GoConqr has a new look! Let us know what you think.

Sign up free

Flashcards

Adrenal Glands

Rahul sharma Endocrine English 25 cards

Cards in this deck (25)

  1. 1Pathophysiology of Acute hypoadrenalism?Adrenal cortex produces 3 steroid hormones. (GFR mnemonic)
    Zona Glomerulosa: Aldosterone: RAAS
    Zona Fasciculata: cortisol: CRH-ACTH
    Zona reticularis: Androgens
    Renin: proteolytic enzyme (Juxtaglomerular apparatus: Renal artery hypotension
    Sympathetic stimulation, Reduced sodium levels in the distal tubal.
    Angiotensin II, Aldosterone: release in response to Angiotensin II, ACTH, K levels.
    The most common cause of adrenal insufficiency is TB (worldwide), Autoimmune (west), others: In Waterhouse-Friderichsen syndrome adrenal haemorrhage occurs secondary to meningococcal septicaemia.
  2. 2Emergency diagnosis of acute hypoadrenalism.Patient may present in Shock:
    Raised pulse, comatose, Postural hypotension, Oliguria, weak, confused. someone on long term steroids who has forgotten their tablets, Known Addison's patient with precipitating factors: infection, trauma, surgery, missed medication. An alternative presentation is with hypoglycaemia.
    If suspected, treat before biochemical results.
  3. 3Emergency management of acute hypoadrenalism.Bloods for cortisol and ACTH ( straight to lab, call ahead), U&Es- High K (check ECG, calcium gluconate if needed), and low Na.
    --Hydrocortisone 100mg IV stat.
    IV fluids bolus, crystalloid or colloid (BP)
    Monitor blod glucose: Hypoglycaemia
    Blood, urine, sputum for culture, then antibiotics if infection concern.
    Glucose IV if hypoglycaemic
    Change to oral steroids after 72 hours if patient's condition is good.
  4. 4Major causes of hypoadrenalism.--Autoimmune (80%) UK
    --TB ( commonest cause worldwide)
    --Adrenal metastases (e.g. from lung, breast and renal cancer)
    --Lymphoma
    --Opportunistic infections in HIV ( CMV, mycobacterium avium)
    --Adrenal Haemorrhage ( waterhouse- Friderichsen syndrome; antiphospholipid syndrome; SLE)
    --Congenital
  5. 5Describe how would you perform short Synacthen test?Do plasma cortisol before and 1/2 h after tetracosactide (Synacthen) 250 microgram IM. Addison's is excluded if 30 min cortisol > 550nmol/L.
    Steroid drugs may interfere with assay (omitted the evening before test).
    Pregnancy and contraceptive pill: cortisol levels may be falsely increase, due to increase cortisol binding globulin (stop 6 weeks prior to test).
  6. 6Describe how would you perform long synacthen test?This is performed for the differentiation of Primary from secondary adrenal failure. The prolonged stimulation of the adrenals by ACTH in this test results in a degree of recovery by adrenal glands which have become atrophic due to pituitary failure; whereas, adrenal glands that are themselves diseased will not respond.
  7. 7Describe how would you perform long synacthen test? and how to interpret these results?--take baseline blood serum cortisol@9 am.
    --IM 1 mg tetracosactide ( synacthen depot).
    --Blood plasma cortisol @1,2,4,8 and 24h.
    Normal: gradual rise with a peak cortisol at 4 to 8 hours.
    Primary adrenal failure: failure to respond or response is not sustained.
    Secondary adrenal failure: A response that rises gradually to a peak at 24 hours ( or prolonged corticosteroid therapy).
  8. 8Explain the process of steroid replacement in the management of Addison's disease to a patient.Corticosteroid treatment replacement for life (hydrocortisone). Avoid giving late (may cause insomnia). Aldosterone is replaced with fludrocortisone. Add extra salt to your diet. Take regular medications (adrenal crisis); Steroid card; wearing bracelet declaring steroid use; prescribing doctor must know of steroid use; adjust medications (increase) before strenuous exercise, an illness or infection, an operation or dental or medical procedure, an accident. give out syringes and IM hydrocortisone if vomiting prevents oral intake. Seek medical help.
  9. 9Describe pathophysiology of Addison's disease.Disease results from decreased production of adrenocortical hormones (aldosterone, cortisol, and dehydroepiandrosterone) as a result of either destruction of the 3 layers of the adrenal cortex (the glomerulosa, fasciculata, and reticularis) or disruption of hormone synthesis. Infiltrating diseases such as tuberculosis or metastasis can also cause destruction of the adrenal medulla.
  10. 10What is Addison's disease?Primary disorder-low circulating adrenal steroids
    High ACTH
    Skin pigmentation (melanocortin receptors
    Hypotension ( loss of aldosterone)
    Weight loss
  11. 11Signs and symptoms of Addison's disease?Weakness, fatigue, and orthostatic hypotension are early symptoms and signs of Addison's disease.
    Weight loss, pigmentation, Anorexia, Nausea, abdominal pain.
    Uncommon: Vitiligo, salt craving, hypoglycaemia, aches and pains.
    Mood: depression, psychosis, low self-esteem
  12. 12Investigations of Addison's disease.Electrolytes
    Serum cortisol
    Serum ACTH
    Sometimes ACTH stimulation testing
    AXR
    CXR
  13. 13What is primary hyperaldosteronism?Primary hyperaldosteronism refers to excess aldosterone production by the adrenal cortex, independent of RAAS, causing increase sodium and water retention, and decrease renin release.
    --either by an aldosterone producing adrenal cortical adenoma. This is Conn's syndrome (2/3 of cases).
    --or bilateral adrenal cortical hyperplasia.
  14. 14What is secondary hyperaldosteronism?Due to high renin from decrease renal perfusion, e.g. in renal artery stenosis, Renin secreting tumour, accelerated HT, diuretics, CCF or hepatic failure.
  15. 15Symptoms and signs of hyperaldosteronism.Often asymptomatic or signs of hypokalaemia (muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, light headedness), polyuria, polydipsia, raised BP but not always.
    Hypertension, hypokalaemia or alkalosis in someone not on diuretics. Na tend to be mildly raised or normal.
  16. 16Describe investigations of hyperaldosteronism.U&E, renin and aldosterone (ideally not on diuretics, hypotensive, steroids, K or laxatives for 4 weeks).
  17. 17Describe HPA (hypothalamic-pituitary- adrenal) axisHypothalamus secretes corticotrophin releasing hormone (CRH)---stimulates anterior pituitary to secrete adrenocorticotrophic hormone (ACTH)---ACTH acts on adrenal glands to stimulate release of cortisol. Cortisol has negative feedback effect: it suppresses the secretion of CRH and ACTH respectively.
  18. 18Describe symptoms and signs of Cushing's syndrome.Persistent excess circulating glucocorticoids.
    Weight gain, proximal myopathy
    -truncal obesity, moon face, buffalo hump,
    -menstrual irregularities, Hirsutism in women and loss of libido in men, secondary hypertension, bruising, DM and osteoporosis.
  19. 19Causes of Cushing's syndrome.1. Exogenous administration of steroids
    2.Puitary adenoma secreting ACTH
    3. Adrenal cortical adenoma
    4. Paraneoplastic syndrome
  20. 20How exogenous administration of steroids causes the Cushing's syndrome?Exogenous administration of steroids to treat other diseases-- the adrenal cortices undergo atrophy because of negative feedback of exogenous glucocorticoids on the HPA axis: the production of CRH and ACTH is suppressed and so the adrenal cortices undergo atrophy.
  21. 21Pituitary adenoma or cushing's diseaseThe second most common cause is a pituitary adenoma secreting ACTH. Cushing's syndrome due to an ACTH secreting pituitary adenoma is called cushing's disease. The adrenal cortices undergo hyperplasia in response to the effect of the circulating ACTH.
  22. 22Adrenal cortical adenomaAn adrenal cortical adenoma which secrets cortisol may also cause cushing's syndrome. The tumour arises from a cell in the zona fasciculata.
  23. 23Investigations of Cushing's syndrome.Random plasma cortisol may mislead, as illness, time of day, and stress influences results.
  24. 24Explain to a patient why they must not stop glucocorticoid therapy suddenly.Do not stop taking oral steroids suddenly if you have been taking them for more than three weeks. Your body normally makes steroid chemicals by itself which are necessary to be healthy. When you take oral steroids for a few weeks or more, your body may reduce or stop making its own steroid chemicals. If you then stop taking oral steroids suddenly, your body does not have any steroids. This can cause various withdrawal symptoms until your body resumes making natural steroids over a few weeks. The withdrawal symptoms can be serious, even life-threatening and include: Weakness, Tiredness, Feeling sick (nausea), Being sick (vomiting), Diarrhoea.
    Tummy (abdominal pain), Low blood sugar (hypoglycaemia), Low blood pressure (hypotension) which can cause dizziness, fainting or collapse.
  25. 25Side effects of long term glucocorticoid therapy and explain how these can be minimised.http://patient.info/health/oral-steroids

Information

Description
Endocrine Flashcards on Adrenal Glands, created by Rahul sharma on 02/10/2016.
Created by
Rahul sharma · Oct 2016
Updated
Nov 7, 2016
Views
0
Rating

More on Adrenal Gland Disorders

Feedback

What is it about?

What do you think of the new look?

How do you like it?