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Flashcards

Adrenal

Liam Musselbrook Medicine English 21 cards

Cards in this deck (21)

  1. 1What is a pheochromocytoma (PCC)?- Catecholamine-secreting tumours
    - Arise from sympathetic paraganglial cells (chromaffin cells)
    - Usually found in the adrenal medulla, 10% are extra-adrenal, 10% are bilateral, 10% are familial (MEN 2a/b, neurofibromatosis, Von Hippel-Lindau)
  2. 2Discuss the presentation of a PCC- Severe/episodic HTN unresponsive to treatment
    - Often vague episodic symptoms which may be worsened by stress, exercise or drugs (B-blockers without alpha blockade)
    - Sweating, heat intolerance, pallor or flushing
    - Headaches, visual disturbances, seizures
    - Palpitations, chest tightness, dyspnoea, postural hypotension
    - Abdominal pain, nausea, constipation
  3. 3Outline the diagnosis of PCC- Three 24 hour collections for raised free metadrenaline & normetadrenaline
    - MRI/CT/functional imaging to locate tumour
  4. 4Outline the management of PCC- Alpha-blockade with pheoxybenzamine
    - B-blockers once alpha blockade established
    - Surgical excision
  5. 5What is Addison's disease?- Primary adrenal insufficiency
    - Destruction of entire adrenal cortex leading to cortisol, aldosterone and sex-steroid deficiencies
  6. 6How can you differentiate Addison's from hypothalamic-pituitary disease?- HPA generally spares aldosterone production
    - Sex steroids are also largely independent of pituitary stimulation
  7. 7Discuss the different aetiologies of Addison's- Autoimmune (80% in the UK)
    - TB: most common worldwide
    - Overwhelming sepsis
    - Metastatic cancer: lung/breast
    - Lymphoma
    - Adrenal haemorrhage (Waterhous-Friderichsen syndrome)
  8. 8What are the symptoms of Addison's disease?- Often vague and non-specific
    - Weight loss, malaise, weakness, myalgia
    - Syncope
    - Depression
  9. 9What are the signs of Addison's?- Pigmentation: especially of new scars and palmar creases
    - Postural hypotension
    - Signs of dehydration
    - Loss of body hair (esp. pubic/axillary)
  10. 10Outline investigations for suspected Addison's and what they will show- U&Es: LOW SODIUM, high potassium, uraemia
    - FBC: anaemia
    - Calcium: raised
    - Glucose: low (lack of cortisol)
    - Short ACTH stimulation/Synacthen test: >550nmol/L excludes Addison's
    - 9am ACTH/cortisol: raised ACTH, low/normal cortisol confirms Addison's
  11. 11What investigations would you do to establish the cause of Addison's?- 21-hydroxylase adrenal autoantibodies: autoimmune
    - CXR: TB
    - Adrenal CT: looking for TB/metastatic disease if antibodies are negative
  12. 12Outline the management of Addison's- Long-term glucocorticoid cover: 15-25mg hydrocortisone daily in 3 doses, give early in day
    - Long-term mineralcorticoid cover is postural hypotension, low Na or high K: fludrocortisone 50-200 micrograms daily
    - Extra steroid doses for strenuous exercise, surgery, febrile illness or trauma
    - Carry 'steroid card' and IM hydrocortisone in case of Addisonian crisis
  13. 13What is an 'Addisonian crisis' and how is it managed?- Severely inadequate levels of cortisol
    - Occurs either as 1st presentation of adrenal disease or triggered by physiological stress
    - Fever, N&V, shock, hypoglycaemia, hyponatraemia and hyperkalaemia
    - Treat with IV fluids and hydrocortisone
  14. 14What is congenital adrenal hyperplasia?- Congenital deficiency in 21-α-hydroxylase (necessary for production of gluco- and mineralcorticoids, but not sex hormones)
    - Aldosterone and cortisol decreased with ACTH increased
    - Testosterone levels are raised
  15. 15Describe the clinical features of congenital adrenal hyperplasia- Virilisation of the external genitalia in females: clitoral hypertrophy and variable fusion of the labia
    - Enlarged penis and pigmented scrotum in males but rarely picked up this way
    - Presents with salt-losing crisis in 80% of males at 1-3 weeks of age
    - In non-salt losing males presents as hypervirilisation: early pubarche, adult body odor, muscular build
  16. 16Outline investigation and management of congenital adrenal hyperplasia- 17-α-hydroxyprogesterone levels: v raised
    - Other features: low sodium, high potassium and metabolic acidosis in salt losers
    - Mx: steroid cover (as per Addison's)
  17. 17What is Conn's syndrome?- Most common in young females
    - Adrenal adenoma causing primary hyperaldosteronism
    - HyperALD leads to sodium and water retention
  18. 18How does Conn's syndrome present?- Mostly asymptomatic
    - HTN: resistant to treatment, may cause headaches
    - Features of hypokalaemia: cramps, weakness tetany, may be polyuria
  19. 19What are the biochemical features of Conn's?- Hypokalaemia, with urinary K+ loss
    - Elevated plasma aldosterone:renin ratio
    - Plasma aldosterone not suppressed by fludrocortisone administration
  20. 20How is Conn's differentiated from adrenal hyperplasia as the cause of primary hyperALD?- Adrenal CT
    - Alternatively can do adrenal scintography
  21. 21Outline the management of Conn's syndrome- Laproscopic adrenalectomy
    - Spironolactone pre-op to control HTN/hypokalaemia

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Medicine (Endocrine) Flashcards on Adrenal, created by Liam Musselbrook on 05/11/2017.
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