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Endocrine 2

Clinical Medicine: Endocrine 2: Pituitary, Calcium, Neuroendocrine

Most common etiology of anterior hypopituitarism mass lesion
HA, vomiting, opthalmoplegia (eye in down and out position), ptosis, mydriasis Pituitary Apoplexy: Acute intrapituitary hemorrhagic vascular events can cause substantial damage to the pituitary and surrounding sellar structures
T/F: Most patients have normal pituitary function with Empty Sella Syndrome True, were you even listening to my presentation?
Most common cause of hyper and hyposecretion of pituitary hormone syndromes in adults Pituitary adenomas, which recall, are benign
Most common presenting feature of adult hypopituitarism Hypogonadism
What blood tests would you do for anterior hypopituitarism? TSH, T4, ACTH
Along with low ACTH and cortisol levels, what differentiates anterior hypopituitarism from primary adrenal insufficiency? Normal potassium, lack of hyperpigmentation
Progressive loss of several or all pituitary hormones with a rapid onset post pituitary apoplexy Panhypopituitarism
Very low IGF-1 is indicative of Growth hormone deficiency.
What are some Tx for anterior hypopituitarism? Removal of pituitary tumors and replacement of hormones
4 endocrine active pituitary adenomas (tumors producing hormones) Prolactinoma, Somatotropinoma, Corticotropinoma, Thyrotropinoma
3 possibilities on secretions of hormones with pituitary adenomas? 1) Excess of 1 hormone 2) Deficiency of 1 hormone 3) Deficiency of all hormones
Preferred imaging study for pituitary? What can you use when that is CONTRA? MRI; CT (pacemaker/metallic implants around brain or eyes
What sight problem can a pituitary tumor cause? What does that impair? Bitemporal hemianopsia...compression of optic nerve medial fibers by tumor impairing peripheral vision on each side
What is diagnostic for Acromegaly? What might you think would be but isn't, and why? IGF-1; Might think GH would be as there is an abundance, but it is pulsated randomly and doesn't correlate with disease severity.
Indolent and often not clinically Dx for 10+ years with acral bony overgrowth; often have MEN 1 genetic abnormalities Acromegaly
Leading cause of death in acromegaly? Cardiovascular
Txs of acromegaly Pituitary microsurgery is TOC
Most common etiology of iatrogenic hypercortisolism Long term steroid use
Difference btwn Cushing's syndrome and Cushing's disease? Syndrome: Excess cortisol from pituitary, adrenal or other sources. Disease: excess pituitary secretion of ACTH
Sx of what? Thin skin, central obesity, moon facies, purple striae, HTN, DM, hyperpigmentation, buffalo hump, hirsutism Chronic cortisol excess
Hematopoietic features of hypercortisolism Leukocytosis, lymphopenia, eosinopenia
Will ACTH be high or low in ACTH independent Cushing's Syndrome? Low (usually from ectopic source or cancer and the high cortisol levels will negatively feedback to pituitary, therefore lowering ACTH)
What happens to 1) Normal 2) Cushing's Disease and 3) Ectopic ACTH Syndrome (ACTH independent Cushing's Syndrome) during a Dexamethasone Supression test? 1) Almost completely suppressed 2) Partially suppressed 3) No response to supression
What is the imaging technique of the most common functional pituitary adenoma? Common Sx include visual-field defects (especially in men), or HA. 90% of women also get microadenomas. MRI is preferred imaging for Prolactinomas.
TOC for prolactinomas Dopamine agonists (Bromocriptine, cabergoline)
T/F: all pituitary microadenomas are of clinical concern and require evaluation of hormonal status GOSH I hate these kind of T/F: FALSE, not all microadenomas are of clinical concern but they DO all require evaluation of hormonal status
Decreased vasopressin, increased dilute urine, hyperosmolality, increased thirst, elevated sodium if water loss Diabetes Insipidus
Increased vasopressin, abnormal concentration of urine, reduced osmolality, hyponatremic Inappropriate ADH
Marked excessive retention of sodium AND water stimulated by a large "effective" blood volume and low cardiac output. What diseases are these seen in? Osmotically inappropriate ADH; seen in CHF, cirrhosis, nephrosis
Hypernatremiuria, hyponatremia, hyperkalemia, increased ADH in response to decreased intravascular volume Primary adrenal insufficiency
Secondary deficiency not associated with thirst, yet polydipsia. Psychogenic DI
Decreased ADH resulting in abrupt onset of polyuria, polydipsia Central Diabetes Insipidus (CDI)
Most common cause of Central Diabetes Insipidus (CDI) 30-50% of CDI cases caused by an autoimmune destruction of ADH -secreting cells in hypothalamus; Idiopathic DI
T/F: DI will always respond to Desmopressin (vasopression challenge test). EC: how does it respond? False, Nephorgenic DI won't respond as it is a kidney disease...Central DI will respond. Responds by reducing thirst and polyuria.
4 effects Desmopressin has on the body in central DI 1) increase urine osmolarity 2) Decrease urine volume 3) Increased body wt (water retention) 4) Decrease plasma osmolarity (diluting plasma and concentrating urine)
Distinguishes primary vs secondary adrenal insufficiency Primary: adrenals not responding to massive amounts of ACTH produced by pituitary trying to stimulate cortisol and ACTH causes HYPERPIGMENTATION; Secondary: Normal RENIN-ANGIOTENSIN SYSTEM, Low ACTH
Most common cause of primary adrenal insufficiency? Other causes? Autoimmune adrenalitis; TB, bilateral adrenal hemorrhage due to anti-coags, HIV, bilateral metastatic infiltration
Sodium down, potassium up, elevated ACTH, eosinophilia, lymphocytosis, low aldosterone with non-specific Sx Chronic primary adrenal insufficiency
What is the difference between regular cortisol/hydrocortisone and florinef? Also treats hypotension with salt retention
What causes an adrenal crisis (acute adrenocortical insufficiency)? Sudden withdrawal from chronic adrenocortical hormone therapy (like for surgery), pituitary apoplexy, injury to both adrenals (trauma, hemorrhage, thrombosis, infx [mengiococcemia])
HA, confusion/coma, elevated temp, HypoTN, Hyperkalemia, hyponatremia, elevated BUN...Tx? Acute adrenocortical insufficiency: IV hydrocortisone
Catecholamine-secreting tumors with paroxymal Sx: tachycardia, diaphoresis, HA, HTN, Hyperglycemia, wt loss, palpitations, Dx by plasma fractionated free metanephrines, associated with MEN 2, Age of onset usually 30-50. Tx? Pheochromacytoma/ Paraganglioma; Tx: Surgery TOC
HTN and hypokalemia, HTN usually due to adrenal incidentaloma. Aldosterone/renin ratio > 67 (<24 excludes Dx). Imaging? Tx? Primary aldosteronism (hyperaldosteronism) as inappropriate high aldosterone secretion that doesn't not suppress in response to sodium. Imaging: Thin section CT of adrenals. Tx: laproscopic adrenalectomy or spirolactone if bilateral
What are the main functions of parathyroid hormone? acts on bones to induce calcium resorption, acts on kidney to enhance calcium resorption and synthesis of 1,25 Vit D; increase in serum ionized calcium and decrease in serum phosphorus
What happens to bone with hyperparathyroidism, continuous over time? Tx? increased osteoclast-mediated bone resorption and osteoporosis. PTH(1-34) is a monotherapy caused a highly significant reduction in fracture incidence.
Primary target organs for most active vitamin D? 1,25 (OH)2D; intestine and bone
What rises and falls with serum phosphorus? Plays a central role in regulation of systemic phosphate homeostasis, vitamin D metabolism, bone mineralization Fibroblast Growth Factor 23 (FGF-23)
Tumor marker in sporadic and hereditary cases of medullary thyroid carcionoma Calcitonin
Physiologically active form of calcium...50% of calcium in plasma free or ionized calcium
If there is a low albumin level, what do you need to check for? Why? Low albumin means low total calcium (but doesn't effect ionized calcium levels. You would want to measure the ionized calcium in this case to get a true calcium level
Responsible for most instances of hypercalcemia in malignancy. No elevated PTH levels. Usually indicative of squamous cell types as well as renal carcinomas (which have massive overproductions of hormone) Parathyroid-related protein PTHrP
At what serum calcium levels do heart arrhythmias occur? Which ones occur? >14 mg/dL; prolonged PR, shortened QT, heart block, asystole, bradyarrhythmias
T/F: It doesn't make a difference, how fast calcium rises..we look at the absolute value risen. False, abrupt rises can have stronger Sx at much more modest levels
80% single adenoma, elevation of PTH and serum calcium in absense of lithium and low urinary calcium excretion, alk phos increase, elevated 1,25 vit D and low 25 vit D. What is the management? PTH mediated hypercalcemia: hyperparathyroidism [HPT]. Management: surgical excision of abnormal parathyroid tissue definitive. In mild, ASx disease and older, some still prefer medical surveillance, but more evidence -> surgery
Which ASx hyperparathyroid patients should have surgery? (6) 1) Estimated GFR <60 2) -2.5 bone density 3) age under 50 4) if surveillance not desirable/possible 5) Calcium >1mg/dL above upper limit 6) Pregnancy
What does a Preoperative 99mTc sestamibi scans do? What else can be monitored during surgery? Predicts location of abnormal gland; Introperative sampling of PTH to confirm removal of suspected adenoma (will decrease to normal)
2 medical alternatives to surgery with primary hyperparathyroidism Bisphosphonates, Calcimimetics
Low urinary calcium excretion, only normal to mildly elevated PTH levels, with a rare genetic component Familial hypocalciuric hypercalcemia
Pathophys of Lithium induced hypercalcemia In treated pts, lithium can shift the PTH secretion curve to the right in response to hypercalcemia, and higher levels of calcium are required to lower PTH secretion, self-perpetuating the cycle
PTH levels reduced, lymphokines/cytokines promote resorption of bone through local destruction Direct Bone Marrow Invasion (leukemia, lymphoma, multiple myeloma
How do you Dx Vitamin D mediated hypercalcemia? First of all, ensure PTH level is low. Obviously they have to have hypercalcemia, but also increased levels of 25(OH)d [not 1,25(OH)2D]. 25D > 100mg/mL
1,25(OH)2D levels are elevated, as this specific type of tissue converts 25 -> 1,25 at an increased rate. EC: What diseases are included with this type of tissue? Granulomatous disease (sarcoidosis, tuberculosis, fungal infections)
2 causes of hypercalcemia related to high bone turnover 1) Hyperthyroidism 2) Immobilization
How do thiazide diuretics cause hypercalcemia? Reduction in urinary calcium excretion and they may "unmask" Dx of hyperparathyroidism
Excessive ingestion of calcium and absorbable antacids causing hypercalcemia Milk Alkali Syndrome
Hypocalcemia initiates development of secondary hyperparathyroidism which stimulates an increase in calcium. What severe disease can cause this hypercalcemia? Chronic renal failure.
The next few slides will be a simple review of hypercalcemia Get it.
Elevated/inappropriately normal PTH and normal 24 hour urine calcium excretion: Primary hyperparathyroidism
Elevated/inappropriately normal PTH and low urine calcium excretion: Familial hypocalciuric hypercalcemia
PTH low and no malignancy Check 1,25 Vit D, other supplements and drugs
PTH low and malignancy with elevated PTHrP, 1,25 Vit D Hypercalcemia of malignancy
PTH low and malignancy with low PTHrP, 1,25 Vit D local osteolytic hypercalcemia
First principle treatment of hypercalcemia normal hydration and loop diuretic
How can hypomagnesemia cause hypocalcemia Hypomagnesia can interfere w/ secretion and peripheral responses to PTH (low/undetectable levels). Low levels of PTH don't stimulate calcium.
What do you need to check in hypocalcemia in acute pancreatitis? Ionized calcium (low albumin levels in pancreatitis)
4 specific things that can cause hypocalcemia and have a HIGH PTH 1) Vit D deficiency 2) PTH resistance syndromes 3) Medications (bisphosphonates, phenytoin) 4) acute pancreatitis (PTH can be high, low, or normal)
T/F: Most transient hypocalcemia will not have a reduction in ionized calcium True
Sx: Tetany including: hypoparathyroidism, acute hyperventilation, hypomagnesemia Any cause of low ionized calcium.
Twitching of circumoral muscles in response to gentle tapping of facial nerve just anterior to ear Chvostek's sign
Carpal spasm may be induced by inflation of blood pressure cuff to 20 mmHg above pt systolic blood pressure for 3 min Trousseau's sign
Tx for hypoparathyroidism replacement of Vit D or 1,25(OH)2D3 and calcium (can be parental)
Most abundant cells in bone, function as mechanoreceptors detecting strain on bone and signalling changes for remodeling, born from osteoblasts Osteocytes
Multinuclated giant cells specialized for resorption of bone. Requires RANKL for activation. Osteoclasts
Cytokine responsible for communication between osteoblasts and osteoclasts RANK ligand or RANKL
Decoy receptor that binds to RANKL preventing interaction w/ RANK and halting osteoclast differentiation Osteoprotegerin (OPG)
7 things that contribute to Osteoporosis 1) Cig consumption (directly toxic to osteoblasts) 2) Calcium nutrition 3) Vit D deficiency 4) lack of physical activity 5) Estrogen deficiency 6) Medications (glucocorticoids etc) 7) Chronic diseases
3 Steps to evaluating Osteoporosis 1) Bone density measurement 2) Risk analysis using FRAX 3) Exclude secondary causes
Biggest risk for osteoporosis? Previous fragility fracture after 40
Variables on FRAX (13). He did emphasize we needed to know these. Age, gender, height, weight, previous fracture, parent fractured hip, current smoker, glucocorticoids, RA, secondary osteoporosis, 3+ alcoholic drinks a day, femoral neck BMD, T score
What test should you use when assessing for moderate risk (10-20%) of osteoporosis? XRAY looking for compression fracture on spine
T/F: Vitamin D supplementation prevents and treats osteoporosis but not osteomalacia False, treats osteomalacia, but not osteoporosis
slows remodeling cycle, enhances mineralization of bone matrix Anti-resorptive agents
Stimulates bone remodeling by increasing bone formation through the osteoblast Anabolic agent
T/F: Estrogens are no long used for osteoporosis or CVD prevention True, simply used as a symptomatic drug for menopause
What drug would you use for osteoporosis if there is a strong history of breast Ca in the family? Raloxifene
First line therapy for Tx of post-menopausal osteoporosis? How do they work? Do you use it for the rest of pts life? Bisphosphonates; inhibit attachment of osteoclast to bone matrix and enhance programmed cell death; discontinue w/in 5 years to prevent bone loss
Weird side effect of bisphosphonates (yes I realize this question is in the eye of the beholder) Atypical femur fractures
Nasal spray that increases bone density, reduces vertebral fractures... Calcitonin
PTH analog requiring adequate vitamin and calcium intake and dramatically increases bone density except in the distal radius (anabolic) (seriously, it is substantial) Teriparatide injection (RDNA origin)
Fully human monoclonal antibody specifically binds to RANKL with high affinity improving bone mineral density. Reserved for pts intolerant/nonresponsive to bisphosphonates Denosumab
Decreased bone density from defective mineralization...ex: Rickets in children. Indications: Low 25 vit D, hypocalcemia, hypophophatemia, elevated bone alk phos Osteomalacia
Bone lesions of increased turnover with disorganized osteoid formation. Sx: bone pain/deformity, kyphosis, elevated bone alk phos, elevated Ca, classic bone scan/XRay features. Major fall risk w/ gait disturbance Paget's Disease of Bone: Osteitis Deformans
T/F: Pathologist cannot distinguish between benign and malignant NETs (neuroendocrine tumors) unless metastases is present True
Tumors found 64% in the GI (small intestine and rectum) and 28% pulmonary Carcinoid
5 things that give GI NETs a poor prognosis 1) Liver/lymph node metastases 2) elevated alk phos 3) primary size/speed of growth 4) Vascular invasion 5) High mitotic counts/necrosis
Low 5-HT (serotonin) content, occasionally secrete ACTH or 5-HTP, may metastasize to bone; doesn't usually cause "carcinoid syndrome" Foregut turmors
High serotonin content, most frequently cause carcinoid syndrome when they mets, release serotonin and tachykinins, no 5-HTP or ACTH, usually multiple, 80% in ileum, less mets to bone Midgut carcinoids; usually in small intestine or colon
Rarely contain serotonin, cause carcinoid syndrome, or secrete 5-HTP or ACTH, but do have numerous peptides. Mets to bone Hindgut tumors; rectum, transverse and descending colon
Flushing DD: (6) (I included the main ones) 1) Emotional 2) Food ingestion 3) Meds 4) Rosacea 5) Menopause 6) Carcinoid
What is the urticarial eruption associated with NETs called? Mastocytosis
Carcinoid syndrome Sx 1) Watery diarrhea 2) Flushing 3) Wheezing 4) Cardiac manifestations (97% have TRICUSPID INSUFFICIENCY [louder w/inspiration, holosystolic, big neck veins], fibrotic plaques on right side)
Main Dx tool for carcinoid syndrome Urinary 5-HIAA excretion rate (would be elevated)
2 Tx for pancreatic endocrine tumors (with hormone excesses) 1) Correct gastric acid hypersecretion and hypoglycemia 2) Surgical resection if feasible (often isn't)
60-90% malignant tumor w/ PUD Sx (H. pylori neg, multiple ulcers, refractory to Tx, diarrhea). Dx: Fasting hypergastrinemia (rule out pernicious anemia); gastrin level >1000 and pH <2 when off anti-secretory meds PET: Gastrinoma (Zollinger-Ellison Syndrome)
Tx for Gastrinoma (Zollinger-Ellison Syndrome) Anti-secretory medications, Whipple surgery if negative for MEN1
Attacks of hypoglycemia, Sx occur w/ fasting, confusion, disorientation, coma, Dx: simultaneous hypoglycemia w/ elevated insulin level; derived from beta cells w/ ectopic insulin secretion; Tx??? Insulinoma; Surgery TOC
Tumor secreting excess vasoactive intestinal polypeptide, 80-90% in pancreas, 37-68% have hepatic metastases at Dx. Sx: large volume diarrhea "pancreatic cholera", hypokalemia, dehydration, flushing, hyperglycemia. Tx? Vipoma; correct dehydration, replace potassium, surgery indicated only if metastases present
T/F: Lanreotide DOES reduce progression of disease more than placebo, but doesn't affect mortality or quality of life with neuroendocrine metastatic tumors True
Single most important prognostic factor in survival for carcinoids (specifically gastrinomas) liver metastases
Manifestations and Genetics of MEN 1 Primary hypeparathyroidism (95%), enteropancreatic tumors, PRL, non-functional adrenal cortical, fore-gut carcinoid, skin angiofibromas; Genetics: autosomal dominant (screen family members)
Manifestations of MEN 2A Genetics: need total thyroidectomy and lymph node dissection as early as first months of life; HYPERTHYROIDISM
Manifestations of MEN 2B earlier onset MEDULLARY THYROIDISM (more aggressive),
Disorders that accompany benign or malignant tumors but are not related directly to mass effects or invasion; atypical manifestations in pt w/cancer should raise suspicion Paraneoplastic syndromes
Some endocrine paraneoplastic syndromes (3) 1) hypercalcemia a) PTHrP b) 1,25 vit D 2) Hyponatremia 3) Cushing's Syndrome
Hirsuitism vs Virilization; What does virilization suggest? Virilization: androgen levels high enough to cause findings like deepening of voice, breast atrophy, increased libido, increased muscle bulk; ominous sign suggesting ovarian/adrenal malignancy. Hirsuitism: FH, excessive male pattern hair growth
Hirsuitism score >8 suggests? Androgen hair growth should be assessed by hormonal evaluation (total and free testosterone >12 indicates virilizing tumor; DHEA >18.5 suggests adrenal tumor
Unilateral, firm, fixed enlargement of breast EXCLUDE Malignancy with mammogram
Fractionated excretion of sodium with pre-renal? Low
Urine osmolality in ATN? Low, high in pre-renal
Created by: crward88



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