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Biochem Exam 5 > Calcium and Phosphate Regulation Part 2 > Flashcards

Calcium and Phosphate Regulation Part 2 Flashcards

1
Q

How can calcium and phosphate homeostasis be disrupted?

A

-dietary deficiency or excess calcium
-mutations in genes for vitamin D receptors
-elevated or decreased PTH
-insensivity of tissues to PTH
-mutation in phosphate transporter molecules
-mutations in FGF23 or regulators of FGF23
-chronic kidney disease

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2
Q

What is hypocalcemia?

A

total serum calcium concentration <8.5mg/dL in the presence of normal plasma protein concentrations or a serum ionized calcium concentration <4.4 mg/dL

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3
Q

What are symptoms of hypocalcemia?

A

-muscle cramping
-increased neuromuscular excitability
-muscle spasm
-fatigue
-cardiac dysfunction
-depression, psychosis, seizures

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4
Q

What is hypoparathyroidism?

A

undersecretion of PTH
-relatively rare

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5
Q

What is the most common cause of hypoparathyroidism?

A

autoimmune destruction of parathyroids/loss of parathyroids due to thyroidectomy

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6
Q

What does the loss of PTH producing tissue do?

A

hypocalcemia due to decreased calcium uptake in gut/kidney and decrease calcium release from bone

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7
Q

What is Di George syndrome?

A

congenital disease with complete lack of parathyroids at birth

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8
Q

What are the treatments for hypoparathyroidism?

A

calcium and calcitriol supplementation
-PTH 1-84 has now been approved in USA and Europe as treatment

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9
Q

What do constitutively activating mutations in CaSR do?

A

cause autosomal dominant hypocalcemia

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10
Q

What does autosomal dominant hypocalcemia do?

A

CaSR is hypersensitive to extracellular Ca2+ and suppresses PTH production even though Ca2+ levels are low
-decreases Ca2+ resaborption in the kidney and decreases release from bone, uptake in gut
-leads to low serum calcium

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11
Q

What is the treatment for autosomal dominant hypocalcemia?

A

calcium and calcitriol

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12
Q

What is pseudohypoparathyroidism?

A

hypocalcemia due to lack of responsiveness of target tissue to PTH
-serum PTH is high

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13
Q

What causes pseudohypoparathyroidism?

A

mutations in the G proteins important for PTH signaling

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14
Q

What can cause vitamin D deficiency?

A

dietary deficiency, lack of sunlight, and malabsorption of vitamin D

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15
Q

What is rickets?

A

vitamin D deficiency seen in growing children
-impaired bone mineralization/outward curvature of long bones
-insufficiently mineralized vertebrae/curved spine
-disorganized growth plate/growth retardation

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16
Q

What is osteomalacia?

A

vitamin D deficiency in adults
-due to low serum calcium and phosphate

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17
Q

What is VDDR type I?

A

vitamin D dependent rickets type I
-autosomal recessive
-defect in renal 25-OH-vitamin D-1 alpha-hydroxylase
-low serum Ca2+ and phosphate
-high PTH
-very low 1,25 (OH)2D3

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18
Q

What is VDDR type II?

A

vitamin D dependent rickets type II
-autosomal recessive
-defect in vitamin D receptor
-several mutations identified
-low serum Ca2+ and phosphate
-high PTH
-alopecia in some patients
-elevated 1,25(OH)2D3

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19
Q

What is the definition of hypercalcemia?

A

serum total calcium >10.5 mg/dl or ionized calcium >5.4mg/dl

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20
Q

What are the symptoms of hyercalcemia?

A

-fatigue
-electrocardiogram abnormalities
-nausea, vomiting, constipation
-anorexia
-abdominal pain
-hypercalciuria/kidney stone formation
-calcification of soft tissues
-hypercalcemic crisis

21
Q

What is primary hyperparathyroidism?

A

-common endocrine disorder of parathyroid hyperfunction
-makes too much PTH due to formation of benign adenoma
-hypercalcemia
-low phosphate
-high bone turnover
-kidney stones

22
Q

treatment for primary hyperparathyroidism?

A

parathyroidectomy may be recommended

23
Q

What are the two inherited forms of familial primary hyperparathyroidism?

A

MEN 1 and MEN 2

24
Q

What is MEN 1?

A

multiple endocrine neoplasia type I
-inactivation of tumor suppressor gene Menin

25
Q

What is MEN 2?

A

multiple endocrin neoplasia type II
-due to gain of function mutation in RET protooncogene
-AD
-milder than MEN 1

26
Q

Heterozygotes for inactive CaSR=

A

familial hypocalciruic hypercalcemia

27
Q

Homozygotes for CaSR=

A

neonatal severe hyperparathyroidism

28
Q

What is hypercalcemia of malignancy?

A

hypercalcemia due to tumors secreting factors that stimulate bone resorption

29
Q

What is secondary hyperparathyroidism?

A

oversecretion of PTH in response to conditions of hypocalcemia and/or decreases 1,25(OH)2D3

30
Q

What causes secondary hyperparathyroidism?

A

usually chronic renal failure
-could be vitamin D malabsorption

31
Q

Definition of hypophosphatemia:

A

<2.5 mg/dl-4.5 mg/dl

32
Q

Causes of hypophosphatemia:

A

-decreased intestinal absorption of phosphate
-increased urinary excretion
-redistribution of extracellular fluid into cells/tissues

33
Q

What is X linked hypophosphatemic rickets?

A

most common disorder of renal phosphate wasting
-due to mutations in PHEX gene on X chromosome
-X linked dominant

34
Q

What makes PHEX?

A

osteoblasts, osteocytes, and odontoblasts

35
Q

What does PHEX do normally?

A

inhibit FGF23 production

36
Q

What do XLH mutation of PHEX lead to?

A

inappropriately elevated FGF23 production

37
Q

What happens when FGF23 is mutated?

A

reduce renal reabsorption of phosphate
-lead to renal phosphate wasting

38
Q

What is XLH treatment?

A

-phosphate supplementation/high dose calcitriol
-limb deformations may need surgery

39
Q

What is ADHR?

A

autosomal dominant hypophosphatemic rickets
-rare form of inherited rickets
-due to mutations in FGF23 that alter cleavage site so it cannot be activated

40
Q

What is ARHR?

A

autosomal recessive hypophosphatemic rickets
-mutations in Dmp1
-lead to overproduction of FGF23

41
Q

What is HHRH?

A

hereditary hypophosphatemic rickets with hypercalcuria
-rare inherited form
-due to heterozygous or homozygous loss of function mutations in type II sodium phosphate cotransporter NaPiIIc

42
Q

What is the treatment for HHRH?

A

phosphate supplements alone (NOT CALCITRIOL)

43
Q

What is TIO?

A

tumor induced osteomalacia
-acquired syndrome of renal phosphate wasting
-cause alteration in Pi metabolism that mimic hypophosphatemic rickets

44
Q

What can help treat TIO?

A

surgical resection of tumor
-may also require supplementation with phosphate and calcitriol

45
Q

What are symptoms of acute hyperphosphatemia?

A

-hypocalcemia
-suppress 1 alpha hydroxylase activity in kidney

46
Q

What are symptoms of chronic hyperphosphatemia?

A

-soft tissue calcification, renal failure, secondary hyperparathyroidism, renal osteodystrophy

47
Q

What are some causes of hyperphosphatemia?

A

-acute phosphate load
-decreased urinary excretion
-redistribution to extracellular space
-genetic causes of hyperphosphatemia

48
Q

Treatments for hyperphosphatemia:

A

administration of phosphate binding salts

49
Q

Why does calcium and phosphate apply to dental care?

A

-need to be aware of how they impact the patient
-increased incidence of periodonitis/periapical abcesses
-vit-D depended rickets have dental abnormalities
-enlarged pulp chambers

Biochem Exam 5 (12 decks)

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