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Endo > Disorders of Calcium and Parathyroid Gland > Flashcards

Disorders of Calcium and Parathyroid Gland Flashcards

1
Q

How is calcium distributed in the serum?

A

40% protein bound
10% complexed (citrate or phosphate ions)
50% ionized

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2
Q

What form of Ca is free and bioavailable?

A

ionized

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3
Q

Clinically, what is measured to determine Ca level?

A

total serum Ca

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4
Q

How does PTH affect bone?

A

increased Ca mobilization

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5
Q

How does PTH affect the kidneys?

A

increases calcium reabsorption from DCT

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6
Q

How does PTH affect intestines?

A

indirectly enhances the absorption of calcium by increasing the production of activated vitamin D

(up-regulates 1-alpha-hydroxylase)

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7
Q

What enzyme activates vitamin D?

A

1-alpha-hydroxylase

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8
Q

Where is Ca-sensing R found?

A

parathyroid
kidney
C cells of thyroid
bone

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9
Q

Stimulation of Ca-sensing receptor results in:

A

intracellular cascade to decrease PTH secretion

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10
Q

What is the appropriate workup for hypercalcemia?

A
  1. check albumin and total Ca TWICE

2. check PTH

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11
Q

PTH dependent causes of hypercalcemia?

A
  1. hyperparathyroidism
  2. familial hypocalciuric hypercalcemia
  3. medication induced
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12
Q

PTH independent causes of hypercalcemia?

A
  1. tumor induced
  2. granulomatous diseases
  3. multiple myeloma
  4. hyperthyroidism or adrenal failure
  5. medication induced
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13
Q

What meds may cause PTH-related hypercalcemia?

A

Li, HCTZ

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14
Q

What meds may cause PTH-unrelated hypercalcemia?

A

vit D toxicity
vit A
milk-alkali

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15
Q

80-85% of primary hyperthyroidism is caused by:

A

adenoma

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16
Q

What is the appropriate lab workup for primary hyperparathyroidism?

A
  1. Ca, albumin
  2. PTH
  3. 25-OH vitamin D
  4. 24h urine Ca, to differentiate from FHH
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17
Q

What are appropriate imaging studies for primary hyperparathyroidism?

A
  1. thyroid US
  2. Tc-sestamibi scan
  3. DXA
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18
Q

What causes familial hyperparathyroidism?

A

inactivating mutation of CaSR, with 100% penetrance

*note: the mutation in present in the parathyroid and kidneys, which causes calcium retention

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19
Q

What lab abnormalities are expected in familial hyperparathyroidism?

A

mildly increased serum Ca, hypocalciuria, slight elevation in PTH

20
Q

What is the trx for familial hyperparathyroidism?

A

none

21
Q

Results from long-standing secondary hyperparathyroidism:

A

tertiary hyperparathyroidism

22
Q

Most common malignancies causing hypercalcemia?

A

breast and sq cell carcinoma

also causes by lung, lymphoma, thyroid, kidney, prostate, multiple myeloma, pancreas…

23
Q

What are causes of hypercalcemia in malignancy?

A
  1. suppression of PTH due to PTH-related protein (which binds to common receptor)
  2. bony mets or bone destruction
  3. activation of osteoclasts by cytokines/TNFalpha
24
Q

What is the initial treatment for acute hypercalcemia?

A
  1. Address volume status**
  2. saline diuresis +/- furosemide (once volume status corrected)
  3. calcitonin
  4. bisphosphonates
25
Q

What hypercalcemic patients would be treated with steroids?

A

myeloma, granulomatous disease and vit D toxicity

**inhibit 1-alpha-hydroxylase

26
Q

Major causes of secondary PTH elevation:

A
  1. hypocalcemia
  2. hyperphosphatemia
  3. vit D deficiency
27
Q

Clinical signs of hypocalcemia:

A
  1. agitation
  2. hyperreflexia
  3. convulsions
  4. HTN
  5. long QT
28
Q

Causes of low PTH hypocalcemia?

A

hypoparathyroidism
Mg deficiency
phosphate excess

29
Q

Causes of high PTH hypocalcemia?

A

Severe vit D deficiency
renal failure
resistance to vit D or PTH

30
Q

In acute hypocalcemia, always correct:

in addition to the low Ca, duh

A

low Mg (if present)

*treat low Ca with Ca gluconate

31
Q

Long term management of hypocalcemia?

A
  1. oral Ca salts
  2. vit D
  3. HCTZ (increases reabs of Ca in distal tubule)
32
Q

What is MEN?

A

AD syndrome characterized by 2 or more endocrine tumors; may be benign or malignant and functional or non-functional

33
Q

Where do tumors present in MEN1

A
  1. parathyroid
  2. pancreas
  3. pituitary
34
Q

What are signs/symptoms of MEN1?

A

kidney stones, recurrent peptic ulcers, fasting hypoglycemia, hypogonadism, galactorrhea

35
Q

What labs would be abn in MEN1?

A 
gastrin
Ca/PTH
insulin/glucose
PRL
IGF-1
ACTH/cortisol
36
Q

What are the average ages for the following MEN1 tumors:

  • -pituitary
  • -insulinoma
  • -gastrinoma
A

38
25
35

37
Q

How does a parathyroidectomy affect patients with primary hyperparathyroidism and gastrinoma?

A

improves hypercalcemia

decreases gastrin

38
Q

Important clinical features of MEN2B?

A
  1. mucosal neuromas (~100%)
  2. marfanoid habitus
  3. pheochromocytoma
  4. medullary thyroid carcinoma (~100%)
39
Q

What gene is affected in MEN2?

A

RET

40
Q

Epidemiology of:
MEN1
MEN2A
MEN2B

A 
MEN1 = 2nd-3rd decade
MEN2A = adults
MEN2B = early onset
41
Q

Important clinical features of MEN2A?

A
  1. medullary thyroid carcinoma (~100%)
  2. pheochromocytoma
  3. primary hyperparathyroidism
42
Q

MEN2B is associated with MORE malignant:

compared to 2A

A

medullary thyroid carcinoma

43
Q

Signs/symptoms of MEN2A and MEN2B

A

thyroid nodules, HTN, “spells”, diaphoresis

44
Q

Abn labs in MEN2A and MEN2B

A
  1. calcitonin, CEA
  2. plasma and urine metanepherines
  3. chromogranin A
45
Q

Definitive treatment of MEN2A and MEN2B

A

thyroidectomy with lymph nose dissection

Endo (28 decks)

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