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Pathology 2 Thyroid, ParaTh, Adrenals > Disorders of Parathyroid glands > Flashcards

Disorders of Parathyroid glands Flashcards

1
Q
A
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2
Q

from where is the parathyroid derived?

A

from the third and fourth branchial pouches.

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3
Q

how many parathyroid glands are there?

what cells compose the parathyroid gland?

A

4

oxyphil and chief cells

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4
Q

what do chief cells synthesize?

A

PTH

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5
Q

what are the functions of PTH?

A
  1. Activates osteoclasts (mobilizes Ca from bone)
  2. Increases resorption of calcium from renal tubules.
  3. Increases the conversion of vitamin D to its active form.
  • Increases Ca absorption from GIT.
    1. Increases urinary phosphate excretion.
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6
Q

how does PTH maintain ionized calcium levels in blood?

A
  • Increases bone resorption and
  • Renal and GIT resorption of calcium
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7
Q

PTH secretion is controlled by what?

A

Level of free ionized calcium in blood stream

  • PTH secretion stimulated by hypocalcemia
  • PTH secretion suppressed by hypercalcemia
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8
Q

what does Total Serum calcium represent?

A

bound calcium + free calcium

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9
Q

what is the activated form of calcium?

A

free calcium

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10
Q

What are the effect of hypoalbuminemia on calcium levels?

A
  • Causes decreased total serum calcium
    • Due to a decrease in Ca bound to albumin.
  • Normal free Ca levels, normal PTH
  • No evidence of tetany**.
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11
Q

what is the effect of respiratory or metabolic alkalosis on calcium levels?

A
  • Alkalosis increases negative charges on albumin.
  • Extra negative charges bind some of the free Ca
  • Total serum calcium remains normal
  • Decreased free calcium, increased PTH
  • Patient develops tetany**
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12
Q

who secretes Calcitonin?

what stimulates the synthesis of calcitonin?

A

C cells of thyroid

hypercalcemia

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13
Q

what are the actions of calcitonin?

A
  • Inhibits bone resorption by inhibiting the activity of osteoclasts.
  • Inhibits absorption of calcium from intestine.
  • Net effect = decreased calcium levels
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14
Q

what are the 2 Disorders of Parathyroid glands?

A
  1. Hyperparathyroidism
  2. Hypoparathyroidism
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15
Q

Hyperparathyroidism (HPTH) can divide into 2 types?

A
  1. Primary Hyperparathyroidism
  2. Secondary Hyperparathyroidism
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16
Q

Primary hyperparathyroidism is characterized by what?

usually affects who?

A

Unregulated overproduction* of PTH by the parathyroid leading to hypercalcemia.

50 y/o women

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17
Q

what are the 2 types of primary hyperparathyroidism?

A

sporadic

associated with MEN I or II

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18
Q

what is a Parathyroid adenoma’s gross findings?

which parathyroid gland is usually affected

A

A benign tumor, Solitary & well circumscribed.

Right inferior parathyroid gland is most often involved

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19
Q

what are the parthyroid glands micro findings?

A
  • Composed of sheets of chief cells with no intervening fat.
  • Remainder of the gland plus all other glands show atrophy.
  • due to suppression of PTH by hypercalcemia.
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20
Q

what is this test called?

what is it showing?

A

parathyroid Tc99 scan

parathyroid adenoma

22
Q

how many glands are affected by primary parathyroid hyperplasia?

what are the micro findings?

A

all 4 glands

chief cell hyperplasia with sparse fat tissue.

23
Q

what is this showing?

A

parathyroid hyperplasia

25
Q

most cases of hyperparathyroidism are?

A

asymptomatic and found incidentally

26
Q

what are the Primary Hyperparathyroidism Renal Clinical findings?

A
  • Calcium oxalate stones = nephrolithiasis (most common presentation**)
  • Nephrocalcinosis (causes polyuria and renal failure).
27
Q

what are the Primary Hyperparathyroidism GIT Clinical findings?

A
  • Peptic ulcer disease: calcium stimulates gastrin release which increases gastric acid.
  • Acute pancreatitis: calcium activates phospholipases
  • Constipation: Most common** GI complaint (hypomotility)
28
Q

what are the Primary Hyperparathyroidism Bones Clinical findings?

what will you see in micro findings?

A

Osteitis Fibrosa Cystica

  • Cystic and hemorrhagic bone lesion
  • Caused by increased osteoclastic activity
  • Commonly involves the jaw and fingers

Aggregates of osteoclasts, reactive giant cells and hemorrhage mimicking neoplasm.

Called the “brown tumor” of hyperparathyroidism

29
Q

What are the Primary Hyperparathyroidism Eye Clinical findings?

A
  • Band keratopathy in the limbus of the eye
  • Due to Metastatic calcifications
30
Q

What are the Primary Hyperparathyroidism CVS Clinical findings?

A
  • Diastolic hypertension
  • calcium increases muscular contraction in the peripheral resistance vessels.
31
Q

What are the Primary Hyperparathyroidism CNS Clinical findings?

A

Depression and seizures (Metastatic calcification)

32
Q

what are the Laboratory findings found in Primary HyperParaThyroidism?

A
  • Increased serum PTH
  • Increased serum calcium = hypercalcemia
  • Decreased serum phosphate = hypophosphatemia
33
Q

what is this showing?

A

parathyroid hyperplasia

35
Q

what are the Primary Hyperparathyroidism GIT Clinical findings?

A
  • Peptic ulcer disease: calcium stimulates gastrin release which increases gastric acid.
  • Acute pancreatitis: calcium activates phospholipases
  • Constipation: Most common** GI complaint (hypomotility)
36
Q
A
37
Q

how does Malignancy induced hypercalcemia happen?

A
  • Bone metastasis with activation of osteoclasts
  • Ectopic secretion of PTH related protein (SCC of lung, RCC)
  • Multiple myeloma: ↑ secretion of osteoclast activating factor (IL-1) by plasma cells.
38
Q

how does Sarcoidosis happen?

A

Macrophages in granuloma synthesize 1 alpha hydroxylase, causing Hypervitaminosis D

39
Q

what is the most common cause of secondary hyperparathyroidism?

A

chronic renal failure

40
Q

what do you see in the labs for 2ry hyperparathyroidism?

A

Decreased calcium, increased PTH, increased phosphate.

41
Q

what is Primary hypoparathyroidism?

A

Refers to hypofunction of parathyroid gland leading to hypocalcemia.

42
Q

what is the etiology of 1ry hypoparathyroidsm?

A
  • Previous thyroid surgery (most common cause)
  • Di George syndrome: congenital absence of parathyroid glands
  • Autoimmune hypoparathyroidism
  • Hypomagnesemia: required for PTH activation
43
Q

PTHrP is always made by ?

A

the tumor, not the body

44
Q

Reduction in total and ionized calcium levels in 1ry hypoparathyroidism results in what?

A
  • Tetany
  • Calcification of basal ganglia
  • Due to metastatic calcification
  • Increased phosphorus drives Ca into brain
  • Cataracts
  • Candida infection (?cause)
  • Prolonged QT interval
45
Q

why does tetany happen in 1ry hypoparathyroidism?

A

due to decreased ionized calcium.

  • Decreased ionized Ca causes partial depolarization of nerve and muscle

A smaller stimulus is required to initiate an action potential.

46
Q

what 2 signs can you find in 1ry hypoparathyroidism?

A
  1. Carpopedal spasm: thumb flexes into palm
  2. Chovestek’s sign: facial twitch after tapping the facial nerve.
47
Q

what Laboratory findings are indicative of 1ry hypoparathyroidism?

A
  1. Low PTH
  2. Hypocalcemia
  3. Hyperphosphatemia
48
Q

what is Pseudohypoparathyroidism?

A

Sex linked inherited disease.

Characterized by end organ resistance (kidney) to PTH.

49
Q

what do patients with pseudohypoparathyroidism have?

A
  • Mental retardation
  • Calcification of basal ganglia
  • Short 4th and 5th metacarpals** (knuckle-knuckle- dimple – dimple sign)
  • Short stature and other skeletal abnormalities.
50
Q

what are the lab findings in pseudohypoparathyroidism?

A

Hypocalcemia, hyperphosphatemia and normal or high PTH.

51
Q

what are 4 other causes of hypocalcemia?

A
  1. Acute pancreatitis: Calcium bound to fatty acids in enzymatic fat necrosis.
  2. Hypovitaminosis D: Chronic renal failure: MCC
  3. Hypoalbuminemia: MCC of hypocalcemia
  4. Hypomagnesemia
52
Q

fill the blanks

A

Pathology 2 Thyroid, ParaTh, Adrenals (10 decks)

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