Describe the effect of an anterior pituitary adenoma on regulation of the hypothalamic-pituitary (HP) axis (SIGS 7.1b).
producing tumors = effects of the overproduced hormone, smaller size (i.e. prolactinoma); non-producing tumors = mass effects, larger size
Describe the endocrine disorders seen in MEN-1, including clinical features and morphologic findings of affected organs (SIGS 7.1b).
3P's: Primary hyperparathyroidism (hypercalcemia, nephrolithiasis), Pituitary adenoma (varies), Pancreatic tumors (gastrinoma is most common; gastric ulcers)
Describe the actions of PTH in the regulation of calcium by the kidney. (SIGS 7.1a)
Low/intermittent levels: anabolic effects on osteoblasts and osteoclasts (indirect) to build bone; chronically high: catabolic effects;
Contrast alterations in blood and urine levels of calcium, phosphate, vitamin D, and alkaline phosphatase in hyper- and hypoparathyroidism. (SIGS 7.1a)
Hypo: Ca+ low, Vit. D. low, alk phos low, phosphate high, PTH low ;hyper: Ca+ high, Vit D high, alk phos high, phosphate low, PTH high
Relate the physiologic process of bone resorption to the management of osteoporosis with parathyroid hormone analogues (teriparatide). (SIGS 7.1a)
synthetic PTH; regulates calcium metabolism from bone to promote bone growth (other meds promote bone density by prohibiting bone resorption); intermittent use
Characterize the utility of imaging techniques in the evaluation of parathyroid disease (Sigs 7.1a).
US: quick/easy/cheap to check size; Nuclear med: Tc-99m test of choice to characterize hot/cold lesion based on metabolic activity; DEXA: bone density
Evaluate lifestyle and integrative approaches to bone health, including vitamins, minerals, specific medicinal foods (fish; soy; tea), weight-bearing exercise, and mind-body techniques.
See image
Describe the pathophysiology of type 1 diabetes mellitus (T1DM) and diabetic ketoacidosis (DKA). (SIGS 7.2a)
antibodies to beta-islet cells-> decr. insulin production-> low glucose in cells-> use of glycogen/FA-> ketone bodies->buildup-> acidic->DKA
Identify the associated clinical features in patients with T1DM and DKA. (SIGS 7.2a)
polyuria, polydipsia, polyphagia, weight loss, DKA (delirium, Kussmaul respirations, abdominal pain/nausea/vomiting, dehydration, fruity breath)
Rationalize serologic and genetic testing done at the time of new-onset T1DM. (SIGS 7.2a)
Screen for HLA subtypes; Serologic testing for presence of auto-antibody types
Explain the pathogenesis of T1DM with emphasis on the genetic and environmental causes. (SIGS 7.2a)
See image: HLA or insulin gene mutations; Environmental triggers: diet, viruses, drugs/toxins, stresses
Classify the ACTH-dependent and ACTH-independent endogenous causes of Cushing syndrome. (SIGs 7.2b)
Dependent: high ACTH, high cortisol (Cushing Disease)- pituitary adenoma ; Indep: low ACTH, high cortisol (Cushing's syndrome)- adrenal adenoma/corticosteroids)
Rationalize the use of 24-hour urine free cortisol (UFC), late-night salivary cortisol and the low-dose overnight dexamethasone suppression test (DST) in the screening for Cushing syndrome. (SIGs 7.2b)
24 hour: cortisol over time (most accurate); late-night: cortisol usually lowest then; Low dose dexameth.: should suppress cortisol (high= cushing)
Contrast the indications for and efficacy of surgery and pharmacologic androgen inhibitors in the treatment of Cushing syndrome. (SIGS 7.2b)
Surgery always recommended to remove hormone producing tumor to decr excess hormone production; pharm if surgery is contraindicated (ketoconazole; metyrapone)
Contrast primary and secondary hypogonadism and correlate them to low testosterone. (SIGS 7.3b)
Primary: issue w/ gonads-> decr. testosterone production; Secondary: issue w/ ant. pituitary-> decr. LH & FSH production
