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Examen

NSG 3600 Med Surg III: NSG 3600 Exam 2 Unit 3: (Complex Metabolic Problems Adrenal/DI/SIADH/Thyroid tumors)Updated Solution

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Subido en
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Escrito en
2025/2026

• Pituitary o Located on the inferior aspect of the brain and is divided into anterior and posterior lobes. The gland is controlled by the hypothalamus, which is an adjacent area of the brain o Gland that secretes hormones that influence growth, metabolism and regeneration o Releases ACTH which stimulates the adrenal to release cortisol o Pituitary signals releases ACTH (adrenocorticotropin hormone) signals adrenal glands to release Cortisol (-) fdbck system • Anterior Pituitary o Hypersecretion of anterior pituitary gland results in Cushing syndrome • Posterior Pituitary o ADH (anti diuretic hormone) and is also called arginine vasopressin it is a hormone made by the hypothalamus in the brain and is stored in the posterior pituitary gland it tells your kidneys how much water to conserve.  ADH constantly regulates and balances the amount of water in your blood stream.  Oxytocin for pregnancy • The adrenal glands secrete compounds like cortisone, adrenaline • Gland o Secretes hormone into blood  Too much  slows down  Not enough  makes more  breakdown in (-) feedback system CONGENTIAL ADRENAL HYPERPLASIA • NORMAL: Pituitary releases ACTH ACTH signals adrenal glands to produce certain amts of cortisol • Present from birth where the enzyme is missing the pituitary is releasing ACTH adrenal glands are not getting the message and so less cortisol is being produced o the pituitary gland is not getting the message as well and so the keeps on producing that ACTH so there's a breakdown in a negative feedback system • Occurs when the enzyme needed for cortisol production is lacking because of a gene defect o Pituitary  ACTH  Adrenal glands  cortisol – normal o Pituitary  ACTH (Adrenal Glands don’t get message)  Leads to decreases in cortisol level = Increase in ACTH because the pituitary gland isn’t getting message, so the negative feedback loop is messed up o Present from birth and results in a low cortisol levels and high levels of male hormones  @ risk for Adrenal crisis bc they have very low levels of cortisol • Patho/etiology o Circulating cortisol levels are inadequate to provide negative feedback to the anterior pituitary gland  ACTH secretion is elevated o Usually follows an autosomal recessive inheritance pattern • Dx o In infancy (at birth) o Visualization of the genitalia  Masculinization – child has development of male characteristics • CM o Visualization of genitalia in infants o Females – more pronounced in females as they get older Facial hair much like a beard  Deeper voice  Baldness  Masculine distribution of pubic hair  Growth of the clitoris to resemble a penis  Deposition of proteins in the skin and muscles like that of males o Males  Same as female  Harder to diagnose due to expected for males  Dark scrotum • Tx o Medications: Corticosteroids (glucocorticoids)  Long-term steroid use: (education)  be aware of cardiovascular wise they are at risk for hypertension, thrombophlebitis, thromboembolism, and accelerated atherosclerosis  immunologic wise they are at high risk for infection  ophthalmic side effects include glaucoma and corneal lesions  Adrenal insufficiency /crisis – we're looking at low cortisol levels which is a key factor or a key manifestation of CAH • Extreme fatigue, N/V • Weight loss, Decreased appetite • Darkening of the skin • Low BP & blood sugar • Abdominal pain •  from stopping suddenly Adrenal Cortex (produces) • Cortisol o Helps control the body’s use of fats, proteins, and carbohydrates o Suppresses inflammation o Regulates blood pressure o Increases blood sugar o Can also decrease bone formation • Aldosterone o Tells kidneys to absorb more sodium into the bloodstream • Release potassium into the urine (regulates BP) • Androgen o Assist ovaries produce estrogen and testes produce testosterone HYPER/HYPO aldosterone is a refers to water balance (controls water) conserve body sodium

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Subido en
5 de junio de 2026
Número de páginas
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Escrito en
2025/2026
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