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Endo > SM_190b: Calcium / Parathyroid / Bone > Flashcards

SM_190b: Calcium / Parathyroid / Bone Flashcards

(62 cards)

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1
Q

Describe Ca homeostasis and actions of PTH

A

Ca homeostasis and actions of PTH

  • Kidney -> Ca, which inhibits PTH
  • Bone -> PO4
  • Negative feedback from Ca and 1,25 Vitamin D on PTH
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2
Q

Describe etiologies of hypercalcemia

A

Hypercalcemia

  • Vitaminosis D and A
  • Immobility
  • Thyrotoxicosis
  • Adrenal insufficiency
  • Milk alkali syndrome, multiple myeloma
  • Infections: granulomatous (TB, fungal)
  • Neoplasms
  • Sarcoidosis
  • Thiazides and other meds
  • Rhabdomyolysis / renal FHH
  • AIDS
  • PTH, paraproteinemias

VITAMIN TRAP

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3
Q

PTH dependent hypercalcemia is commonly caused by ___ and ___

A

PTH dependent hypercalcemia is commonly caused by primary hyperparathyroidism and familial hypocalciuric hypercalcemia

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4
Q

Non-PTH dependent hypercalcemia is commonly caused by ____

A

Non-PTH dependent hypercalcemia is commonly caused by malignancy

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5
Q

Hypercalcemia presents with ___, ___, ___, and ___

A

Hypercalcemia presents with stones, bones, groans, and psychogenic overtones

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6
Q

Describe clinical features of hypercalcemia

A

Hypercalcemia clinical features

  • Nephrolithiasis / nephrocalcinosis
  • Arthralgias, myalgias, weakness
  • Abdominal pain, constipation, nausea / vomiting
  • Neurologic impairment: mild to severe
  • Polyuria
  • Shortened QT interval
  • Increased symptoms with higher Ca levels (such as Ca ≥ 12 mg/dL)

(stones, bones, groans, and psychogenic overtones)

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7
Q

Hypercalcemia therapy first line is ____

A

Hypercalcemia therapy first line is to stop any offending medications / supplements

  • Hydration
  • Loop diuretics (furosemide) if indicated to induce calciuresis
  • IV bisphosphonates (pamidronate, zoledronate)
  • Calcitonin
  • Glucocorticoids
  • Dialysis
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8
Q

____ is the most common outpatient cause of hypercalcemia

A

Primary hyperparathyroidism is the most common outpatient cause of hypercalcemia

  • Commonly in ≥ 50 years old
  • Onset in childhood suggests hereditary disorder such as MEN 1 or 2A
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9
Q

Primary hyperparathyroidism is most commonly caused by ___

A

Primary hyperparathyroidism is most commonly caused by benign solitary parathyroid adenoma

  • 85%: benign solitary parathyroid adenoma
  • 5%: 2 adenomas present
  • 10%: multiple gland hyperplasia (sporadic vs MEN 1 / 2A)
  • Parathyroid malignancy is rare
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10
Q

Describe mechanism of primary hyperparathyroidism

A

Primary hyperparathyroidism mechanism

  • Lack of negative feedback from Ca and 1,25 Vitamin D to PTH
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11
Q

Normal to high PTH and high Ca is ___

A

Normal to high PTH and high Ca is hyperparathyroidism

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12
Q

Low PTH and low Ca is ____

A

Low PTH and low Ca is hypoparathyroidism

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13
Q

Low PTH and high Ca is ___

A

Low PTH and high Ca is non-PTH hypercalcemia

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14
Q

Describe lab features of primary hyperparathyroidism

A

Primary hyperparathyroidism lab features

  • High serum Ca with normal to elevated PTH
  • Often low phosphorus levels present
  • High / normal urine Ca: high serum Ca spills over into urine
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15
Q

Primary hyperparathyroidisim renal manifestations include ____ and ____

A

Primary hyperparathyroidisim renal manifestations include polyuria and nephrolithiasis / nephrocalcinosis

  • Nephrolithiasis / nephrocalcinosis especially if 24 hr urine Ca > 300 mg
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16
Q

Describe bone manifestations of primary hyperparathyroidism

A

Primary hyperparathyroidism bone manifestations

  • Osteoporosis / fractures / low bone mineral density
  • Leads to more cortical bone loss (forearm) over trabecular
  • Severe manifestations (osteitis fibrosa cystica) are rare: periosteal resorption in distal phalanges, bone cysts / brown tumors
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17
Q

Salt and pepper skull occurs in ____

A

Salt and pepper skull occurs in Salt and pepper skull occurs in hyperparathyroidism

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18
Q

Describe primary hyperparathyroidism treatment

A

Primary hyperparathyroidism treatment

  • If asymptomatic: observe
  • If symptomatic and / or progression likely: surgery
  • Calcimimetics (cinacalcet): lower serum Ca by decreasing PTH secretion
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19
Q

Calcimimetics (cinacalcet) lower serum Ca by ____

A

Calcimimetics (cinacalcet) lower serum Ca by decreasing PTH secretion

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20
Q

Both primary hyperparathyroidism and familial hypocalciuric hypercalcemia have ____ and ____

A

Both primary hyperparathyroidism and familial hypocalciuric hypercalcemia have high serum Ca and normal to elevated PTH

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21
Q

Describe familial hypocalciuric hypercalcemia

A

Familial hypocalciuric hypercalcemia

  • Autosomal dominant
  • One allele of CaSR inactivated
  • Hypercalcemia is mild
  • Hypocalciuria
  • PTH slightly elevated
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22
Q

Describe neonatal severe hyperparathyroidism

A

Neonatal severe hyperparathyroidism

  • Autosomal recessive
  • Both CaSR alleles inactivated
  • Severe hypercalcemia
  • Hypocalciuria
  • PTH elevated
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23
Q

Fractional excretion of Ca: FeCa = ____

A

Fractional excretion of Ca: FeCa = [(UCa x PCr) / (UCr x PCa)] x 100

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24
Q

FeCa ____ in familial hypocalciuric hypercalcemia

A

FeCa < 1% in familial hypocalciuric hypercalcemia

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25
Look for ___ in familial hypocalciuric hypercalcemia
Look for low urine Ca in familial hypocalciuric hypercalcemia * Use 24 hour collection: calculate FeCa * FMHx (autosomal dominant): relative with hypercalcemia, hypercalcemia known in infancy * Treatment: observation, NO surgery
26
Humoral hypercalcemia mechanisms are \_\_\_\_, \_\_\_\_, and \_\_\_\_
Humoral hypercalcemia mechanisms are PTHrP, local bone resorption, and ectopic Vitamin D
27
Describe PTHrP mechanism of humoral hypercalcemia of malignancy
PTHrP mechanism of humoral hypercalcemia of malignancy * PTh related peptide: factor primarily involved with chondrocyte replication at the growth plate * Binds to PTH receptor * Highly expressed in fetus and breast milk * Commonly produced by squamous cell carcinoma of lung / neck / head and carcinoma of kidney and ovary Measure PTHrP
28
Describe local bone resorption mechanism of humoral hypercalcemia of malignancy
Local bone resorption mechanism of humoral hypercalcemia of malignancy * Via tumor cell production of osteolytic factors * Multiple myeloma, breast cancer, prostate cancer, lymphoma Check imaging (bone scan, X-rays)
29
Describe ectopic Vitamin D mechanism of humoral hypercalcemia of malignancy
Ectopic Vitamin D mechanism of humoral hypercalcemia of malignancy * Ectopic Vitamin D 1,25-(OH)2 production: due to ectopic production of 1-alpha-hydroxylase, leukomia / lymphoma / renal cell cancer / granulomatous disease (TB, sarcoidosis) Measure Vitamin D 1,25-(OH)2 level
30
Evaluation for humoral hypercalcemia of malignancy includes \_\_\_\_, \_\_\_\_, and \_\_\_\_
Evaluation for humoral hypercalcemia of malignancy includes measuring PTHrP, checking imaging (bone scan / X-rays), and Vitamin D 1,25-(OH)2 production
31
Describe the diagnostic algorithm for hypercalcemia
Diagnostic algorithm for hypercalcemia
32
Most commonly a low reported Ca is \_\_\_
Most commonly a low reported Ca is NOT true hypocalcemia
33
Correct serum Ca for \_\_\_\_
Correct serum Ca for albumin \< 4.0 mg / dL * Serum Ca is bound to circulating proteins: 40% bound to albumin and other proteins * Low albumin leads to low total serum Ca measurement but the free (ionized) Ca is normal
34
Corrected Ca = \_\_\_\_\_
Corrected Ca = total measured Ca + [(4 - albumin) x 0.8] * Add 0.8 to the total measured Ca for every 1 point the albumin is below 4
35
Describe clinical features of hypocalcemia
Hypocalcemia clinical features * Neuromuscular irritability * Paresthesias * Chvostek's / Trousseai's signs * Laryngospasm * Bronchospasm * Prolonged QT interval * Seizures * Tetany
36
Hypoparathyroidism can be \_\_\_\_, \_\_\_\_, or \_\_\_\_
Hypoparathyroidism can be destruction, congenital, or functional * Destruction: surgical, autoimmune, destruction by ionizing radiation / infiltration * Congenital (abnormal development): DiGeorge, velo-cardio-fascial syndrome * Functional: hypomagnesemia (PTH secretion is dependent on Mg)
37
Describe hypocalcemia in renal failure
Hypocalcemia in renal failure * Loss of renal responsiveness to PTH results in increased urinary Ca loss and decreased P excretion: develop secondary hyperparathyroidism * Hyperphosphatemia reduces Ca solubility * Reduced 1-alpha hydroxylase activity with reduced 1,25-(OH)2 Vitamin D production
38
Loss of renal responsiveness to PTH results in ____ urinary Ca loss and ____ P excretion
Loss of renal responsiveness to PTH results in increased urinary Ca loss and decreased P excretion
39
Describe treatment for hypocalcemia
Hypocalcemia treatment * Ca (IV, oral) * Vitamin D * Calcitriol (Vitamin 1,25 D): in hypoparathyroidism, Vitamin D resistant rickets, renal failure * Parathyroid hormone (Natpara)
40
Describe diagnostic algorithm for hypocalcemia
Hypocalcemia diagnostic algorithm
41
Rickets / osteomalacia are ____ due to \_\_\_\_, \_\_\_\_, or \_\_\_\_
Rickets / osteomalacia are defect in bone mineralization due to Vitamin D deficiency, Ca deficiency, and P deficiency * P deficiency: malabsorption, phosphorus wasting conditions
42
Describe pathogenesis of Vitamin D deficiency in rickets and osteomalacia
Vitamin D deficiency in rickets and osteomalacia 1. Chronic low Vitamin D 2. Decrease in Ca absorption from gut 3. Decrease in serum Ca and increase in PTH (secondary hyperparathyroidism) 4. Increased urinary Ca reabsorpion and PO4 excretion 5. Increased bone resorption Serum Ca is preserved at expense of bone Hypocalcemia and hypophosphatemia present only if severe long-standing Vitamin D deficiency
43
In Vitamin D deficiency causing rickets and osteomalacia, ____ is preserved at expense of bone
In Vitamin D deficiency causing rickets and osteomalacia, serum Ca is preserved at expense of bone
44
Rickets / osteomalacia clinical features are \_\_\_\_, \_\_\_\_, and \_\_\_\_
Rickets / osteomalacia clinical features are skeletal deformities, bone pain / fragility / fractures, and muscular hypotonia / weakness * Bone pain, fragility, fractures: effect of secondary hyperparathyroidism
45
Descibe Vitamin D sources
Vitamin D sources * Sun: need UVB rays to make Vitamin D * Diet * Limitations: where you live, body surface exposure, sunscreen, skin cancer risk, naturally dark skin tone, older age (less efficient at making Vitamin D)
46
Describe major causes of Vitamin D deficiency
Vitamin D deficiency causes * lack of intake exposure * Decreased skin synthesis * Decreased bioavailability: intestinal malabsorption (Celiac), obesity * Increased intestinal losses
47
Vitamin D 25-OH represents the ____ and should be measured to \_\_\_\_
Vitamin D 25-OH represents the storage form and should be measured to diagnose Vitamin D deficiency
48
Vitamin D 1,25-(OH)2 is the ____ form
Vitamin D 1,25-(OH)2 is the active form * Due to secondary hyperparathyroidism: Vitamin D converted to this form * Body tries to maintain this level in the normal range as much as possible
49
Describe treatment of rickets / osteomalacia
Rickets / osteomalacia * Vitamin D2 (ergocalciferol): prescription * Vitamin D (cholecalciferol): over the counter * Ca: diet / supplements * Calcitriol (Vitamin D 1,25(OH)2) if indicated: prescription * Phosphate (if indicated)
50
Osteoporosis is \_\_\_
Osteoporosis is compromised bone strength prediposing to increased risk of fracture * Bone strength: bone density and bone quality
51
Osteoporosis is T-score \_\_\_\_
Osteoporosis is T-score ≤ -2.5 (DXA) (osteopenia is -2.5 \< x \< 1)
52
Describe pathogenesis of osteoporosis
Pathogenesis of osteoporosis * Resorption \> formation, increased bone loss, low peak bone mass * Poor bone quality, low bone density, propensity to fall
53
Peak bone mass is \_\_\_\_
Peak bone mass is maximum bone mass or density achieved during a lifetime * Strongest predictor of BMD in old age is BMD at younger age * Skeletal sites reach maturity at different ages
54
\_\_\_ is used to measure bone strength
DXA is used to measure bone strength * T-score: SD compared to young adults * Z-score: SD compared to age/sex-matched controls
55
As age increases, bone density ____ and fracture risk \_\_\_\_
As age increases, bone density decreases and fracture risk increases
56
Describe osteoporosis prevention
Osteoporosis prevention * Maximize peal bone density achieved in adolescence: physical activity, adequate Ca and Vitamin D * Minimize other causes: amenorrhea / hypogonadism, tobacco, alcohol, medications, eating disorders * Health lifestyle interventions possible at any age
57
Antiresorptive osteoporosis therapy consists of \_\_\_\_, \_\_\_\_, \_\_\_\_, \_\_\_\_, and \_\_\_\_
Antiresorptive osteoporosis therapy consists of bisphosphonates, denosumab, selective estrogen receptor modulators, estrogen, and calcitonin (post-menopausal women, men ≥ 50 years old)
58
Anabolic therapy for osteoporosis includes \_\_\_\_, \_\_\_\_, and \_\_\_\_
Anabolic therapy for osteoporosis includes teriparatide, abaloparatide, and romosozumab (postmenopausal women, men ≥ 50 years old)
59
Paget's disease is ____ caused by \_\_\_\_
Paget's disease is hyperdynamic bone remodeling caused by increased osteoclast and osteoblast activity * Etiology: viral (paramyxovirus) * Often asymptomatic * Detection by elevated alkaline phosphattase or incidental radiologic exam
60
Severity of Paget's disease correlates with \_\_\_
Severity of Paget's disease correlates with rise in alkaline phosphatase level * Alkaline phosphatase is not specific to bone: osteoblasts, liver or intestine * If of bone origin: represents any state of high bone turnover
61
Describe clinical features of Paget's disease
Paget's disease clinical features * Characteristic features on radiograph and bone scan * Degenerative changes: pain, nerve compression / entrapment, hearing loss * Labs: normal serum Ca, normal P, normal PTH, high alkaline phosphatase * Bony deformities * Pathologic fracture with minimal trauma * Increased bone vascularity: high output CHF * Small risk of osteosarcoma development
62
Paget's Disease therapy involves \_\_\_
Paget's Disease therapy involves treatment to relieve symptoms and prevent complications * NSAIDs / PT for pain * Bisphosphonate therapy: cyclic oral or IV therapy highly effective in normalizing alkaline phosphatase levels and diminishing disease progression * Calcitonin shown to decrease disease progression

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