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Endocrine & Reproduction II Exam #2 > Parathyroid Pathology > Flashcards

Parathyroid Pathology Flashcards

1
Q

Which 3 cell types exist in the parathyroid glands?

What is their histology?

A

Chief cells: central round, uniform nuclei. Light pink/white cytoplasm w/ secretory granules.

Oxyphil cells: smaller, darker nuclei. Eosinophilic granular material (mitochondria). Less endocrinologically active.

Adipose cells

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2
Q

What are the 3 major functions of PTH? How?

A

Releases Ca++ from bone by activating osteoclast activity (increased [Ca++].

Acts on kidney to hold Ca++ and increase vitamin D levels.

Acts on the SI to increase absorption of Ca++.

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3
Q

What is the relationship between calcium and phosphorus levels?

A

Inverse correlation

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4
Q

How do the parathyroid glands know when to adjust [Ca++] (to increase or decrease)?

A

The CaSR (calcium-sensing receptor) regulates the amount of PTH secreted from the gland.

Low serum Ca++ = increased PTH
High serum Ca++ = decreased PTH

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5
Q

What are the 3 major causes of primary hyperparathyroidism? Which is most common?

A

Adenoma - most common
Primary hyperplasia
Parathyroid carcinoma - least common

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6
Q

What are the levels of PTH and [Ca++] like in primary hyperparathyroidism?

A

Both are elevated

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7
Q

What are the symptoms of primary hyperparathyroidism?

What is the major cause of these symptoms?

A

Painful bones: osteoporosis/osteitis fibrosis cystica
Renal stones: nephrolithiasis
Abdominal groans: constipation, gallstones
Psychic moans: depression, lethargy, seizures

Protracted hypercalcemia

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8
Q

Osteitis fibrosis cystica (von Recklinghausen’s disease of bone) include which 4 features?

It may look similar to…

A

Begins as a brown tumor

Osteoclast-driven bone destruction

Small fractures

Hemorrhage and reactive tissue

May look similar to metastatic disease! This is rare for initial presentation, though.

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9
Q

How is primary hyperparathyroidism detected?

A

Not usually symptomatically - usually from high Ca++ on normal blood work. PTH is then ordered and found to be high, too.

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10
Q

What cells make up a parathyroid adenoma?

How many are there usually?

They might be surrounded by…

A

Parathyroid chief or oxyphil cells

Typically solitary

Can be surrounded by a rim of normal parathyroid tissue

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11
Q

What gene mutation may cause parathyroid adenomas? Which type of mutation is most common?

A

MEN1 - somatic mutations (20-30%) are more common than germline

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12
Q

How many glands does parathyroid hyperplasia typically affect?

What might be responsible for it?

Primary parathyroid hyperplasia is much less common than…

A

Typically multiple glands

MEN syndromes may be responsible

Secondary > primary parathyroid hyperplasia

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13
Q

What feature is used to distinguish between adenoma and primary hyperplasia?

A

Adenomas affect 1 gland usually, which primary hyperplasia affects multiple

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14
Q

What is the treatment for parathyroid adenoma?

How can it be predicted to be successful?

A

Parathyroidectomy

Intraoperative monitoring of PTH

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15
Q

What is the signature sign of parathyroid carcinoma?

Which 3 features are “highly suggestive”?

A

Metastasis

Invasion of adjacent tissues
Vascular invasion
Elevated PTH post-operation

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16
Q

Which causes of hypercalcemia tend to cause more symptoms?

A

Non-parathyroid (malignancy) - mental status changes, N/V, EKG changes (shortened QT interval)

17
Q

What are 4 non-parathyroid-related causes of hypercalcemia?

A

Malignancy - most common

Vit. D excess - granulomatous disease, hypervitaminosis

Excess calcium ingestion

Medications - thiazide diuretics

18
Q

What are the levels of PTH and [Ca++] in non-parathyroid-related hyperparathyroidism?

A

Low/normal PTH, but elevated [Ca++]

19
Q

What are the 2 mechanisms of hypercalcemia of malignancy?

What are their underlying causes and associated cancers?

A

Humoral hypercalcemia of malignancy (HHP)

  • PTHrP (80%): analogous to PTH and produced in squamous carcinomas (can be others)
  • Vit. D-mediated from lymphomas

Local osteolytic hypercalcemia: release of Ca++ due to osteoclastic bone resorption.

  • breast carcinoma
  • myeloma
20
Q

What is the main cause of secondary parathyroid hyperplasia?

A

Kidney disease

21
Q

What is the mechanism of secondary parathyroid disease?

A

Poor kidney function leads to decreased calcitrol and increased phosphorus.
This leads to decreased Ca++, which acts on the CaSR: increased PTH, PTH mRNA and proliferation.
All leads to increased serum PTH.

22
Q

What is renal osteodystrophy?

What is seen on XR? Under what circumstance?

A

Dissecting osteitis in hyperparathyroidism.

“Rugger jersey sign” in renal osteodystrophy due to secondary hyperparathyroidism.

23
Q

What causes calciphylaxis? What does it lead to?

A

Secondary hyperparathyroidism (renal dz), which leads to extensive calcification and occlusion of blood vessels and resultant ischemia.

May lead to clots, infection and ulcers.

24
Q

What causes tertiary hyperparathyroidism?

A

Tertiary hyperparathyroidism is a state of excessive secretion of PTH after a long period of secondary hyperparathyroidism and resulting in a high blood calcium level. It reflects development of autonomous (unregulated) parathyroid function following a period of persistent parathyroid stimulation.

25
Q

What are some clinical features of hypocalcemia? (4)

What are some PE findings of hypocalcemia? (3)

A

Clinical

  • behavioral changes/stupor
  • numbness
  • muscle cramps, spasms
  • convulsions

PE

  • Trousseau sign: carpopedal spasm on inflation of BP cuff
  • Chovstek sign: facial twitching when tapping on facial n.
  • prolonged QT interval
26
Q

What are 2 causes of primary hypoparathyroidism?

A

Iatrogenic (surgical)

Autoimmune

27
Q

What are 3 causes of congenital hypoparathyroidism?

A

DiGeorge syndrome - defects of the 3rd and 4th pharyngeal pouches

Activating CaSR germline mutations

Familial isolated hypoparathyroidism - precursor of PTH cannot become functional PTH

28
Q

What genetic change is seen in DiGeorge syndrome?

What 3 types of abnormalities are seen?

A

Chr. 22q11.2 deletion

Immune deficiency: thymic hypoplasia or aplasia (infection)
Heart outflow defects: Truncus Arteriosus, Tetralogy of Fallot (cyanosis)
Parathyroid hypoplasia or aplasia: hypocalcemia (tetany)

29
Q

Loss of function mutation in CaSR leads to:

Gain of function mutation in CaSR leads to:

A

LoF - Familial hypocalciuric hypercalcemia

GoF - Autosomal dominant hypoPTH (hypercalciuric hypocalcemia)

30
Q

Main problem in familial hypocalciuric hypercalcemia =

What causes the hypocalciuria and hypercalcemia?

A

The body never thinks there is enough Ca++, even when there is.

Hypercalcemia - PTH is turned on
Hypocalciuria - reduced renal excretion

31
Q

Main problem in autosomal dominant hypoparathyroidism (hypercalciuric hypocalcemia) =

What causes the hypocalcemia and hypercalciuria?

A

The body thinks there is plenty of Ca++, even when there is not.

Hypocalcemia - PTH turned off
Hypercalciuria - increased renal excretion

32
Q

What is Pseudohypoparathyroidism (calcium and phosphorus levels)?

What is the underlying pathogenesis?

A

Hypocalcemia and hyperphosphatemia, despite elevated PTH.

Resistance to PTH

  • related to GPCR pathways
  • may affect other hormone pathways
33
Q

What is the step-by-step pathogenesis of Pseudoparathyroidism? (4)

A
  1. Renal tubular cells do not respond to PTH.
  2. PTH cannot elicit an increase in Ca++, causing hypocalcemia.
  3. Hypocalcemia results in increased PTH.
  4. PTH cannot elicit an increase in Ca++.
34
Q

What are the major features of Albright’s hereditary osteodystrophy? (3)

A

Short stature and obesity
Shortened phalanges of UE
Shortened phalanges of LE

May also see dental abnormalities, subcutaneous ossification, cataracts, seizures and tetany.

35
Q

What are the levelf of PTH and Ca++ in Pseudohypoparathyroidism?

A

Elevated PTH, but low Ca++

Endocrine & Reproduction II Exam #2 (10 decks)

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