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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
osteoitis fibrosa cystica
The hallmark of severe hyperparathyroidism, rare. | -Combination of: increased osteoclast activity, peritrabecular fibrosis, and cystic brown tumors
26
Describe osteopersosis.
Increased osteoclast activity, resulting in decreased bone mass. Preferentially involving phalanges, vertebrae, and femur.
27
What is dessecting osteitis?
Because osteoclast activity in hyperparathyroidism first eats through cortical bone, they then tunnel centrally through the trabeculae and create a railroad track appearance.
28
Why do brown tumors develop?
(Osteoperotic) bone loss leads to microfractures and secondary hemorrhages --> influx of macrophages and reparative fibrous tissue --> creating a (brown) mass of reactive tissue.
29
Why are brown tumors brown?
Vascularity, hemorrhage, and hemosiderin deposition (common in cystic generation).
30
Three organs (other than skeletal system) that are affected by hyperparathyroidism.
1. Nephrolithiasis (dt PTH induced hyperCa) 2. Nephrocalcinosis (calcification of tubules/interstitium) 3. Calcification in stomach, lungs, myocardium, blood vessels
31
What is the most common cause of asx hypercalcemia (discovered only bc of routine blood draw) v. sx hypercalcemia.
hyperparathyroidism (asx) v. malignancy (sx)
32
Location of solid tumors common causing hypercalcemia.
Lung, breast, H//N, renal
33
Main hematologic malignancy causing hypercalcemia.
Multiple myeloma.
34
Main cause of hypercalcemia of malignancy.
typcially caused by tumor secretion fo PTH-related peptide (PTHrP)
35
Labs in primary hypercalcemia.
PTH - increased Ca - increased Phosphate - hypo
36
Clinical sx of primary hyperparathyroidism
Bone disease/pain, nephrolithiasis, GI sx, CNS sx, Neuromuscular, Cardiac (AV/MV calcification)
37
- Hyperplastic parathyroid glands, may be asymmetric. | - Increased number of chief cells (diffuse or multinodular)
Secondary hyperparathyroidism
38
Most common cause of secondary hyperparathyroidism
renal failure - (any condition that causes overactive PT gland that leads to chronic hypoCa)
39
Where can metastatic calcification in secondary hyperparathyroidism be seen?
lungs, heart, stomach, blood vessels
40
Define calciphylaxis
vascular calcification --> ischemic damage to skin and other organs.
41
Treatment of secondary hyperparathyroidism
Vit D supplements and phsophate binders
42
When parathyroids become autonomous and excessive
Tertiary hyperparathyroidism
43
Treatment of tertiary hyperparathyroidism
removal of parathyroids
44
Most common cause of hypoparathyroidism
Accidental surgical removal during thyroidectomy.
45
Causes of autoimmune hypoparathyroidism
autoimmune polyendocrine syndrome type 1
46
___ = chronic mucocutaneous candidiasis + primary adrenal insufficiency
autoimmune polyendocrine syndrome type 1 (APS1)
47
GOF mutation in calcium sensing receptor gene (CASR) causes what?
AD hypoparathyroidism
48
Function of CASR
PTH suppression = hypoCa
49
Difference between AD and AR Familial Isolated Hypoparathyroidism
``` AD = mutation in PTH maturation AR = LoF mutation of GCM2 (needed for PT devleopment) ```
50
Clincial manfestation of hypocalcemia
Tetany! Mental status chagne, paradoxical calcifications (basal ganglia --> parkinsonian likemvmt disorder), lens and catraract formation, heart (QT prolongation), denta abnormalities
51
What is end organ resistance to PTH
Pseudohypoparathyroidism
52
Lab presentation of pseudohypoparathyroidism
PTH - normal or increased Ca - decreased Phosphate - hyperphosphatemia
53
Lab presentation of hypoparathyroidism
PTH - decreased Ca - decreased Phosphate - hyperphosphatemia

Endocrine Two (16 decks)

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