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Endocrine Two > Parathyroid Pathology > Flashcards

Parathyroid Pathology Flashcards

1
Q

A cell with central, round, uniform nuclei. It has light to dark pink cytoplasm, sometimes clear from glycogen - “water clear”. Contain secretory granules.

A

Chief Cells

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2
Q

What is in secretory granules of Chief Cells?

A

PTH

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3
Q

A cell with acidophilic cytoplasm, tightly packed with micotchondria.

A

Oxyphil cells

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4
Q

What type of granules do oxyphil cells have?

A

Glycogen granules. Sparse/absent secretory granules.

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5
Q

Size of oxyphil cells compared to chief cells.

A

Oxyphil slightly larger than chief.

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6
Q

Function of the parathyroid. What type of conditions stimulate hormone release?

A

Regulates calcium by synthesizing and secreting PTH when free calcium levels are low.

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7
Q

Name the four functions of PTH

A
  1. Increase renal tubular reabsorption of Ca
  2. Increase urinary phosphate excretion
  3. Increase conversion of Vit D to active dihydroxy form in kidneys (augment GI Ca absorption)
  4. Release Ca and phosphorus from bone.
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8
Q

What inhibits the parathyroid?

A

High calcium levels inhibit PTH secretion.

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9
Q

Causes of hypercalcemia with increased PTH concentration (four).

A
  1. Hyperparathyroidism - (a) Primary (adenoma > hyperplasia). (b) Secondary. (c) Tertiary.
  2. Familial hypocalciuric hypercalcemia.
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10
Q

Causes of hypercalcemia with decreased PTH concentration (five).

A
  1. Hypercalcemia of malignancy
  2. Vit D toxicity
  3. Immobilization
  4. Thiazide diuretics
  5. Granulomatous disease (sarcoidosis)
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11
Q

Describe the main differences between the causes of primary, secondary, and tertiary hyperparathyroidism.

A
  • Primary - autonomous over production of PTH (adenoma)
  • Secondary - Compensatory hypersecretion of PTH in response to prolonged hypocalcemia (CKF) –> overactive PT glands.
  • Tertiary - hypersecretion fo PTH after cause of prolonged hypoCa is corrected (post renal transplant)
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12
Q

Predominant Sex of those with primary hyperparathyroidism.

A

female (4:1)

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13
Q

Most common cause of primary hyperparathyroidism.

A

Parathyroid Adenoma

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14
Q

Two main molecular defects and two main familial syndromes that play a role in development of sporadic parathyroid (?) adenoma.

A

Molecular: Cyclin D1 inversion, MEN1/RET mutation
Familial: MEN1/2, Familial hypocalciuric hypercalcemia

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15
Q

Normal function of Cyclin D1 and MEN1.

A

Cyclin D1 - major regulator of cell cycle

MEN1 - tumor suppressor gene

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16
Q

Describe genetic cause of familial hypocalciuric hypercalcemia.

A

LoF mutations in parathyroid Calcium-Sensing Receptor Gene (CASR), leading to decreased sensitivity to extracellular calcium.

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17
Q

A solitary, well-circumscribed tumor that is hypercellular - with little to no fat - composed of uniform chief cells, few (or predominantly) nests of larger oxyphil cells.

A

Parathyroid adenoma

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18
Q

Describe PTgland that surrounds the parathyroid adenoma.

A

Usually normal in size or shrunken form feedback inhibition by elevated Ca.

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19
Q

Describe the edge of a parathyroid adenoma.

A

Usually there is a rim of nonneoplastic parathyroid tissue, generally separated by a fibrous capsule.

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20
Q

If a parathyroid adenoma is composed of primarily oxyphil cells, what is it called?

A

Oxyphil adenoma

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21
Q

Main morphological difference between parathyroid hyperplasia and parathyroid adenoma.

A

Hyperplasia involves all four glands. Adenoma is usually one gland.

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22
Q

Morphology of parathyroid hyperplasia.

A

ALL FOUR GLANDS are classically INVOLVED with weight of all glands > 1gm. Hypercellular with little to no fat.

23
Q

What type of cell hyperplasia is seen in parathyroid hyperplasia?

A

Chief cell hyperplasia - diffusely or multinodular.

24
Q

Although a very rare cause of hypercalcemia, what is the critical diagnostic criteria for parathyroid carcinoma?

A
  • **Necessary for diagnosis: Invasion of surrounding tissues and/or metastasis.
  • Looks like a normal parathyroid.
25
Q

osteoitis fibrosa cystica

A

The hallmark of severe hyperparathyroidism, rare.

-Combination of: increased osteoclast activity, peritrabecular fibrosis, and cystic brown tumors

26
Q

Describe osteopersosis.

A

Increased osteoclast activity, resulting in decreased bone mass. Preferentially involving phalanges, vertebrae, and femur.

27
Q

What is dessecting osteitis?

A

Because osteoclast activity in hyperparathyroidism first eats through cortical bone, they then tunnel centrally through the trabeculae and create a railroad track appearance.

28
Q

Why do brown tumors develop?

A

(Osteoperotic) bone loss leads to microfractures and secondary hemorrhages –> influx of macrophages and reparative fibrous tissue –> creating a (brown) mass of reactive tissue.

29
Q

Why are brown tumors brown?

A

Vascularity, hemorrhage, and hemosiderin deposition (common in cystic generation).

30
Q

Three organs (other than skeletal system) that are affected by hyperparathyroidism.

A
  1. Nephrolithiasis (dt PTH induced hyperCa)
  2. Nephrocalcinosis (calcification of tubules/interstitium)
  3. Calcification in stomach, lungs, myocardium, blood vessels
31
Q

What is the most common cause of asx hypercalcemia (discovered only bc of routine blood draw) v. sx hypercalcemia.

A

hyperparathyroidism (asx) v. malignancy (sx)

32
Q

Location of solid tumors common causing hypercalcemia.

A

Lung, breast, H//N, renal

33
Q

Main hematologic malignancy causing hypercalcemia.

A

Multiple myeloma.

34
Q

Main cause of hypercalcemia of malignancy.

A

typcially caused by tumor secretion fo PTH-related peptide (PTHrP)

35
Q

Labs in primary hypercalcemia.

A

PTH - increased
Ca - increased
Phosphate - hypo

36
Q

Clinical sx of primary hyperparathyroidism

A

Bone disease/pain, nephrolithiasis, GI sx, CNS sx, Neuromuscular, Cardiac (AV/MV calcification)

37
Q
  • Hyperplastic parathyroid glands, may be asymmetric.

- Increased number of chief cells (diffuse or multinodular)

A

Secondary hyperparathyroidism

38
Q

Most common cause of secondary hyperparathyroidism

A

renal failure - (any condition that causes overactive PT gland that leads to chronic hypoCa)

39
Q

Where can metastatic calcification in secondary hyperparathyroidism be seen?

A

lungs, heart, stomach, blood vessels

40
Q

Define calciphylaxis

A

vascular calcification –> ischemic damage to skin and other organs.

41
Q

Treatment of secondary hyperparathyroidism

A

Vit D supplements and phsophate binders

42
Q

When parathyroids become autonomous and excessive

A

Tertiary hyperparathyroidism

43
Q

Treatment of tertiary hyperparathyroidism

A

removal of parathyroids

44
Q

Most common cause of hypoparathyroidism

A

Accidental surgical removal during thyroidectomy.

45
Q

Causes of autoimmune hypoparathyroidism

A

autoimmune polyendocrine syndrome type 1

46
Q

___ = chronic mucocutaneous candidiasis + primary adrenal insufficiency

A

autoimmune polyendocrine syndrome type 1 (APS1)

47
Q

GOF mutation in calcium sensing receptor gene (CASR) causes what?

A

AD hypoparathyroidism

48
Q

Function of CASR

A

PTH suppression = hypoCa

49
Q

Difference between AD and AR Familial Isolated Hypoparathyroidism

A 
AD = mutation in PTH maturation
AR = LoF mutation of GCM2 (needed for PT devleopment)
50
Q

Clincial manfestation of hypocalcemia

A

Tetany!
Mental status chagne, paradoxical calcifications (basal ganglia –> parkinsonian likemvmt disorder), lens and catraract formation, heart (QT prolongation), denta abnormalities

51
Q

What is end organ resistance to PTH

A

Pseudohypoparathyroidism

52
Q

Lab presentation of pseudohypoparathyroidism

A

PTH - normal or increased
Ca - decreased
Phosphate - hyperphosphatemia

53
Q

Lab presentation of hypoparathyroidism

A

PTH - decreased
Ca - decreased
Phosphate - hyperphosphatemia

Endocrine Two (16 decks)

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