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Applied Biochemistry > Hormonal Control of Calcium and Phosphate: Part 2 > Flashcards

Hormonal Control of Calcium and Phosphate: Part 2 Flashcards

1
Q

Hypocalcemia

A

low serum calcium

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2
Q

Hypercalcemia

A

high serum calcium

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3
Q

Hypophosphatemia

A

low serum phosphate

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4
Q

Hyperphosphatemia

A

high serum phosphate

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5
Q

Calcium and Phosphate Homeostasis can be

Disrupted in Many Different ways: (7)

A

•Dietary deficiency or excess of calcium, (phosphate), vitamin D
•Mutations in genes for Vitamin D receptor, 25-OH-vitamin D 1α-
hydroxylase enzyme
•Elevated or decreased PTH (parathyroid tumors, CaSR mutations,
agenesis of parathyroid glands, loss of parathyroid tissue due to
thyroid surgery)
•Insensitivity of tissues to PTH (inactivating mutations in G-proteins
important for PTH receptor signaling)
•Mutations in phosphate transporter molecules (NaPi-IIc)
•Mutations in FGF23 or regulators of FGF23 (Dmp1, PHEX)
•Chronic kidney disease

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6
Q

Chronic kidney disease affects Ca2+ /Pi homeostasis because

A

impaired kidney function interferes with Ca2+ and Pi reabsorption

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7
Q

Hypocalcemia - blood calcium concentration…

A

below normal range (<1.1-1.35 mM ionized calcium)

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8
Q

Symptoms of hypocalcemia (depending on rapidity of onset and whether hypocalcemia is mild or severe): (6)

A
  • Muscle cramping
  • Muscle spasms
  • Increased neuromuscular excitability
  • Fatigue
  • Cardiac dysfunction
  • Depression, psychosis, seizures
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9
Q

causes of hypocalcemia (6)

A

inadequate PTH production
syndromes with component of hypoparathyroidism
PTH resistance
inadequate vitamin D
vitamin D resistance or synthesis defects
miscellaneous

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10
Q

SKIPPED

Inadequate PTH production examples (7)

A

•PTH gene mutations
•Hypoparathyroidism due to parathyroid agenesis/X-linked
hypoparathyroidism
•Parathyroidectomy as a complication of thyroid surgery
•Constitutively active CaSR mutations (OMIM# 601198)
(autosomal dominant hypocalcemia)
•Autoimmune (e.g. Antibodies that activate the CaSR)
•Post radiation therapy
•Tumors that metastasize to parathyroid

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11
Q

SKIPPED

Syndromes with component of hypoparathyroidism examples (5)

A 
•DiGeorge syndrome 
•HDR (hypoparathyroidism, deafness, renal anomalies) 
syndrome 
•Kenney-Caffey syndrome 
•Sanjad-Sakati syndrome 
•Kearns-Sayre syndrome
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12
Q

SKIPPED
Vitamin D resistance or synthesis defects
(Vitamin D dependent Rickets) example (1)

A

•Mutations in VDR or 1αhydroxylase

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13
Q 
SKIPPED
Miscellaneous examples (3)
A

•Drugs (e.g. i.v. bisphosphonate therapy in patients with
vitamin D insufficiency/deficiency)
•Osteoblastic metastases
•Acute pancreatitis

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14
Q

Hypoparathyroidism(undersecretion of PTH) is relatively

A

rare (<200,000 cases in USA)

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15
Q

Hypocalcemia with serum PTH inappropriately low for

A

hypocalcemic state

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16
Q

Most common cause of hypoparathyroidism

A

autoimmune destruction of parathyroids/loss of parathyroids due to thyroidectomy

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17
Q

Loss of PTH producing tissue results in

A

hypocalcemia due to
decreased Ca2+ uptake in gut/kidney, decreased Ca2+
release from bone

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18
Q

Di George Syndrome –

A

congenital disease with complete lack of

parathyroids at birth

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19
Q

Hypoparathyroidism Treatment: no approved — replacement therapy

A

hormonal

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20
Q

Conventional treatment of hypoparathyroidism– mainly

A

calcium and calcitriol [1,25 (OH)2D3] supplementation (but can increase risk of kidney stones due to hypercalciuria)

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21
Q

(2) have been in clinical trials - PTH
1-84 now approved in USA/Europe as adjunctive
treatment for patients not well controlled with
conventional therapy

A

PTH 1-34 and PTH 1-84

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22
Q

Hypoparathyroidism Associated with

Activating CaSR Mutations

A

Autosomal dominant hypocalcemia - ADH

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23
Q

Constitutively activating mutations in CaSR cause

A

autosomal dominant hypocalcemia

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24
Q

CaSR signals constitutively even though Ca2+ levels are

A

low (i.e.parathyroid “misreads” Ca2+ levels as high and inappropriately suppresses PTH)

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25
Q

Decreases Ca2+ reabsorption in kidney (more excreted in

urine) and decreases release from bone, uptake in gut, etc which leads to

A

low serum Ca2+

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26
Q

Treatment of Hypoparathyroidism Associated with

Activating CaSR Mutations

A

mainly calcium and calcitriol [1,25 (OH)2D3]
supplementation but there can be complications of hypercalciuria
(too much calcium in urine) with Ca2+ supplementation

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27
Q

Pseudohypoparathyroidism

A

Insensitivity to PTH

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28
Q

Pseudohypoparathyroidism is hypocalcemia due to

A

not due to lack of PTH but due to lack
of responsiveness of target tissues to PTH (hence
“pseudohypoparathyroidism”)

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29
Q

in pseudohypoparathyroidism, serum PTH is high as

A

parathyroid gland keeps trying to

respond to correct the low serum Ca2+

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30
Q

Pseudohypoparathyroidism is due to mutations in

A

G proteins important for PTH signaling

esp. Gsalpha

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31
Q

Pseudohypoparathyroidism is —

A

rare

approx 0.7 per 100,000

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32
Q

More common cause of hypocalcemia than hypoparathyroidism

A

vitamin D deficiency

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33
Q

Vitamin D Deficiency can be due to (3)

A

dietary deficiency,
lack of sunlight,
malabsorption of vitamin D

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34
Q

Lack of vitamin D inhibits

A

Ca2+ and Pi uptake in gut (due to

downregulation of calcium and phosphate transport proteins, Calbindins, TRPV6, NaPi-IIb)

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35
Q

Vitamin D Deficiency in children leads to

A

rickets

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36
Q

rickets (3)

A
  • Impaired bone mineralization/outward curvature of long bones (bowing)
  • Insufficiently mineralized vertebrae/curved spine
  • Disorganized growth plate/growth retardation
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37
Q

Vitamin D Deficiency in adults leads to

A

osteomalacia

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38
Q

osteomalacia

A

failure of osteoid to fully calcify - soft bones

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39
Q

osteomalacia is due to

A

low serum calcium and phosphate

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40
Q

Low serum Ca2+ / Pi normally requires what kind of vitamin D deficiency?

A

long term severe

deficiency of Vit D

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41
Q

characteristic of vitamin D deficient rickets

A

Metaphyseal cupping (flaring)/”fuzzy growth plate

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42
Q

VDDR type I is also known as

A

pseudovitamin D deficiency rickets

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43
Q

VDDR type I inheritance

A

AR

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44
Q

VDDR type I is a defect in

A

renal 25-OH-vitamin D-1α-hydroxylase

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45
Q

VDDR type I is low

A

serum Ca, Pi

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46
Q

VDDR type I is high

A

PTH

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47
Q

VDDR type I is very low

A

1,25(OH)2D3

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48
Q

VDDR type II is also known as

A

hereditary vitamin D resistant rickets

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49
Q

VDDR type II inheritance

A

AR

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50
Q

VDDR type II is a defect in

A

vitamin D receptor (VDR)

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51
Q

VDDR type II several — identified

A

mutations

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52
Q

VDDR type II is low

A

serum Ca, Pi

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53
Q

VDDR type II is high

A

PTH

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54
Q

VDDR type II: — in some patients

A

alopecia

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55
Q

VDDR type II is elevated

A

1,25(OH)2D3

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56
Q

pseudohypoparathyroidism
(lack of responsiveness to PTH)
•Mutation in — gene involved in PTH receptor signaling

A

GNAS

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57
Q

Hypoparathyroidism (under production of PTH)
•Parathyroid agenesis (Di George syndrome)
•Autoimmune destruction of —
•Loss of parathyroid tissue during — —-
•Activating CaSR mutations which inappropriately

A

parathyroid
thyroid surgery
suppress PTH secretion

58
Q

Vitamin D Deficient Rickets is due to

A
  • Dietary/ malabsorption

* Low sunlight

59
Q

Vitamin D Dependent Rickets
•Type I - Mutation in
•Type II – Mutation in

A

renal 25-OH- vitamin D-1α-hydroxylase

Vitamin D receptor

60
Q

Hypercalcemia –

A

blood calcium concentration higher

than normal range (>1.1-1.35mM ionized)

61
Q

symptoms of hypercalcemia (7)

A
  • Fatigue
  • Electrocardiogram abnormalities
  • Nausea, vomiting, constipation
  • Anorexia
  • Abdominal pain
  • Hypercalciuria/kidney stone formation
  • Calcification of soft tissues – (e.g. vasculature).
62
Q

Hypercalcemic crisis occurs at — ionized serum

calcium

A

> 2.5mM (emergency situation – can lead to, anuria/oliguria,

coma, somnolence)

63
Q

causes of hypercalcemia (3)

A

elevated PTH levels
elevated 1,25(OH)2D3 levels
miscellaneous

64
Q

SKIPPED

cause of elevated PTH levels in hypercalcemia (5

A
  • Primary Hyperparathyroidism
  • Familial hyperparathyroidism (MEN, FHH, HPT-JT)
  • Inactivating mutations of CaSR
  • Secondary to hypophosphatemia
  • Secondary to parathyroid tumors
65
Q

SKIPPED

causes of Elevated 1,25(OH)2D3 levels in hypercalcemia (1)

A

Hypervitaminosis D (vitamin D intoxication)

66
Q

SKIPPED

miscellaneous causes of hypercalcemia (2)

A

•Hypercalcemia of malignancy – due to tumor production of
factors which stimulate bone resorption (e.g. PTHrP)
•Severe dehydration – will increase serum Ca2+ concentration
without changing total blood calcium

67
Q

Primary Hyperparathyroidism (PHPT) is a relatively common

A

endocrine disorder of parathyroid

hyperfunction (PTH oversecretion) (1 in 500 – 1 in 1000)

68
Q

Usually, 1 of 4 parathyroid glands makes too much PTH

due to

A

development of benign adenoma resulting in

excessive PTH synthesis/secretion (85% of cases)

69
Q

Hypercalcemia

A

PTH hypersecretion not adequately
inhibited by normal negative feedback response to
elevated Ca2+

70
Q

in Primary Hyperparathyroidism (PHPT),
•Phosphate usually —
•High — —-
•Kidney stones due to

A

low (decreased renal reabsorption)
bone turnover (increased resorption and formation)
hypercalciuria

71
Q

treatment of Primary Hyperparathyroidism (PHPT)

A

parathyroidectomy

72
Q

MEN1 (2)

A

•Due to inactivation of tumor suppressor gene Menin (gene
name MEN, One copy of gene is mutated, but “second hit”
needed for tumor formation
•Rare: 2-3 per 100,000 (accounts for ~2% of 1o HPT cases)

73
Q

MEN2A (3)

A
  • Due to gain of function mutation in RET protooncogene
  • AD inheritance
  • Generally milder than MEN1
74
Q

Mutations in MEN result in

A

neoplastic tumors in several endocrine tissues (and other tissues), including parathyroids – i.e. more PTH secretion

75
Q

Heterozygotes for inactive CaSR have

A

familial

hypocalciuric hypercalcemia

76
Q

in familial primary hyperthyroidism, CaSR doesn’t signal even though

A

Ca2+ levels are high (i.e.
parathyroid misreads Ca2+ levels as being low) therefore
PTH is inappropriately elevated

77
Q

familial primary hyperthyroidism results in

A

elevated serum Ca2+ and lower than normal Pi

78
Q

Familial Primary Hyperparathyroidism is largely

A

asymptomatic

79
Q

Familial Primary Hyperparathyroidism homozygotes have

A

neonatal severe hyperparathyroidism

NSHPT

80
Q

neonatal severe hyperparathyroidism

(NSHPT) is potentially

A

fatal - requires parathyroidectomy

81
Q

Hypercalcemia can occur due to

A

tumors secreting factors that
stimulate bone resorption (e.g.
breast cancer, myeloma)

82
Q

Some cancers, e.g. (2)
secrete PTHrP - mimics PTH
actions

A

squamous

carcinomas, some breast cancers,

83
Q

Causes severe problems due to (2)

A

bone degradation and elevated

serum calcium

84
Q

Hypercalcemia of Malignancy can be

A

life threatening

85
Q

Secondary Hyperparathyroidism

A

Oversecretion of PTH in response to conditions of

hypocalcemia and/or decreased 1,25(OH)2D3

86
Q

most common cause of Secondary Hyperparathyroidism

A

chronic renal failure

87
Q

why is chronic renal failure the most common cause of secondary hyperparathyroidism

A

ailing kidneys can’t produce much 1,25(OH)2D3, which normally inhibits PTH, and do not excrete Pi adequately, resulting in insoluble calcium phosphate forming and removal of Ca2+ from circulation

88
Q

Secondary Hyperparathyroidism can also be caused by

A

vit D malabsorption

89
Q

Secondary Hyperparathyroidism treatment

A

aimed at correctly the underlying cause of the hypocalcemia

90
Q

Secondary Hyperparathyroidism is usually improved in patients who undergo

A

kidney transplant

91
Q

In patients with chronic renal failure- (4)

A

dietary P restriction,
VitD supplements,
phosphate binders,
calcimimetics (stimulate CaSR)

92
Q

Hypophosphatemia

A

Phosphate levels lower than normal range (<0.8-1.5mM)

<2.5-4.5mg/dL

93
Q

Hypophosphatemia is relatively common- occurs in

A

5% of hospitalized
patients (increases to 30% in alcoholics and patients w/
severe sepsis)

94
Q

causes of Hypophosphatemia (3)

A

Decreased intestinal absorption of phosphate
Increased urinary excretion
Redistribution from extracellular fluid into cells/tissues

95
Q

SKIPPED

Decreased intestinal absorption of phosphate (5)

A

•Dietary Vitamin D deficiency/low sun exposure
•Vitamin D receptor defects/synthetic defects
•Malabsorption of vitamin D (Celiac Disease, Crohn’s disease,
bowel resection, gastric bypass, chronic diarrhea, etc.)
•Nutritional deficiencies (alcoholism, anorexia, starvation)
•Antacids containing aluminum/magnesium

96
Q

SKIPPED

Decreased intestinal absorption of phosphate (4)

A
  • Renal phosphate wasting disorders
  • Primary and secondary hyperparathyroidism (i.e. increased PTH)
  • Mutations in FGF23 (PHEX or Dmp1)
  • Mutations in NaPi-IIc (sodium/phosphate cotransporter gene)
97
Q

SKIPPED
Increased urinary excretion
Redistribution from extracellular fluid into cells/tissues (3)

A

•Hungry bone syndrome (increased demand for calcium and
phosphate for bone formation after parathyroidectomy)
•Refeeding syndrome (after starvation)
•Treatment of diabetic ketoacidosis

98
Q

Rickets/Osteomalacia are Diseases

Associated with

A

Hypophosphatemia

99
Q

X-linked Hypophosphatemic

Rickets (XLH) is the most common disorder of

A

renal phosphate wasting, (3.9–5

per 100,000 live births)

100
Q

features of XLH (4)

A

growth retardation, rachitic/ osteomalacic bone

disease, dental abscesses, weak bones (fractures)

101
Q

XLH is due to

A

mutations in PHEX gene on X-chromosome (phosphate-

regulating gene with homologies to endopeptidases on the X chromosome)

102
Q

XLH inheritance pattern

A

x linked dominant

103
Q

how many mutations described of XLH?

A

> 400

104
Q

PHEX produced by (3)

A

osteoblasts, osteocytes, odontoblasts

105
Q

PHEX normally inhibits

A

FGF23 production

106
Q

XLH mutations of PHEX lead to

A

inappropriately elevated
FGF23 production, even though serum phosphate is low
(mainly by osteocytes)

107
Q

FGF23 reduces

A

renal reabsorption of phosphate (leads to

renal phosphate wasting - i.e. more excreted in urine)

108
Q

XLH results in

  • — serum Pi
  • — (2ry to reduced renal phosphate reabsorption)
  • — 1,25(OH)2D3 (should be elevated with low serum Pi, but inhibited by FGF23)
A

low
phosphaturia
low

109
Q

XLH Treatment (2)

A

Phosphate supplementation

high dose calcitriol

110
Q

XLH treatment response to treatment depends on

A

age of patient at time of initiation

111
Q

XLH may require surgical intervention to correct

A

limb deformities

112
Q

Treatment of XLH can be reduced to

A

lower doses of phosphate and/or calcitriol or no medications in some adults

113
Q

Clinical trials started using — — as a new

therapy for XLH

A

FGF23 antibodies

114
Q

ADHR: (2)

A

•Rare form of inherited hypophosphatemic rickets- symptoms
similar to XLH
•Due to mutations in FGF23 that alter cleavage site so it
cannot be proteolytically inactivated – FGF23 stays active
longer

115
Q

ARHR: (4)

A

•Recessively inherited hypophosphatemic rickets - symptoms
similar to XLH
•Due to mutations in Dmp1
•Dmp1 expressed by osteocytes and negatively regulates
FGF23
•Mutation in Dmp1 leads to overproduction of FGF23

116
Q

HHRH

A

Hereditary Hypophosphatemic Rickets with Hypercalciuria

117
Q

HHRH is a rare inherited form of

A

hypophosphatemic rickets

118
Q

HHRH due to

A

heterozygous or homozygous loss of function
mutations in type II sodium phosphate cotransporter
NaPiIIc (gene name SLC34A3

119
Q

HHRH is clinically similar to

A

XLH but with elevated levels of 1,25

(OH)2D3

120
Q

treatment of HHRH

A

phosphate supplements alone (not calcitriol)

121
Q

XHL, ADHR, and ARHR1 lead to increased

A

FGF23

122
Q

HHRH is due to reduced function of

A

Na+ dependent phosphate transporter which is a

target gene of FGF23

123
Q

Tumor Induced Osteomalacia (TIO) is an acquired syndrome of

A

renal phosphate wasting

124
Q

Factors secreted into circulation by tumors
cause alterations in Pi metabolism that
mimic

A

hyophosphatemic rickets

125
Q

Serum biochemistry of TIO is the same as for

A

hypophosphatemic rickets

126
Q

Children with TIO display

A

rickets-like

features

127
Q

FGF23 levels go down with

A

surgical
resection of tumor – may require
supplementation with phosphate and
calcitriol

128
Q

Symptoms of acute (short term) hyperphosphatemia: (2)

A

•Hypocalcemia (muscle tetany, etc.) (due to calcium precipitating with phosphate in soft tissues, reducing serum calcium)
•Suppresses 1 α-hydroxylase activity in kidney, lowering
1,25D3 levels, which further exacerbates hypocalcemia by
reducing Ca2+ uptake in gut/renal reabsorption

129
Q

Chronic hyperphosphatemia symptoms: (2)

A

•Soft tissue (incl. vasculature) calcification, renal failure, 2ry
hyperparathyroidism, renal osteodystrophy.
•Hyperphosphatemia from renal failure plays a key role in
development of secondary hyperparathyroidism

130
Q

Symptoms of hyperphosphatemia mainly related to

A

knock-on effects on calcium homeostasis

131
Q

causes of hyperphosphatemia (4)

A

Acute Phosphate load (increased intestinal uptake)
Decreased urinary excretion
Redistribution to extracellular space
Genetic causes of hyperphosphatemia (Familial Tumoral calcinosis)

132
Q

SKIPPED

Acute Phosphate load (increased intestinal uptake) (2)

A
  • Phosphate containing laxatives/enemas

* Rapid administration of phosphate (oral, I.V. rectal)

133
Q

SKIPPED

Decreased urinary excretion (3)

A
  • Renal insufficiency/failure
  • Secondary to hypoparathyroidism /pseudohypoparathyroidism
  • Vitamin D intoxication
134
Q

SKIPPED

Redistribution to extracellular space (2)

A
  • Metabolic/respiratory acidosis/diabetic ketoacidosis

* Severe systemic infections

135
Q

SKIPPED

Genetic causes of hyperphosphatemia (Familial Tumoral calcinosis) (3)

A
  • Inactivating mutations in FGF23
  • Inactivating mutations of Klotho (FGF23 receptor)
  • Others
136
Q

Treatment of hyperphosphatemia involves administration of

A

phosphate binding salts – calcium, magnesium, aluminum. Aluminum avoided in patients with renal failure

137
Q

Dentists should understand how disorders of Ca2+ / Pi

metabolism

A

impact the patient (e.g. short stature, weak,

undermineralized skeleton, defects in alveolar bone)

138
Q

Increased incidence of periodontitis/periapical abcesses

suggested in patients with

A

hypophosphatemic

rickets/osteomalacia

139
Q

Some patients with Vit D-dependent rickets have dental

abnormalities - such as

A

thin enamel, hypomineralization→

microscopic cracks harbor bacteria → frequent cavities.

140
Q

Patients with hypercalcemia of malignancy often treated

with

A

high dose bisphosphonates – risk of developing BONJ

141
Q

what are commonly seen with hyperphosphatemia?

A

Poor muscle tone (hypotonia)/ muscle weakness are

common/ seizures can occur

Applied Biochemistry (52 decks)

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