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Neuroendocrine I: Exam 3 > Calcium and Phosphate Homeostasis > Flashcards

Calcium and Phosphate Homeostasis Flashcards

1
Q

Symptoms of Hypocalcemia

A
  • Hyperreflexia
  • Spontaneous twitching
  • Muscle cramp
  • Numbness
  • Chvostek sign
  • Trousseau sign
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2
Q

What is the Chvostek sign?

A
  • Twitching of the facial muscles elicited by tapping on facial nerve near anterior ear
  • Due to hypocalcemia
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3
Q

What is the Trousseau sign?

A
  • Carpopedal spasm upon inflation of a blood pressure cuff

- Due to hypocalcemia

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4
Q

Symptoms of Hypercalcemia

A
  • Decreased QT interval
  • Constipation
  • Lack of appetite
  • Polyuria
  • Polydipsia
  • Muscle weakness
  • Hyporeflexia
  • Lethargy
  • Coma
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5
Q

How does hypocalcemia influence membrane excitability?

A
  • Low extracellular Ca2+ reduces activation threshold for Na+ channels making it easier to evoke an AP –> increases membrane excitability
  • Generation of spontaneous AP = physical basis of hypocalcemic tetany (spontaneous muscle contractions)
  • Produces tingling & numbness (on sensory neurons) and spontaneous muscle twitches (on motoneurons and muscle)
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6
Q

How does hypercalcemia influence membrane excitability?

A
  • High extracellular Ca2+ raises activation threshold for Na+ channels making it difficult to evoke an AP –> decreases membrane excitability and ability to produce spontaneous AP
  • NS depressed and reflex responses are slowed
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7
Q

How can the forms of Ca2+ in plasma be altered?

A
  1. Changes in [plasma protein] - increase [plasma protein] results in increased total [Ca2+]
  2. Changes in [anion] results in a change in the fraction of Ca2+ complexed w/ anions - increase [Pi] results in decreased ionized [Ca2+]
  3. Acid/base abnormalities - acidemia (excess H+) results in an increase in free ionized Ca2+ b/c less is bound to albumin and in alkalemia, the opposite occurs b/c more Ca2+ bound to albumin
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8
Q

Regulation of PTH: chronic hypercalcemia

A
  • Causes decreased synthesis and storage of PTH

- Increased breakdown of stored PTH and release of inactive PTH fragment into circulation

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9
Q

Regulation of PTH: chronic hypocalcemia

A
  • Causes increased synthesis and storage of PTH

- Hyperplasia of parathyroid glands (secondary hyperparathyroidism)

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10
Q

Actions of PTH and Vitamin D on bone

A
  • PTH receptors located on OSTEOBLASTS
    a. Short term –> bone formation via direct action on osteoblast
    b. Long term –> increase bone resorption via indirecct action on osteoclasts mediated by M-CSF, IL-6 and RANKL released from osteoblast
  • Vitamin D –> acts w/ PTH to stimulate osteoclast activity and bone resorption through osteoblasts
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11
Q

Actions of PTH and Vitamin D on bone: RANKL and OPG lvls

A
  • PTH: increases RANKL and decreases OPG secretion from osteoblasts
  • Vitamin D: increases RANKL secretion from osteoblasts
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12
Q

Actions of PTH on the kidney

A
  • Stimulates 1alpha-hydroxylase activity to promote the formation of active vitamin D
  • Stimulates Ca2+ reabsorption at thick ascending limb of Henle’s loop and distal tubule
  • Inhibits Pi reabsorption at proximal tubule by inhibiting NPT2a expression
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13
Q

Actions of Vitamin D on intestines

A
  • Increases Ca2+ absorption by upregulating the transcription of:
    a. Epithelial Ca2+ channel TRPV6 –> increased entry of Ca2+ from lumen into cell
    b. Calbindin –> reservoir/shuttle for ICF Ca2+ to bring to plasma side
    c. Plasma membrane Ca2+ ATPase –> allows Ca2+ to reach plasma
    d. Plasma membrane Na+/Ca2+ exchanger

-Increases Pi absorption by upregulating transcription of Na+/K+ ATPase and Na+-Pi cotransporter

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14
Q

Actions of Vitamin D on kidneys

A

-Promotes Pi reabsorption at proximal tubules by stimulating NPT2a expression

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15
Q

Actions of Vitamin D on the parathyroid gland

A
  • Directly inhibits PTH gene expression

- Directly stimulates Ca2+ Sensing Receptor gene expression

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16
Q

Actions of Calcitonin

A
  • high lvls of Ca2+ stimulate its release by parafollicular C cells in the thyroid gland
  • Decreases Ca2+ and Pi concentrations by:
    a. Inhibiting bone resorption (at high lvls of circulating calcitonin) –> receptors expressed on OSTEOCLASTS resulting in decreased activity and number of osteoclasts
    b. reduces Ca2+ uptake in kidneys
17
Q

Effects of estradiol-17beta on Ca2+/Pi regulation

A
  • Stimulates intestinal Ca2+ absorption
  • Stimulates renal tubular Ca2+ reabsorption
  • Promotes survival of osteoblasts and apoptosis of osteoclasts –> bone formation
18
Q

Effects of adrenal glucocorticoids (e.g. cortisol) on Ca2+/Pi regulation

A
  • Promotes bone resorption
  • Promotes Ca2+ wasting
  • Inhibits intestinal Ca2+ absorption
  • Pts treated w/ high lvls of glucocorticoids can develop glucocorticoid-induced osteoporosis
19
Q

Primary hyperparathyroidism

A

-Caused by an adenoma of the parathyroid gland which is over-producing PTH causing hypercalcemia/hypophosphatemia by:

a. Increased bone resorption (Ca2+ & Pi released to blood)
b. At the kidney it is increasing Ca2+ reabsorption, Pi excretion, and activation of vitamin D
c. Increased activation of vitamin D –> increased Ca2+ absorption by intestinal mucosa

20
Q

Expected lab values (PTH, Ca2+, Pi and vitamin D) compared to normal in: Primary hyperparathyroidism

A
  • PTH: increased
  • Ca2+: increased
  • Pi: decreased
  • Vitamin D: increased
21
Q

Expected lab values (PTH, Ca2+, Pi and vitamin D) compared to normal in: Secondary hyperparathyroidism due to renal failure

A
  • PTH: increased –> secondary to low [Ca2+]
  • Ca2+: decreased
  • Pi: increased ** –> kidneys unable to properly excrete Pi and decreased activity of 1alpha-hydroxylase
  • Vitamin D: decreased
22
Q

Expected lab values (PTH, Ca2+, Pi and vitamin D) compared to normal in: Secondary hyperparathyroidism due to vitamin D deficiency

A
  • PTH: increased –> secondary to low [Ca2+]
  • Ca2+: decreased
  • Pi: decreased ** –> lack of vitamin D causes decreased ability to absorb Ca2+ and Pi
  • Vitamin D: decreased
23
Q

Expected lab values (PTH, Ca2+, Pi and vitamin D) compared to normal in: Hypoparathyroidism

A
  • PTH: decreased
  • Ca2+: decreased (hypocalcemia)
  • Pi: increased (hyperphosphatemia) –> due to decreased ability to excrete at kidney
  • Vitamin D: decreased
24
Q

Symptoms of Hypoparathyroidism

A

Most associated w/ hypocalcemia:

  • Muscle spasm or cramping
  • Numbness, tingling or burning (esp around mouth and fingers)
  • Seizures
  • Poor teeth development and mental deficiency in kids
25
Q

Albright hereditary osteodystrophy (Pseudohypoparathyroidism type 1a)

A
  • Inherited autosomal dominant disorder in which the Gs for PTH in bone and kidney is defective
  • Hypocalcemia and hyperphosphatemia develop but there is an increase in PTH (PTH resistance)
  • Administration of exogenous PTH produces no phosphaturic response and no increase in urinary cAMP lvls
26
Q

Expected lab values (PTH, Ca2+, Pi and vitamin D) compared to normal in: Albright hereditary osteodystrophy

A
  • PTH: increased ***
  • Ca2+: decreased
  • Pi: increased
  • Vitamin D: decreased
27
Q

Symptoms/phenotype of Albright hereditary osteodystrophy (Pseudohypoparathyroidism type 1a)

A
  • Short stature
  • Short neck
  • Obesity
  • Subcutaneous calcification
  • Shortened MT and MCs
28
Q

Humoral hypercalcemia of malignancy

A

-Tumor produces PTH-related peptide (PTHrP) which can bind and activate some of the same receptors of PTH to elicit a similar profile to primary hyperparathyroidism (hypercalcemia/hypophosphatemia):

a. Increased bone resorption (Ca2+ & Pi released to blood)
b. At the kidney - increasing Ca2+ reabsorption and Pi excretion

BUT it differs in that there is a decrease in PTH and vitamin D lvls due to negative feedback on PTH and inability to stimulate the activation of 1alpha-hydroxylase

29
Q

Expected lab values (PTH, Ca2+, Pi and vitamin D) compared to normal in: Humoral hypercalcemia of malignancy

A
  • PTH: decreased
  • Ca2+: increased
  • Pi: decreased
  • Vitamin D: decreased
30
Q

Familial Hypocalciuric hypercalcemia (FHH)

A

-Autosomal dominant disorder resulting in a mutation which inactivates the Ca2+ Sensing Receptors in the parathyroid gland and ascending limb of the kidney –> unable to sense [Ca2+] and not able to properly inhibit PTH secretion or determine to secrete/reabsorb Ca2+:

a. decreased urinary Ca2+ excretion (hypocalciuria)
b. increased serum [Ca2+] (hypercalcemia)

31
Q

Expected lab values (PTH, Ca2+, Pi and vitamin D) compared to normal in: Familial Hypocalciuric Hypercalcemia

A
  • PTH: normal to increased
  • Serum Ca2+: increased
  • Urine Ca2+: decreased
  • Pi: normal
  • Vitamin D: normal
32
Q

Congenital pseudovitamin D-deficient/vitamin D-dependent rickets type I versus type II

A
  • Type I due to decrease in 1alpha-hydroxylase –> unable to produce active vitamin D
  • Type II due to decrease in vitamin D receptor –> unable to elicit effects of vitamin D but have normal lvls of active vitamin D
33
Q

Clinical manifestations of osteomalacia

A

Nutritional deficiency in vitamin D could be caused by GI disorder resulting in malabsorption, suboptimal nutrition or inadequate sun exposure

  • Bone pain and muscle weakness
  • Bone tenderness
  • Fracture
  • Muscle spasms, cramps, + Chvostek’s sign, tingling/numbness (hypocalcemia)
34
Q

Expected lab values (PTH, Ca2+, Pi, vitamin D, urine, bone) compared to normal in: Vitamin D deficiency (rickets vs osteomalacia)

A
  • PTH: increased (secondary hyperparathyroidism)
  • Ca2+: normal to decreased
  • Pi: decreased
  • Vitamin D: decreased (very low serum 25-OH, vitamin D –> decreased absorption of Ca2+ and Pi)
  • Urine: increased Pi and cAMP
  • Bone: increased resorption in osteomalacia

Neuroendocrine I: Exam 3 (18 decks)

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