Chapter 23: Parathyroid Flashcards Preview

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Flashcards in Chapter 23: Parathyroid Deck (89):
1

Where are the superior parathyroids found?

Lateral to the recurrent laryngeal nerves (RLNs), posterior surface of superior portion of gland, above inferior thyroid artery

2

Superior parathyroids develop from what

4th pharyngeal pouch; associated with thyroid complex

3

Inferior parathyroids develop from what

3rd pharyngeal pouch; associated with thymus

4

Where are the inferior parathyroids found?

- Medial to RLNs, more anterior, below inferior thyroid artery

5

Parathyroids: which ones are more likely to have a variable location and more likely to be ectopic?

Inferior parathyroids

6

Where are the inferior parathyroids occasionally found?

In the tail of the thymus (most common ectopic site) and can migrate to the anterior mediastinum

7

Ectopic sites of inferior parathyroids

Tail of thymus, anterior mediastinum, intra-thyroid, near tracheoesophageal groove

8

% population that have all parathyroid glands

90%

9

Artery: blood supply to both superior and inferior parathyroid glands

Inferior thyroid artery

10

Increases serum calcium

PTH

11

Four physiologic effects of PTH

- Increases kidney Ca reabsorption in the DCT, decreases kidney PO4 absorption
- Increased osteoclasts in bone to release Ca (and PO4-)
- Increased VitD production in kidney (increased 1-OH hydroxylation) -> increased Ca-binding protein in intestine -> increased intestinal Ca absorption

12

Increases intestinal Ca and PO4 absorption by increasing calcium-binding protein

Vitamin D

13

- Decreases serum Ca
- Decreases Ca resorption (osteoclast inhibition)
- increases urinary Ca and PO4 excretion

Calcitonin

14

Normal Ca level

8.5 - 10.5 (ionized 4.4 - 5.5)

15

Normal PTH level

5 - 40 pg/mL

16

Normal PO4 level

2.5 - 5.0

17

Normal Cl- level

98 - 107

18

Most common cause of hypoparathyroidism

Previous thyroid surgery

19

- Women, older age
- Due to autonomously high PTH

Primary hyperparathyroidism

20

Dx: primary hyperparathyroidism

Increased Ca, decreased PO4-, Cl- to PO4- ratio > 33; increased renal cAMP; HCO3- secreted in urine

21

ABG in primary hyperparathyroidism

Hyperchloremic metabolic acidosis

22

Bone lesions from Ca resorption; characteristic of hyperparathyroidism

Osteitis fibrosa cystica (brown tumors)

23

Symptoms of primary hyperparathyroidism

Most patients have no symptoms -> increased calcium found on routine lab work for some other problem or on checkup

24

Muscle weakness, myalgia, nephrolithiasis, pancreatitis, PUD, depression, bone pain, pathologic fractures, mental status changes, constipation, anorexia

Primary hyperparathyroidism
- HTN can result from renal impairment

25

Diagnostic workup for primary hyperparathyroidism

- H&P. Elevated Ca thru 2-3 detrminations.
- CXR: look for bony mets, sarcoid, pulmonary tumors
- Excretory urogram: nephrolithiasis, renal tumors
- Serum protein electrophoresis to r/o multiple myeloma
- 24-hr urinary ca determination
- r/o MEN
- Check PTH level

26

Indications for surgery: primary hyperparathyroidism

- Symptomatic disease
- Asymptomatic disease with Ca > 13, decreased Cr clearance, kidney stones, substantially decreased bone mass

27

Primary hyperparathyroidism: % pts with single adenoma

80% of patients

28

Primary hyperparathyroidism: % pts with multiple adenomas

Occur in 4% of patients

29

Primary hyperparathyroidism: % patients with diffuse hyperplasia

Occurs in 15% of patients with MEN 1 or 2a have 4-gland hyperplasia

30

Hyperparathyroidism: very rare, can get high Ca levels

Parathyroid adenocarcinoma

31

Treatment: parathyroid adenoma

Resection; inspect other glands to rule out hyperplasia or multiple adenomas

32

Treatment: parathyroid hyperplasia

- Do not biopsy all glands -> risks hemorrhage and hypoparathyroidism
- Tx: resect 3 1/2 glands or total parathryoidectomy and autoimplantation

33

Treatment: parathyroid Ca

Need radical parathyroidectomy (need to take ipsilateral thyroid lobe)

34

Treatment: primary hyperparathyroidism in pregnancy

Surgery in 2nd trimester; increased risk of stillbirth if not resected

35

What are benefits of intra op frozen section in primary hyperparathyroidism?

Can confirm that the tissue taken was indeed parathyroid

36

What are benefits of intra op PTH levels?

Can help determine if the causative gland is removed (PTH should go to

37

Where do you check for missing glands in hyperparathyroidism?

Check inferiorly in thymus tissue (MC ectopic location, can remove tail of the thymus and see if PTH drops), near carotids, vertebral body, superior to pharynx, thyroid

38

What if you still cannot find the parathyroid glands when you checked all ectopic locations?

Close and follow PTH; if PTH still increased, get sestamibi scan to localize

39

At reoperation for a missing gland, where do you look?

The most common location for the gland is normal anatomic position

40

What causes hypocalcemia post op in primary hyperparathyroidism?

From bone hunger or failure of parathyroid remnant / graft

41

Hypocalcemia postop primary hyperparathyroidism: Normal PTH, decreased HCO3-

Bone hunger

42

Hypocalcemia postop primary hyperparathyroidism: decreased PTH, normal HCO3-

Aparathyroidism

43

Primary hyperparathyroidism: most commonly due to missed adenoma remaining in the neck

Persistent hyperparathyroidism (1%)

44

What can cause recurrent hyperparathyroidism after surgery for primary hyperparathyroidism?

- Occurs after a period of hypocalcemia or normocalcemia
- Can be due to new adenoma formation
- Can be due to tumor implants at the original operation that have now grown.
- Need to consider recurrent parathyroid cancer

45

Risks of reoperation in primary hyperparathyroidism

Associated with increased risk of RLN injury, permanent hypoparathyroidism

46

- Will have preferential uptake by the overactive parathyroid gland
- Good for picking up adenomas but not 4-gland hyperplasia
- Best for trying to pick up ectopic glands

Sestamibi scan

47

- Seen in patients with renal failure
- Increased PTH in response to low Ca
- Most do not need surgery (95%)
- Ectopic calcification and osteoporosis can occur

Secondary hyperparathyroidism

48

Tx: secondary parathryoidism

- Ca supplement, vitamin D, control diet PO4, PO4-binding gel, decreased aluminum
- Surgery for bone pain (MC indication), fractures, or pruritus (80% get relief)

49

MC indication for surgery in secondary hyperparathyroidism

Bone pain

50

What does surgery involve in secondary hyperparathyroidism?

Surgery involves parathyroidectomy with autotransplantation or subtotal parathyroidectomy

51

- Renal disease now corrected with transplant but still overproduces PTH
- Has similar lab values as primary hyperparathyroidism (hyperplasia)
Tx: subtotal (3 1/2 glands) or total parathyroidectomy with autoimplantation

Tertiary hyperparathyroidism

52

Patients have increased serum Ca and decreased urine Ca (should be increased if hyperparathyroidism)

Familial hypercalcemic hypocalciuria

53

What causes familial hypercalcemic hypocalciuria?

Caused by defect in PTH receptor in distal convoluted tubule of the kidney that causes increased resorption of calcium

54

Dx: Ca 9-11, have normal PTH (30-60), decreased urine Ca

Tx?

Familial hypercalcemic hypocalciuria

Tx: nothing (Ca generally not that high in these patients); no parathyroidectomy

55

Because of defect in PTH receptor in the kidney, does not respond to PTH

Pseudohypoparathyroidism

56

- Rare cause of hypercalcemia
- Increased Ca, PTH, and alkaline phosphatase (can have extremely high Ca levels)

Parathyroid Cancer

57

MC location for metastases in parathyroid cancer

Lung

58

Tx: parathyroid cancer

Wide en bloc excision (parathyroidectomy and ipsilateral thyroidectomy)

59

5-year survival rate: parathyroid cancer

50%

60

Mortality in parathyroid cancer

Due to hypercalcemia

61

Recurrence rate of parathyroid cancer

Recurrence in 50%

62

- Derived from APUD cells
- Neoplasms can develop synchronously or metachronously
- Autosomal dominant, 100% penetrance

Multiple endocrine neoplasia syndromes

63

Components of MEN-one

Pituitary adenoma
Parathyroid hyperplasia
Pancreatic islet cell tumors

64

Usually first part to become symptomatic in MEN one

Parathyroid hyperplasia

65

Tx: parathyroid hyperplasia in MEN-one

4-gland resection with autotransplantation

66

#1 pancreatic islet cell tumor in MEN-one

Gastrinoma #1 - 50% multiple, 50% malignant; major morbidity of syndrome

67

#1 pituitary adenoma in MEN-one

Prolactinoma #1

68

How do you begin to treat MEN-one?

Need to correct hyperparathyroidism 1st if simultaneous tumors

69

Components of MEN-IIa

Parathyroid hyperplasia
Medullary CA of thyroid
Pheochromocytoma

70

MC symptom of medullary CA of thyroid

Diarrhea

71

#1 cause of death in MEN-IIa patients

Medullary CA of thyroid

72

Usually first part to be symptomatic in MEN-IIa

Medullary CA of thyroid

73

MEN-2a:
- Nearly all patients; diarrhea most common symptom; often bilateral
- #1 cause of death in these patients
- Usually 1st part to be symptomatic

Medullary CA of thyroid

74

MEN-2a: often bilateral, nearly always benign

Pheochromocytoma

75

How do you begin to treat MEN-2a?

Need to correct pheochromocytoma 1st if simultaneous tumors

76

Components of MEN-2b

- Medullary CA of thyroid
- Pheochromocytoma
- Mucosal neuromas
- Marfan's habitus, musculoskeletal abnormalities

77

How do you begin to treat MEN-2b?

Need to correct pheochromocytoma 1st if simultaneous tumors

78

Gene affected: MEN one

MENIN gene

79

Gene affected: MEN2a and 2b

RET proto-oncogene

80

Disease phenotypes related to mutation of the RET proto-oncogene

MEN2a (60%), MEN2b (5%), FMTC (35%)

81

Germline mutations in cysteine codons of extracellular and transmembrane domains of RET

MEN2a

82

Germline activating mutation in tyrosine kinase domain or RET

MEN2b

83

Germline mutations in cysteine codons of extracellular or transmembrane domains of RET

FMTC

84

Causes of hypercalcemia

- Malignancy
- Hyperparathyroidism
- Hyperthyroidism
- Familial hypercalcemia hypocalciuria
- Immobilization
- Granulomatous disease (sarcoidosis or tuberculosis)
- Excess vitamin D
- Milk alkali syndrome
- Thiazide diuretics

85

Breakdown of hypercalcemia in malignancy

- Hematologic (25%): lytic bone lesions
- Nonhematologic (75%): cancers that release PTHrP (small cell lung CA, breast CA)

86

Inhibits osteoclasts (used with malignancies or failure of conventional treatment); has hematologic, liver, and renal side effects

Mithramycin

87

Usually secondary to another surgery in patients with pre-existing hyperparathyroidism
- Tx?

Hypercalcemic crisis

Tx: fluids (normal saline) and furosemide (Lasix)

88

How does breast cancer metastases to bone cause hypercalcemia?

Release PTHrP (rP = related peptide); can cause hypercalcemia
- This is NOT due to bone destruction
- Associated with increased urinary cAMP (from action of PTHrP on kidney)

89

What do hematologic malignancy do to bone?

These can cause bone destruction with increased Calcium (urinary cAMP will be low)