Endocrine Pharmacology

*Glucocorticoids ONLY increase NEUTROPHIL count by causing demargination, all other WBC count goes down.

*Cortisol precursors are increased because lack of the 21 alpha hydroxylase, halts Normal synthesis of cortisol<Decrease in Cortisol levels>ACTH secretion stimulation>Adrenal Hyperplasia(Including fasicularis and reticulars, with no hyperplasia of Glomerulosa),hyperplasia of reticularis>Excessive androgen>Virilization,hirsutism,Femal Pseudohermaphroditism.*So we want to Supress excess ACTH secretion and thus avoid effects associated withe excessive androgen production.+Obv glucorticoids would help with Hypotension too.*Weak glucocorticoid could also compensate for some mineralocorticoid deficiency(In 21a hydroxylase def, aldosterone is also decreased>Hyponatremia,Hyperkalemia), on the other hand we want strong enough glucocorticoid to supress ACTH.*Hydrocortisone is often used.

*Specific nucleotide sequence that is recognized by a steroid hormone receptor-hormone complex.*remember steroids bind to Intracellular receptors and moves into the nucleus and mediates effects by influencing gene transcription(needs more time to give effect, but effects also last longer)

*Because it is glucocorticoid with Low-protein binding>Can cross placenta.(Glucocorticoids can increase Synthesis of surfactant)

*Because we want good surface activity on mucous membranes and we want to avoid systemic effects Beclomethasone and budesonide readily penetrate the airway mucosa but have very short half-lives after they enter the blood, so that systemic effects and toxicity are greatly reduced.

*Dexamethasone, it also has longest lasting effect and 0 salt-retaining effect.

*Addison's disease is adrenal failure where Both Cortisol and Aldosterone are decreased>Hence effects described.*So we need combo like Cortisol(Primary glucocorticoid)+Fludrocortisone(Primary Mineralocorticoid, synthetic analog of aldosterone with very little glucocorticoid activity too).*FA wants you to know that Fludrocortisone can exacerbate Heart failure.+Underlying cause should be investigated/corrected TB/Autoimmune disease

*Competitive inhibitor of Glucorticoid and progesterone RECEPTORS.

*As it inhibits cortisol production but it doesn't inhibit production of cortisol precursors.

*remember Ketoconazole inhibits P450 needed for synthesis of all steroids(Ketzzung action)and we can use this when low steroid levels are desirable/(eg, adrenal carcinoma, hirsutism, breast and prostate cancer). *Aminoglutethimide is another steroid synthesis inhibitor but it blocks the conversion of cholesterol to pregnenolone and also inhibits synthesis of all hormonally active steroids. It can be used in conjunction with other drugs for treatment of steroid producing adrenocortical cancer.

D-cholecalciferol and ergocalciferol are commonly added to calcium supplements and dairy products.Calcitriol, the active 1,25-dihydroxyvitamin D3metabolite, would prevent vitamin D deficiency and is available as an oral formulation. However, because it is not subject to the complex mechanisms that regulate endogenous production of active vitamin D metabolites, it is not suitable for widespread use.

*It activates Calcium Sensing receptors in Parathyroid Gland(mimicks Calcium basically and tells gland that it can chill as calcium is enough, thus PTH secretion decreases).*Obv. this can give Hypocalcemia.*Note that cinacalcet is ALLOSTERIC activator of those receptors.

*In the case of DM2 and GESTATIONAL diabetes(Previously healthy women gets diabetes during pregnancy),First line is ALWAYS DIET MODIFICATION(then you try exercise modification) and only after that Drug therapy.*WEIGHT Loss is good up regulate insulin receptors.*First line DRUG for DM2 is METFORMIN(If not in answer choices pick other ORAL hypoglycemic and LASTLY INSULIN)*In DM1 you have lack of Insulin due to destruction of B-cells secreting them so you need HORMONE REPLACEMENT THERAPY with subcutaneous INSULIN, LOW -carb diet is just adjunct to prevent spikes of glucose levels.*In Gestational DM you begin with WEIGHT loss/Exercise but if it didn't work you go STRAIGHT to Insulin(No oral hypoglycemics)<INSULIN is answer for FIRST LINE PHARMACOtherapy in GDM.

*EXOgenous insulin, not insulinoma

*Because it tests if you know that insulin is anabolic hormoneand they might give case of type 1 diabetic that lost significant amount of weight in short amount of time and that she is HAPPY ABOUT IT, most likely cause would be DECREASED INSULIN DOSE(She was happy about weight loss so she likely reduced the dose on purpose)