Parathyroid Disorders Flashcards

1
Q

PTH acts on

A

Bone, kidneys, and intestines to increase blood calcium levels

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2
Q

The absence of parathyroid glands is

A

Incompatible with life

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3
Q

The parathyroid gland has two types of cells

A

Chief cells and oxyphil cells

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4
Q

What is the main function of chief cells?

A

Manufacturing, storing and rapidly releasing PTH in response to alterations of blood calcium levels

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5
Q

Chief cells stain slightly

A

Eosinophilic

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6
Q

Chief cells contain secretory granules that contain

A

PTH

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7
Q

Which cells are inactive chief cells?

A

Oxyphil cells

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8
Q

Oxyphil cells may take on a water-clear apperance due to the presence of

A

Cytoplasmic glycogen

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9
Q

Oxyphil cells tend to be slightly larger than chief cells, have acidophilic cytoplasm and are tightly packed with

A

Mitochondria

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10
Q

Oxyphil cells have secretory granules that are slightly sparse or

A

Absent

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11
Q

As people get older, what increases in the parathyroid gland?

A

Adipose tissue and oxyphil cells

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12
Q

Wht are the normal serum calcium levels?

A

8.5 to 10.5

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13
Q

What effect does PTH have on bone?

A

Inhibits osteoblast activity and stimulates osteoclast activity aka increases bone resorption

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14
Q

What effect does PTH have on the kidneys?

A

PTH increases calcium reabsorption within the distal convoluted tubules and blocks phosphate reabsorption in the proximal tubules

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15
Q

PTH stimulates the production of what vitamin?

A

D within the proximal tubules

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16
Q

What effect does PTH have on the GI system?

A

Increased calcium reabsorption

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17
Q

What is primary hyperparathyroidism?

A

Autonomous overproduction of PTH. Usually secondary to adenoma or hyperplasia of parathyroid tissue

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18
Q

What is secondary hyperparathyroidism?

A

Hypocalcemia triggers a compensatory increased secretion of PTH (example: kidney disease)

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19
Q

What is tertiary hyperparathyroidism?

A

Consequence of prolonged hypocalcemia even after it is corrected. Even we we correct the hypocalcemia, PTH doesnt go down when it is supposed to.

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20
Q

Hyperparathyroidism is an important cause of?

A

Hypercalcemia

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21
Q

Primary hyperparathyroidism is a common endocrine disorder secondary to

A

Adenomas 85 to 95%
Primary hyperplasia (diffuse or nodular) 5-10%
Parathyroid carcinoma

22
Q

What is the most common cause of primary hyperparathyroidism?

A

Pararhyroid adenoma

23
Q

MEN-1 mutations are associated with?

A

Parathyroid adenoma

24
Q

Overexpression of cyclin D1 secondary to cyclin D1 gene inversions are associated with

A

Parathyroid adenomas

25
Q

What are the symptoms of primary hyperparathyroidism?

A

Painful bones, renal stones, abdominal groans, and psychic moans

26
Q

What are other clinical symptoms of primary parathyroidism?

A

Bone pain secondary to fractures, constipation, nausea, peptic ulcers, pancreatitis, gallstones, depression, lethargy, eventually seizures, myalgias, weakness, fatigue, aortic or mitral valve calcifications

27
Q

parathyroid adenomas are almost always

A

Solitary

-may be present at an ectopic site (mediastinum)

28
Q

Parathyroid adenomas are mostly composed of

A

Polygonal chief cells with small centrally placed nuclei

29
Q

the growth of parathyroid carcinoma is limited to

A

1 gland

30
Q

What is the only criteria for parathyroid carcinoma?

A

Invasion of surrounding tissues and metastasis

31
Q

In parathyroid carcinoma we can appreciate

A

Bands of fibrous tissue between the nests of carcinoma cells

32
Q

What is the leading cause of secondary hyperparathyroidism?

A

Renal failure

33
Q

What are some other secondary causes of secondary hyperparathyroidism?

A

Deficient dietary calcium, steatorrhea, vitamin D deficiency

34
Q

Decreased phosphate excretion is also associated with

A

Secondary hyperparathyroidism

35
Q

What is the main cause of acquired hypoparathyroidism?

A

Surgically acquired

36
Q

Autoimmune hypoparathyroidism is associated with

A

Autoimmune polyendocrine syndrome type 1 along with chronic mucocutaneous candidiasis and primary adrenal insufficiency

37
Q

Autosomal dominant hypoparathyroidism is due to

A

Gain of function mutations in the calcium sensing receptor gene (CASR)

38
Q

Heighened calcium sensing suppresses what?

A

PTH which result in hypocalcemia and hypercalciuria

39
Q

Familial isolated hypoparathyroidism (the autosomal dominant version) is associated with

A

A mutation in the gene encoding PTH precursor peptide

40
Q

The autosomal recessive verison of FIH is associated with?

A

A loss of function mutation in the transcription factor gene glial cells missing-2 (GCM2)

41
Q

What is the deletion in Di George syndrome?

A

22q11.2 deletion

42
Q

Di George syndrome leads to

A

Congenital malformations of the heart, parathyroid and thymus

43
Q

What is the main manifestation of hypocalcemia?

A

Tetany

44
Q

Tetany is characterized by

A

Neuromuscular irritability

45
Q

What other symptoms can be seen in hypoparathyroidism?

A

Perioral numbness
Paraesthesias of the distal extremities and carpopedal spasm
Life-threatening laryngospasm
Generalized seizures

46
Q

What are some classic findings on hypoparathyroidism?

A

Chvostek sign- tapping along the facial nerve induces contractions of the muscles of the eye, mouth or nose

Trousseau sign- carpal spasms produced by occlusion of the circulation to the forearm and hand with a blood pressure cuff for several minutes

47
Q

Hypoparathyroidism can induce

A

Mental status changes

48
Q

Hypoparathyroidi can induce intracranial manifestations like

A

Calcifications of the basal ganglia, parkinsonian-like movement disorders, increased ICP with resultant papilledema

49
Q

Hypoparathyroidism can result in

A

Calcification of the lens and cataract formation

50
Q

What cardiovascular problems can someone with hypoparathyroidism have?

A

Prolongation of the QT interval

51
Q

What dental abnormalities can be seen in hypoparathyroidism?

A

Dental hypoplasia, failure of eruption, defective enamel and root formation, abraded carious teeth