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Endocrine 2 > parathyroid gland path > Flashcards

parathyroid gland path Flashcards

1
Q

what are the 2 cell types that make up the parathyroid glands?
Which predominates

A
  • Chief cells (predominate)

- oxyphil cells

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2
Q

Describe the chief cells

A
  • Central, round, uniform nuclei
  • light pink cytoplasm
  • Sometime they are clear from the glycogen (Water-clear appearance)
  • Secretory granules of PTH
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3
Q

Describe the Oxyphil cells

A
  • slightly larger than chief cells
  • Acidophilic cytoplasm
  • Tightly packed with mitochondria
  • Glycogen granules but NOT secretory granules
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4
Q

Describe the amount of stromal fat in parathyroid glands

A
  • increases up to age 25 then plateaus

- up to 30% of the gland

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5
Q

Function of the parathyroid

A

regulate calcium

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6
Q

What stimulates the synthesis and secretion of PTH

A

decreased levels of free calcium

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7
Q

Explain what PTH does on different parts of the body

A
  • increases renal tubular reabsorption of Ca
  • Increases urinary phosphate excretion
  • Increases conversion of vitamin D to its active dihydoxy form in the kidneys . .. augments GI Ca absorption
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8
Q

what are the causes of hypercalcemia associated with increased PTH

A
  • Primary hyperparathyroidism (adenoma > hyperplasia)
  • Secondary
  • Tertiary
  • Familial hypocalciuric hypercalcemia
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9
Q

What are the causes of hypercalcemia associated with decreased PTH

A
  • Hypercalcemia of malignancy
  • vitamin D toxicity
  • Immobilization
  • thiazide diuretics
  • Granulomatous disease (Sarcoidosis)
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10
Q

What are the 4 causes of primary hyperparathyroidism

A
  • Autonomous overproduction of parathyroid hormone
  • Adenoma
  • Hyperplasia
  • carcinoma
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11
Q

What are the causes of secondary hyperparathyroidism

A
  • Compensatory hypersecetion of PTH in response to prolonged hypocalcemia
  • Chronic renal failure
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12
Q

explain what tertiary hyperparathyroidism is

A
  • hypersecretion of PTH even after the cause of prolonged hypocalcemia is corrected
  • ex: after renal transplant
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13
Q

epidemiology of primary hyperparathyroidism

A
  • usually adults

- More common Women . . . 4:1

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14
Q

How are most cases of primary hyperparathyroidism discovered

A

incidentally on serum electrolyte panel

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15
Q

What is the most common cause of primary hyperparathyroidism

A

a solitary parathyroid adenoma arising sporadically

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16
Q

What are the 2 molecular defects that play a role in sporadic parathyroid adenomas

A
  • Cyclin D1 gene inversions leading to overexpression of Cyclin D1 . . cell cycle regulator
  • MEN1 mutations . . . tumor suppressor gene
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17
Q

what are the genetic syndromes associated with familial hyperparathyroidism

A
  • MEN types 1 and 2 . .. MET1 and RET mutations
  • Familial hypocalciuric hypercalcemia . . rare autosomal dominant . . mutations in parathyroid calcium sensing receptor gene (CASR)- LOSS OF FUNCTION
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18
Q

Morphology of parathyroid Adenoma

A
  • solitary
  • .5-5 gm
  • well circumscribed
  • Glands outside the adenoma are usually normal in size or shrunken from feedback inhibition by elevated calcium
  • hypercellular with little to no fat
  • composed of uniform chief cells
  • Few nests of larger oxyphil cells . .. occasionally composed entirely of them (oxyphil adenoma)
  • usually a rim of compressed, parathyroid gland, generally separated by a fibrous capsule
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19
Q

Parathyroid hyperplasia occurs sporadically or as a component of _______

A

MEN syndrome

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20
Q

describe the involvement of the glands in parathyroid hyperplasia

A
  • Classically all 4 involved
  • may be Asymmetric which can make distinction from adenoma difficult
  • combined weight of all glands rarely >1 gm
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21
Q

Morphology of Parathyroid hyperplasia

A
  • Hypercellular with little to no fat

- Typically see chief cell hyperplasia . . diffusely or multinodular

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22
Q

Describe a parathyroid carcinoma

A
  • enlarge one parathyroid
  • sometimes exceeds 10 gm
  • rare
  • cells can look like normal parathyroid
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23
Q

What do you need for diagnosis of parathyroid carcinoma

A

-invasion of surrounding tissues and/or metastasis

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24
Q

What scan is used to assess the parathyroid glands?

i.e. location, is it solitary or diffuse

A
  • Sestamibi san

- this is a radionucleotide scan where sestamibi is labeled with the radio-pharmaceutical technetium-99

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25
Q

Symptomatic, untreated primary hyperparathyroidism manifests with what 3 skeletal abnormalities?

A
  • Osteoporosis
  • Brown tumors
  • Osteitis fibrosa cystica
26
Q

Describe osteoporosis

A

-decreased bone mass with preferential involvement of phalanges, vertebrae, and proximal femur

27
Q

The increased osteoclast activity in hyperparathyroidism affects what part of the bone

A

cortical bone more severely than medullary

28
Q

What is it called when, in medullary bone, osteoclasts tunnel into and dissest centrally along the length of the trabeculae

A

railroad tracks appearance . . . dissecting osteitis

29
Q

What are brown tumors?

A
  • Microfractures and secondary hemorrhages –>influx in macrophages and reparative fibrous tissue –> mass
  • Brown color from vascularity, hemorrhage, and hemosiderin deposition
30
Q

What is the hallmark of severe hyperparathyroidism and know as generalized osteitis fibrosa cystica?

A
  • increased osteoclast activity
  • Peritrabecular fibrosis
  • cystic brown tumors
31
Q

What is another word for generalized osteitis fibrosa cystica

A

-Recklinghausen disease of bone

32
Q

What are other organ pathologies that occur in primary hyperparathyroidism

A
  • Nephrolithiasis: urinary tract stones
  • Nephrocalcinosis: calcification of the renal interstitium and tubules
  • Calcification may also be seen in the stomach, lungs, myocardium, and blood vessels
33
Q

what are the 2 clinical courses of primary hyperparathyroidism

A
  • Asympsotmatic and identified on routine blood chemistry

- or classic symptoms

34
Q

What is the most common cause of symptomatic hypercalcemia

A

-malignancy

35
Q

What malignancies can cause hypercalcemia

A
  • Solid tumors: lung, breast, head and neck, and renal

- Hematologic: multiple myeloma

36
Q

What do osteolytic tumors secrete to induce hypercalcemia?

What is the other way they can cause hypercalcemia

A

PTH-related peptide (PTHrP)

-metastasis . . cytokine induced bone resorption

37
Q

Labs in primary hyperparathyroidism

A
  • elevated Ca
  • Elevated PTH: this is low if hypercalcemia is caused by non parathyroid disease
  • low phosphate
38
Q

What is the phrase used to describe the symptoms of primary hyperparathyroidism aka hypercalcemia

A

Bones, stones, abdominal groans and psychic moans

39
Q

GI symptoms of hypercalcemia

A
  • constipation
  • nausea
  • peptic ulcers
  • pancreatitis
  • gallstones
40
Q

CNS symptoms of hypercalcemia

A
  • depression
  • lethargy
  • eventually seizures
41
Q

Neuromuscular symptoms of hypercalcemia

A

-weakness and fatigue

42
Q

Cardiac symptoms of hypercalcemia

A

Aortic and/or mitral valve calcifications

43
Q

Secondary hyperparathyroidism is caused by any condition that gives rise to what?

A

chronic hypocalcemia, which in turn leads to compensatory overactivity of the parathyroid glands

44
Q

What is by far the most common cause of secondary hyperparathyroidism?
Give the other causes also

A

-Renal failure

  • inadequate dietary intake of calcium
  • steatorrhea
  • vitamin D deficiency
45
Q

Mechanism by which chronic renal failure induces secondary hyperparathyroidism

A
  • decreased phosphate excretion . . elevated phosphate levels directly depress serum calcium levels
  • Also, loss of renal substance reduces the availability of a-1-hydroxylase which is necessary for the synthesis of the active form of vitamin D which in turn reduces intestinal absorption of calcium
46
Q

Morphology of secondary hyperparathyroidism

A
  • hyperplastic parathyroid glands (decreased fat) . . can be asymmetric
  • Increased number of chief cells (diffuse or mutinodular)
  • “metastatic” calcifications can be seen in lungs, heart, stomach and blood vessels
47
Q

Describe the clinical course of secondary hyperparathyoidism

A
  • usually dominated by the inciting chronic renal failure
  • the hyperparathyroidism per se is usually not as severe or as prolonged as primary
  • Calciphylaxis: vascular calcifications –> ischemic changes to skin and other organs
48
Q

Treatment of secondary hyperparathyroidism

A
  • Vitamin D supplements

- phosphate binders

49
Q

If a patient with secondary hyperparathyroidism, the parathyroids become autonomous and excessive

A

tertiary hyperparathyroidism

50
Q

Treatment for tertiary hyperparathyroidism

A

parathyroidectomy

51
Q

What are the causes of hypoparathyroidism

A
  • SURGICALLY INDUCED
  • autoimmune
  • autosomal dominant hypoparathyroidism
  • Familial isolated hypoparathyroidism
  • Congenital absence of parathyroid glands
52
Q

Autoimmune hypoparathyroidism is associated with what?

A

chronic mucocutaneous candidiasis and primary adrenal insufficiency ( autoimmune polyendocrine syndrome type 1: APS1)

53
Q

Congenital absence of parathyroid glands is also called what if present with thymic defects

A

DiGeorge syndrome

54
Q

Autosomal recessive familial isolated hypoparathyroidism (FIH) is caused by loss of function mutations in what

A

glial cells missing-2 (GCM2)

55
Q

Describe the Tetany changes found with hypocalcemia

A
  • Circumoral or parestesias (tingling) of the distal extremeities and carpopedal spasm
  • When severe: life threatening laryngospasm and generalized seizures
  • Chvostek sign: tap area of facial nerve to induce contractions of the muscles of the eye, mouth and nose
  • Trousseau sign: carpal spasms produced by occlusion of the circulation of the forarm and hand with a blood pressure cuff for several minutes
56
Q

What are the mental status changes associated with hypocalcemia

A
  • emotional instability
  • anxiety
  • depression
  • confusion
  • hallucinations
  • frank psychosis
57
Q

what are the paradoxical calcifications from hypocalcemia

A
  • likely from increased phosphate levels
  • Basal ganglia: parkinsonian like movement disorders
  • Lens and cataract formation
58
Q

Cardio symptoms of hypocalcemia

A

conduction defect: prolongation of QT interval in electrocardiogram

59
Q

What occur when hypocalcemia is present during early development and are highly characteristic of hypoparathyroidism

A

dental abnormalities

60
Q

occurs because of end organ resistance to actions of PTH . . . serum PTH levels are normal or elevated

A

pseudohypoparathyroidism

61
Q

What does pseudohypoparathyroidism present as

A

hypocalcemia and hyperphosphatemia

62
Q

in pseudohypoparathyroidism, there can also be end organ resistance to what?

A

PTH, TSH, and FSH/LH . . . genetic defects in G protein coupled receptors

Endocrine 2 (10 decks)

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