Clinical Medicine: Endocrine 2: Pituitary, Calcium, Neuroendocrine
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| Most common etiology of anterior hypopituitarism | mass lesion
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| 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
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| T/F: Most patients have normal pituitary function with Empty Sella Syndrome | True, were you even listening to my presentation?
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| Most common cause of hyper and hyposecretion of pituitary hormone syndromes in adults | Pituitary adenomas, which recall, are benign
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| Most common presenting feature of adult hypopituitarism | Hypogonadism
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| What blood tests would you do for anterior hypopituitarism? | TSH, T4, ACTH
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| Along with low ACTH and cortisol levels, what differentiates anterior hypopituitarism from primary adrenal insufficiency? | Normal potassium, lack of hyperpigmentation
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| Progressive loss of several or all pituitary hormones with a rapid onset post pituitary apoplexy | Panhypopituitarism
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| Very low IGF-1 is indicative of | Growth hormone deficiency.
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| What are some Tx for anterior hypopituitarism? | Removal of pituitary tumors and replacement of hormones
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| 4 endocrine active pituitary adenomas (tumors producing hormones) | Prolactinoma, Somatotropinoma, Corticotropinoma, Thyrotropinoma
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| 3 possibilities on secretions of hormones with pituitary adenomas? | 1) Excess of 1 hormone 2) Deficiency of 1 hormone 3) Deficiency of all hormones
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| Preferred imaging study for pituitary? What can you use when that is CONTRA? | MRI; CT (pacemaker/metallic implants around brain or eyes
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| 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
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| 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.
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| Indolent and often not clinically Dx for 10+ years with acral bony overgrowth; often have MEN 1 genetic abnormalities | Acromegaly
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| Leading cause of death in acromegaly? | Cardiovascular
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| Txs of acromegaly | Pituitary microsurgery is TOC
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| Most common etiology of iatrogenic hypercortisolism | Long term steroid use
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| Difference btwn Cushing's syndrome and Cushing's disease? | Syndrome: Excess cortisol from pituitary, adrenal or other sources. Disease: excess pituitary secretion of ACTH
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| Sx of what? Thin skin, central obesity, moon facies, purple striae, HTN, DM, hyperpigmentation, buffalo hump, hirsutism | Chronic cortisol excess
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| Hematopoietic features of hypercortisolism | Leukocytosis, lymphopenia, eosinopenia
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| 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)
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| 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
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| 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.
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| TOC for prolactinomas | Dopamine agonists (Bromocriptine, cabergoline)
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| 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
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| Decreased vasopressin, increased dilute urine, hyperosmolality, increased thirst, elevated sodium if water loss | Diabetes Insipidus
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| Increased vasopressin, abnormal concentration of urine, reduced osmolality, hyponatremic | Inappropriate ADH
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| 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
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| Hypernatremiuria, hyponatremia, hyperkalemia, increased ADH in response to decreased intravascular volume | Primary adrenal insufficiency
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| Secondary deficiency not associated with thirst, yet polydipsia. | Psychogenic DI
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| Decreased ADH resulting in abrupt onset of polyuria, polydipsia | Central Diabetes Insipidus (CDI)
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| 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
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| 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.
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| 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)
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| 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
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| Most common cause of primary adrenal insufficiency? Other causes? | Autoimmune adrenalitis; TB, bilateral adrenal hemorrhage due to anti-coags, HIV, bilateral metastatic infiltration
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| Sodium down, potassium up, elevated ACTH, eosinophilia, lymphocytosis, low aldosterone with non-specific Sx | Chronic primary adrenal insufficiency
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| What is the difference between regular cortisol/hydrocortisone and florinef? | Also treats hypotension with salt retention
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| 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])
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| HA, confusion/coma, elevated temp, HypoTN, Hyperkalemia, hyponatremia, elevated BUN...Tx? | Acute adrenocortical insufficiency: IV hydrocortisone
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| 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
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| 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
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| 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
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| 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.
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| Primary target organs for most active vitamin D? | 1,25 (OH)2D; intestine and bone
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| 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)
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| Tumor marker in sporadic and hereditary cases of medullary thyroid carcionoma | Calcitonin
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| Physiologically active form of calcium...50% of calcium in plasma | free or ionized calcium
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| 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
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| 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
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| At what serum calcium levels do heart arrhythmias occur? Which ones occur? | >14 mg/dL; prolonged PR, shortened QT, heart block, asystole, bradyarrhythmias
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| 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
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| 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
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| 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
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| 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)
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| 2 medical alternatives to surgery with primary hyperparathyroidism | Bisphosphonates, Calcimimetics
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| Low urinary calcium excretion, only normal to mildly elevated PTH levels, with a rare genetic component | Familial hypocalciuric hypercalcemia
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| 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
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| PTH levels reduced, lymphokines/cytokines promote resorption of bone through local destruction | Direct Bone Marrow Invasion (leukemia, lymphoma, multiple myeloma
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| 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
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| 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)
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| 2 causes of hypercalcemia related to high bone turnover | 1) Hyperthyroidism 2) Immobilization
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| How do thiazide diuretics cause hypercalcemia? | Reduction in urinary calcium excretion and they may "unmask" Dx of hyperparathyroidism
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| Excessive ingestion of calcium and absorbable antacids causing hypercalcemia | Milk Alkali Syndrome
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| Hypocalcemia initiates development of secondary hyperparathyroidism which stimulates an increase in calcium. What severe disease can cause this hypercalcemia? | Chronic renal failure.
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| The next few slides will be a simple review of hypercalcemia | Get it.
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| Elevated/inappropriately normal PTH and normal 24 hour urine calcium excretion: | Primary hyperparathyroidism
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| Elevated/inappropriately normal PTH and low urine calcium excretion: | Familial hypocalciuric hypercalcemia
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| PTH low and no malignancy | Check 1,25 Vit D, other supplements and drugs
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| PTH low and malignancy with elevated PTHrP, 1,25 Vit D | Hypercalcemia of malignancy
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| PTH low and malignancy with low PTHrP, 1,25 Vit D | local osteolytic hypercalcemia
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| First principle treatment of hypercalcemia | normal hydration and loop diuretic
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| 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.
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| What do you need to check in hypocalcemia in acute pancreatitis? | Ionized calcium (low albumin levels in pancreatitis)
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| 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)
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| T/F: Most transient hypocalcemia will not have a reduction in ionized calcium | True
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| Sx: Tetany including: hypoparathyroidism, acute hyperventilation, hypomagnesemia | Any cause of low ionized calcium.
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| Twitching of circumoral muscles in response to gentle tapping of facial nerve just anterior to ear | Chvostek's sign
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| 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
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| Tx for hypoparathyroidism | replacement of Vit D or 1,25(OH)2D3 and calcium (can be parental)
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| Most abundant cells in bone, function as mechanoreceptors detecting strain on bone and signalling changes for remodeling, born from osteoblasts | Osteocytes
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| Multinuclated giant cells specialized for resorption of bone. Requires RANKL for activation. | Osteoclasts
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| Cytokine responsible for communication between osteoblasts and osteoclasts | RANK ligand or RANKL
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| Decoy receptor that binds to RANKL preventing interaction w/ RANK and halting osteoclast differentiation | Osteoprotegerin (OPG)
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| 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
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| 3 Steps to evaluating Osteoporosis | 1) Bone density measurement 2) Risk analysis using FRAX 3) Exclude secondary causes
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| Biggest risk for osteoporosis? | Previous fragility fracture after 40
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| 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
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| What test should you use when assessing for moderate risk (10-20%) of osteoporosis? | XRAY looking for compression fracture on spine
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| T/F: Vitamin D supplementation prevents and treats osteoporosis but not osteomalacia | False, treats osteomalacia, but not osteoporosis
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| slows remodeling cycle, enhances mineralization of bone matrix | Anti-resorptive agents
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| Stimulates bone remodeling by increasing bone formation through the osteoblast | Anabolic agent
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| T/F: Estrogens are no long used for osteoporosis or CVD prevention | True, simply used as a symptomatic drug for menopause
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| What drug would you use for osteoporosis if there is a strong history of breast Ca in the family? | Raloxifene
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| 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
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| Weird side effect of bisphosphonates (yes I realize this question is in the eye of the beholder) | Atypical femur fractures
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| Nasal spray that increases bone density, reduces vertebral fractures... | Calcitonin
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| 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)
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| Fully human monoclonal antibody specifically binds to RANKL with high affinity improving bone mineral density. Reserved for pts intolerant/nonresponsive to bisphosphonates | Denosumab
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| Decreased bone density from defective mineralization...ex: Rickets in children. Indications: Low 25 vit D, hypocalcemia, hypophophatemia, elevated bone alk phos | Osteomalacia
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| 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
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| T/F: Pathologist cannot distinguish between benign and malignant NETs (neuroendocrine tumors) unless metastases is present | True
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| Tumors found 64% in the GI (small intestine and rectum) and 28% pulmonary | Carcinoid
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| 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
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| Low 5-HT (serotonin) content, occasionally secrete ACTH or 5-HTP, may metastasize to bone; doesn't usually cause "carcinoid syndrome" | Foregut turmors
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| 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
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| 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
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| Flushing DD: (6) (I included the main ones) | 1) Emotional 2) Food ingestion 3) Meds 4) Rosacea 5) Menopause 6) Carcinoid
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| What is the urticarial eruption associated with NETs called? | Mastocytosis
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| 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)
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| Main Dx tool for carcinoid syndrome | Urinary 5-HIAA excretion rate (would be elevated)
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| 2 Tx for pancreatic endocrine tumors (with hormone excesses) | 1) Correct gastric acid hypersecretion and hypoglycemia 2) Surgical resection if feasible (often isn't)
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| 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)
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| Tx for Gastrinoma (Zollinger-Ellison Syndrome) | Anti-secretory medications, Whipple surgery if negative for MEN1
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| 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
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| 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
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| 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
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| Single most important prognostic factor in survival for carcinoids (specifically gastrinomas) | liver metastases
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| 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)
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| Manifestations of MEN 2A | Genetics: need total thyroidectomy and lymph node dissection as early as first months of life; HYPERTHYROIDISM
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| Manifestations of MEN 2B | earlier onset MEDULLARY THYROIDISM (more aggressive),
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| 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
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| Some endocrine paraneoplastic syndromes (3) | 1) hypercalcemia a) PTHrP b) 1,25 vit D 2) Hyponatremia 3) Cushing's Syndrome
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| 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
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| 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
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| Unilateral, firm, fixed enlargement of breast | EXCLUDE Malignancy with mammogram
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| Fractionated excretion of sodium with pre-renal? | Low
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| Urine osmolality in ATN? | Low, high in pre-renal
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