrenal –> renal artery –> abdominal aorta

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3
Q

Venous supply adrenal glands

A

Right adrenal vein drains directly into the IVC

Left adrenal vein drains into the renal vein then into the IVC

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4
Q

Lymphatic supply to adrenal glands

A

Para-aortic nodes

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5
Q

Development of adrenal glands

A

Cortex –> derived from mesoderm

Medulla –> derived from renal crest/ ectodermal tissue

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6
Q

Nervous supply to adrenal glands

A

Cortex –> hormonal control

Medulla –> sympathetic stimulation from splanchnic nerve from thoracic segment

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7
Q

Adrenal gland consists of two parts

A
  1. Outer adrenal cortex (90%)

2. Inner adrenal medulla (10%)

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8
Q

Three zones of the adrenal cortex and what it secretes?

A
  1. Zona glomerulosa –> mineralocorticoids
  2. Zona fasciculata –> glucocorticoids
  3. Zona reticularis –> androgens

Glomerulosa –> clusters
Fasciculata –> arranged in cords
Reticularis –> networks around blood sinusoids

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9
Q

Types of cells in the adrenal medulla?

A

Two cell types:

  1. Nor-epinephrine producing cells 20%
  2. Epinephrine producing cells 80%

Produces catecholamines

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10
Q

3 hormones secreted by the cortex

A

Mineralocorticoids –> aldosterone
Glucocorticoids –> cortisol
Androgens –> DHEA

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11
Q

Aldosterone production

A 
Produced by zona glomerulosa 
Sodium/BP homeostasis 
Release is stimulated by three factors 
- angiotensin II
- high plasma potassium 
- ACTH
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12
Q

Regulation of aldosterone production

A

Blood pressure falls/ low plasma sodium
Detected by juxtagkomerular cells of the kidney
Secrete renin in response
Plasma renin carries out the conversion of angiotensinogen produced by the liver to active angiotensin I
Angiotensin I is subsequently converted to angiotensin II by angiotensin converting enzyme found in the lungs
Angiotensin II is a potent vasoconstrictor that constricts the blood vessels
Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex
Aldosterone causes the tubules of the kidney to increase the reabsorption of sodium and water into the blood to raise blood pressure . At the same time potassium is excreted and potassium levels fall in the blood.

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13
Q

Hypo-pituitary-adrenal axis

A
  1. CRH is secreted by the hypothalamus
  2. Stimulates the anterior pituitary to release ACTH
  3. This hormone acts on the zona fasciculata and reticularis of the adrenal cortex which secretes cortisol
  4. Cortisol has a negative feedback system on the hypothalamus and AP to inhibit CRH & ACTH release
    Affected by stress, illness and time of day
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14
Q

Cortisol release is in what rhythm?

A

Circadian rhythm

  • rate of secretion changes throughout a 24 hr period
  • highest levels of cortisol are released earliest in the morning -6am
  • falls through the day
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15
Q

Right adrenal

A

Pyramidal in shape

Anterior to diaphragm

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16
Q

Definition of Adrenal insufficiency

A

Inadequate adreno cortical function

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17
Q

Causes of primary insufficiency

A

Addisons disease
Congenital adrenal hyperplasia
Adrenal TB malignancy

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18
Q

Causes of secondary adrenal insufficiency

A

Lack of ACTH stimulation
Iatrogenic (excess steroid use)
Pituitary or hypothalamic disorders

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19
Q

Definition of addisons disease

A

Autoimmune destruction of adrenal cortex causes decreased cortisol production and aldosterone deficiency

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20
Q

Clinical features of addisons disease

A 
Tanned 
Tired 
Weight loss
Dizziness 
Low BP 
Suspect addisons in all with unexplained abdominal pain or vomiting
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21
Q

Diagnosis of addisons disease

A

Suspicious biochemistry
- decreased sodium and increase potassium
-hypoglycaemia due to decreased cortisol
Short synACTHen test
“if you think a gland is deficient you stimulate it”
- measure plasma cortisol before and 30 minutes after an IV injection of ACTH
- cortisol normally would increase in addisons there is no increase
ACTH levels
- should be increased
- causes skin pigmentation
- High ACTH levels POMC also produces melanin

22
Q

Treatment for addisons disease

A

Do not delay treatment to confirm diagnosis

  • hydrocortisone as cortisol replacement (15-25mg in 2-3 doses)
    • If unwell then IV first, then tablets, try to mimic diurnal variation “twice daily, higher dose in the morning, smaller dose in the afternoon”
  • fludrocortisone as aldosterone replacement (50-200ug PO)
23
Q

What do patients need to know about steroid replacement

A
  • Sick day rules “double your dose” in febrile illness, stress or injury
  • Prescribing doctors/dentists/surgeons must now about steroid use (Need to wear identification e.g card and wrist band)
  • Can’t stop steroids suddenly
  • Add 5-10mg of hydrocortisone to daily intake before strenous activity/exercise
24
Q

Exogenous steroid use causing secondary adrenal insufficiency mechanism

A

Exogenous steroids also feedback to the HPA axis and switch off own production of cortisol
Gradually wear of steroids to re sensitise the pituitary and adrenal cortex

25
Clinical features of exogenous steroid use
Similar to addisons except - skin pale (no increased ACTH) - aldosterone production intact (regulated by RAAS)
26
Treatment if exogenous steroid use
Treat with hydrocortisone as fludrocortisone (aldosterone replacement) is unnecessary
27
Definition of Cushings syndrome
Clinical state produced by chronic glucocorticoid excess + loss of the normal feedback mechanisms of the HPA axis and loss of circadian rhythm of cortisol secretion
28
Causes of Cushings
``` ACTH dependent causes: - Cushings disease (bilateral adrenal hyperplasia from an ACTH secreting tumour) - ectopic ACTH production - rarely - ectopic CRH production ACTH independent causes: - adrenal adenoma/cancer -adrenal nodular hyperplasia - iatrogenic -pharmacological doses of steroids ```
29
Symptoms of Cushings
- Weight gain - Mood change (depression, lethargy, irritability - Proximal weakness - Gonadal dysfunction (irregular menses) - Acne
30
Signs of Cushings
- Central obesity - Plethoric, moon face - Buffalo neck hump - Supraclavicular fat distribution - Skin and muscle atrophy - Bruises easily - Purple abdominal striae - Osteoporosis
31
Diagnosis of Cushings
``` Step 1: Establish cortisol excess: “too much, so suppress” -Dexamethasone suppression testing -24 hour urinary free cortisol -Late night salivary cortisol ``` Step 2: Establish source of cortisol excess: 1. meausure ACTH a) If normal or High then do a CRH stimulation test ii. If no change in ACTH do a CT chest/abdo/pelvis (ectopic ACTH) ii If exagerated rise in ACTH do a pituitary MRI (pituitary ACTH source) b) If undetecable do an adrenal CT scan
32
Management of Cushings
Surgical - transphenoidal pituitary surgery - laparoscopic adrenalectomy- adrenal source - removal of ACTH source Medical - Metyrapone/ketoconazole (inhibts cortisol production) - short term measure
33
Iatrogenic Cushings syndrome mechanism
- commenest cause of cortisol excess - prolonged steroid use - chronic suppression of piuitary ACTH production and results in adrenal atrophy
34
Implications of cushings SYNDROME
- Unable to respond to stress - need exra doses when ill/surgical procedure - cannot stop suddenly - gradual withdrawl of steroid therapy if>4-6 weeks
35
Definition of primary hyperaldosteronism
-Autonomous production of aldosterone independent of its regulators (angiotensin II/potassium) causes increased sodium and water retention
36
Causes of primary hyperaldosteronism
- Single aldosterone adrenal adenoma (Conn’s syndrome)40% or - bilateral adrenalcorticol hyperplasia 60%
37
Clinical features of primary hyperaldosteronism
- Significant hypertension - Hypokaelaemia (in up to 50%) - Alkalosis (urinary secretion of H+)
38
Diagnosis of primary hyperaldosteronism
Think Conns if: - Hypertension associated with hypokaelamia - Refractory hypertension e.g despite >3 hypertensive drugs - Hypertension occurring before 40 years of age U&E's ( for hypokaelamia, alkalosis) Renin and aldosterone ration – best screening tool - Before screening stop medications if possible (definitely stop beta blocker and MR antagonists) - Elevated aldosterone and decreased renin Saline suppression test (“if you think a gland is excessive then suppress it”) o Volume expansion should suppress renin and aldosterone o 2L saline over 4 hours o 4h aldosterone >270pmol/l highly suspicious o Aldosterone will still be high!! CT or MRI of the adrenals to localise the cause - If CT/ MRi shows a unilateral adenoma  adrenal vein sampling from both adrenals. If one side shows >3 fold increase in aldosterone production and adenoma is likely and surgical excision is indicated
39
Management of Primary hyperaldosteronism
Surgical - Unilateral laproscopic adrenalectomy - Only if adrenal adenoma - Cure of hypokalaemia - Cures hypertension in 30-70% cases Medical - In bilateral adrenal hyperplasia - Use MR antagonists (spironolactone or eplerenone- newer selective antagonist which doesn’t cause gynaecomastia) - Or amiloride (blocks Na reabsorption by kidney)
40
Secondary hyperaldosteronism cause
Due to a high renin and high aldosteronism from decreased renal perfusion e.g renal artery stenosis, accelerated hypertension, diuretics or hepatic failure
41
Phaechromocytoma definition
Catecholamine secreting tumour of the adrenal medulla or extra-adrenal neural crest cells such as sympathetic ganglua (paraganglioma)
42
Causes of phaechromocytoma
Rule of tens - 10% malignant - 10% extra-adrenal - 10% bilateral - 10% familial - Von Hippel-Lindau syndrome, Men II, Neurofibromatosis I
43
Clinical features of pheochromocytoma
- Hypertension (intermittent in 50%, persists in 25%) - Episodes of headache, palpitations, pallor and sweating - THINK if pale AND sweaty as also vasoconstriction - Also tremor, anxiety, nausea, vomiting, chest or abdo pain - Crises last 15 minutes - Often well in between crises
44
Diagnosis of Phaechromocytoma
``` - Measure 24 urinary catecholamines o At least twice - Plasma catecholamines o Only if high index of suspicion - Imaging o CT abdomen o MIBG scan (chromaffin seeking analogue) –uptake scan ```
45
Management of phaechromocyoma
- Pre-operative treatment “patient prepped for surgery then surgeon handles pheo then catecholamines bind to receptors and patient dies” therefore: - Alpha-blockade - Phenoxygenzaine or doxazosin
46
Adrenal incidentaloma definition
True incidentaloma is an incidentally detected lesion with no pathophysiological significance, and needs to be differentiated from incidentally detect but clinically relevant masses
47
Importance of incidentaloma
Important to determine whether the incidentally discovered adrenal mass is: - malignant - functioning and associated with excess hormonal secretion
48
Differential diagnosis of incidentaloma
- cortisol secreting adrenal adenoma (cushings) - mineralocorticoid-secreting adrenal adeoma - androgen secreting adenoma - CAH
49
Investigations of adrenal incidentaloma
- Clinical assessment for symptoms and signs of excess hormone secretion - urinary free cortisol and overnight dexamethasone suppresion - urinary free catecholamines - aldosterone/renin ratio
50
Management of incidentaloma
- up to 20% may develop hormonal excess during follow up - unlikely if 4cm (likely malignant) - imaging features suggestive of malignancy (lack of clearly defined borders) Non surgical - repeat MRI at 6 and 12 months - repeat biochemical screening annualy

Endocrine (7 decks)

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