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Endo II - Path (Tobin) > Lecture 3: Parathyroid Pathology > Flashcards

Lecture 3: Parathyroid Pathology Flashcards

1
Q

In early infancy and childhood, the parathyroid glands are composed almost entirely of what cell type?

A

Chief cells

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2
Q

What are the 3 histological characteristics of the Chief Cells of the parathyroid glands?

A
  • Central round, uniform nuclei
  • Light pink or white cytoplasm (water-clear appearance)
  • Secretory granules
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3
Q

Which cells of the parathyroid hormone contain large amounts of cytoplasmic glycogen and secretory granules containing PTH?

A

Chief cells

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4
Q

Which cells of the parathyroid gland have an acidophilic cytoplasm and are tightly packed with mitochondria?

A

Oxyphil cells

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5
Q

In order to maintain calcium homeostasis, what are the 4 actions of PTH?

A
  1. ↑ renal reabsorption of Ca2+
  2. ↑ conversion of Vit D —> active 1,25(OH)2D form in kidneys
  3. ↑ urinary phosphate excretion
  4. Augments GI Ca2+ absorption
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6
Q

Secondary hyperparathyroidism is a compensatory hypersecretion of PTH in response to prolonged hypocalcemia, most commonly in the setting of what?

A

Chronic renal failure

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7
Q

What are 3 causes of PRIMARY hyperparathyroidism; which is most common?

A
  1. Adenoma **most common*****
  2. Primary Hyperplasia
  3. Parathyroid carcinoma
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8
Q

Which 2 molecular defects/mutations have an established role in the development of sporadic parathyroid adenomas?

A
  1. Cyclin D1 gene overxpression (due to Cyclin D1 Inversion)
  2. MEN1 mutations
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9
Q

*MEN1* mutations are associated with parathyroid adenomas in which 2 ways?

Which way is more common?

A
  • Germline mutations causing familial MEN1 and can manifest w/ parathyroid adenomas
  • MORE common is _SPORADIC**_ parathyroid adenomas, with SOMATIC*** MEN1 mutations
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10
Q

Which 2 genetic syndromes are associated with familial parathyroid adenoma;

What is the associated gene mutated in each?

A
  • MEN type 1 associated w/ MEN1
  • MEN type 2 associated w/ RET
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11
Q

Familial hypocalciuric hypercalcemia is a rare disorder due to _which genetic mutation_?

What is the mode of inheritance?

A
    • CASR
    • - Loss-of-function mutation in parathyroid calcium-sensing receptor gene
    • Autosomal dominant
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12
Q

What is the typical *microscopic finding* in parathyroid adenomas?

What is the dominant cell type?

A
  • A: Polygonal cells (Chief cells that are uniform, w/ small, centrally placed nuclei)
  • A few nests of larger oxyphil cells are present as well
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13
Q

What is “endocrine atypia” in relation to the morphology of some parathyroid adenomas?

A

-A: Not uncommon to find bizarre and pleomorphic nuclei; this is not a criterion for malignancy

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14
Q

What type of parathyroid adenoma may resemble a Hurthle cell tumor in the thyroid?

A

-A: Oxyphil adenoma (uncommon)

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15
Q

Which _morphological feature of the normal parathyroid glands_ is inconspicous/missing in adenomas and hyperplasia?

A
  • A: Adipose tissue
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16
Q

How does parathyoid adenoma differ vs. hyperplasia ?

(in # of glands involved?)

A
  • A: Affects ONLY 1 lobe

- Adenoma are almost always solitary ( affects only _1_ lobe),

- _Hyperplasia_ almost always present in _multiple_ glands

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17
Q

What morphologic change** distinguishes parathyroid **ADENOMA vs parathyroid hyperplasia?

A
  • A: NORMAL rim of parathyroid tissue typically surrounds an an adenoma ,
  • Hyperplasia does NOT have a normal rim of parathyroid tissue
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18
Q

What are the only reliable diagnostic criteria for parathyroid carcinoma?

A

- A:

  1. Metastasis = most telltale sign! ***
  2. Invasion of surrounding tissues or vasculature
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19
Q

Parathyroid carcinomas are often hard to distinguish from _______?

A
  • A: Adenomas
  • Why? Both are solitary and enclosed by fibrous capsule
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20
Q

What 3 interrelated skeletal abnormalities can manifest as a result of symptomatic, untreated hyperparathyroidism?

A
  • A:
  1. Osteoporosis
  2. Brown tumors ****
  3. Osteitis fibrosa cystica
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21
Q

The osteoporosis associated with symptomatic, untreated hyperparathyroidism preferentially involves which 3 bones?

A

- A:

1. Phalanges

2. Vertebrae

3. Prox. femur

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22
Q

The osteoclast activity associated with hyperparathyroidism affects what type of bone more severly?

A

- A: Cortical bone

(i.e., subperiosteal and endosteal surfaces)

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23
Q

In untreated hyperparathyroidism, what do the osteoclasts do in medullary bone?

Create what appearance?

A
  • Tunnel into and dissect centrally along the length of the trabeculae
  • Create appearance of rail-road tracks aka dissecting osteitis
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24
Q

What are the 3 hallmarks of severe hyperparathyroidism and is known as generalized osteitis fibrosa cystica (von Recklinghausen disease of bone)?

A
  • Osteoclast-driven bone destruction –> microfractures + hemorrhage
  • Peritrabecular fibrosis
  • Cystic brown tumors (STARTS as a brown tumor)
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25
Q

What is the pathophysiological process underlying the development of brown tumors?

A
  • A: Bone loss predisposes to ==> microfractures and 2’ hemorrhages
  • which elicits influx of macrophages and ingrowth of reparative fibrous tissue creating a mass
26
Q

- Q: PTH-induced hypercalcemia may lead to the formation of ______________ & ___________

A
  • A: Urinary tract stones (nephrolithiasis) & Nephrocalcinosis (calcification of the renal interstitium and tubules)
27
Q

The cystic brown tumors of osteitis fibrosis cystica can resemble what?

A

Metastatic disease

28
Q

What is the most common cause of asymptomatic hypercalcemia?

A

- A: Primary hyperparathyroidism

29
Q

What is the most frequent cause of symptomatic hypercalcemia in adults?

A

Malignancy (i.e., breast, lung, head/neck and renal cancers)

30
Q
  • Q: Osteolytic tumors induce hypercalcemia by which most common mechanism?
A

- A: PTHrP secretion

PTH-related peptide (PTHrP)

31
Q

What are the levels of PTH and Ca2+ like in PRIMARY hyperparathyroidism?

A
  • A: BOTH HIGH
  • ↑ PTH + ↑Ca2+
  • When Ca2+ levels are ↑, levels of PTH should be ↓ due to negative feedback
32
Q

Other than Ca2+ and PTH, what other lab values can point to PTH excess?

A
  • Hypophosphatemia
  • ↑ urinary excretion of both calcium and phosphate
33
Q

What 5 GI manifestations may result from 1’/PRIMARY hyperparathyroidism?

(increased PTH secretion and hypercalcemia hyperparathyroidism)

A
  1. Constipation
  2. Nausea
    • Peptic ulcers
    • Pancreatitis
    • Gallstones
34
Q

What are 3 CNS alterations of 1’ hyperparathyroidism?

(increased PTH secretion and hypercalcemia)

A
  1. Depression
  2. Lethargy
  3. Eventually seizures
35
Q

What are 2 neuromuscular abnormalities may result from PRIMARY hyperparathyroidism?

A
  1. Weakness
  2. Fatigue
36
Q

What are 2 cardiac manifestations may result from PRIMARY hyperparathyroidism?

A
  1. Aortic calcification
  2. Mitral calcification

Or BOTH

37
Q

Nephrolithiasis and Bone disease are abnormalities most directly related to what setting of primary hyperparathyroidism?

A

↑↑↑ PTH

(hyperparathyroidism)

38
Q

Fatigue, weakness, pancreatitis, metastatic calcifications, and constipation are abnormalities most directly attributable to what in the setting of PRIMARY hyperparathyroidism?

A

- A: Hypercalcemia

39
Q

What is the most common cause of SECONDARY hyperparathyroidism and list 3 other causes?

A
  1. Renal failure = most common****
  2. Vit D deficiency
  3. Inadequate dietary intake of Ca2+
  4. Steatorrhea (malabsorption of ADEK
40
Q

What are 5 causes of hypercalcemia which are associated with ↓ [PTH]?

A
    • Hypercalcemia of malignancy
    • Vit D toxicity
    • Immobilization
    • Thiazide diuretics
    • Granulomatous disease (sarcoidosis)
41
Q

What is the morphology of the parathyroid glands in secondary hyperparathyroidism?

A

-A: hyperplastic

(as a result of reactive hyperplasia)

42
Q

The skeletal abnormalities are usually not as severe or as prolonged in of SECONDARY hyperparathyroidism. This is known as what?

(as compared to primary hyperparathyroidism)

A
  • A: Renal osteodystrophy
43
Q

SECONDARY hyperparathyroidism may present as what IMAGE FINDING?

A
  • A: “Rugger Jersey Sign”

(Renal osteodystrophy associated w/ SECONDARY hyperparathyroidism)

44
Q

What is Calciphylaxis in the setting of secondary hyperparathyroidism?

A

-A: Extensive calcification and occlusion of blood vessels w/ resultant ischemia

45
Q

-Q: Vitamin D mediated- hypercalcemia of malignancy are seen with what type of tumors?

A
  • A: Lymphomas
46
Q

Local osteolytic hypercalcemia is associated with what 2 types of tumors?

(due to the release of Ca2+ as a result of osteoclastic _bone_ resorption)

A
  1. Breast carcinoma
  2. Myeloma
47
Q

Acquired hypoparathyroidism is almost always a consequence of what?

A

- A: Surgery

48
Q

Autoimmune hypoparathyroidism is often associated with what underlying condition?

A

Auto-immune polyendocrine insufficiency syndrome type 1 (APS1)

49
Q

Auto-immune polyendocrine insufficiency syndrome type 1 (APS1) is due to mutations in what gene?

A

Autoimmune regulator (AIRE) gene

50
Q

When does Auto-immune polyendocrine insufficiency syndrome type 1 (APS1) typically present and what are the manifestations of this disease?

A
  • During childhood w/ onset of candidiasis
  • Followed several years later by hypoparathyroidism
  • Then adrenal insufficiency during adolescence
51
Q
  • Q: Autosomal-Dominant hypoparathyroidism is caused by gain-of-function mutations in which gene?
A

- A: CASR gene

Calcium-sensing receptor (CASR) gene

52
Q

Inappropriate CASR activity in autosomal-dominant hypoparathyroidism leads to what serum and urine calcium levels?

A

- A: HYPOcalcemia and HYPERcalciuria**

53
Q

Familial isolated hypoparathyroidism (FIH) can be inherited via AD or AR patterns.

How does each differ and which mutation is seen?

A
  • AD = due to mutation in gene encoding PTH precursor peptide, which impairs its processing to the mature hormone
  • AR = due to loss-of-function mutations in the transcription factor gene glial cells missing-2 (GCM2), essential for parathyroid development
54
Q

Congenital absence of parathyroid glands can occur in conjunction with what?

A
  1. Thymic aplasia
  2. Cardiovascular defects
  3. Part of 22q11 deletion syndrome (i.e., DiGeorge Syndrome)
55
Q

What is the hallmark of hypocalcemia?

A
  • A: Tetany

(aka neuromuscular irritability or MUSCLE SPAMS)

56
Q

What are 3 intracranial manifestations which may result from chronic hypocalcemia?

A
    • Calcifications of the basal ganglia
    • Parkinsonian-like movement disorders
    • ↑ ICP —> papilledema
57
Q

What are _2 eye manifestations_ may occur in the setting of hypocalcemia?

A
  1. Lens Calcification
  2. Cataract formation
58
Q

What is an ECG Finding of hypocalcemia?

A

- A: Prolonged QT interval

Conduction defect –> prolongation of the QT interval on ECG

59
Q

What is the pathophysiology of Pseudohypoparathyroidism?

A
  • A: E__n_d-organ RESISTANCE_

(due to the actions of PTH)

60
Q
  • Q: One form of Pseudohypoparathyroidism also shows resistance to what other hormones?

- Q: Why?

A
  • A:
  1. TSH
  2. FSH/LH
  • A: Due to PTH acting thru a GPCR **
61
Q
  • Q: What are the serum levels of Ca2+, PTH, and PO43-, in Pseudohypoparathyroidism?
A
  1. ↓ HYPOcalcemia
  2. ↑ PTH *** WTF***
  3. ↑ HYPERphosphatemia
62
Q

Which condition presents with hypocalcemia despite a high serum PTH?

A
  • A: Pseudohypoparathyroidism

[WTF]

Endo II - Path (Tobin) (6 decks)

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