ASN QBank Pearls - Mineral Bone Disease Flashcards

1
Q
  • bone composition shows LOW bone mass

- NORMAL primary mineralization

A

osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  • bone composition shows LOW bone mass

- HIGH secondary mineralization

A

adynamic bone disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • bone composition shows NORMAL or INCREASED bone mass
  • DECREASED secondary mineralization
  • INCREASED osteoid volume
A

secondary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  • wide osteoid seams with significant DECREASE in the rate of mineralization
  • absence of cell activity and endosteal fibrosis
  • aluminum disease is frequently associated with
A

osteomalacia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

the Endocrine Society guidelines recommend vitamin D insufficiency/deficiency for whom?

A

high-risk populations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

tumor-induced osteomalacia (TIO) is typically caused by

A

benign mesenchymal tumors of vascular or skeletal origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  • abnormal bone mineralization
  • increased alkaline phosphatase
  • long term, osteomalacia and associated fractures

is caused by?

A

chronic hypophosphatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

calcitriol levels in TIO are

A

LOW, despite hypophosphatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

MOST common renal manifestation of sarcoidosis

A

hypercalciuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

topiramate inhibits which enzyme?

A

carbonic anhydrase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

topiramate is a/w

A
  • proximal RTA
  • distal RTA
  • calcium phosphate stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

is a/w urinary crystals and is the MCC of nephrolithiasis

A

atazanavir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

triamterene is a/w

A

urinary crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

orlistat is a/w

A

enteric hyperoxaluria and urinary calcium oxalate crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • hypotension
  • hyperkalemia
  • hypocalcemia
  • heart block
  • cardiac arrest
  • at risk if AKI or CKD
A

hypermagnesemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hypomagnesemia

  • renal magnesium wasting
  • HIGH urinary Ca2+
A

thick ascending limb of LOH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hypomagnesemia

  • renal magnesium wasting
  • LOW urinary Ca2+
A

early distal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hypomagnesemia

  • renal magnesium wasting
  • normal urinary Ca2+
A

late distal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

patients who are at highest risk of hypocalcemia at initiation of cinacalcet

A

those with already low Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how soon after starting cinacalcet should you measure Ca2+ level?

A

1 week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

PTH level in milk-alkali syndrome (aka Ca2+-alkali syndrome)

A

suppressed (LOW)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

AD hypocalcemia (ADH) is commonly caused by

A

activating mutation of CaSR gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

majority of AD hypocalcemia (ADH) patients are asymptomatic and therefore are not diagnosed until

A

adulthood, when hypocalcemia is noted

24
Q
  • hypocalcemia
  • seizures
  • neuromuscular irritability during periods of stress, such as a febrile illness (may be mislabeled as febrile seizures)
A

symptomatic children with AD hypocalcemia (ADH)

25
Q
  • Ca2+ 6-8 mg/dL, but as low as 5 mg/dL
  • normal/slightly low PTH
  • high/high normal UCa2+ excretion (rather than expected low excretion)
  • recurrent nephrolithiasis and nephrocalcinosis (worse during treatment with vitamin D and calcium 
supplementation)
  • no previous normal serum Ca2+ values
  • low Mg2+ (in some patients)
A

AD hypocalcemia (ADH)

26
Q

how to confirm diagnosis of AD hypocalcemia (ADH)?

A

analysis for mutation in CaSR gene

27
Q

systemic medial calcification of the arterioles that leads to ischemia and subcutaneous necrosis

A

calciphylaxis (calcific uremic arteriolopathy)

28
Q

what factors are implicated in the genesis of calciphylaxis (calcific uremic arteriolopathy)?

A
  • hyperparathyroidism
  • active vitamin D administration
  • hyperphosphatemia
  • elevated Ca2+ x PO4- product
29
Q

what medications have been implicated as significant risk factors for the development of calciphylaxis (calcific uremic arteriolopathy)?

A
  • warfarin
  • calcium-based binders
  • vitamin D analogs
  • systemic glucocorticoids
30
Q

how can calciphylaxis (calcific uremic arteriolopathy) develop in the setting of warfarin use?

A

inhibition of vitamin K-dependent carboxylation of matrix GLA protein (MGP)

31
Q

what does matrix GLA protein (MGP) normally do?

A

it’s a mineral-binding extracellular matrix protein that actively inhibits calcification of arteries

32
Q

potential side effect of sodium thiosulfate

A

HAGMA

33
Q

mechanism for HAGMA d/t sodium thiosulfate

A

unknown

34
Q

key regulator of phosphate homeostasis

A

FGF-23

35
Q

FGF-23 is produced by

A

bone osteocytes

36
Q

FGF-23 is stimulated by rises in serum

A

phosphorus (in CKD)

37
Q

FGF-23 acts on numerous downstream targets in an attempt to normalize serum phosphorus levels; these targets include what?

A
  • increases PTH secretion
  • decreases Na+-dependent phosphate reabsorption by the proximal tubule
  • decreases 1-α hydroxylase activity
38
Q

FGF-23 excess has been a/w an increased risk for

A

cardiovascular mortality

39
Q

the use of calcium-containing phosphate binders have been shown to increase mortality in treatment of hyperphosphatemia compared to the use of?

A

non-calcium-containing phosphate binders

40
Q

what are the physiologic processes that predispose to metastatic calcification?

A
  • chronic metabolic acidosis leaching calcium and phosphate from bones
  • severe SHPT
  • intermittent metabolic alkalosis during HD that predisposing to soft tissue precipitation of calcium salt
  • elevated calcium-phosphate product
41
Q

treatment for calciphylaxis (calcific uremic arteriolopathy)

A
  • sodium thiosulfate IV
  • non-calcium-containing phosphate binders
  • daily dialysis with low calcium dialysate
  • aggressive wound care
  • adequate pain control
  • stop vitamin D analogs
  • lower PTH < 300 with cinacalcet or parathyroidectomy
  • stop IV iron
42
Q

which medications for SHPT have not been shown to improve patient survival?

A

cinacalcet and paricalcitol

43
Q

what procedure for SHPT has been shown to improve patient survival?

A

parathyroidectomy

44
Q

should patients with CKD stages 3-5 and evidence of CKD-MBD undergo BMD testing?

A

NO

45
Q

why shouldn’t patients with CKD stages 3-5 and evidence of CKD-MBD undergo BMD testing?

A
  • does not predict fracture risk as it does in general population
  • does not predict type of renal osteodystrophy
46
Q

based on KDIGO guidelines, when should patients with CKD stages 3-5 undergo bone biopsy?

A
  • unexplained fractures
  • persistent bone pain
  • unexplained hypercalcemia
  • unexplained hypophosphatemia
  • possible aluminum toxicity
  • before giving bisphosphonates to patients with CKD-MBD
47
Q

what is MOST likely to occur during the first year after a patient has a parathyroidectomy?

A

increase in all-cause hospitalizations; mostly d/t hypocalcemia

48
Q

cinacalcet decreases PTH concentration by an average of what percentage even in patients with SHPT?

A

47%

49
Q

what are some of the symptoms of SHPT?

A
  • bone pain
  • myopathy
  • pruritus
50
Q

calcimimetics such as cinacalcet work by

A

increase sensitivity of CaSR for calcium which upregulates the calcium-sensing and vitamin D receptors in the parathyroid gland

51
Q
  • short fourth and fifth metacarpals
  • rounded facies
  • ?AD inheritance
  • a/w TSH resistance
  • high PTH
  • low calcitriol
  • low Ca++
  • high phosphate
A

pseudohypoparathyroidism type 1A

52
Q

condition with phenotypic appearance of pseudohypoparathyroidism type 1A, but biochemically NORMAL

A

pseudoPSEUDOhypoparathyroidism

53
Q

MCC of increased urinary Ca++ excretion w/o an apparent underlying etiology

A

idiopathic hypercalciuria

54
Q

patients with colon resection and ileostomy can have bicarbonate loss in the ileostomy effluent which leads to formation of an acidic urine, and in addition to low urine volume puts them at risk for

A

uric acid stones

55
Q
  • bone complication from overproduction of PTH
  • increased PTH can be result of parathyroid adenoma, MEN type 1, MEN type 2A, parathyroid Ca, and renal osteodystrophy from ESRD
A

osteitis fibrosa cystica (OFC)

56
Q

what are the indications for parathyroidectomy in primary hyperparathyroidism?

A
  • Ca++ > 1 mg/dl about ULN
  • CrCl < 60 ml/min
  • bone density > 2.5 SD and/or previous fragility fracture
  • < 50 yoa