Pathophysiology 01 - Module 1 - Stress and Adaptation module 1-4

NURSING 2PF3 Module 1: Stress and Adaptation 3 o T-Helper 2 Shift: Depresses the activity of the T-helper 1 cells (thereby decreasing cell-mediated immunity) and promotes the activity of T-helper 2 cells (increasing humoral immunity)  Cardiovascular: o Enhances the effects of the catecholamines (Epi and NE) - Excessive cortisol (or excessive corticosteroid administration):  Cushing Disease  Excessive production of ACTH by the pituitary leading to excessive cortisol  Cushing syndrome  All other causes of excessive cortisol production (e.g. adrenal tumors, non-pituitary ACTH-secreting tumor)  Altered fat metabolism  Cushingoid signs  Subclavicular fat pad “buffalo hump” and round, plethoric “mood face”  Hyperglycemia (steroid diabetes),  Excessive sodium retention and potassium excretion (glucocorticoids have some mineralocorticoid properties)  Hypertension, edema, and hypokalemia  Poor wound healing and susceptibility for infections.  Protein breakdown  muscle wasting and weakness; thin, wrinkled skin, may cause destruction of bone proteins (osteoporosis)  Accompanying increase in androgen levels  hirsutism, acne, and menstrual irregularities (e.g. amenorrhea)  Emotional disturbances  Pendulous abdomen (hanging loosely); abdominal striae (stretch marks); ecchymosis (small hemorrhagic spot in the skin); purpura (purple coloured patches in skin)  Treatment: Correct the source of hypercortisolism - Insufficient cortisol: See Addison’s Disease (below) 3. Adrenal androgens/Gonadocorticoids Dehydroepiandrosterne [DHEA] and DHEA-sulphate - Primarily synthesized by the zona reticularis and the zona fasciculate - Circulate mostly bound to albumin - Main effects:  DHEA and DHEA-sulphate are converted to testosterone and estrogens  Weak androgens  Too much DHEA (in females) can lead to an increase in virilisation (development of male characteristics) or hirsutism (excessive harriness). Often this is seen in PCOS (poly-cystic ovarian syndrome) - Congenital adrenal hyperplasia (CAH) (adrenogenital syndrome)  Caused by an autosomal recessive trait in which a deficiency exists in any of the enzymes necessary for the synthesis of cortisol  cortis