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Musculoskeletal Physiopathology > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

What is hyperparathyroidism?

A

Parathyroid gland hyperplasia

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2
Q

What are the two types of hyperparathyroidism?

A

Primary and secondary

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3
Q

___% of primary hyperparathyroidism is caused by parathyroid adenoma

A

85%

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4
Q

85% of primary hyperparathyroidism is caused by…

A

parathyroid adenoma

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5
Q

Some cases of ___ are heritable involving a mutation of the parathyroid CASR gene

A

primary hyperparathyroidism

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6
Q

___% of primary hyperparathyroidism involves hyperplasia of all four glands

A

10%

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7
Q

With primary hyperparathyroidism, secretion of PTH is ___

A

increased

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8
Q

In cases of primary hyperparathyroidism, PTH will remain elevated despite increasing ___ levels

A

calcium

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9
Q

Increased PTH in bone ___ osteoclastic activity and ___ osteoblastic activity

A

increases osteoclastic activity and decreases osteoblastic activity

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10
Q

Increased PTH in kidneys ___ calcitriol

A

increases

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11
Q

Increased calcitriol in kidneys ___ calcium and ___ phosphate

A

conserves calcium and excretes phosphate

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12
Q

Increased calcitriol in bone ___ osteoclastic activity and ___ osteoblastic activity

A

increases osteoclastic activity and decreases osteoblastic activity

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13
Q

Increased calcitriol to the GI increases ___

A

calbindin

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14
Q

Calbindin in the GI increases ___ absorption

A

calcium

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15
Q

Increased PTH in kidneys increases ___

A

calcitriol

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16
Q

What are the calcium levels found in primary hyperparathyroidism?

A

Elevated and continue to increase

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17
Q

How does the parathyroid gland respond to elevated calcium with primary hyperparathyroidism?

A

Parathyroid gland isn’t functioning normally so PTH production remains high
(normally, high calcium reduces PTH)

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18
Q

With primary hyperparathyroidism, there is ___ osteoclastic activity and ___ osteoblastic activity

A

increased osteoclastic activity and decreased osteoblastic activity

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19
Q

With primary hyperparathyroidism, the kidneys have ___ reabsorption of calcium

A

increased

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20
Q

With primary hyperparathyroidism, the kidneys have ___ excretion of phosphate

A

increased

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21
Q

With primary hyperthyroidism, the kidneys have ___ calcitriol production

A

increased

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22
Q

With primary hyperparathyroidism, the intestines have increased ___

A

calbindin

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23
Q

What are the examples of osteitis that can come of primary hyperparathyroidism?

A
  • Dissecting osteitis
  • Osteitis fibrosa
  • Osteitis fibrosa cystica
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24
Q

Describe dissecting osteitis resulting from primary hyperparathyroidism

A
  • Osteoclasts stimulated by increased PTH
  • Cut cones into subperiosteal and endosteal surfaces of cortical bone
  • Collagen is laid down adjacent to trabeculae
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25
Q

Describe osteitis fibrosa resulting from primary hyperparathyroidism

A
  • Accelerated bone remodeling
  • Trabeculae resorbed
  • Marrow replaced by fibrous tissue, macrophages, areas of hemorrhage from microfractures, and reactive bone
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26
Q

Describe osteitis fibrosa cystica resulting from primary hyperparathyroidism

A
  • Brown tumors which contain osteoclastic giant cells
  • Other radiographically visible bone changes
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27
Q

Cones have been cut into subperiosteal and endosteal surfaces of cortical bone and collagen has been laid down adjacent to trabeculae
What condition is being described?

A

Dissecting osteitis (due to primary hyperparathyroidism)

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28
Q

Bone remodeling is accelerated, trabeculae is resorbed, and bone marrow has been replaced by fibrous tissue, macrophages, areas of hemorrhage from microfractures, and reactive bone
What condition is being described?

A

Osteitis fibrosa (due to primary hyperparathyroidism)

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29
Q

Brown tumors in the bone containing osteoclastic giant cells are present with other visible bone changes
What condition is being described?

A

Osteitis fibrosa cystica (due to primary hyperparathyroidism)

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30
Q

The following are clinical manifestations of what disease?

  • Hypercalcemia
  • Impaired renal function and eventual renal failure (due to persistent hypercalcemia)
  • Kidney stones
  • Peptic ulcers
  • Musculoskeletal pain
  • Fracture
A

Primary hyperparathyroidism

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31
Q

The following are radiographic findings of what disease?

  • Osteolysis
  • Loss of cortical definition
  • Frayed, irregular, “lace like” appearance
  • Subperiosteal resorption
  • Brown tumor
  • Soft tissue calcifications
A

Primary hyperparathyroidism

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32
Q

What are the long term radiographic characteristics of primary hyperparathyroidism?

A
  • Osteolysis
  • Loss of cortical definition
  • Frayed, irregular, “lace like” appearance
  • Subperiosteal resorption
  • Brown tumor
  • Soft tissue calcifications
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33
Q

Which of the two types of heterotrophic calcifications are present in cases of primary hyperparathyroidism?

A

Metastatic

34
Q

What are the treatments for primary hyperparathyroidism?

A
  • Surgical removal of the parathyroid gland adenoma(s)
  • Follow up tests to assess bone mineral density and renal function
35
Q

Secondary hyperparathyroidism is typically a result of ___

A

chronic renal failure

36
Q

___ is a result of chronic renal failure, but may also occur in cases of vitamin D deficiency, intestinal malabsorption, and Fanconi syndrome

A

Secondary hyperparathyroidism

37
Q

With secondary hyperparathyroidism, renal retention of phosphate is ___

A

increased (hyperphosphatemia)

38
Q

With secondary hyperparathyroidism, there is ___ calcitriol produced by kidneys

A

inadequate

39
Q

With secondary hyperparathyroidism, there is ___ calbindin and dietary calcium absorption

A

decreased

40
Q

Overtime of secondary hyperparathyroidism, elevated PTH secretion leads to ___ of the parathyroid glands

A

hyperplasia of the parathyroid glands

41
Q

Parathyroid hyperplase is caused by long standing secondary hyperparathyroidism due to renal failure
Does parathyroid hyperplasia reverse following a kidney transplant?

A

Usually does not

42
Q

What is the treatment for secondary and tertiary hyperparathyroidism?

A

Generally, a parathyroidectomy

43
Q

What is renal osteodystrophy?

A

Skeletal effect of secondary/tertiary hyperparathyroidism; chronic kidney disease causes weakening of bones

44
Q

Renal osteodystrophy is common in ___ patients

A

long-term dialysis patients

45
Q

What are the two major lesions of renal osteodystrophy?

A
  • Osteitis fibrosa
  • Osteomalacia
46
Q

How does renal osteodystrophy present in the spine?

A
  • Generalized deossification
  • Trabecular accentuation
  • Condensation in the end plates called “rugger-jersey” spine (stripes through vertebral bodies)
47
Q

Hyperphosphatemia can lead to ___ in soft tissues

A

metastatic calcifications

48
Q

40% of adults with adynamic variant of renal osteodystrophy are treated with ___
50% of adults with ARO are treated with ___

A

40% hemodialysis
50% peitoneal dialysis

49
Q

Renal osteodystrophy is characterized by reduction in cellular activity in bone
What is the result of this change?

A
  • Fewer osteoclasts and osteoblasts
  • Old bone accumulates and is not remodeled
  • Bone becomes more brittle and prone to fracture
50
Q

Most patients with renal osteodystrophy show some combination of…

A

osteitis fibrosa, osteomalacia, osteosclerosis, and adynamic variant of renal osteodystrophy

51
Q

What are five treatments for renal osteodystrophy due to secondary/tertiary hyperparathyroidism?

A
  • Treatment for renal failure
  • Drug therapy to control phosphate levels
  • Vitamin D supplementation
  • Calcimimetics
  • Parathyroidectomy may be required
52
Q

What is the most common cause of hypoparathyroidism?

A

Idiopathic parathyroid atrophy

53
Q

What are some less common causes of hypoparathyroidism?

A
  • 1% of primary hyperparathyroidism patients who have a parathyroidectomy will get hypoparathyroidism
  • Radioactive iodine therapy
  • Familial hypoparathyroidism (X-linked recessive or autosomal recessive)
54
Q

Hypoparathyroidism involves ___ PTH secretion

A

deficient

55
Q

A patient presents with the following clinical manifestations:

  • Hyperactive reflexes
  • Spontaneous muscle contractions
  • Convulsions
  • Laryngeal spasm with airway obstruction
  • Severe muscle cramps
  • Mild tingling in hands and feet due to neuromuscular excitability
  • Depression, paranoia, psychosis

What is the likely disease?

A

Hypocalcemia due to hypoparathyroidism

56
Q

What is the treatment for hypoparathyroidism?

A

Vitamin D and calcium supplementation

57
Q

What is pseudohypoparathyroidism?

A

End-organ insensitivity to PTH due to mutation on GNAS1 gene on chromosome 20q

58
Q

Albright hereditary osteodystrophy is a phenotype of…

A

pseudohypoparathyroidism

59
Q

A patient presents with the following:

  • Short stature
  • Obesity
  • Intellectual disability
  • Subcutaneous calcifications
  • Congenital anomalies of bone

What is the likely cause?

A

Albright hereditary osteodystrophy (pseudohypoparathyroidism)

60
Q

pseudohypoparathyroidism

What congenital anomalies of bone occur with Albring hereditary osteodystrophy?

A
  • Short metacarpals and metatarsals
  • Underdeveloped enamel; delayed tooth eruption
61
Q

When do gigantism and acromegaly occur in the maturation of the skeleton?

A

Gigantism occurs in skeletally immature individuals
Acromegaly occurs once the growth plates close

62
Q

How common is gigantism/acromegaly?

A

Relatively rare: 3 in 1 million
More common in females (3:2)

63
Q

What hormone is increased by gigantism/acromegaly?

A

Human growth hormone

64
Q

What is a somatotroph adenoma?

A

Pituitary tumor that makes growth hormone

65
Q

What are some effects of somatotroph adenoma?

A
  • Growth hormone hypersecretion
  • Adenohypophyseal hypofunction
66
Q

What is the difference between a microadenoma and a macroadenoma found in the pituitary gland?

A

Microadenoma is less than 1cm, macroadenoma is 1cm or more

67
Q

Besides pituitary tumor/somatotroph adenoma, what can cause gigantism/acromegaly?

A

Growth hormone supplementation

68
Q

Increased growth hormone in gigantism will lead to…

A

proportional overgrowth in all tissues

69
Q

Increased growth hormone in acromegaly will lead to…

A

widening of the bones, but not elongation, and thickening of soft tissues ie. heel pad

70
Q

When chondrocytes and osteoblasts increase replication due to growth hormone, what is the result?

A

Increased growth in size

71
Q

How does involvement of insulin-like growth factor-1 (IGF-1) help increase cellular metabolism and replication in gigantism/acromegaly?

A
  • Inhibits apoptosis
  • Makes hypoglycemic environment
72
Q

When do IGF-1 levels peak normally in life?

A

Late teens to early twenties

73
Q

If a patient has gradually increasing facial robusticity/coarsening of features, increased nose size, and increased size of hands and feet, what is suspected?

A

Acromegaly

74
Q

What are some facial features of acromegaly?

A
  • Glabellar enlargement
  • Facial prognathism: Increased space between teeth, dental malalignment
  • Increased nose size
74
Q

What are some clinical manifestations of acromegaly besides visible characteristics?

A
  • Diabetes mellitus type 2 sequela
  • Hypofunctioning pituitary
  • Organ enlargement
  • Cardiovascular, cerebrovascular, and respiratory issues can be fatal
75
Q

What are some issues that arise with hypofunctioning pituitary gland with acromegaly?

A
  • Secondary reproductive issues
  • Visual issues
76
Q

What is an example of organ enlargement found in those with acromegaly?

A

Cardiomegaly

77
Q

What are some radiographic characteristics of facial features in those with acromegaly?

A
  • Frontal bossing
  • Prognathism
  • Widening of bones (non-specific)
  • Spade tuft deformities
  • Increase in the sella turcica
78
Q

If a patient’s radiographs present with the following, what is suspected?

  • Frontal bossing
  • Prognathism
  • Widening of bones
  • Spade tuft deformities
  • Increase in the sella turcica
  • Increased thickness of soft tissues where visible
A

Acromegaly

79
Q

If a patient’s heel pad is especially thick and their gloves or hats don’t fit, what is suspected?

A

Acromegaly

80
Q

What are some treatments for acromegaly/gigantism?

A
  • Pituitary adenoma removal
  • Radiation therapy (if surgery is contraindicated)
  • Somatostatin therapy (GH antagonist)
81
Q

If you have a patient that had gigantism, what is your biggest concern for them now?

A

Cardiovascular issues

Musculoskeletal Physiopathology (15 decks)

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