Parathyroid Disorders Flashcards

1
Q

What are the main organs involved in calcium and phosphate homeostasis?

A

Bone, kidneys, gastrointestinal tract

These organs work together to regulate levels of calcium and phosphate in the body.

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2
Q

What hormone regulates plasma calcium and phosphate levels?

A

Parathyroid hormone (PTH)

PTH plays a critical role in maintaining calcium and phosphate balance.

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3
Q

What is the role of vitamin D in calcium-phosphate homeostasis?

A

Regulates calcium and phosphate absorption and metabolism

Vitamin D is essential for the proper utilization of calcium and phosphate.

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4
Q

What is the function of fibroblast growth factor-23 (FGF23)?

A

Inhibits renal phosphate reabsorption and vitamin D synthesis

FGF23 helps to regulate phosphate levels in the body.

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5
Q

What is the reference range for total calcium in blood?

A

8.6 to 10.2 mg/dL; 2.2 to 2.6 mmol/L (SI)

These values indicate the normal concentration of calcium in the bloodstream.

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6
Q

What percentage of calcium in the blood is ionized (active form)?

A

~ 50%

Ionized calcium is the biologically active form of calcium.

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7
Q

What is the reference range for ionized calcium?

A

4.5 to 4.9 mg/dL; 1.12 to 1.23 mmol/L (SI)

Ionized calcium levels are critical for various physiological functions.

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8
Q

What is the reference range for serum phosphate?

A

3 to 4.5 mg/dL; 0.97 to 1.45 mmol/L (SI)

Serum phosphate levels are vital for energy storage and bone health.

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9
Q

How is calcium absorbed in the intestine?

A

Transcellular active transport and paracellular passive process

Calcium absorption is regulated by vitamin D and occurs mainly in the duodenum and upper jejunum.

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10
Q

What is the role of osteoblasts in bone mineralization?

A

Secrete collagen I and express alkaline phosphatase (ALP)

Osteoblasts are essential for the formation and mineralization of bone.

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11
Q

What hormone is synthesized by the chief cells of the parathyroid glands?

A

Parathyroid hormone (PTH)

PTH is crucial for calcium homeostasis and is stimulated by low calcium levels.

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12
Q

What is the effect of FGF23 on phosphate transporters in the proximal convoluted tubule (PCT)?

A

Decreases expression of phosphate transporters

This leads to increased renal phosphate excretion.

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13
Q

What is the primary mechanism of calcium reabsorption in the kidneys?

A

Proximal convoluted tubule (65%) and thick ascending limb (25%)

Calcium reabsorption is regulated by sodium and PTH.

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14
Q

What is the role of calcitonin in calcium homeostasis?

A

Lowers blood calcium levels

Calcitonin is secreted by the thyroid gland and counteracts the effects of PTH.

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15
Q

What is the active form of vitamin D?

A

1,25-dihydroxycholecalciferol (calcitriol)

Calcitriol is crucial for calcium and phosphate absorption in the intestines.

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16
Q

What is the primary site of phosphate absorption in the intestine?

A

Throughout the small intestine

Phosphate absorption is also regulated by vitamin D.

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17
Q

True or False: Osteoclasts are responsible for bone resorption.

A

True

Osteoclasts break down bone tissue, releasing calcium and phosphate into the bloodstream.

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18
Q

What is the effect of PTH on bone resorption?

A

Stimulates bone resorption

PTH increases calcium levels in the blood by promoting the activity of osteoclasts.

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19
Q

What condition can result from mutations in the PHEX gene?

A

Increased plasma FGF23 levels

This can lead to hypophosphatemia and related disorders.

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20
Q

Fill in the blank: The primary excretion of calcium occurs through the _______.

A

bile

Calcium excretion in the intestine is larger than that in the kidney.

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21
Q

What is the role of sodium-potassium ATPase in phosphate absorption?

A

Maintains sodium gradient for sodium-phosphate transporters

This gradient is crucial for the active transport of phosphate in the intestines.

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22
Q

What is the impact of chronic kidney disease on calcium and phosphate homeostasis?

A

Increased phosphate retention and decreased calcium levels

This can lead to secondary hyperparathyroidism and bone disorders.

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23
Q

What is PTH?

A

Parathyroid hormone, synthesized and stored in glands, responds within minutes to hypocalcemia

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24
Q

Where are the parathyroid glands located?

A

Posterior aspect of the thyroid, sometimes five glands

25
Q

What does decreased serum calcium stimulate?

A

Stimulates osteoclasts to resorb bone, releasing calcium into the blood

26
Q

What are the effects of PTH on the kidneys?

A

Reduces calcium clearance and increases synthesis of 1,25-dihydroxyvitamin D; promotes excretion of phosphate

27
Q

What is the role of calcium and vitamin D in relation to PTH?

A

They provide negative feedback to PTH

28
Q

What is primary hyperparathyroidism?

A

Condition where a parathyroid adenoma produces excess PTH, leading to excess calcium

29
Q

What are the classic symptoms associated with primary hyperparathyroidism?

A
  • Stones
  • Bones
  • Groans
  • Thrones
  • Psychiatric Overtones
30
Q

How is primary hyperparathyroidism diagnosed?

A
  • Elevated calcium
  • Elevated PTH
  • Sestamibi scan
  • 24-hour urinary calcium
31
Q

What is the treatment for primary hyperparathyroidism?

A

Parathyroidectomy

32
Q

What is secondary hyperparathyroidism?

A

Condition characterized by normal or low calcium levels and elevated PTH, often due to chronic kidney disease

33
Q

How is secondary hyperparathyroidism diagnosed?

A

Exclude normocalcemic primary hyperparathyroidism and measure vitamin D levels

34
Q

What causes tertiary hyperparathyroidism?

A

Progression from secondary hyperparathyroidism to autonomous overproduction of PTH

35
Q

What is familial hypocalciuric hypercalcemia?

A

Condition due to inactivating mutation of gene for calcium-sensing receptor, leading to excessive renal calcium re-uptake

36
Q

What is the most common cause of hypoparathyroidism?

A

Removal or damage to parathyroid glands during neck surgery

37
Q

What is pseudohypoparathyroidism?

A

Condition with tissue resistance to PTH due to defective Gs protein in the kidney

38
Q

What are the phenotypes associated with pseudohypoparathyroidism?

A
  • Albright Hereditary Osteodystrophy (type 1a)
  • Normal PTH with defective Gs protein imprinted from father
  • Phenotypes: short 4th & 5th metatarsals and metacarpals, rounded faci, intellectual disability
39
Q

What are the signs and symptoms of hypercalcemia?

A
  • Fatigue
  • Depression
  • Mental confusion
  • Anorexia
  • Nausea/vomiting
  • Constipation
  • Increased urine output
  • Short QT on EKG
40
Q

What is the treatment for hypercalcemia?

A
  • Hydration
  • Furosemide
  • Bisphosphonates
  • Calcitonin
  • Glucocorticoids
  • Dialysis
41
Q

What causes vitamin D intoxication?

A

Ingestion of 40-100x normal physiologic amounts of vitamin D

42
Q

What are the management strategies for hypercalcemia associated with high bone turnover?

A
  • Avoid excessive sunlight exposure
  • Limit vitamin D and calcium intake
43
Q

What is the treatment for hypocalcemia?

A

Oral calcium and vitamin D, may add thiazide diuretics

44
Q

What are the components of MEN-1 syndrome?

A
  • Parathyroid
  • Pancreas
  • Pituitary
  • Adrenal
45
Q

What are the components of MEN-2A syndrome?

A
  • Medullary thyroid carcinoma
  • Pheochromocytoma
  • Parathyroid
46
Q

What are Chovstek’s and Trousseau signs indicative of?

A

Hypocalcemia

47
Q

what is the role of FGF23

A

suppression of PTH

48
Q

what region of the nephron does PTH act on to increase Ca reabsorption

49
Q

how does PTH indirectly increase GI reabsorption of calcium

A

promotes synthesis of Vit. D

50
Q

T or F: Vit. D. is a steroid hormone

51
Q

PTH increases the expression of what enzyme to promote Vit. D. activiation

A

25-hydroxcyvitamin D 1-alpha hydroxylase

52
Q

Henry Whitaker, whom you diagnosed w/ Vit. D. deficiency, presents to your clinic 6 months later with progressive Vit. D deficiency symptoms. However, he claims he has been compliant w/ his Vit. D. supplements. He has a medical history opioid abuse and a PE revealed epigastric tenderness. you suspect a hepatobiliary disease may be the culprit for this pts. clinical presentations. Explain why you as the physician would screen this pt. for hepatobiliary diseases in the context of a pseudo-Vit. D deficiency.

A

Vit. D. is converted into its active form in the PCT stimulated by PTH
However, in order for Vit. D. to be used where it is needed in the body, it must first be secreted into bile and reabsorbed by entero hepatic circulation. Given the pt.’s h/o opioid abuse, choletheiasis should be considered if epigastric tenderness is present.

53
Q

what effect does Vit. D have on the kidneys

A

increased phosphate reabsorption

54
Q

Chronically elevated levels of Calcium increases the risk for kidney stones in the CD which can lead to what hormonal disease?

A

nephrogenic DI

55
Q

describe the pathogenesis of primary hyperparathyroidism.

A

excessive secretion of PTH by the parathyroid gland; lab-work up would reveal hypercalcemia, elevated PTH, and hypophosphatemia

56
Q

what is the pathogenesis of secondary hyperparathyroidism

A

excess PTH secondary to prolonged hypocalcemia
main causes: Vit. D. deficiency, CKD

57
Q

what characterizes tertiary hyperparathyroidism?

A

advanced progression of poorly controlled secondary hyperparathyroidism

58
Q

composite a list of conditions that can cause hypoparathyrodism

A

Direct Injury to the PTG: iatrogenic (such as surgery) or idiopathic (like autoimmune)
hypomagnesemia
DiGeorge Syndrome
Gestational hypocalcemia
maternal hyperparathyroidism
Decreased sensitization to PTH: receptors defects within the PTG or PTH sensitive tissues
CKD
Vit. D deficiency

59
Q

T or F: Tumor Lysis syndrome and rhabdomyolysis can cause transient hyperparathyroidism

A

false
The PTH-related effect of cellular lysis is the release of intracellular phosphate and myoglobin breakdown; the former causes acute hyperphosphatemia while the latter contributes to hypocalcemia