Endocrine Pathology

*PUBERTAL GYNECOMASTIA which is a NORMAL finding.<This is way more common then kleinfelter, but they will give you other clues like Normal size of Testes,Penis, Normal Hair development,Normal Testosterone,estrogen,FSH,LH.<Which will help you to rule of Kleinfelter.

While Bitemporal hemianopia is often tested(As pituitary adenoma can compress optich chiasm), MOST common symptom is HEADACHE and it can be tested too.*MOST common pituitary adenoma is PROLACTINOMA(Derived from LACTOTROPHS-ACIDOPHILS)
*Second most common is NON-functioning tumors that present with signs of PANHYPOpituitarism(can even cause STOMACH pain,fatigue,excessive thirst/urination,basically any sign caused by decreased hormone levels of ANY Hormone from pituitary) along with signs of mass-effect(bitemporal hemianopsia,headache).*Somatotroph ademona secreting GH is third most common.

*HYPERpigmentation(ACTH has melanocyte stimulating properties) with bitemproal hemianopsia after bilateral adrenalectomy is giveaway for NELSON syndrome which is condition caused by ENLARGEMENT of previously existing ACTH secreting tumor(Derived from basophils-adrenocorticotrophs),this process happens trough HyperTROPHY(Increase in MASS) y your pituitary secretes more ACTH because with adrenalectomy we removed negative feedback from cortisol.Treatment:TARGETED radiation therapy or Surgery.

*Increased GH>Increased cell growth of proliferation>Increased risk of cancer(especially COLORECTAL Cancer/Polyps).*Most common cause of death in patients with pituitary tumor secreting GH is Heart failure(due to hyperTROPHY), hypertrophy in response to GH is also what contributes to LARYNGEAL/TONGUE swelling(Contributing to DEEPER voice) and development of colorectal polyps/cancer.*Gigantism is when GH secreting hormone affects persons BEFORE epiphysela plates close(>MORE LINEAR GROWTH>GIGANT) vs ACROMEGALY happens when epiphyesal plates have already closed(So you mainly increase width of bones usually HANDS and feet get larger/thicker and facial features become more coarse, especially MANDIBLE is affected>Separation of teeth on lower jow)..*GH has pulsatile secretion and thus isn't really used for diagnosis instead we use IGF1 levels(mediates effects of GH and is stable) but they might also hint you on GH secreting tumor if GH serum levels did NOT decrease in response to oral glucose(Normally hyperglycemia>Decreased GH secretion).MRI showing mass could also help(remember BODYBUILDER can be getting GH/IGF1 from exogenous sources for gains)*Treatment should BEGIN with SURGERY(remove adenoma), but they often test the fact that Long-acting Somatostatin analog(OCTREOTIDE) can be used for treatment and you should also know that growth hormone RECEPTOR antagonist known as PEGVISOMANT.*Dopamine AGONISTS(like carbergoline) can be used too.

*He likely has dwarfism(laron syndrome) and thus his GH receptors can NOT be activated by GH, hence GH can't promote IGF1 from LIVER(HY)secretion to mediate its effects and so you get less feedback inhibition and so you get INCREASED serum GH with DECREASED IGF1.

*LOSS of function of G-protein coupled calcium receptors in parathyroid glands results in receptors that need to sense MORE calcium to suppress PTH secretion and thus those patients usually get Slight elevation of PTH that results in increased serum Calcium(HYPERcalcemia) by DECREASING calcium excretion(This also promotes reabsorbtion of magneseium>HYPERMagnesemia).In hyperparathyroidism URINE calcium usually increases because PTH increases overall load of calcium in the blood(i.e NET gain of calcium is so much that even though PTH decreases calcium excretion still the amount that was delivered to kidney and was filtered is greated than normal urine calcium levels) while here as elevation of PTH and calcium levels is mild, inhibitory effects of PTH on calcium excretion predominate>DECREASED urine calcium(+This is also contributed by Calcium sensing receptors in KIDNEY itself)

*DI causes NET loss of ONLY water(Just like FEVER does) leading to EUVOlemic HYPERnatremia(Volume is maintained by compensatory mechanisms controlling fluid depletion), POsm/Na increases because TBW decreases while TBNa stays the same, so as Na concentration increases in ECF which btw was contracted(You loose fluid in kidneys from ECF), water in ICF will move towards greater concentration of Na in ECF leading to contraction of ICF.*Because you don't really give a fuck so we give thiazide diuretics(+/-Amilorde) to promote volume loss(HYPERtonic loss of Na) so your body will increase reabsorption of Na/Water in PROXIMAL convoluted tubule, kinda same principle is utilized when we use NSAID-INDOMETHACIN as this guy will constrict afferent arteriole>Less perfusion>Your kidney will try to compensate by increased Proximal tubule reabsorbtion(Basically your kidney will try to hold on to every bit of water and Na and thus decrease the amount that is lost in urine).NOTE however that in CENTRAL DI preffered treatment is DESMOPRESSIN ACETATE(basically synthetic ADH) because here you just supplement what is missing and you are done.*Adequate hydration is CRUCIAL in both of those conditions.*ALSO Note if they ask about FIRST step in treatment of NEPHROGENIC DI look at stem if patient is on offending drug(Like LITHIUM for Bipolar disorder, first thing you should do is REMOVE the offending agent and substitute it with alternative)

*Eccentric hypertophy>DILATED cardiomyopathy.

Do water deprivation test, serum Na will decrease while urine osmolarity will increase in psychogenic polydypsia(Can be due to schyziphrenia) vs No real improvement with SIADH(Can be caused by CYCLOPHOSPHAMIDE,Head trauma,Small cell lung cancer)

*Target of destruction is CYTOCHROME P450 enzyme-21 hydroxylase.vsTB is most common cause of Addison disease in developing countries.

When first it was described as primary adrenal insufficiency, the most common cause was tuberculosis of the adrenal gland. Now the majority of patients have adrenal autoantibodies and are thought to have autoimmune Addison’s disease. Autoimmune adrenalitis may occur by itself (isolated autoimmune Addison’s disease) or it may occur with other autoimmune endocrine diseases. Two major patterns of autoimmune polyendocrine syndromes have been described. In addition to autoimmune adrenitis, patients with autoimmune polyendocrine syndrome type (APS1) have chronic mucocutaneous candidiasis and abnormalities of the skin, nails, and teeth (ectodermal dystrophy). APS1 is also known as APECED (autoimmune polyendocrinopathy, candidiasis, and Ectodermal dystrophy). In addition patients have other autoimmune disorders including autoimmune hypoparathyroidism, idiopathic hypogonadism, and pernicious anemia. APS1 result from mutations of the autoimmune regulator (AIRE) gene, the product of which is expressed primarily in the thymus.

Autoimmune polyendocrine syndromes type 2 (APS2) is not associated with candidiasis, ectodermal dysplasia, or autoimmune hypoparathyroidism.
Instead, autoimmune adrenalitis is present with autoimmune thyroiditis (Hashimoto’s thyroiditis) or type 1 diabetes mellitus.

*Because it ties with physiology(POMC breaks into MSH and ACTH , thus when we increase synthesis of ACTH from POMC we also increase MSH which stimulates melanin production), also HYPERpigmentation is ONLY characteristic for PRIMARY adrenal insufficiency(In secondary and tertiary ACTH levels are actually DOWN not up).*Very HY to know,they develop HYPERkalemic metabolic acidosis(Lack of aldosterone>Less H and K excreted)

*CORTISOL(choose this over aldosterone which is deficient in this case too but acute lack of cortisol is what leads to this life-threatening acute condition).CLASSIC case they love is MENINGOCOCCEMIA(Like N.meningitis infects college student who now presents with neck stiffness and Deep purple NON-blanchable rash)>HEMORRHAGE into adrenal glands>ACUTE primary adrenal insufficiency.(<No hyperpigmentation because it usually kills you before you have chance to increase synthesis of melanin enough)*STRESS can precipitate this condition in patients with PRIMARY CHRONIC adrenal insufficiency(Addison disease) because stress increases demand on cortisol.

*Whenever you have PRIMARY adrenal insufficiency, metyrapone test(11 B hydroxylase inhibitor that blocks turning of 11DeOxyCortisol into cortisol), ACTH will increase even more but 11 deoxycortisol levels still remain low(Because problem is in your adrenal gland cells)cortisol levels will decrease even more, contrast this with increased 11deoxycortisol+LOW ACTH levels,coupled with decreased cortsiol with metyrapone stimulation test in patient with secondary adrenal insufficiency.

*In addison disease you would expect to see that because CELLS of adrenal gland are killed and thus cells that secrete aldosterone are killed too(>Less H and K excretion)vsIn SECONDARY causes you don't see those abnormalities because zona glomerulosa does NOT need ACTH to produce aldosterone(It needs Angiotensin2), so even though your cortisol is low, your aldosterone is fine and you don't usually develop hyperkalemic metabolic acidosis.*Remember LOW ACTH levels is the problem in secondary(hence no hyperpigmentation)vs*Dead adrenal is problem in primary(>leading to compensatory increase in ACTH>HYPERpigmentation)