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Adrenal insufficiency
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Adrenal insufficiency

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adrenal insufficiency

adrenal insufficiency

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  • 1.  Medulla secretes epinephrine and norepinephrine into adrenal veins when stimulated Cortex secretes steroids regulating metabolism, vascular tone, cardiac contractility, TBW/Na/K balance, androgenic function
  • 2.  Cyclic secretion controlled by time of day, HPA axis, renin-angiotensin system, serum potassium levels Stress increases basal glucocorticoid and mineralocorticoid levels 5-10 fold › Occurs within minutes
  • 3.  Basal failure results in adrenal insufficiency › Leads to insidious wasting disease Stress failure results in adrenal crisis Life-threatening Absence of glucocorticoids is most critical
  • 4.  Three classes: › Glucocorticoids › Mineralocorticoids › Androgenic steroids
  • 5.  Regulate fat, glucose, protein metabolism Cathecholamine and β-adrenergic receptor synthesis Maintain vascular tone and cardiac contractility Control endothelial integrity/vascular permeability
  • 6.  Cortisol › Controlled by HPA axis › Hypothalamus  CRH and arginine vasopressin in circadian rhythm (max: 2 -4am) › Anterior Pituitary  ACTH › Adrenal cortex  cortisol › Peak @ 8am; declines throughout day
  • 7.  Cortisol › 25mg produced daily (non-stressed) › 5-10% free and physiologically active › The rest: bound to cortisol-binding globulin  Becomes uncoupled in times of stress › Negatively feeds back to control hypothalamus  Role in adrenal insufficiency
  • 8.  Regulated via renin-angiotensin system & serum potassium levels › Diminished GFR  juxtaglomerular apparatus release of prorenin › Aldosterone release  Na & H2O resorption at distal tubules (K is lost) › Minor hyperkalemia can stimulate aldosterone secretion directly
  • 9.  Controlled by ACTH Diurnal pattern (like cortisol) Significant source of androgens in females › Can cause signs/symptoms seen in adrenal insufficiency
  • 10. 1. Primary = failure of adrenal glands2. Secondary = failure of HPA axis › Usually due to chronic exogenous glucocorticoid administration › pituitary failure1. Tertiary = Hypothalamic dysfunction
  • 11.  Loss of all three types of adrenal steroids 90% of glands must be destroyed to manifest clinically › High functional reserve Adrenoleukodystrophy = X-linked inherited d/o of very-long-chain fatty acid metabolism › Progressive neurological symptoms from demyelination
  • 12.  Addison disease = autoimmune d/o Thrombosis/hemorrhage › Sepsis, DIC, antiphospholipid syndrome Infiltrative diseases › Bilateral cancer metastasis › Amyloidosis, hemosiderosis (rare)
  • 13.  TB = infectious cause worldwide HIV = infectious cause 50% have degree of destruction › Only 5% have clinical symptoms of Adrenal Insufficiency › CMV infection, ketoconazole use, macrophage-released cytokines are risk factors
  • 14.  HPA axis failure › deficiency of glucocorticoids and adrenal androgens › mineralcorticoids are unaffected Most common cause=chronic exogenous glucocorticoid › suppresses diurnal CRH/AV release › both time- and dose-related › reversible  recovery may take up to a year
  • 15.  Less common causes › Postpartum necrosis (Sheehan syndrome) › Adenoma hemorrhage(s) › Pituitary destruction from head trauma › associated focal neurological changes, visual deficits, diabetes insipidus or panhypopituitarism
  • 16.  Short course (2-3 weeks) is unlikely to suppress the HPA axis Daily doses of prednisone 5mg or less are unlikely to cause secondary insufficiency
  • 17. CLINICAL PRESENTATION Nonspecific › Fatigue, anorexia, weight loss, loss of libido Neurological › Headaches, visual changes, diabetes insipidus Gastrointestinal › Pain, nausea, vomiting, diarrhea
  • 18. CLINICAL PRESENTATION Hypotension/Orthostasis Cachexia › Thin axillary and pubic hair in women Hypoglycemia Normocytic anemia, lymphocytosis, eosinophilia
  • 19. CLINICAL PRESENTATION Hyperpigmentation › Pressure points, axilla, palmar creases, perineum, oral mucosa › Usually seen early in primary AI Pallor out of proportion to anemia › Seen in secondary AI
  • 20. CLINICAL PRESENTATION Hyponatremia › Primary = lack of aldosterone & Na wasting › Secondary = vasopressin secretion & H2O loss Hyperkalemia › Only occurs in primary › mild with associated azotemia & metabolic acidosis
  • 21. CLINICAL PRESENTATION Life-threatening emergency May be primary or secondary HYPOTENSION › Typically resistant to catecholamine and IVF resuscitation
  • 22. CLINICAL PRESENTATION Abrupt adrenal failure usually from gland hemorrhage or thrombosis › Anticoagulation › DIC › Sepsis (Waterhouse-Friderichsen syndrome) › Usually have abdominal and flank pain › Can resemble ruptured AAA
  • 23. CLINICAL PRESENTATION Catastrophic HPA axis failure › Head trauma › Hemorrhage of pituitary adenoma › Post-partum herniation (Sheehan syndrome) › Usually neurological deficits, headaches, visual field cuts and diabetes insipidus
  • 24.  Short corticotropin stimulation test › Get baseline level › Inject 250mcg cosyntropin (IV or IM) › Measure plasma cortisol level in 30 minutes › Measure plasma cortisol level in 60 minutes › Excluded if basal or test level is > 525 nmol/L Plasma cortisol levels between 8am-9am › Level <83 nmol/L rules IN › Level >525 nmol/L rules OUT
  • 25.  Admit: stimulation test
  • 26.  Base the dose of suppressive therapy on the severity of the stressful event. Use glucocorticoids only (no mineralocorticoids) 100mg bolus of IV hydrocortisone followed by infusion of 200mg IV over next 24 hours Correct volume and sugar deficits with D5NS Dexamethasone is of no utility
  • 27.  Unexplained hyponatremia and hyperkalemia with hypotension unresponsive to catecholamine and fluid administratio  receive 100mg hydrocortisone intravenously