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Endocrinology/Nutrition > 03b: Calcium > Flashcards

03b: Calcium Flashcards

1
Q

Calcium in the plasma is in which forms? Star the form that’s utilized by the body to maintain cellular functions and neuromuscular activity.

A
  1. Free ions* (50%)
  2. Bound to plasma proteins (40%)
  3. Diffusible complexes (10%)
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2
Q

List the calcium-regulating hormones (calciotropic hormones) that are responsible for maintaining the serum calcium within the normal range

A
  1. PTH
  2. Calcitonin
  3. Vit D
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3
Q

When the pH is below 7.4, (more/less) calcium is bound to albumin, thus a (higher/lower) fraction is in the ionized form.

A

Less

Higher

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4
Q

Equation for total serum calcium corrected for albumin

A

(4.0-albumin)(0.8) + total Ca

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5
Q

The concentrate of calcium ions in the extracellular fluid is kept constant by the regulation of:

A
  1. Intestinal absorption
  2. Bone mobilization
  3. Tubular reabsorption
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6
Q

T/F: In adults, less than half of the calcium in the diet is absorbed.

A

True - usually between 20 and 30% (may be higher in increased demand states like pregnancy/lactation, growing kids)

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7
Q

The hormone that is most responsible for regulating intestinal calcium absorption

A

1,25-dihydroxy vit D

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8
Q

The amount of phosphorus in the normal adult is about (X) kg, of which (Y)% is in the skeleton.

A 
X = 1
Y = 85
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9
Q

When determining serum P levels, it is important that a level be obtained under which condition? Why?

A

Fasting

There are decreases in plasma P with the ingestion of CHO (due to increase insulin secretion) and P levels can rapidly rise after a meal.

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10
Q

T/F: only 10% of dietary phosphorus is absorbed

A

False - Dietary phosphorus is efficiently absorbed (60%) by the small intestine in a passive manner

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11
Q

1,25(OH)2D (increases/decreases) phosphorus absorption in the which part of GI tract?

A

Increases

Small intestine (ileum, jejunum)

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12
Q

The major control of phosphorus economy is exerted by which organ system?

A

Kidneys

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13
Q

During exposure to sunlight, (X) undergoes a photochemical reaction to form (Y).

A 
X = 7-dehydroxycholesterol (provitamin D3; cholesterol precursor)
Y = previtamin D3
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14
Q

Once formed, previtamin D3 undergoes either (X) or (Y) process

A 
X = isomerization to vitamin D3 
Y = photoisomerization (via absorbing solar radiation) into biologically inert compounds (lumisterol and tachysterol )
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15
Q

T/F: increased pigmentation will increase the capacity of the skin to produce vitamin D3

A

False - melanin competes w provitamin D3 for solar radiation

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16
Q

(X) is the major circulating form of vitamin D. Where is it made?

A

X = 25-hydroxyvitamin D

Liver

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17
Q

Obese patients are often vitamin D deficient because:

A

sequestration of vitamin D in their body fat

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18
Q

T/F: 1,25(OH)2D is the vitamin D metabolite that is measured to determine the vitamin D status of a patient.

A

False - 25(OH)D

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19
Q

(X) form of vit D interacts with (specific/nonspecific) receptor known as (Y). What kind of receptor is it?

A

X = 1,25(OH)2D
Specific
Y = the vitamin D receptor (VDR)

Nuclear

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20
Q

1,25(OH)2D interacts with (X) receptor; and the complex interacts with (Y).

A 
X = VDR 
Y = Retinoid-X R (RXR)
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21
Q

PTH has which actions on kidney?

A
  1. Increase Ca reabs; increase P clearance

2. Increase 1,25(OH)2D synthesis (to increase Ca absorption from gut)

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22
Q

1,25(OH)2D increases Ca absorption in the which part of GI tract?

A

Mainly duodenum (lesser extent in jejunum and ileum)

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23
Q

T/F: The biologically active

portion of the PTH molecule resides in the last 34 amino acids.

A

False - first 34 AA

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24
Q

The action of PTH at a cellular level involves which signaling pathway?

A

Adenylate cyclase/cAMP pathway

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25
Q

PTH increases Ca mobilization from bone by directly (inducing/inhibiting) (X) on (Y) cells.

A

Inducing
X = RANKL
Y = osteoblasts

(interacts with RANK and stimulates preosteoclasts to become active mature osteoclasts)

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26
Q

T/F: Calcitonin is produced by the parathyroid gland.

A

False - by C cells in thyroid

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27
Q

(X) cells have calcitonin receptor. The activity of these cells is (increased/decreased) upon the hormone’s binding.

A

X = mature, active osteoclasts

Decreased

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28
Q

(X) is a factor made by (osteoclasts/osteoblasts/osteocytes). Its major function is to (increase/decrease) P excretion in kidney by internalization of (Y) transporter.

A

X = FGF-23
Osteoclasts and osteocytes;
Increase
Y = Na-P

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29
Q

Preferred range of 25-(OH) vit D blood level is (X) ng/mL

A

X = 40-60

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30
Q

Circulating concentrations of 1,25(OH)2D3 are useful for which purpose?

A

To determine disorders in metabolism of 25(OH)D to 1,25(OH)2D

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31
Q

T/F: The serum assay for calcitonin is especially valuable for evaluating disorders in Ca, P, and bone metabolism.

A

False - only really valuable for determining presence of C-cell (medullary) tumor in thyroid

32
Q

64 y.o. F with mild renal failure has very low 1,25(OH)2D levels. Assuming she is otherwise healthy and renal function is only mildly impaired, what could be causing the low vit D level?

A

Hyperphosphatemia (serum P directly inhibits 1-hydroxylase even if kidney’s capacity to produce 1,25(OH)2D is adequate)

33
Q

List some hypercalcemic disorders that are associated with an acquired disorder in the
metabolism of 25(OH)D to 1,25(OH)2D.

A
  1. Hyper-PTH
  2. Chronic granulomatous disorders (sarcoid, TB, silicosis; granulomatous tissue has capacity to produce 1,25(OH)2D in unregulated manner)
34
Q

List two causes of acquired hypo-PTH. Star the more common one.

A
  1. Surg removal/damage after thyroid surg*

2. SEVERE hypo-Mg (chronic alcoholics with poor nutrition)

35
Q

List the classification of causes for hypercalcemia

A
  1. PTH-related (hyper-PTH)
  2. Malignancy-related (PTHrP secretion)
  3. Vit D-related (excess ingestion)
  4. Disorders w high bone turnover (ex: hyperthyroid)
  5. Chronic renal failure (chronic 2o hyper-PTH)
36
Q

Major cause of hyper-PTH:

A

Solitary adenoma (85%)

37
Q

FHH (Familiar Hypocalciuric Hypercalcemia) is due to (X) mutation in (Y). What’s the mechanism behind the hypercalcemia?

A 
X = point
Y = Ca sensor in parathyroid chief cells

Inhibition of PTH release occurs at higher serum Ca levels (new equilibrium)

38
Q

Gold standard sites for DEXA (bone densitometry).

A
  1. Lumbar spine (90% trabecular/metabolically active bone)

2. Proximal femur

39
Q

DEXA: T-score is useful in estimating (X). For each T-score decrease by one, (X) (increases/decreases) by (Y).

A

X = fracture risk
Increases
Y = factor of 2 (doubled)

40
Q

WHO definition of Normal Bone Density:

A

T-score above -1

41
Q

WHO definition of Osteopenia (low bone mass):

A

T-score between -1 and -2.5

42
Q

WHO definition of Ostoporosis:

A

T-score of -2.5 or below

43
Q

WHO definition of severe Ostoporosis:

A

T-score of -2.5 or below PLUS presence of fragility fracture

44
Q

The Z-score is useful in

comparing:

A

Patient’s bone density with the average expected density for a given age

45
Q 
Estrogen and selective estrogen
receptor modulators (i.e. raloxifene) (increase/decrease) (X) bone process by which mechanism?
A

Decrease
X = resorption

Bind estrogen Rs in osteoblasts and decreasing RANKL

46
Q

Denosumab is a monoclonal antibody which (increases/decreases) (X) bone process by which mechanism?

A

Decreases
X = resorption

Preventing the interaction between RANK and RANKL by 
binding RANKL (mimicks osteoprotegerin)
47
Q

Bisphosphonates (ex: alendronate, risedronate,

ibandronate and zoledronic acid) (increase/decrease) (X) bone process by which mechanism?

A

Decrease
X = resorption

Directly impairing osteoclast function (bind Ca hydroxyapatite, taken up by osteoclasts, and inhibit Farnesyl pyrophosphate synthase)

48
Q

How do thiazide diuretics impact bone formation/resorption?

A

Decrease resorption by decreasing PTH (via increasing renal Ca reabsorption)

49
Q

Proton pump inhibitors, such as omeprazole, (increase/decrease) (X) bone process by which mechanism?

A

Increase
X = resorption

decrease gastric acid and may decrease absorption of calcium carbonate (thus increasing PTH)

50
Q

List some drugs that may increase bone resorption by altering vit D metabolism or Ca absorption/excretion.

A
  1. Anticonvulsants (phenytoin, phenobarbital)
  2. Glucocorticoids
  3. PPIs
  4. Loop diuretics
51
Q

Currently, the only FDA-approved osteoporosis therapy that is anabolic to bone is:

A

Teriparatide (synthetic PTH analog - given in pulses)

52
Q

Second most common metabolic bone disease in older adults is (X). It’s characterized by (high/low) production of (Y).

A

X = Paget’s disease
High
Y = thick, more fragile and vascular bone (deformities, pain, neuro issues)

53
Q

Most frequent genetic mutation linked to Paget’s disease is in (X) gene, found in (Y)% of patients with familial Paget’s.

A 
X = sequestosome 1 
Y = 30
54
Q

T/F: Most common clinical picture of Paget’s is patient with focal bone pain and neuro symptoms (ex: radiculopathy).

A

False - most commonly asymptomatic; but most common Sx is bone pain

55
Q

T/F: In Paget’s, the affected area often shows signs of inflammation.

A

True (dolor, calor, rubor, tumor)

56
Q

Pt with high serum level of (X) is confirmed to be muscle (not liver) in origin. What step is taken next to rule out/in Paget’s disease?

A

X = alk phos

Nuclear medicine bone scan (identify “hot spots”); further evaluation via plain x-rays

57
Q

List some meds that have been approved for Paget’s disease treatment.

A

Anti-resorptives - Calcitonin and bisphosphonates (etidronate, tiludronate)

58
Q

The most dreaded complication of Paget’s disease is:

A

osteosarcoma

59
Q

T/F: Osteoporosis does not cause bone pain.

A

True

60
Q

T/F: Osteomalacia does not cause bone pain.

A

False - throbbing, aching pain (check by pressing on sternum)

61
Q

Trousseau’s sign used to assess (X). Explain the procedure to elicit the sign.

A

X = latent tetany (ex: carpo-pedal spasm)

Inflate BP cuff to between P systole and diastole - elicits tetany (locally causing alkalosis, causing ionized Ca to decrease)

62
Q

Chvostek sign used to assess (X). Explain the procedure to elicit the sign.

A

X = latent tetany (hypocalcemia)

tap facial nerve - twitching of mouth

63
Q

55 yo F with hypercalcemia. What are the two most likely etiologies?

A
  1. 1o Hyper-PTH

2. Malignancy (breast esp)

64
Q

(X) levels can be used to distinguish hyper-PTH from malignancy (PTHrP). (Y) levels can also be telling.

A 
X = PTH
Y = P (will be normal/high in malignancy due to down-regulation of PTH)
65
Q

PTHrP secreted by (X) cells

A

X = squamous (carcinoma)

66
Q

Pt with sarcoid or other granulomatous disease may have (hyper/hypo)-calcemia. Why?

A

Hypercalcemia

Activated macrophages in granulomas cause unregulated conversion of 25-hydroxy vit D to 1,25-dihydroxy vit D

67
Q

Young patient presenting with bowed legs and normal Ca/vit D levels. What would you check next? What’s at the top of your DDx?

A

Phosphate

If low, hypophosphatemic rickets

68
Q

Hypophosphatemic rickets: (X) inheritance pattern of point mutation in (Y).

A 
X = AD or X-linked
Y = FGF-23
69
Q

Adult patient with unrelenting, throbbing bone pain has normal Ca levels but very low P levels. What’s at the top of the differential?

A 
Oncogenic osteomalacia (a benign or malignant tumor that
makes FGF 23)
70
Q

Point mutation of alpha-1 hydroxylase results in which disorder?

A

Vit D-dependent Rickets Type I

71
Q

Mutation/dysfunction of VDR results in which disorder?

A

Vit D-dependent Rickets Type II (aka vit D-resistant Rickets)

72
Q

Global alopecia is a classic sign of which (inherited/acquired) cause of (hyper/hypo)-calcemia?

A

Inherited; hypocalcemia

Vit D-dependent Rickets Type II

73
Q

Vit D-dependent Rickets Type II: (hyper/hypo)-calcemia, (high/low) levels of 25-hydroxy vit D, (high/low) levels of 1,25 vit D, (high/low) levels of PTH, and (hyper/hypo)-phosphatemia.

A

Hypocalcemia
High; high; high
Hypophosphatemia

74
Q

Major cause of hypocalcemia in hospital setting

A

Low albumin

75
Q

Abnormal soft tissue calcification (esp of basal ganglia) is seen in which disorder?

A

Pseudohypoparathyroidism

76
Q

Pt with unexplained (hyper/hypo)-calcemia can be almost definitively diagnosed with (X) if you notice “dip” of 4th and 5th metacarpals.

A

Hypocalcemia

X = Pseudohypoparathyroidism

77
Q

Pt with Pseudo-pseudo-hypoparathyroidism differs from one with Pseudohypoparathyroidism in that:

A
  1. PO4, Ca, PTH all normal (PTH still working), despite remaining skeletal deformities/mental retardation
  2. Gene came from dad, instead of mom

Endocrinology/Nutrition (10 decks)

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