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Endocrine > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

Name the three layers of the adrenal cortex, how they are regulated and what they secrete

A

Zona glomerulosa
Regulated by angiotensin II & (plasma) K+
Secrete mineralocorticoids (aldosterone)
————————————————————————————
Zona fasciculata
Regulated by ACTH
Secrete glucocorticoids (cortisol)
————————————————————————————
Zona reticularis
Regulated by ACTH
Secrete adrenal androgens (DHEA)

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2
Q

Name the cells of the adrenal medulla and what they produce

A

Chromaffin cells
Catecholamines (epinephrine & norepinephrine)

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3
Q

What substance are all corticosteroids (aldosterone, cortisol, DHEA, testosterone…) derived from?

A

Cholesterol

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4
Q

Describe the HPA axis (cortisol & androgen production regulation)

A

Hypothalamus secretes corticotrophin releasing hormone (CRH)
Anterior pituitary secretes adrenocorticotropic hormone (ACTH)
Adrenal cortex secretes cortisol (& small amounts of DHEA)

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5
Q

Describe the regulation of the HPA axis

A

Negative feedback control of CRH & ACTH
Variation of CRH secretion with illness, stress and time of day

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6
Q

Briefly describe the RAAS system

A

Drop in blood pressure →
Kidneys release renin →
Angiotensinogen converted to angiotensin I →
Angiotensin I converted to angiotensin II by ACE →
Aldosterone secreted by adrenal cortex →
Salt retention & Increase in BP

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7
Q

Aldosterone is secreted in response to what level of plasma K+

A

High K+

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8
Q

Describe the main actions of cortisol
(Cardiac, renal, CNS, bone, connective tissue, metabolic, immunological)

A

CARDIAC - Increased CO & BP
RENAL - Increased renal blood flow & GFR
CNS - Decreased libido, mood lability
BONE - Accelerated osteoporosis
CONNECTIVE TISSUE - decreased wound healing
METABOLIC - Increased blood glucose, lipolysis & proteolysis
IMMUNOLOGICAL - Decreased inflammatory response

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9
Q

Name some conditions that are treated with glucocorticoids

A

Asthma, RA, UC, Crohn’s, sarcoidosis

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10
Q

Where are mineralocorticoid receptors located (4)

A

Kidneys
Gut
Salivary glands
Sweat glands

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11
Q

Describe the main actions of aldosterone

A

Na/K balance (K/H excretion, Na reabsorption)
Extracellular volume & blood pressure regulation

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12
Q

Adrenal insufficiency aetiology

A

Primary insufficiency
- Addison’s disease
- Congenital adrenal hyperplasia
- Adrenal infection e.g. TB
- Adrenal malignancy
- Bilateral adrenal haemorrhage (sepsis, anti-coagulants)
- Bilateral adrenalectomy
- Bilateral adrenal infiltration e.g. haemochromatosis

Secondary/ tertiary insufficiency
- Excess exogenous steroids
- Pituitary/ hypothalamic disorders causing lack of ACTH

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13
Q

Define primary adrenal insufficiency

A

Destruction of the entire (>90%) adrenal cortex causing decreased production of adrenocortical hormones (glucocorticoids, mineralocorticoids, and adrenal androgens)

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14
Q

Primary adrenal insufficiency/ Addison’s disease clinical presentation

A
  • Anorexia, fatigue, lethargy
  • Loss of appetite, salty food cravings
  • Dizziness & low bp
  • Abdominal pain, vomiting, diarrhoea
  • Skin & oral mucosa pigmentation (excess ACTH)
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15
Q

What clinical sign differentiates primary from secondary adrenal insufficiency and what does it indicate

A
  • Skin & oral mucosa pigmentation
  • Caused by excess ACTH from the pituitary gland
    • ACTH molecule contains sequence for MSH within it
    • ACTH is degraded by proteases eventually exposing MSH
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16
Q

What is the most common cause of adrenal insufficiency in infants (< 6 months)

A

Congenital adrenal hyperplasia

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17
Q

Primary adrenal insufficiency/ Addison’s disease bloods findings

A
  • Adrenal autoantibodies positive in 70%
    • Biochemistry - ↓ Na+, ↑ K+, may be hypoglycaemic
      (especially in paediatrics)
    • ACTH levels very high (results in skin pigmentation)
    • Renin/aldosterone levels - ↑↑ renin, ↓ decreased
      aldosterone
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18
Q

Primary adrenal insufficiency/ Addison’s disease ‘stimulation’ test

A

Short synacthen test
- Measure plasma cortisol before IV/IM ACTH injection
- Measure plasma 30 mins after IV/IM ACTH injection
- Normal baseline cortisol >250 nmol/L,
- Normal post ACTH cortisol >550 nmol/L

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19
Q

Investigations to determines the aetiology for primary adrenal insufficiency

A
  • 17-OH-Progesterone blood levels (High in CAH)
  • 21-OH antibody (Addison’s, anti-phospholipid syndrome)
  • CT adrenals (infection/ infiltration/ haemorrhage/
    malignancy)
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20
Q

Primary adrenal insufficiency/ Addison’s treatment

A
  • Hydrocortisone as cortisol replacement
    • If unwell IV first
    • Usually 15-30mg PO daily in divided doses
    • Try and mimic diurnal rhythm (higher dose in morning)
  • Fludrocortisone as aldosterone replacement
    • Careful monitoring of BP and K+
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21
Q

Primary adrenal insufficiency/ Addison’s disease ‘sick day rules’

A

Increase steroid replacement when unwell or undergoing other stress e.g. preoperative

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22
Q

Adrenal crisis treatment

A
  • 0.9% IV NaCl (normal saline)
  • 100mg IV hydrocortisone
  • Cardiac monitoring
  • ?underlying cause/precipitant
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23
Q

Adrenal crisis definition/ aetiology

A

Acute, severe glucocorticoid deficiency caused by either

  • stress in a patient with underlying adrenal insufficiency or
  • sudden discontinuation of glucocorticoids after prolonged glucocorticoid therapy
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24
Q

Congenital adrenal hyperplasia definition/ aetiology

A
  • Inherited group of disorders characterised by a deficiency in one of the enzymes necessary for cortisol synthesis
  • 90% due to an autosomal recessive 21⍺-hydroxylase deficiency
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25
Q

Congenital adrenal hyperplasia pathophysiology

A
  • 21⍺-hydroxylase deficiency prevents the production of aldosterone and cortisol
  • Increased volume of precursors will be diverted into the androgen pathway → increased testosterone and dihydrotesterone
  • Reduced cortisol stimulates ACTH release and cortical hyperplasia
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26
Q

Classic vs non-classic CAH clinical presentation

A

Classic CAH

  • Presents at birth or shortly after
  • Genital ambiguity (virilisation) in females
  • Adrenal failure - collapse, hypotension, hypoglycaemia, poor weight gain
    • Biochemical patten of Addison’s disease

Non-classic CAH

  • Partial 21⍺-hydroxylase deficiency
  • Presents later (adolescence/adulthood) (hyperandrogenaemia)
    • Precocious puberty
    • Hirsutism
    • Acne
    • Oligomenorrhoea, infertility or sub-fertility
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27
Q

Congenital adrenal hyperplasia investigations

A
  • Basal (or stimulated) 17-OH progesterone
    • would be high as it is converted by 21⍺-hydroxylase
      (which is deficient)
  • Genetic analysis
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28
Q

Congenital adrenal hyperplasia management

A

Paediatrics

  • Glucocorticoid replacement
  • Mineralocorticoid replacement in some
  • Surgical correction
  • Achieve maximal growth

Adults

  • Glucocorticoid replacement, avoiding steroid over-replacement
  • Control androgen excess
  • Restore fertility
29
Q

Secondary/ tertiary adrenal insufficiency is different from primary adrenal insufficiency in two ways. Name these.

A

No excess ACTH => no skin pigmentation
Intact aldosterone production => less hypotension

30
Q

Secondary vs tertiary adrenal insufficiency

A

Secondary: lack of production of ACTH by the pituitary gland
Tertiary: lack of CRH secretion by the hypothalamus

31
Q

Secondary/tertiary adrenal insufficiency investigations

A

Insulin tolerance test
CRH stimulation test (secondary vs primary)
MRI of hypothalamus & pituitary gland

32
Q

Secondary/tertiary adrenal insufficiency treatment

A

Hydrocortisone replacement alone
(Fludrocortisone unnecessary)

33
Q

Cushing’s syndrome vs disease

A

Cushing’s syndrome - increased cortisol
Cushing’s disease - increased cortisol (cushing’s syndrome) due to functioning pituitary adenoma

34
Q

Cushing’s syndrome aetiology

A

ACTH dependant
- Cushing’s disease (pituitary adenoma)
- Ectopic ACTH secretion (e.g. SCLC)
- Ectopic CRH secretion (e.g. medullary thyroid carcinoma)

ACTH independent
- Exogenous steroids (most common)
- Adrenal adenoma or carcinoma
- Adrenal corticol nodular hyperplasia
- Mccune-Albright syndrome

  • Pseudo-Cushing’s (severe depression/ alcoholism)
35
Q

Differences in adrenal enlargement in ACTH dependent vs independent Cushing’s syndrome

A

ACTH dependent - (usually) diffuse enlargement
ACTH independent - (usually) nodular enlargement

36
Q

Cushing’s syndrome clinical presentation - excess cortisol effects (ACTH independent & dependant)

A

Inflammation & (central) fat deposition
- Facial plethora & swelling (‘moon face’)
- Central obesity
- Dorsocervical fat pad
- Conjunctival oedema (chemosis)

————————————————————————————

Increased blood sugars, lipolysis & proteolysis
- Proximal myopathy
- Glycosuria/ diabetes mellitus

————————————————————————————

Decreased collagen formation & wound healing
- Thin skin
- Easy bruising
- Striae

————————————————————————————

Increased bone resorption & decreased bone formation
- Osteoporosis

————————————————————————————

Cortisol effects on CNS
- Depression/psychosis

————————————————————————————

Cortisol effects on cardio & renal (increased CO & BP)
- Hypertension

37
Q

Cushing’s syndrome clinical presentation - excess ACTH & androgen effects (ACTH dependant)

A

Increased ACTH
- Skin pigmentation

Increased adrenal androgens
- Acne
- Virilization/ hirsutism
- Oilgo/ammenorhea
- Frontal balding

38
Q

Cushing’s syndrome first line screening test & 3 other screening tests available (to establish excess cortisol)

A

First line - Overnight dexamethasone suppression test

  • Normal: cortisol <50 nmol/l next morning
  • Abnormal: cortisol >130 nmol/l

Other screening tests - 24hr urine free cortisol, diurnal cortisol variation, late night salivary cortisol test

39
Q

Cushing’s syndrome diagnostic test

A

Low dose dexamethasone suppression test
- 2 day 2mg/day dexamethasone
- Normal: cortisol <50 nmol/l 6 hours after last dose
- Cushing’s: cortisol >130 nmol/l

+ Repeat to confirm

40
Q

Cushing’s syndrome aetiology focused investigations

A

1) Serum ACTH (ACTH dependent vs independent)
2a) If serum ACTH high
=> pituitary MRI (pituitary adenoma)
=> biochemical tests e.g. CRT +/- HDDST (ectopic ACTH/ CRH)
2b) If serum ACTH low
=> exogenous steroids??
=> Adrenal glands CT

41
Q

Cushing’s syndrome management

A

Aetiology based
- Pituitary adenoma => hypophysectomy +/- radiotherapy
- Adrenal adenoma => adrenalectomy
- Ectopic => remove source +/- radiotherapy OR bilateral adrenalectomy
- If all other treatments fail => metyrapone (/Ketoconazole/Pasireotide)

42
Q

Explain the effect of prolonged high dose steroid therapy on the pituitary gland & adrenal gland.

A

Initially there is an excess of cortisol (iatrogenic Cushing’s)
This causes chronic suppression of pituitary ACTH secretion
This then leads to adrenal atrophy & suppression
If they then suddenly stop taking the steroids it could lead to an adrenal crisis

43
Q

Define primary hyperaldosteronism

A

Autonomous production of aldosterone independent of its regulators (angiotensin II/ plasma K+), causing elevated aldosterone & hypertension

44
Q

Describe the (cardiac) effects of excess aldosterone

A

Sodium retention in the kidneys
Excessive cardiac collagen formation, inflammation & fibrosis
Abnormal endothelial function & increased oxidative stress
Baroreceptors dysfunction & increased sympathetic outflow

=> Increased BP, LVH & atheroma formation (^ CV risk)

45
Q

Primary hyperaldosteronism aetiology

A
  • Adrenal adenoma (conn’s syndrome)
  • Bilateral adrenal hyperplasia (most common)
  • Genetic mutation (rare)
46
Q

Primary hyperaldosteronism clinical presentation

A

Significant hypertension
Hypokalaemia (~30% cases)
Alkalosis

47
Q

Primary hyperaldosteronism investigations

A

1) Plasma aldosterone: renin ratio
2) If ratio raised => saline suppression test
3) If limited suppression => Primary aldosteronism

4) Adrenal CT to demonstrate adenoma
5) If present => adrenal vein sampling
(to confirm adenoma is source of aldosterone excess)

48
Q

Primary hyperaldosteronism management

A

Adrenal adenoma
- Unilateral laparoscopic adrenalectomy
(Cures hypokalaemia & may cure hypertension)

Bilateral adrenal hyperplasia
- mineralocorticoid receptor antagonists (e.g. spironolactone)

49
Q

Adrenal adenomas can be benign (functioning/ non functioning) or malignant. If you identified an adrenal adenoma on CT, what would make you likely to surgically remove it?

A
  • If functional lesion ie. Produces cortisol (Cushing’s) or aldosterone (conn’s) OR
  • If large adenoma (thought to be at risk of malignancy)
50
Q

When giving fludrocortisone to a patient. What would you consider giving first?

A

IV fluids e.g. saline (to prevent sudden fluid overload)

51
Q

What happens to aldosterone, cortisol & dihydrotestosterone production in 21α hydroxylase deficiency (CAH)

A

Mineralocorticoid/ Aldosterone - none/low
Glucocorticoid/ cortisol - none/low
Adrenal androgens/ dihydrotestosterone - normal/high

52
Q

Secondary hyperaldosteronism definition

A

Increased adrenal production of aldosterone in response to nonpituitary, extra-adrenal stimuli such as renal hypo perfusion

53
Q

Secondary hyperaldosteronism aetiology & pathophysiology

A

Reduced blood flow due to:
- Obstructive renal artery disease (eg, atheroma, stenosis)
- Renal vasoconstriction (in accelerated hypertension)
- Oedematous disorders (e.g. HF, cirrhosis with ascites)
Leads to excess renin & hence angiotensin II

54
Q

Secondary hyperaldosteronism clinical presentation

A

Hypertension

55
Q

Secondary hyperaldosteronism investigations

A
  • Renin/aldosterone ratio: high aldosterone AND high renin
  • Imaging: doppler US or CT angiogram to look for for renal artery stenosis/ obstruction
56
Q

Secondary hyperaldosteronism management

A

Treat cause!
Mineralocorticoid receptor antagonists (Spironolactone)

57
Q

Adrenal cortex tumours are likely benign adenomas. What would make you suspect adrenocortical carcinoma (a very rare malignancy)

A
  • Medical history of Li-fraumeni syndrome
  • Functional, virilising tumour
  • Haemorrhage, necrosis, atypical mitoses & invasion
58
Q

A patient presents with an adrenal cortex tumour and fever, what is a differential diagnosis

A

Adrenocortical carcinoma with necrosis
(necrosis causes fever)

59
Q

What is a phaeochromocytoma

A

Catecholamine-secreting tumour
Typically derived from chromaffin cells of adrenal medulla

60
Q

Phaeochromocytoma vs paraganglioma

A

Phaeochromocytoma - adrenal medulla
Paraganglioma - extra-adrenal, sympathetic chain

61
Q

What would make you suspect a familial condition associated with a phaeochromocytoma/paraganglioma

A
  • Younger patient
  • Paraganglioma or BILATERAL phaeochromocytoma
62
Q

Phaeochromocytoma/paraganglioma clinical presentation

A
  • Insidious onset
  • Classical triad -hypertension, headache, hyperhidrosis (3H’s)
  • Other symptoms - postural hypotension, tachycardia, pyrexia, SOB, palpitations, anxiety, weight loss, constipation (excess catecholamines effect)
63
Q

Why is phaeochromocytoma known as the ‘10% tumour’?

A

10% extra-adrenal (more commonly familial)
10% bilateral (more commonly familial)
10% malignant
10% not classic triad (hypertension, headache, sweating)
>10% familial

64
Q

Complications of a phaeochromocytoma/paraganglioma

A

LV heart failure (due to overstimulation of cardiac muscle)
Myocardial necrosis (due to cardiac muscle injury)
Stroke (due to hypertension & arrhythmias)
Shock (due to cardiomyopathy => Cardiogenic shock)
Paralytic ileus of bowel (due to sympathetic overstimulation)

65
Q

What biochemical changes can be expected in phaeochromocytoma/paraganglioma

A

Hyperglycaemia (sympathetic overstimulation)
Hypokalaemia (due to K cell influx, more likely with vomiting), Hypercalcaemia
High Hb concentration (erythrocytosis)
Lactic acidosis - in absence of shock

66
Q

What would make you suspect and investigate for a phaeochromocytoma/paraganglioma

A

Resistant hypertension
Young person with hypertension
Classic triad of symptoms (3H’s)
Family history
Adrenal incidentalomas

67
Q

Phaeochromocytoma/paraganglioma investigations

A

CONFIRM CATECHOLAMINE EXCESS
- 2 x 24 hr urinary metanephrines (sensitive)
- Plasma metanephrites, ideally at time of symptoms (specific)

CONFIRM TUMOUR
- MRI abdomen or whole body (neck for paraganglioma)
- MIBG scan
- PET scan

68
Q

Phaeochromocytoma/paraganglioma treatment

A

PRE-OP (a before b)
- Full ⍺-blockade (phenoxybenzamine/ doxazosin)
- Then once stable, full β-blockade (propranolol/atenolol etc)
- Fluid &/ blood replacement
- High salt diet

DEFINITIVE
- laparoscopic excision (or de-bulking if not possible)
- chemo/ radio-labelled MIBG if malignant

POST-OP
- Genetic testing & long-term follow up/monitoring

69
Q

Genetic conditions associated with phaeochromocytoma/paraganglioma

A

•Multiple Endocrine Neoplasia 2 (MEN2A/MEN2B)
•Von-Hippel-Lindau syndrome
•Succinate dehydrogenase mutations
•Neurofibromatosis
•Tuberose sclerosis

Endocrine (22 decks)

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