Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Adrenal cortical disorderspptx


  • Be the first to comment

  • Be the first to like this

Adrenal cortical disorderspptx

  1. 1. Adrenal Cortical Disorders
  2. 2. Learning outcomes Describe the clinico-pathological affects of adrenal cortical hyperfunction Describe the clinico-pathological affects of adrenal cortical hypofunction
  3. 3. Adrenocortical Hyperfunction/ Hyperadrenalism Cushing syndrome; ACTH-independent Conn syndrome; Hyperaldosteronism Adrenogenital syndrome; Excessive androgens
  4. 4. Cushing Syndrome Disorder caused by high levels of glucocorticoids either of exogenous or endogenous origin
  5. 5. Adrenals in Cushing Syndrome Exogenous: bilateral cortical atrophy due to suppression of endogenous ACTH Endogenous: adrenal cortical hyperplasia, which may be; Diffuse Type; (in 70%of cases) Cortex diffusely thickened and yellow due to increase in the size and number of lipid-rich cells in zonae fasciculata and reticularis Nodular Type; Bilateral glands may weigh from 30- 50 gm and shows 0.5 to 2.0cm, yellow nodules scattered throughout hyperplastic cortex
  6. 6. Hyperaldosteronism Primary or Secondary hyperaldosteronism: Primary Hyperaldosteronism: autonomous overproduction of aldosterone, with resultant suppression of renin-angiotensin system and decreased plasma renin activity, causes includes; Aldosterone-producing unilateral adrenal adenoma (Conn syndrome) (80%) in less than 1%, surgically curable form of hypertension Primary adrenocortical nodular hyperplasia (15%) in children/young adults, best managed with medicine
  7. 7. Hyperaldosteronism Secondary hyperaldosteronism Aldosterone release as a consequence of any high renin state as in: Renal ischemia due to decreased renal perfusion; e.g arteriolar nephrosclerosis, renal artery stenosis Arterial hypovolemia and edema; e.g congestive heart failure, cirrhosis, nephrotic syndrome Pregnancy; caused by estrogen-induced increases in plasma renin substrate
  8. 8. Adrenocortical Insufficiency Primary adrenocortical insufficiency - Acute insufficiency (Adrenal crisis) - Chronic insufficiency (Addison disease) Secondary adrenocortical insufficiency - Due to decreased stimulation of the adrenals resulting from a deficiency of ACTH release from the pituitary gland
  9. 9. Primary Adrenocortical Insufficiency Acute Adrenocortical Insufficiency, occurs in; - Massive adrenal hemorrhage - Sudden with drawls of long term corticosteroid therapy - Stress in patient with underlying chronic adrenal insufficiency Chronic Adrenocortical Insufficiency, causes Includes: - Autoimmune adrenalitis - Tuberculous adrenalitis - Infarction - Acquired immune deficiency syndrome (AIDS) - Metastatic cancers
  10. 10. Primary Acute Adrenocortical Insufficiency Massive adrenal hemorrhage: It destroys adrenal cortex, can be seen in; - Patients maintained on anticoagulants - Postoperative patients who develop DIC - Pregnancy Waterhouse-Friderichsen syndrome Classically associated with Neisseria meningitidis septicemia, can be caused by pseudomonas , pneumococci and haemophilus influenza infection, probably due to endotoxin- induced vascular injury with associated DIC
  11. 11. Primary Acute Adrenocortical Insufficiency Sudden with drawal of long term corticosteroid therapy or failure to increase its dosage in response to an acute stress; May precipitate adrenal crisis, because of inability of the atrophic adrenals to produce glucocorticoids Stress in patient with chronic adrenal Insufficiency; Such as infections, trauma, or surgical procedures may precipitate an acute adrenal crisis, manifested by intractable vomiting, abdominal pain, hypotension, coma, and vascular collapse Death follows rapidly unless corticosteroids are replaced immediately
  12. 12. Primary Chronic Adrenocortical Insufficiency Autoimmune Adrenalitis (Addison disease) 60-70% Autoimmune destruction of steroid producing cells, caused by mutations in autoimmune Regulator gene(AIRE) Autoimmune Polyendocrinopathy Syndrome (APS) Coexist, Hashimoto thyroiditis, pernicious anemia, type I DM, and idiopathic hypoparathyroidism Shrunken adrenals cortex Shows scattered residual cortical cells in a collapsed network of connective tissue infiltrated by lymphocytes
  13. 13. Secondary Adrenocortical Insufficiency Secondary to disorder of hypothalamus or pituitary; Metastatic cancer, infection, infarction or radiations that, reduces the output of ACTH, this leads to hypoadrenalism without hyperpigmentation because melanotropic hormone levels are low Gross; adrenals reduced to a thin rim of uniform atrophic flat, yellow cortex which surrounds an intact medulla Microscopy; atrophy of cortical cells with loss of cytoplasmic lipid, in the zonae fasciculata and reticularis
  14. 14. Pathogenesis of Hypoadrenalism Clinical manifestation occurs when at least 90% of the adrenal cortex is destroyed Primary hypoadrenalism; due to primary adrenal disease; - increased levels of ACTH precursor hormone stimulate melanocytes, results in hyperpigmentation of skin and mucosal surfaces (not in secondary adrenocortical insufficiency) - decreased aldosterone activity, results in potassium retention and sodium loss, with resultant hyperkalemia, hyponatremia, volume depletion, and hypotension Secondary hypoadrenalism; deficient cortisol and androgen output but normal or near-normal aldosterone synthesis, occasionally hypoglycemia as a result of glucocorticoid deficiency and impaired gluconeogenesis
  15. 15. References Robbins Basic Pathology 10th edition by Kumar Abbas Aster