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05 Endo > Calcium Bone Disorders > Flashcards

Calcium Bone Disorders Flashcards

1
Q

only __ of bone is metabolically active

A

1% (only ionized calcium is metabolically active)

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2
Q

t/f serum ionized ca > serum ca and albumin

A

true

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3
Q

normal range of calcium levels

A

ionized ca 4.65-5.25 mg/dl

total serum ca: 8.5-10.5 mg/dl

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4
Q

what is pseudohypocalcemia

A

total plasma ca is low but ionized ca is normal

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5
Q

what is pseudohypercalcemia

A

elevation in the serum total ca concentration without any rise in serum ionized ca concentration

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6
Q

corrected ca

A

measured total ca + (0.8 x (4.0-albumin))

serum total calcium concentration falls approximately 0.8 mg/dl for every 1 g/dl reduction in serum albumin concentration

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7
Q

pth effects

A

works on bone to increase osteoclast activity
works on kidney to increase ca reabsorption in kidney
works indirectly on intestines to increase ca absorption from food (with help of vitd)

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8
Q

hepatic conversion of vit d

A

enzyme: cyp27a1 or sterol 27-hydroxylase
product: 25-hydroxyvitamin D (inactive)

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9
Q

renal conversion of vit d

A

enzyme: cyp27b1 or 25-dihydroxyvitamin d1-1-alpha hydroxylase
product: 1,25oh2d or calcitriol (active)

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10
Q

vitamin d supplements

A 
vitd2 (ergocalciferol): 10,000-50,000 iu
vit d3 (cholecalciferol): 400-5,000 iu
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11
Q

what produces calcitonin

A

nonfollicular cells of the thyroid (c cells)

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12
Q

calcitonin effects

A

decreases tubular reabsorption of ca
impairs osteoclast mediated absorption
tumor marker for neuroendocrine diseases

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13
Q

calcium homeostasis

A

calcium levels are high: ca inhibits pth, thyroid will release calcitonin
calcium levels are low: parathyroid glands will release pth (no inhibition)

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14
Q

hormonal response to hypophosphatemia

A

low plasma po4 -> inc calcitriol -> absorption of ca and phosphate in the intestine

page 4

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15
Q

conidtions that affect mineral homeostasis

A 
primary hyperparathyroidism (inc pth)
granulomatous disease (inc vitd)
vit d deficiency (dec vitd)
chronic renal disease (inc phosphate)
hypoparathyroidism (dec pth)
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16
Q

most common causes of hypercalcemia

A

primary hyperparathyroidism

malignancy

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17
Q

mechanisms that elevate body ca

A

accelerated bone resorption
excessive gi absorption
dec renal excretion of ca

page 5

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18
Q

complications of hypercalcemia

A 
osteoporosis and fractures
pancreatitis
kidney stones
hypertension
cardiac arrythmias
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19
Q

effects of ca on ecg

A

high ca = qt interval shorten

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20
Q

diagnosis of hypercalcemia step 1

A

check repeat serum ca

correct ca for albumin

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21
Q

diagnosis of hypercalcemia step 2

A

check for clinical signs: moans, groans, stones, and psychotic overtones

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22
Q

diagnosis of hypercalcemia step 3

A

measure intact pth

elevated: phpt (primary hyperpth)
mild to upper normal: phpt or familal hypocalciuric hypercalcemia
low normal or low: non pth-mediated hypercalcemia

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23
Q

definition of phpt

A

elevation of serum ionized calcium in the setting of an inappropriate elevation of pth

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24
Q

management of hypercalcemia

A 
volume expansion with isotonic saline
loop diuretic
calcitonin
biphosphonates
glucocorticoids
denosumab
calcimimetics
hemodialysis
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25
Q

imaging studies for hypercalcemia

A

parathyroid sestamibi scan

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26
Q

criteria for parathyroid surgery

A 
< 50 yo
serum ca 1.0 mg/dl above normal
(+) kidney stones or nephrocalcinosis
elevated 24h urine ca collection
reduced kidney fn
presence of vertebral fractures and osteoporosis
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27
Q

t/f inferior parathyroids are more likely to be ectopic

A

true, due to abnormal migration during embryogenesis

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28
Q

t/f patients with phpt are risk free after surgery

A

false, they’re at risk for rapid influx of ca back into the bone due to the loss of stimulation by pth aka hungry bone syndrome = can lead to hypocalcemia

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29
Q

t/f most cases of hypocalcemia are autoimmune

A

false, 75% of cases are acquired

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30
Q

notable causes for low pth

A

parathyroid agenesis
di george syndrome
activating casr mutations

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31
Q

PE signs and symptoms for hypopth

A 
trosseau's sign (hand)
chvostek's sign (facial nerve)
hyperreflexia
laryngeal spasm
seizures
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32
Q

complications of hypopth

A 
hypercalcemia and hypercalciuria
impairment of well being and mood
cognitive dysfunction
basal ganglia calcifications
cataract
increased bone mass
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33
Q

what is pseudohypoparathyroidism

A

patients have an elevated PTH but the target organs are not responsive to the effects

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34
Q

vitamin d levels

A

deficient: < 50 nmol/ml or < 20 ng/ml
insufficient: 50-70 nmol/ml or 20-30 ng/mg
sufficient: 75-125 nmol/ml or 30-50 ng/ml
toxicity: >375 nmol/ml or >150 ng/ml

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35
Q

management in acute symptomatic hypocalcemia

A

iv calcium gluconate

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36
Q

other treatments for hypocalcemia

A

vit d repletion
high oral calcium intake (diet and supplement)
parenterally administered pth
magnesium

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37
Q

key regulator for phosphorus homeostasis

A

fgf23 + klotho, overproduced in ckd due to consistently elevated phosphate levels

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38
Q

physiological role and function of fgf23

A

short term: kidney
long term: intestines

result in return to normal serum phosphorus levels

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39
Q

normal phosphorus homeostasis

A

elevated phosphorus -> inc fgf23, dec 1,25oh2d3 -> dec ca in blood

dec ca in blood + dec calcitriol + inc phosphorus -> inc pth

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40
Q

chronic stimulation of parathyroid glands

A

ckd -> phosphate levels are constantly elevated -> inc fgf23 and pth

low ca levels and low 1,25oh2d3 -> inc pth -> parathyroid gland hyperplasia

41
Q

t/f the abnormalities in secondary hyperparathyroidism covers all the abnormalities in ckd-mbd

A

true

42
Q

what stage of ckd can ckd-mbd develop

A

stage 2, egfr = 60-89 ml/min

universal in stage 5

43
Q

clinical manifestations of ckd-mbd

A

abnormalities in bone turnover, mineralization, volume linear growth, or strength
extra-skeletal calcification

44
Q

fgf23 lowering therapy

A

phosphate restriction
phosphate biners
cinacalcet hydrochloride
parathyroidectomy

45
Q

fgf23 increasing therapy

A

active vit d

iv iron

46
Q

treatment of secondary hyperparathyroidism: treatments of hyperphosphatemia

A

dietary phosphate restricion (dairy, red meats, sodas)

use non-calcium containing phosphate binders to maintain normal serum phosphate

47
Q

treatment of secondary hyperparathyroidism: treatment of vitd

A

cholecalciferol or ergocalciferol

NOT calcitriol, will further increase fgf

48
Q

treatment of secondary hyperparathyroidism: treatment of hypocalcemia

A

mild and asymptomatic: not treated

treat vit d deficiency

49
Q

treatment of secondary hyperparathyroidism: treatment of persistent hyperpth

A

calcimimetics
calcitriol
vit d analogs
parathyroidectomy

50
Q

cause of tertiary hyperpth

A

excessive secretion of pth after long standing hyperpth leading to hypercalcemia

persistent hyperpth and development of hypercalcemia after renal transplant

51
Q

treatment for tertiary hyperpth

A

parathyroid surgery

calcimimetics-cinacalcet (SE: nausea)

52
Q

moa of calcimimetics-cinacalcet

A

bind to and activate the calcium-sensing receptor in the parathyroid gland inhibiting pth

53
Q

clinical manifestations of vitamin d deficiency

A

low vitd and ca

high pth

54
Q

groups at risk for vit d deficiency

A 
breastfed infants
older patients
dark skin
patients with malabsorption syndromes
obese patients
55
Q

treatment for people without vitd deficiency

A

600-800 iu per day

56
Q

treatment for patients with normal absorptive capacity

A

100 units / 2.5 mcg until normal levels

57
Q

treatment for patients with serum 25ohd <12 ng/ml

A

1250 mcg of vit d2 or d3 orally once/week for 6-8 wks

+ 20 mcg of vit d3 daily after

58
Q

treatment for patients with serum vit d 12-20 ng/ml

A

20-25 mcg daily

59
Q

diagnostic test for non-pth mediated hypercalcemia

A

measure pthrp and vit d metabolites

60
Q

results for pthrp and vitd metabolites

A

elevated pthrp: humoral hypercal of malignancy

elevated 1,25d: lymphoma, sarcoid, tb

61
Q

possible diagnoses for normal pthrp and vitd

A 
multiple myeloma
hyperthyroidism
vit a intoxication or other supplements
lithium
thiazides
62
Q

t/f tb patients can take large quantities of vit d

A

false, if large quantities of 1,25oh2d3 are produced, a spillover effect can occur and result in hypercalcemia

63
Q

treatment of choice for patients wit chronic granulomatous diseases and lymphoma

A

glucocorticoids

prednisone 20-40 mg/day

64
Q

glucocorticoids moa

A

decreases intestinal absorption of dietary calcium due to excess vit d
decreases calcitriol production

65
Q

most common cause of low-normal/low pth non-pth mediated hypercalcemia

A

humoral hypercalcemia of malignancy

66
Q

treatmeent for humoral hypercalcemia of malignancy

A

bisphosphonates limit bone resorption

denosumab is a monoclonal antibody to rankl

67
Q

what is paget’s disease

A

localized bone remodeling disorder characterized by increased bone resorption and accelerated bone formation

68
Q

progression of paget’s disease

A

overactive osteoclastic bone resorption -> compensatory increase in osteoblastic new bone formation -> structurally disorganized mosaic of woven and lamellar bone

69
Q

initial osteolytic phase of paget

A

prominent bone resorption and hypervascularization

“blade of grass” lesion

70
Q

second phase of paget

A

haphazardly woven bone

fibrous ct may replace normal bone marrow

71
Q

final sclerotic phase of paget

A

bone resorption declines progressively leading to a hard, dense, less vascular pagetic bone

72
Q

clinical manifestations of paget

A

usually asymptomatic with incidental findings of elevated alp or skeletal abnormality

symptoms: bone pain, secondary arthritis, fractures in the femur, compression of surrounding tissue

73
Q

PE findings in paget

A 
bowing of extremity
short stature with simian stance
extremity with an area of warmth and tenderness to palpation
bony deformities
leg length discrepancy
74
Q

imaging findings in paget

A 
bone resorption (black)
sclerosis (hyperdense)
cotton wool appearance = osteoporosis circumscripta
picture frame lesion
ivory vertebra

diffuse isotope uptake in bone scan

75
Q

biochemical findings in paget

A

test of choice: ALP

elevated bone turnover markers
normal ca and phosphate

76
Q

bone resorption markers

A

ctx

dpd, pyd, ntx, tacp

77
Q

bone formation markers

A

oc, alp, balp, p1np

p1cp

78
Q

treatment for paget

A

-dronates and calcitonin

79
Q

t/f osteoporosis occurs more as people age but is not a natural part of aging

A

true

80
Q

signs and symptoms of osteoporosis

A

back pain caused by fractured or collapsed vertebra
loss of height over time
stooped posture
bone fracture that occurs more easily than expected

81
Q

complications of fractures

A

hip fractures: dvt and pe
vertebral fractures: restrictive lung disease
lumbar fractures: abdominal distention, early satiety, constipation

82
Q

who should be screened for osteoporosis

A

women >65, men >70
postmenopausal women and men 50-69 with risk factors
fragility fracture at any age
height loss of 2 cm
all postmenopausal women with at least one who risk factor

83
Q

screening tool for osteoporosis

A

frax screening tool
peripheral bone density test
osteoporosis screening tool for asians*

84
Q

gold standard test for osteoporosis

A

dxa scan (central bone mineral density test)

lumbar spine, total proximal femur, femoral neck

85
Q

bmd scores in young adults

A

normal: within 1 sd
osteopenia: 1-2.5 sd below
osteoporosis: =2.5 sd
severe osteoporosis: = 2.5 sd

86
Q

tscore compared to bmd scores for 30 yo adult

A

normal: >/= -1 sd
osteopenia: -1 to -2.5
osteoporosis: at or below -2.5
severe osteoporosis: at or below -2.5 with >/= 1 fractures

87
Q

indications for vertebral imaging

A

all women >/= 70 yo, men >/= 80 yo if the tscore is <1
women 65-69, men 75-79 if t score is <1.5
postmenopausal women 50-64, men 50-69 with risk factors

88
Q

indication for pharmacologic treatment in osteoporosis

A

history of hip/vertebral fracture
osteoporosis based on bmd measurement
high risk postmenopausal women and men >/= 50 yo with tscores -1.0 and -2.5
adults with condition/taking medication that is associated with low bone mass or bone loss

89
Q

osteoporosis medications that can stop bone loss

A

estrogens

raloxifene

90
Q

osteoporosis medications that can reduce vertebral fractures and further bone loss

A

calcitonin, pth, denosumab, strontium

91
Q

moa of bisphosphonates

A

impairs ability of osteoclasts to form ruffled border and promote osteoclast apoptosis

92
Q

moa of denosumab

A

antibody that binds to rankl -> osteoclast activity and survival is inhibited

can cause hypocalcemia

93
Q

moa of teriparatide

A

anabolic agent that works like pth when administered intermittently

94
Q

t/f estrogen/progestin therapy can be given to women with a history of heart disease and stroke

A

false

95
Q

indications for estrogen agonist/antagonist (raloxifene)

A

risk for vertebral fractures

risk for invasive breast cancer in postmenopausal women with osteoporosis

96
Q

indications for calcitonin

A

hypercalcemia: IM/SC

reduce re-occurrence of vertebral fractures: intranasal

97
Q

indications for strontium ranelate

A

when other osteoporosis medicines are unsuitable

for vertebral and nonvertebral fractures

98
Q

duration of osteoporosis treatment

A

3-5 years

discontinue bisphosphonates: stable bmd, no fractures, low risk for fractures

99
Q

complications of bisphosphonates

A

atypical femoral fractures

osteonecrosis of the jaw

05 Endo (16 decks)

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