Endocrine

Question 1

What is acute adrenal insufficiency (adrenal crisis)?

Answer 1

Etiology: adrenal hemorrhage or infarction; acute illness/injury/surgery in pt w/ chronic adrenal insufficiency or long-term glucocorticoid use
RF: underlying primary adrenal insufficiency (Addison disease) or suppression of HPA axis due to chronic glucocorticoid use
Presentation: hypotension/shock; nausea, vomiting, abdominal pain; weakness, fever
Tx: hydrocortisone or dexamethasone; high flow IVF

Question 2

What is primary hyperparathyroidism?

Answer 2

Etiology: parathyroid adenoma (most common), hyperplasia, carcinoma, increased in MEN1 and 2A
Presentation: asymptomatic (most common); mild, nonspecific symptoms (eg fatigue, constipation), abdominal pain, renal stones, bone pain, neuropsychiatric symptoms
Dx: hypercalcemia, hypophosphatemia, elevated or inappropriately normal PTH, elevated 24h urinary ca excretion
Indications for parathyroidectomy: age <50yo, symptomatic hypercalcemia; complications - osteoporosis (T score < -2.5, fragility fracture), nephrolithiasis/calcinosis, CKD (GFR <60);
elevated risk of complications - calcium >/= 1mg/dl above normal, urinary ca excretion >400mg/day

Question 3

What is thyroid storm/hyperthyroidism?

Answer 3

Precipitating factors: thyroid or non-thyroid surgery, acute illness (eg trauma, infection), childbirth; acute iodine load (eg iodine contrast)
Presentation: fever as high as 40-41.1C (104-106F); tachycardia, hypertension, CHF, cardiac arrhythmias (eg atrial fibrillation); agitation, delirium, seizure, coma; goiter, lid lag, tremor, warm and moist skin; nausea, vomiting, diarrhea, jaundice
Tx: beta blocker (eg propranolol) to decrease adrenergic manifestations; PTU (to block new hormone synthesis) followed by iodine solution (SSKI) (to block release; given 1h later to prevent excess I incorporation into TH); glucocorticoids (eg hydrocortisone) to decrease peripheral T4 to T3 conversion and improve vasomotor stability; identify trigger and treat, supportive care

Question 4

What is hypocalcemia?

After confirmation, next step is to check PTH level to distinguish between low PTH-assoc. conditions (eg parathyroid surgery, polylglandular autoimmune) and elevated PTH-assoc. conditions (eg vit D deficiency, chronic kidney disease).

Answer 4

Causes: neck sugery (parathyroidectomy), pancreatitis, sepsis, tumor lysis syndrome, acute alkalosis, chelation: blood (citrate binds ionized ca) transfusion, EDTA, foscarnet
Presentation: muscle cramps, Chvostek and Trousseau signs, paresthesias (tingling and numbness), hyperreflexia/tetany, seizures; QT interval prolongation
Pts w/ impaired hepatic function are at increased risk due to decreased clearance of citrate by the liver.
Lactate, foscarnet, and EDTA can chelate calcium in the blood
Tx: IV calcium gluconate/chloride

Question 5

What is papillary thyroid cancer?

Answer 5

Most common thyroid epithelial malignancy
Characterized by slow spread into local tissues and regional lymph nodes
Pathology: large cells w/ ground glass cytoplasm; pale nuclei w/ inclusion bodies and central grooving; and grainy, lamellated calcification known as psammoma bodies
Tx: surgical resection; postoperative adjuvant therapies for pts at increased risk of recurrence include radioiodine ablation and suppressive doses of thyroid hormone

Question 6

What is follicular thyroid cancer?

Answer 6

Second most common thyroid epithelial malignancy
Peak incidence of 40-60yo
Presentation: firm thyroid nodule
Thyroid scintigraphy usually shows a nonmetabolically active “cold” nodule
Dx: surgically excised nodule - invasion of tumor capsule and/or blood vessels; invasion pattern accounts for tendency of FTC to metastasize via hematogenous spread and to distant tissues (eg bone, lung)

Question 7

What is thyroid lymphoma?

Answer 7

Uncommon, though high incidence in pts w/ pre-existing chronic lymphocytic (Hashimoto) thyroiditis (ie chronic hypothyroidism, positive antithyroid peroxidase antibody)
Presentation: rapidly enlarging, firm goiter assoc. w/ compressive symptoms (eg dysphagia, hoarseness); systemic B sxs (fever, night sweats, wt loss); retrosternal extension (prominent venous distension, facial redness=Pemberton sign)

Question 8

What is Riedel thyroiditis?

Answer 8

Progressive fibrosis of thyroid gland and surrounding tissues
Resulting fibrotic mass may resemble malignancy, but sxs are chronic and slowly progressive rather than acute

Question 9

What is constitutional growth delay?

Answer 9

Characterized by delayed growth spurt, delayed puberty, and delayed bone age.

Question 10

What is glucose 6 phosphatase deficiency (type 1 glycogen storage disease/von Gierke disease)?

Answer 10

Caused by deficient glucose 6 phosphatase in liver, kidney, intestinal mucosa which results in impaired conversion of glycogen to glucose, leading to glycogen accumulation in affected organs
Presentation: 3-4mo, hypoglycemia (seizures), lactic acidosis (due to buildup in liver); DOLL LIKE FACE, thin extremities, short stature, LARGE LIVER
No spleen and heart involvement
Labs: hyperuricemia, hyperlipidemia

Question 11

What is euthyroid sick syndrome?

Answer 11

AKA “low T3 syndrome”; any pt w/ acute, severe illness

Labs: decreased total and free T3 levels, normal TSH and T4

Question 12

What is subclinical hypothyroidism?

Answer 12

Elevated TSH

Normal T4, T3 (until late stages)

Question 13

What is chronic lymphocytic (Hashimoto) thyroiditis?

Answer 13

Form of hypothyroidism; subclincal hypothyroidism may convert to overt hypothyroidism
Presentation: symmetrically enlarged non-tender thyroid
Labs: antithyroid peroxidase and anti-thyroglobulin antibodies
High titers of anti-tpo assoc. w/ increased risk of miscarriage
Tx: levothyroxine

Question 14

Estrogen and TH.

Answer 14

Oral E decreases clearance of thyroxine-binding globulin, leading to elevated TBG levels.
Pt w/ nl thyroid fxn can readily increase thyroxine production to saturate increased number of TBG binding sites.
Hypothyroid pts are dependent on exogenous thyroid replacement and cannot compensate resulting in decreased free thyroxine and increased TSH. So, higher dosing of levothyroxine may be required.

Question 15

Radioactive iodine uptake (RAIU) scintigraphy

Answer 15

Increased in cases of hormone overproduction (graves)

Low/undetectable in cases of release of preformed hormone (painless thyroiditis)

Question 16

Water deprivation test.

Answer 16

Urine osm >600 suggest primary polydipsia due to intact ADH and ability to concentrate urine in absence of water intake.
Less than 600 = diabetes insipidous
Desmopression distinguishes between central and nephrogenic DI.
Central DI: >50% increase in urine osmolality w/ desmopressin; Tx: intranasal desmopressin
Nephrogenic DI: minimal change in urine osmolality w/ desmopression

Question 17

Thyrotoxicosis.

Answer 17

Causes increased sensitivity to catecholamines due to increased expression of beta-1 adrenergic receptors as well as changes in proteins controlling post beta-1 adrenergic receptor activity.
It DOES NOT stimulate catecholamine production.

Question 18

What is metabolic syndrome?

Answer 18

At least 3/5 are met: 
BP >130/80
Fasting glucose >100-110 
Abdominal obesity (M: waist circum >40in; W: >35in)
Triglycerides >150
HDL (M: <40, W: <50)

Question 19

Diabetic neuropathy.

Answer 19

Small fiber injury: predominance of positive sxs (eg pain, paresthesias, allodynia)
Large fiber injury: predominance of negative sxs (numbness, loss of proprioception and vibration sense, diminished ankle reflexes)

Question 20

Hypercalcemia.

Answer 20

Nephrolitihiasis, osteoporosis, nausea, constipation, neuropsychiatric symptoms (confusion, stupor, coma); (“stones, bones, abdominal moans, psychic groans”)
Tx: severe - calcitonin (inhibits osteoclast-mediated bone resorption, quickly reduces serum Ca concentrations and can be admnistered w/ saline)
Bisphosphonates also inhibit bone resorption and provide a sustained reduction in ca levels. however their effect is delayed usually occuring over 2-4d and they are typically given after initial administeration of saline and calcitonin

Question 21

What is painless (silent) thyroiditis?

Answer 21

Variant of chronic lymphocytic (Hashimoto) thyroiditis
Presentation: self-limited hyperthyroid phase, then hypothyroid phase
Low uptake on RAIU scan
Labs: thyroid peroxidase autoantibodies
Tx: beta blocker for hyperthyroid symptoms

Question 22

What is methimazole?

Answer 22

Decreases TH production

Used in thyrotoxicosis

Question 23

What is radioactive iodine?

Answer 23

Causes radiation-induced destruction of thyroid follicular cells
Leads to clincial and biochemical resolution of hyperthyroidism over the subsequent 6-18 weeks
Can lead to permanent hypothyroidism w/in months in >90% of pts (Graves)
In contrast, when used to treat toxic nodular goiter and toxic adenoma, the radioisotope is taken up only by the autonomous thyroid tissue, and the function of the remaining normal tissue is usually adequate to prevent permanent hypothyroidism
Used in thyrotoxicosis

Question 24

What is Gauchers disease?

Answer 24

Most common lysosomal storage disease 
Due to GLUCOcerebrosidase deficiency resulting in accumulation of glucocerebrosidase in lipid-laden MACROPHAGES of different tissues - 
BM: anemia + thrombocytopenia
Splenomegaly > hepatomegaly
Bone: bone pain 
FFT, delayed puberty 
Tx: enzyme replacement

Question 25

Primary hyperparathyroidism and HTN.

Answer 25

Primary hyperparathyroidism can cause HTN, arrhythmias, ventricular hypertrophy, and vascular and valvular calcification.

Question 26

Hypothyroidism and metabolic abnormalities.

Answer 26

Causes- Hyperlidemia: due to decreased LDL surface receptors and/or decreased LDL receptor activity Hypertriglyceridemia: due to decreased lipoprotein lipase activity Hyponatremia: due to decreased free water clearance Asx elevation of creatinine and serum transaminases

Question 27

Glucose control in DM.

Answer 27

Pts who have an elevated HbA1c despite good control of fasting glucose may have POSTPRANDIAL hyperglycemia. Combined regimen including a long-acting basal insulin (to control baseline/fasting glucose) and a rapid-acting mealtime insulin (to control postprandial glucose) may be needed to provide optimal control.

Question 28

Hyperthyroid drugs.

Answer 28

``` Antithyroid drugs (methimazole, PTU) are used in pts w/ mild disease who are likely to have a permanent remission. Also used in preparation for treatment w/ radioactive iodine in pts w/ significant hyperthyroidism or who are at increased risk of complications. ```

Question 29

What is acute thyrotoxic myopathy?

Answer 29

Presentation: severe distal or proximal muscle weakness; muscle atrophy DTR are frequently normal Tx: treatment of hyperthyroidism usually improves the myopathy

Question 30

Genitalia in classic congenital adrenal hyperplasia.

Answer 30

Newborn girls: ambiguous genitalia, ranging from clitoromegaly appears as underdeveloped phallus w/ a displaced urethral meatus; nonpalpable gonads as ovaries are intraabdominal and testes are not present Labioscrotal folds may be partially or completely fused Interal organs are female, no testes Newborn boys: normal or sometimes hypervirilized genitalia w/ palpable testes

Question 31

What is 5 alpha reductase deficiency?

Answer 31

Causes defective conversion of testosterone to dihydrotesterone Classically presents in genotypically male newborns (46XY) w/ female or undervirilized external genitalia. Testosterone level is normal.

Question 32

What is androgen insensitivity syndrome?

Answer 32

Due to a defect in the androgen receptor | Presents in a genotypically male newborn (46XY) w/ undervirilized ambiguous or female external genitalia

Question 33

What is glucagonoma?

Answer 33

Necrolytic migratory erythema (indurated plaques w/ scaling + central clearing on face, groin, + extremities) + diarrhea, wt loss, and anemia. Dx: glucagon >500 Imaging: CT scan or MRI to localize tumor and evaluate for mets

Question 34

Tissue transglutaminase IgA antibodies

Answer 34

Seen in dermatitis herpetiformis, typically assoc. w/ celiac disease Skin manifestations: grouped, intensely pruritic papules and vesicles on the extensor surfaces of the elbows, knees, back, and butt.

Question 35

DKA

Answer 35

Worsening hyperglycemia and metabolic acidosis can manifest as abdominal pain, altered mentation, and hyperventilation. Dx: based on clinical presentation and beside capillary blood glucose Tx: aggressive IV hydration and insulin

Question 36

Primary aldosteronism (Conn's syndrome)

Answer 36

HTN, metabolic alkalosis, hypokalemia, mild hypernatremia | Tx: aldosterone antagonists (spironolactone, eplerenone)

Question 37

Subacute (de quervain's) thyroiditis.

Answer 37

Hypothyroid | Tx: beta blockers to control thyrotoxic sxs and NSAIDs for pain relief

Question 38

Whatis suppurative thyroiditis?

Answer 38

Infectious. Rare condition causing high-grade fever and pain at thyroid gland. Gland may be palpably enlarged due to abscess formation. However, pts are usually euthyroid as involvment of the thyroid gland is focal.

Question 39

Fetal hyperglycemia

Answer 39

Fetus cannot produce insulin during the 1st trimester and therefore cannot protect itself from hyperglycemia.

Question 40

Neonatal hypoglycemia

Answer 40

After delivery, fetal insulin production takes time to decrease whereas maternal glucose exposure ends as soon as the umbilical cord is clamped. This often results in a period of neonatal hypoglycemia until insulin levels normalize. Hypoglycemia is the most common complication among infants of DM mothers.

Question 41

Pheochromocytoma

Answer 41

Can be precipitated by increases in abdominal pressures (tuor palpation, positional changes), surgical procedures, anesthetic agents Non-selective beta blockers can cause a state of unopposed alpha adrenergic stimulaton leading to vasoconstriction and paradoxical HTN. Therefore, alpha adrenergic blockers (phenoxybenzamine) should be administered prior to beta blockers.

Question 42

Precocious puberty

Answer 42

Onsest of secondary sex characteristics (eg pubic/axillary hair, cystic acne, accelerated growth) in girls age <8 and boys age <9) Central precocious puberty: results from early activation of the hypothalamic pituitary gonadal axis; pulsatile GnRH secretion stimulates elevated FSH and LH levels Peripheral precocious puberty: LOW FSH and LH; caused by gonadal or adrenal release of excess sex hormones; basal levels of FSH and LH are low due to neg fb and remain low following GnRH agonist stimulation MRI of the brain to evaluate for hypothalamic or pituitary tumor. If idiopathic central PP, GnRH therapy, it desensitizes the pituitary and suppresses FSH and LH secretion to slow pubertal progression, prevent premature epiphyseal plate fusion, and maximize height potential.

Question 43

Central adrenal insufficiency

Answer 43

Pts w/ cushingoid appearance are more likely to have a suppressed HPA axis. Following glucocorticoid discontinuation, normal HPA axis function may not fully return for up to 6-12 months.

Question 44

Hypothyroid myopathy

Answer 44

Myalgias, proximal muscle weakness, elevated serum CK Features of hypothyroidism (fatigue, delayed reflexes) Dx: TSH, T4 levels

Question 45

Refeeding syndrome

Answer 45

Carb ingestion whether enteral or IV, causes pancreatic insulin secretion and cellular uptake of P, K, and Mg. P is the primary deficient electrolyte as it is required for energy (ATP). Deficiencies in P and Mg potentiate cardiac arrhythmias in a heart already atrophic from prolonged malnutrition. Therefore, aggressive initiation of nutrition w/o adequate electrolye repletion can quickly precipitate cardiopulmonaory failure. Aldosterone + cortisol are high during starvation but less so during refedding. They do not directly mpact P or Mg uptake.

Question 46

What is milk alkali syndrome?

Answer 46

Caused by excessive intake of calcium and absorbable alkali (eg ca carbonate preparation used in pts w/ osteoporosis); resulting hypercalcemia causes renal vasoconstriction and decreased glomerular blood flow; inhibition of NKCl transporter and impaired ADH acitivity lead to loss of Na and free water. It can be seen in pts taking calcium bicarbonate for osteoporosis. Clinical finding: symptomatic hypercalcemia, AKI, metabolic akalosis. Thiazides are assoc. w/ MILD hypercalcemia. Not event to get to symptomatic hypercalcemia.

Question 47

What is hypercalcemia of immobilzation?

Answer 47

Insidious, Due to increased osteoclastic bone resorption Onset usuallly around 4w after immbolizaitoins, althought pts w/ chronic renal insufficiency may develop hypercalcemia in as little as 3d RF: pre-existig high rate of bone turnover (younger pts, Paget disease) Suppressed PTH Tx: bisphosphonates inhibit osteoclastic bone resorption and are effective in tx

Question 48

Albumin + Calcium

Answer 48

40% of Ca bound to albumin Hypoalbuminemia: lowers the total Ca level so measured ca levels are corrected upward based on extent of hypoalbuminemia Hyperalbuminemia: assoc. w/ increase in total ca In either case, total ionized fraction is unaffected + pt will not have ca-related sxs directly related to the change in albumin levels

Question 49

Hyperthyroidism + Calcium

Answer 49

Untreated hyperthyroid pt are at increasd risk for rapid bone loss from increased osteoclastic activity in the bone cells. Leading to osteoporosis and increased risk of fracture. Pts can also develop hypercalcemia and hypercalciuria due to increased bone turnover. Untreated hyperthyroid pts are also at risk for cardiac tachyarrhythmias, including a fib.

Question 50

What is congenital hypothyroidism?

Answer 50

Infants initially appear normal at birth, but gradually develop apathy, weakness, hypotonia, large tongue, sluggish movement, abdominal bloating, and an umbilical hernia. For this reason, screening newborns for hypothyroidism, along with phenylketonuria and galactosemia, is standardly performed in all states.

Question 51

Diabetic nephropathy

Answer 51

Target HbA1c <7% Intensive BP control is assoc. w/ reduced progressive of DN. Ideal BP <130/80 ACE-i and ARBs are preferred antihypertensive drugs These agents lower systemic BP and reduce intraglomerular pressure, which may be renoprotective

Question 52

What is thyroglobulin?

Answer 52

Produced only by thyroid tissue (either normally functioning or malignant). Serum thyroglobulin measurements are used as a tumor marker once the normally functioning thyroid tissue is removed. Rising levels indicated recurrence of differentiated thyroid cancer. Levothyroxine suppresses TSH release (neg FB). B/c TSH stimulates thyroid tissue growth, levo supplementation to suppress TSH (i.e., by causing a mildly hyperthytroid state) may help prevent thyroid cancer recurrence.

Question 53

Vitamin D deficiency

Answer 53

Pts w/ osteomalacia due to vit. D deficiency have low or low-normal serum ca, low serum P, increased serum PTH, low plasma 25OHvit D levels, and elevated ALP. Unlike in osteoporosis, most pts complain of bone pain and muscle weakness. XR: decreased bone density w/ thinning of cortex and pseudofractures (Looser zones).

Question 54

Prolactinoma + TSH

Answer 54

TSH may be NORMAL or low; depends on compressive effect on thyrotroph cells.

Question 55

What is familial hypocalciuric hypercalcemia?

Answer 55

Caused by a mutation in the calcium sensing receptor. Benign disorder characterized by asymptomatic hypercalcemia, elevated or inappropriately normal PTH levels and low urinary calcium excretion. It can be differentiated from primary hyperparathyroidism, which has increased urinary ca excretion, by the urine calcium/creatinine clearance ratio.

Question 56

Congenital hypothyroidism

Answer 56

Assoc. w/ neurodevelopmental injury if not recognized and treated early. Decreased activity, hoarse cry, and jaundice are commonly assoc. w/ congenital hypothyroidism, but majority of infants are asx. Thyroid dysgenesis is the most common cause of congenital hypothyroidism worldwide.

Question 57

Hyperthyroidism + RAIU

Answer 57

In hypertyroidism, increased RAIU suggests denovo thyroid hormone synthesis, whereas decreased RAIU suggests release of preformed hormone (eg thyroiditis) or exogenous hormone intake. Thyrotoxicosis due to exogenous TH is characterized by low serum thyroglobulin levels. Wt loss supplements contain TH derived from porcine or other animal sources.

Question 58

DKA

Answer 58

Best markers indicating resolution of DKA are serum anion gap and beta-hydroxybutyrate levels The serum AG estimates the unmeasured anion concentration in the blood and returns to normal w/ disappearance of ketoacid anions. BH is not measured by the nitroprusside test so it needs to be measured directly with serum assay of BH.

Question 59

Nonclassical congenital adrenal hyperplasia

Answer 59

Occurs secondary to 21 hydroxylase deficiency Increase in 17OH progesterone Sufficient mineralocorticoids and glucocorticoids Increase in testosterone Causes gonadotropin-independent precocious puberty; pts can have premature secondary sex characteristics (pubic hair, cystic acne), accelerated growth and bone age, and low/normal LH

Question 60

Evaluation of adrenal insufficiency?

Answer 60

Should include 8AM serum cortisol and plasma ACTH In addition, an ACTH stimulaton test (cosyntropin test) can identify pt w/ primary adrenal insufficiency (and most pts w/ central adrenal insufficiency) and should be performed in the initial evaluation. Urinary cortisol levels are decreased, but sensitivity is too low for use in initial diagnosis

Question 61

Dexamethasone suppression test.

Answer 61

Dexamethasone suppresses release of ACTH from the pituitary, which subsequently reduces adrenal cortisol production. The dexamethasone suppression test is used to evaluate hypercortisolism not primary adrenal insufficiency.

Question 62

What is cushing syndrome?

Answer 62

Wt gain, psych sxs, hirsutism, HTN, hyperglycemia Initial step in eval of Cushing syndrome is to confirm hypercortisolism w/ a 24h urine free cortisol, late night salivary cortisal assay, and/or low dose dexamethasone test If hypercortisolism is confirmed, ACTH levels are measured to differentiate ACTH-dependent (Cushign disease - pituitary) from ACTH-independent (eg small cell lung cancer, primary adrenal disease) causes

Question 63

Hyperaldosteronism

Answer 63

Ratio of plasma aldosterone to plasma renin is useful for primary evaluation.

Question 64

Euthryroid state: elevated T4, normal TSH TH is normally bound to TBG, transthyretin, and albumin Only free TH is biologically active Changes in binding protein levels can affect the total circulating pool of TH, but if the axis is intact, free hormone levels are unchanged.

Answer 64

Estrogen (pregnancy, OCP, HRT) increases the level of T4 binding globulin by decreasing its metabolism and increasing synthesis in the liver. As additional TBG binds more TH, TH production increases to maintain euthyroid state. This effect is seen in pregnancy and in pts on OCP or menopausal estrogen replacement. Total TH levels are elevated, but pts w/ normal hypothalamic pituitary thyroid function maintain a euthyroid state and normal free T4 and TSH level.

Question 65

Hirsutism

Answer 65

Rapid onset hirsutism (<1y) w/ virilizaiton (eg temporal balding, excessive muscular development, enlarged clitoris) suggests very high androgen levels due to an androgen-secreting neoplasm of the ovaries or adrenal glands Ovaries naturally secrete: T, androstenedione, and dehydroepiandrosterone (DHEA) Adrenals: T, androstenedione, DHEA, and DHEAS Therefore, women w/ androgen-producing tumor should be evaluated w/ serum T and DHEAS levels Ovarian source - elevated T and normal DHEAS (more common) Adrenal source - elevated DHEAS (less common) DHEAS and DHEA have negligible intrinsic androgenic action but are converted to adrostenedione and subsequently to testosterone in peripheral tissues.

Question 66

Type II DM + CVD

Answer 66

Metform is recommended 1st line med for most pts w/ type 2 DM. Options for add-on tx in pts w/ established cardiovascular disease: -GLP1 agonists: decreased cardiovas events, induce signficant wt loss -SGLT2 ihibitors: assoc. w/ decreased BP, decreased risk for HF and cardiovasc events, minor wt loss

Question 67

Insulin and sulfonylureas

Answer 67

Not shown to reduce risk of cardiovascular events

Question 68

Thiazolidinediones

Answer 68

Assoc. w/ possible wt gain. | Cause fluid retention, which can lead to symptomatic HF in pts w/ underlying heart disease

Question 69

DPP4 inhitibors

Answer 69

Less effective than GLP1 agonists Have minimal effect on wt Not assoc. w/ a decreased risk of cardiovasc events

Question 70

PTH-related protein

Answer 70

From malignant tumor cells, causes hypercalcemia

Question 71

Hypoparathyroidism

Answer 71

Treatment of chronic hypoparathyroidism is w/ calcium and vit D, but calcium and phosphorus must be closely monitored. A calcium phosphorus product (serum ca x serum p) >55 increases the risk of soft tissue calcification. Calcification in the basal ganglia can cause extrapyramidal manifestations.

Question 72

Hypothyroidism + carpal tunnel syndrome

Answer 72

CTS is common in pts w/ hypothyroidism and is frequently bilateral. Hypothyroidism causes soft tissue thickening and mucinous infiltration, which can lead to compression of the median nerve w/in the carpal tunnel. Tx: levothyroxine

Question 73

CTS + renal disease

Answer 73

Pts w/ ESRD on hemodialysis frequently develop CTS due to accumulaton of dialysis-related amyloid. When CTS occurs, it is more common in the arm used for vascular access (eg access graft, arteriovenous fistula) suggesting a contribution of vascular steal or venous HTN. ESRD can also lead to pathologic calcification w/ deposition of calcium phosphate, which can compress the nerve.