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Endo Repro Exam > Clinical Calcium Disorders > Flashcards

Clinical Calcium Disorders Flashcards

1
Q

normal calcium range

A

8.4 - 10.2 mg/dL

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2
Q

hypercalcemia - clinical features

A

*sings and symptoms vary on degree of hypercalcemia and acuity (chronic vs. acute)
*bones, stones, thrones, groans, psychic overtones, PLUS HEART:
1. bones: osteoporosis, bone pain
2. stones: hypercalciuria, nephrolithiasis, nephrocalcinosis, impaired glomerular filtration
3. thrones: polyuria
4. groans: constipation, anorexia, vomiting, peptic ulcer disease, acute pancreatitis
5. psychic overtones: lethargy, drowsiness, confusion, disorientation, irritability, depression, stupor, coma
6. HEART: shortened QT segment, HTN, bradycardia

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3
Q

basic rules of hypercalcemia

A

*PTH is most important lab test in pts with hypercalcemia
*you expect a LOW PTH in presence of HIGH calcium (due to negative feedback)

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4
Q

PTH-dependent causes of hypercalcemia

A
  1. primary hyperparathyroidism
  2. familial hypocalciuric hypercalcemia

*PTH-dependent = elevated corrected calcium and normal to elevated PTH levels

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5
Q

PTH-independent causes of hypercalcemia

A
  1. CANCER (skeletal metastases, paraneoplastic syndromes)
  2. hyperthyroidism
  3. vitamin D intoxication
  4. granulomatous disease (sarcoidosis, TB, etc)
  5. milk alkali syndrome
  6. lithium therapy
  7. vitamin A intoxication

*PTH-independent = elevated corrected calcium and LOW PTH (PTH levels should be low when serum calcium is high)

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6
Q

primary hyperparathyroidism - overview

A

*most common cause of hypercalcemia
*due to increased secretion of PTH; primary means that the problem is at the level of the parathyroid glands
*various forms:
-benign adenoma
-parathyroid hyperplasia (enlargement of all 4 glands)
-parathyroid carcinoma
-MEN syndrome

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7
Q

primary hyperparathyroidism - laboratory evaluation

A

*high calcium
*elevated or inappropriately normal PTH
*low phosphate
*high alkaline phosphatase (ALP) from increased bone turnover
*hypercalciuria on 24h urine calcium collection

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8
Q

primary hyperparathyroidism - imaging evaluation

A

*goal = localize the gland; can be accomplished via various scans
1. radionuclide scan with technetium-99m (Sestamibi)
2. 4D parathyroid CT scan
3. ultrasound
4. bone density (DXA) to evaluate for surgery indication

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9
Q

primary hyperparathyroidism - treatment

A

*observation
*surgery
*cinacalcet: sensitizes calcium sensing receptor (CaSR) in parathyroid gland to circulating calcium to lower PTH secretion; generally reserved for non-surgical candidates

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10
Q

primary hyperparathyroidism - major indications for surgery

A

*indications for surgery:
1. calcium 11.5 mg/dL or higher
2. kidney stones, hypercalciuria, declining GFR
3. osteoporosis
4. age < 50 years

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11
Q

osteitis fibrosa cystica (complication of hyperparathyroidism)

A

*chronically high PTH = osteoblasts produce RANK-L, which stimulates osteoclasts and increases bone breakdown
*over time, cystic bone spaces fill with brown fibrous tissue or “brown tumor,” consisting of osteoclasts & hemosiderin deposits from hemorrhages
*these cyst-like tumors are painful and classically associated with primary hyperparathyroidism
*findings: lytic lesions on X-ray; fatty infiltration of bone marrow
*aka von Reckinghausen disease of bone

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12
Q

familial hypocalciuric hypercalcemia (FHH) - overview

A

*a CaSR (calcium sensing receptor) mutation makes the parathyroid glands less sensitive to Ca2+ levels → a higher-than-usual Ca2+ concentration is required to inhibit PTH release
*autosomal DOMINANT

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13
Q

familial hypocalciuric hypercalcemia (FHH) - clinical features

A

*asymptomatic hypercalcemia
*do NOT experience Ca2+-related problems (no osteoporosis, kidney problems, or EKG changes)
*exam tip-off: family history of failed parathyroid surgery in first-degree relatives; genetics = autosomal dominant

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14
Q

familial hypocalciuric hypercalcemia (FHH) - diagnosis

A

*very LOW urine Ca2+
*increased serum Ca2+
*normal/mildly elevated PTH

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15
Q

familial hypocalciuric hypercalcemia (FHH) - treatment

A

*none
*warn family members to avoid parathyroid surgery for hypercalcemia

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16
Q

how to differentiate primary hyperparathyroidism vs. familial hypocalciuric hypercalcemia (FHH)

A

use the URINE CALCIUM to differentiate:
*primary hyperparathyroidism = HYPERCALCIURIA (high levels of calcium in urine)
*familial hypocalciuric hypercalcemia (FHH) = very LOW levels of calcium in urine

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17
Q

PTH-independent causes of hypercalcemia: HYPERTHYROIDISM

A

*elevated T4/T3 stimulates osteoclasts to break down bone, releasing calcium into the blood

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18
Q

PTH-independent causes of hypercalcemia: CANCER

A
  1. lytic lesions/bony metastases: breast, bone, multiple myeloma
    -direct damage to bone causes calcium to leak into circulation
    -SPEP + UPEP for multiple myeloma is a standard part of the evaluation of PTH-independent hypercalcemia
  2. paraneoplastic: breast, squamous cell carcinoma of the lung
    -some cancers can secrete PTH-rP, which structurally looks and acts like PTH
    -PTH-rp (PTH related peptide) stimulates osteoclasts to break down bone
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19
Q

PTH-independent causes of hypercalcemia: VITAMIN D INTOXICATION

A

*increased vitamin D = increased calcitriol
*labs: high 25-vit D, high or normal calcitriol

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20
Q

PTH-independent causes of hypercalcemia: GRANULOMATOUS DISEASE (TB, sarcoidosis, etc)

A

*increased amount of 1-alpha-hydroxylase (the enzyme that catalyzes the conversion of 25-vit D to calcitriol in the kidney)
*note - for sarcoidosis, ACE level is often elevated

21
Q

PTH-independent causes of hypercalcemia: other mechanisms

A
  1. milk alkali syndrome: excessive calcium intake with an alkali (ex. Tums)
  2. lithium therapy: increases PTH release (four-gland hyperplasia)
  3. thiazide treatment: increased renal reabsorption of calcium in the DCT
  4. vitamin A intoxication: increased bone resorption
22
Q

which diuretic is associated with hypercalcemia

A

*thiazide diuretics (cause high serum calcium, low urine calcium)
*ex: HCTZ

23
Q

lab evaluation of hypercalcemia (general)

A

*check PTH and calcium (plus albumin for calcium correction)

*if high PTH and high calcium: check a 24h urine calcium (low urine Ca2+ = FHH)

*if LOW PTH and high calcium, check:
-PTHrP
-SPEP and UPEP
-calitriol
-25-vitamin D
-consider: TSH, vitamin A

24
Q

management of hypercalcemia (general)

A

*treat underlying cause/avoid exacerbating medications
*acute tx = IV FLUIDS
*other options:
-biphosphonates (zoledronic acid): inhibit bone resorption
-calcitonin: inhibits osteoclast activity and inhibits renal calcium reabsorption (calcium resistance / tachyphylaxis develops after 48-72 hours)
-loop diuretics: LOOPS LOSE CALCIUM
-glucocorticoids for granulomatous disease

25
Q

hypocalcemia - clinical features

A

*INCREASED NEUROMUSCULAR EXCITABILITY:
-paresthesias (hands, lips & tongue)
-tetany
-cramping
-muscle spasm
-hyperreflexia
-seizures
-anxiety/depression
*physical exam findings: CHOVSTEK SIGN & TROUSSEAU SIGN

26
Q

trousseau sign

A

*inflation of blood pressure cuff leading to carpal spasm
*physical exam finding associated with hypocalcemia

27
Q

Chvostek sign

A

*ipsilateral facial muscle twitching by tapping the facial nerve
*physical exam finding associated with hypocalcemia

28
Q

EKG change associated with hypocalcemia

A

*QT prolongation
*can predispose to Torsades de Pointes

29
Q

causes of hypocalcemia

A

*hypoparathyroidism
*CKD/hyperphosphatemia
*vitamin D deficiency
*hypomagnesemia
*malabsorption
*precipitation/binding: blood transfusions, acute pancreatitis
*medications
*pseudohypoparathyroidism
*pseudo-pseudohypoparathyroidism

30
Q

hypoparathyroidism - overview

A

*most common cause of hypocalcemia
*various causes:
1. damage to parathyroid glands during parathyroid and/or thyroid surgery
2. autoimmune destruction (autoimmune polyglandular syndrome)
3. DiGeorge syndrome

31
Q

hypoparathyroidism - labs

A

*low PTH
*low calcium
*high phosphate (less PTH → increased renal reabsorption of phosphate → high phosphate)

32
Q

DiGeorge Syndrome

A

*22q11 deletion; associated with:
1. hypocalcemia (due to parathyroid hypoplasia or absence)
2. cardiac anomalies (conotruncal); get an echo
3. hypoplastic thymus
4. craniofacial/ENT abnormalities (low set, posteriorly rotated ears; wide-set eyes; bulbous nasal tip; palatal or laryngotracheal abnormalities)
5. developmental delay
6. immunodeficiency (T cells)
7. problem with pharyngeal pouches 3-4

33
Q

hypocalcemia due to chronic kidney disease (CKD)

A

*damage to renal tissue → less 1-alpha hydroxylase → decreased conversion of 25-vit D to calcitriol
*decreased renal clearance of phosphate: excess phosphate binds to calcium to create deposits of Ca, which removes calcium from the serum → hypocalcemia
*secondary & tertiary hyperparathyroidism

34
Q

hypocalcemia due to secondary hyperparathyroidism in CKD

A

*low serum calcium in CKD → PTH secretion
*over time, this leads to high PTH and low/normal serum calcium

35
Q

tertiary hyperparathyroidism in CKD

A

*seen only in end-stage renal disease (ESRD)
*prolonged secondary hyperparathyroidism → hypertrophy of parathyroid glands
*over time, leads to really high PTH levels, causing high calcium

36
Q

hypocalcemia due to vitamin D deficiency

A

*vitamin D deficiency is very common
*mechanism: low 25-vit D → low calcitriol → inability to increase serum calcium via calcitriol → hypocalcemia
*people with increased skin pigmentation have higher risk
*common etiologies of low vitamin D: decreased sun exposure, low dietary intake, liver disease, gut malabsorption, CKD

37
Q

hypocalcemia due to magnesium deficiency

A

*magnesium is required for proper PTH secretion and mediates tissue responsiveness to PTH
*low magnesium → reduced PTH secretion and reduced renal responsiveness to PTH
*risk factors: low dietary intake, chronic alcohol use
*in patients with hypocalcemia & hypomagnesemia: serum calcium won’t respond until magnesium is corrected

38
Q

hypocalcemia due to blood transfusions

A

*transfused blood contains citrate (prevents stored blood from clotting)
*citrate precipitates calcium out of the serum
*presents as severe, acute hypocalcemia (seizures)

39
Q

hypocalcemia due to acute pancreatitis

A

*release of pancreatic enzymes break down adipose tissue → high serum lipids
*lipids decrease magnesium and bind to free calcium, removing calcium from circulation

40
Q

hypocalcemia due to loop diuretics

A

*LOOPS LOSE CALCIUM
*loop diuretics such as furosemide → increased renal calcium excretion → increased calcium in urine, decreased calcium in serum

41
Q

other medications that can cause hypocalcemia

A

*bisphosphonates
*cincalcet
*foscarnet

42
Q

pseudohypoparathyroidism - overview

A

*mutation in GNAS1 (encodes alpha subunit of G protein): PTH can’t activate cAMP when binding to receptor → no signal transduction → no response to PTH by bone/kidney
*lots of types, but most important = Type 1a: autosomal dominant, maternal transmission of mutation; example of imprinting
*pts can have resistance to other G-protein coupled hormones
*labs: low Ca2+, high phosphorous, high PTH

43
Q

pseudohypoparathyroidism - labs

A

*serum calcium = LOW
*serum phosphorous = HIGH
*PTH = HIGH

44
Q

type 1a pseudohypoparathyroidism - clinical features

A

*short, broad thumb nails
*short 4th and 5th digits
*stunted growth

45
Q

pseudo-pseudohypoparathyroidism - overview

A

*autosomal dominant
*exam findings consistent with type 1a pseudohypoparathyroidism BUT with normal PTH and calcium
*defective G protein is inherited from father but mom’s normal allele can maintain responsiveness to PTH

46
Q

treatment of hypocalcemia (general)

A

*correct for albumin if indicated to ensure true hypocalcemia
*remember to check for/treat hypomagnesemia
*treat underlying cause, if able
*acute/symptomatic = IV calcium gluconate
*chronic/asymptomatic - oral calcium

47
Q

treatment of acute, symptomatic hypocalcemia

A

*IV calcium gluconate
*hypocalcemia = nerve irritability = ECG changes, seizures, bronchospasm; treat with IV medication to prevent these potentially fatal complications

48
Q

treatment of chronic, asymptomatic hypocalcemia

A

*oral calcium:
1. calcium carbonate, calcium acetate (replaces calcium)
2. calcitriol (helps body absorb the calcium replacement)

Endo Repro Exam (31 decks)

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