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Endocrine Exam > Parathyroid Gland Pathology > Flashcards

Parathyroid Gland Pathology Flashcards

1
Q

What do chief cells look like?

A
  • Central round, uniform nuclei
  • Light pink or white cytoplasm
  • Secretory granules
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2
Q

What do oxyphil cells look like?

A
  • Smaller, darker nuclei
  • Eosinophilic granular material
  • Less endocrinologically active
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3
Q

What is the principle function of the parathyroid gland?

A
  • Calcium homeostasis
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4
Q

What does the parathyroid hormone do?

A
  • Directly releases calcium from bone

- Exerts effects on the kideny

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5
Q

What effects does parathyroid hormone have on the kidneys?

A
  • Calcium resorption –> blocks phosphate resorption

- Conversion of 25(OH)D to 1,25(OH)2D in the kidney –> further mobilizes calcium from bone and intestine

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6
Q

How does the parathyroid gland know what to do?

A
  • Calcium-sensing receptor (CaSR) regulates the amount of PTH secreted from the parathyroid glands
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7
Q

What does low serum calcium result in?

A
  • Increased PTH secretion
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8
Q

What does high serum calcium result in?

A
  • PTH repression
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9
Q

What is the most common cause of primary hyperparathyroidism?

A
  • Adenoma
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10
Q

What are the symptoms of primary hyperparathyroidism?

A
  • Painful bones
  • Renal stones
  • Abdominal groans
  • Psychic moans
  • “Bones, stones, groans, and moans”
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11
Q

What causes the painful bones in primary hyperparathyroidism?

A
  • Osteoporosis

- Osteitis fibrosis cystica

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12
Q

What causes the abdominal groans in primary hyperparathyroidism?

A
  • Constipation

- Gallstones

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13
Q

What causes the psychic moans in primary hyperparathyroidism?

A
  • Depression
  • Lethargy
  • Seizures
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14
Q

What is osteitis fibrosis cystica?

A
  • Starts as a brown tumor
  • Osteoclast-driven bone destruction
  • Small fractures
  • Hemorrhage and reactive tissue
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15
Q

What is the main way that primary hyperparathyroidism is diagnosed?

A
  • In an asymptomatic patient, through routine bloodwork
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16
Q

What is a parathyroid adenoma?

A
  • Benign neoplasm of parathyroid chief or oxyphil cells
  • Typically solitary
  • Can be surrounded by a rim of normal parathyroid tissue
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17
Q

What happens to the other parathyroid glands in a parathyroid adenoma?

A
  • The other glands atrophy due to the abnormal levels of PTH and calcium
18
Q

What is parathyroid hyperplasia?

A
  • Almost always present in multiple glands
  • Secondary hyperplasia is MUCH more common
  • No normal rim of parathyroid tissue
19
Q

What may be responsible for parathyroid hyperplasia?

A
  • MEN syndromes (rare sporadic forms)
20
Q

How do you tell the difference between adenoma and hyperplasia?

A
  • One gland affected: adenoma

- Multiple glands affected: hyperplasia

21
Q

What is the treatment for an adenoma?

A
  • Surgery excision

- Within minutes of excision, hormone levels with fall

22
Q

What is the telltale sign of parathyroid carcinoma?

A
  • Metastasis

- Highly suggestive sings: invasive of adjacent tissue and vascular invasion

23
Q

What does the hypercalcemia cause in hyperparathyroidism?

A
  • Most likely to be asymptomatic or have subtle symptoms

- Most commonly due to parathyroid adenoma

24
Q

What does hypercalcemia cause in non-parathyroid sources?

A
  • More likely to be overt/symptomatic

- Mental status changes, N/V, EKG changes – shortened QT interval

25
Q

What the humoral hypercalcemia of malignancy?

A
  • PTHrP –> analogous to PTH seen in squamous carcinomas

- Vitamin D-mediated –> lymphomas

26
Q

What is local osteolytic hypercalcemia?

A
  • Release of calcium - osteoclastic bone resorption (breast carcinoma and myeloma)
27
Q

What causes high PTH levels and low calcium levels?

A
  • Secondary hyperplasia due to reduced kidney function
28
Q

What is the typical endpoint in secondary hyperplasia?

A
  • 4-gland hyperplasia
29
Q

What is renal osteodystrophy?

A
  • Dissecting osteitis in hyperparathyroidism

- In secondary hyperparathy, renal osteodystrophy can lead to “Rugger Jersey Sign”

30
Q

What is calciphylaxis?

A
  • Secondary hyperparathyroidism can lead to extensive calcification and occlusion of blood vessels with resultant ischemia
31
Q

What happens in tertiary hyperparathyroidism?

A
  • After prolonged hypocalcemia, the parathyroid goes into autopilot and continuously pumps out PTH, even after calcium levels are fixed
32
Q

What are some clinical features of hypocalcemia?

A
  • Behavioral disturbance/stupor
  • Numbness and paresthesias
  • Muscle cramps, spasms
  • Convulsions
33
Q

What are some physical exams signs of hypocalcemia?

A
  • Trousseau sign positive
  • Chvostek sign positive
  • Prolonged QT interval on ECG
34
Q

What are some causes of acquired primary hypoparathyroidism?

A
  • Iatrogenic

- Autoimmune

35
Q

What are some causes of congenital primary hypoparathyroidism?

A
  • DiGeorge syndrome
  • CASR germline mutations (activating) – familial hypocalcemic hypercalciuria
  • Familial isolated hypoparathyroidism
36
Q

What is DiGeorge syndrome?

A
  • Developmental defects in 3rd to 4th pharyngeal pouches

- Parathyroid glands may be absent or underdeveloped

37
Q

What is CASR germline mutations (activating) – familial hypocalcemic hypercalciuria?

A
  • Hyperactive calcium-sensing receptors
38
Q

What is familial isolated hypoparathyroidism?

A
  • Precursor PTH can’t get all the way to functional PTH
39
Q

What happens in an inactivating CaSR mutation?

A
  • Thinks there isn’t enough calcium even when there is
  • Turns on PTH causing hypercalcemia
  • Reduces renal excretion causing hypocalciuria
40
Q

What happens in activating CaSR mutation?

A
  • Thinks there is plenty of calcium even when there isn’t
  • Turns off PTH causing hypocalcemia
  • Increases renal excretion causing hypercalcemia
41
Q

What is psedohypoparathyroidism?

A
  • Normal or elevated PTH
  • Hypocalcemia
  • Hyperphosphatemia
42
Q

What causes pseudohypoparathyroidism?

A
  • Resistance to PTH
  • Related to G-protein receptor pathways
  • Can affect other hormone pathways: TSH, LH/FSH

Endocrine Exam (11 decks)

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