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PARATHYROID DISORDERS (based on T) Flashcards

1
Q

How many parathyroid glands are there and where are they located?

A

There are 4 parathyroid glands: 2 superior glands (almost always posterior to the upper portions of the thyroid lobes) and 2 inferior glands (variable location, often posterior to the lower thyroid or in the mediastinum).

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2
Q

What is the primary function of parathyroid hormone (PTH)?

A

The primary function of PTH is to maintain extracellular fluid calcium concentration within a narrow normal range.

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3
Q

What are the three properties of parathyroid glands vital to homeostasis?

A
  1. Short-term: Rapidly secretes PTH in response to changes in blood calcium. 2. Intermediate-term: Synthesizes, processes, and stores large amounts of PTH in a regulated manner. 3. Long-term: Replicates when chronically stimulated (e.g., chronic kidney disease).
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4
Q

What are the key actions of PTH on the kidneys?

A
  1. Stimulates calcium reabsorption 2. Inhibits phosphate transport and promotes phosphate excretion 3. Stimulates synthesis of 1,25 (OH)2D3 (active vitamin D)
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5
Q

What are the key actions of PTH on bones?

A
  1. Bone formation: Intermittent, low doses 2. Bone resorption: Continuous, high doses
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6
Q

What is the key action of PTH on the intestine?

A

PTH promotes calcium absorption in the proximal intestine via calcitriol (1,25 OH2 Vitamin D).

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7
Q

What are the two main types of PTH receptors and where are they found?

A
  1. PTH1 receptor: Binds PTH & PTHrp, found in bones, kidneys, breast, skin, heart, pancreas. 2. PTH2 receptor: Binds PTH but not PTHrp, found in CNS, cardiovascular, and gastrointestinal systems.
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8
Q

What are the two main categories of hypercalcemia based on PTH levels?

A
  1. High Calcium, High (or Inappropriately Normal) PTH: Primary hyperparathyroidism (adenoma, hyperplasia, MEN 1/2A, carcinoma), lithium therapy, familial hypocalciuric hypercalcemia. 2. High Calcium, Low PTH: Malignancy, vitamin D-related disorders, high bone turnover, renal failure.
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9
Q

What is the first step in evaluating hypercalcemia?

A

Determine whether it is acute or chronic (chronic is >3 months and often due to hyperparathyroidism or MEN syndromes).

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10
Q

What is the most common cause of primary hyperparathyroidism?

A

Parathyroid adenoma (75-80% of cases).

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11
Q

What are the major causes of primary hyperparathyroidism?

A
  1. Parathyroid adenoma (75-80%) 2. Diffuse parathyroid hyperplasia (20%) 3. Parathyroid carcinoma (<1%) 4. MEN 1 and MEN 2A (rare).
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12
Q

What are the clinical manifestations of hypercalcemia?

A

‘Stones, bones, abdominal moans, and psychic groans’: 1. Stones: Nephrolithiasis, nephrocalcinosis, dehydration 2. Bones: Bone pain, osteoporosis, osteitis fibrosa cystica 3. Abdominal moans: Nausea, vomiting, constipation, pancreatitis 4. Psychic groans: Cognitive impairment, fatigue, muscle weakness.

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13
Q

What are the skeletal manifestations of hyperparathyroidism?

A
  1. Generalized bone demineralization 2. Subperiosteal resorption (most sensitive finding) 3. Brown tumors 4. Osteopenia/osteoporosis 5. ‘Salt and pepper’ skull on X-ray.
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14
Q

What are the renal manifestations of hyperparathyroidism?

A
  1. Recurrent calcium nephrolithiasis 2. Nephrocalcinosis 3. Renal failure due to impaired concentration ability.
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15
Q

What imaging study is used to localize parathyroid adenomas?

A

99m Sestamibi scan.

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16
Q

What are the indications for parathyroid surgery in primary hyperparathyroidism?

A
  1. Symptoms of hypercalcemia (e.g., nephrocalcinosis, urolithiasis, fractures). 2. Serum calcium >1 mg/dL above normal. 3. Creatinine clearance <60 cc/min or urinary calcium excretion >400 mg/day. 4. Bone Mineral Density (BMD) T-score < -2.5 at spine, hip, or distal radius. 5. Age <50 years.
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17
Q

What are the MEN syndromes associated with hyperparathyroidism?

A
  1. MEN 1 (Wermer’s Syndrome): Hyperparathyroidism, pituitary tumors, pancreatic tumors (Zollinger-Ellison Syndrome). 2. MEN 2A: Pheochromocytoma, medullary thyroid carcinoma, parathyroid tumors. 3. MEN 2B: MEN 2A features plus multiple neuromas.
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18
Q

What are some cardiovascular findings in hypercalcemia?

A
  1. Hypertension 2. Shortened QT interval 3. Cardiac arrhythmias.
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19
Q

What is asymptomatic primary hyperparathyroidism?

A

Biochemically confirmed hyperparathyroidism (elevated or inappropriately normal PTH with hypercalcemia) without signs or symptoms.

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20
Q

What are the guidelines for monitoring asymptomatic primary hyperparathyroidism?

A
  1. Serum calcium: Annually 2. Serum creatinine: Annually 3. Renal function: eGFR annually, 24-hour biochemical stone profile if stones are suspected 4. Bone Mineral Density (BMD): Every 1-2 years.
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21
Q

What is the cause of Familial Hypocalciuric Hypercalcemia (FHH)?

A

Inactivating mutation of the calcium-sensing receptor (CASR) in the parathyroid gland and kidneys.

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22
Q

What are the lab findings in Familial Hypocalciuric Hypercalcemia (FHH)?

A

Normal to high PTH, high calcium, low phosphorus.

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23
Q

What is the inheritance pattern of Familial Hypocalciuric Hypercalcemia (FHH)?

A

Autosomal dominant.

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24
Q

At what age does Familial Hypocalciuric Hypercalcemia (FHH) typically present?

A

First decade of life.

25
Is surgery or medical therapy usually needed for Familial Hypocalciuric Hypercalcemia (FHH)?
No, it is most often not needed.
26
What percentage of renal calcium is reabsorbed in Familial Hypocalciuric Hypercalcemia (FHH)?
>99%.
27
How does renal calcium reabsorption compare in primary hyperparathyroidism?
<99% calcium reabsorption.
28
What are the causes of hypercalcemia with low PTH?
Malignancy-related causes, such as solid tumors with metastasis (breast), solid tumors with humoral mediation (lung, kidney), and hematologic malignancies (multiple myeloma, lymphoma, leukemia).
29
What are the expected lab results in malignancy-related hypercalcemia?
High calcium, low phosphorus, low iPTH, high PTHrP (more likely), low 1,25 (OH)2 D.
30
How do lab findings differ in true primary hyperparathyroidism?
PTH is high, and 1,25 (OH)2 D is high.
31
What can cause hypercalcemia related to vitamin D?
Vitamin D intoxication, increased 1,25 (OH)2 D from sarcoidosis or granulomatous disease, idiopathic hypercalcemia of infancy.
32
What is the threshold for diagnosing vitamin D intoxication?
25-hydroxyvitamin D assay >100 ng/mL.
33
What is the treatment for vitamin D intoxication?
Hydrocortisone 100 mg/day.
34
What are some causes of hypercalcemia associated with high bone turnover?
Hyperthyroidism, immobilization, thiazide diuretics, vitamin A intoxication.
35
What are some causes of hypercalcemia associated with renal failure?
Severe secondary hyperparathyroidism, aluminum intoxication, milk-alkali syndrome.
36
What is the most common cause of secondary hyperparathyroidism?
Chronic kidney disease (CKD).
37
What other conditions can cause secondary hyperparathyroidism?
Osteomalacia, vitamin D deficiency, pseudohypoparathyroidism.
38
What is the role of FGF-23 in chronic kidney disease-related secondary hyperparathyroidism?
FGF-23 inhibits renal 1-alpha hydroxylase, decreasing 1,25 (OH)2 D production and leading to secondary increase in PTH.
39
What are the clinical manifestations of secondary hyperparathyroidism?
Bone pain, ectopic calcification, renal osteodystrophy.
40
What are the treatments for secondary hyperparathyroidism?
Dietary phosphate restriction, calcitriol, phosphate binders, cinacalcet.
41
What causes tertiary hyperparathyroidism?
Development of autonomous PTH adenoma due to chronic overstimulation of hyperplastic PTH glands (e.g., chronic renal insufficiency).
42
What is the treatment for tertiary hyperparathyroidism?
Often requires parathyroid surgery.
43
What are severe clinical manifestations of hypercalcemia?
Cardiac arrhythmia, ventricular tachycardia, arrest, coma.
44
What is the management of severe hypercalcemia (>13 mg/dL)?
Hydration and bisphosphonates to counteract increased bone resorption.
45
What are some therapies for severe hypercalcemia?
Hydration with normal saline, bisphosphonates (pamidronate, zoledronate), denosumab.
46
What is the cause of hypoparathyroidism?
Deficiency of PTH, ineffective PTH, or overwhelmed parathyroid function.
47
What are the main categories of hypoparathyroidism causes?
PTH absent (hereditary or acquired), PTH ineffective (e.g., CKD, lack of active vitamin D), PTH overwhelmed (e.g., severe hyperphosphatemia, rhabdomyolysis, tumor lysis syndrome).
48
What is the most common cause of acquired hypoparathyroidism?
Total thyroidectomy where more than three parathyroid glands are removed.
49
What is a major electrolyte disorder associated with hypoparathyroidism?
Hypocalcemia.
50
What are some clinical manifestations of acute hypocalcemia?
Neuronal irritability, latent tetany (Chvostek’s and Trousseau’s signs), paresthesias, muscle cramps, laryngeal spasms, seizures.
51
What are Chvostek’s and Trousseau’s signs?
Chvostek’s: Facial twitching when tapping the cheek. Trousseau’s: Carpopedal spasm induced by inflating a BP cuff.
52
What are some chronic manifestations of hypocalcemia?
Basal ganglia calcification (Fahr’s syndrome), impaired intellectual ability, dry skin, brittle nails, enamel hypoplasia, subcapsular cataracts, CHF/cardiomyopathy.
53
What is pseudohypoparathyroidism?
Hypocalcemia due to renal resistance to PTH, often associated with Albright’s hereditary osteodystrophy.
54
What are the features of Albright’s hereditary osteodystrophy?
Short stature, round face, brachydactyly, heterotopic calcification.
55
What are the treatments for hypocalcemia?
IV calcium gluconate for acute cases, oral calcium supplements (carbonate or citrate), vitamin D supplementation.
56
What is the goal of hypoparathyroidism treatment?
Maintain serum calcium in the low-normal range without causing hypercalciuria to avoid nephrolithiasis and decreased GFR.
57
What is the emergency treatment for severe symptomatic hypocalcemia?
Slow IV push of calcium gluconate or continuous IV calcium drip.
58
What can be given to minimize renal calcium losses in hypoparathyroidism?
Thiazide diuretics.

AAA-MEDICINE (ENDOCRINE) (10 decks)

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