Hyperparathyroidism Flashcards

1
Q

Structure and Function of the Parathyroid Glands (3).

A
  1. 4 Parathyroid Glands in 4 Corners of Thyroid Gland.
  2. Chief Cells in the Glands.
  3. PTH Release in Response to Hypocalcaemia.
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2
Q

Functions of Parathyroid Hormone (4).

A
  1. Increase Osteoclast Activity in Bones.
  2. Increase Calcium Absorption from the Gut.
  3. Increase Calcium Absorption from the Kidneys.
  4. Increase Vitamin D Activity.
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3
Q

Synergistic Activity of Vitamin D.

A
  1. Increases Calcium Resorption from the Intestines.

2. PTH activates Vitamin D.

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4
Q

What is Primary Hyperparathyroidism?

A

Uncontrolled PTH produced directly by a tumour of the parathyroid glands, leading to hypercalcaemia.

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5
Q

Management of Primary Hyperparathyroidism.

A

Surgical Removal of the Tumour.

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6
Q

Aetiology of Primary Hyperparathyroidism.

A
  1. 80% - Solitary Adenoma.
  2. 15% - Hyperplasia.
  3. 4% - Multiple Adenoma.
  4. 1% - Carcinoma.
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7
Q

Clinical Presentation of Primary Hyperparathyroidism.

A
  1. Elderly Female.
  2. Unquenchable Thirst.
  3. Inappropriately Normal/RaisedPTH.
  4. Majority = Asymptomatic.
  5. Hypercalcaemia.
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8
Q

Associations of Primary Hyperparathyroidism (2).

A
  1. Hypertension.

2. MEN I and II.

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9
Q

Investigations of Primary Hyperparathyroidism (6).

A
  1. Raised Calcium.
  2. Low Phosphate.
  3. Raised/Inappropriately Normal PTH.
  4. X-Ray : Pepperpot Skull.
  5. Technetium-MIBI Subtraction Scan.
  6. Urine Calcium : Creatinine Clearance Ratio > 0.01.
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10
Q

Management of Primary Hyperparathyroidism (3).

A
  1. Definitive - Total Parathyroidectomy.
  2. Conservative - No End Organ Damage AND Age > 50 AND Calcium < 0.25 mmol/L above the upper limit of normal.
  3. If surgery is not suitable, Cinacalcet.
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11
Q

Mechanism of Action of Cinacalcet.

A

Calcimimetic - ‘mimics’ action of Calcium on tissues by allosteric activation of a Calcium-sensing receptor.

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12
Q

What is Secondary Hyperparathyroidism?

A

Insufficient Vitamin D or CKD leads to low absorption of Calcium from the intestines, kidneys and bones causing hypocalcaemia - hyperplasia of chief cells.

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13
Q

Management of Secondary Hyperparathyroidism (2).

A
  1. Correct Vitamin D Deficiency.

2. Perform a renal transplant to treat renal failure.

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14
Q

Aetiology of Secondary Hyperparathyroidism.

A
  1. Low Vitamin D.

2. CKD.

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15
Q

Investigations of Secondary Hyperparathyroidism (4).

A
  1. PTH Elevated.
  2. Calcium Low/Normal.
  3. Phosphate Elevated in CKD and Low in Vitamin D Deficiency.
  4. Vitamin D Low.
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16
Q

Indications for Surgery in Secondary Hyperparathyroidism (3).

A
  1. Bone Pain.
  2. Persistent Pruritus.
  3. Soft Tissue Calcifications.
17
Q

What is Tertiary Hyperparathyroidism?

A

Secondary Hyperparathyroidism continues for a long period of time, leading to hyperplasia of the glands.

18
Q

Pathophysiology of Tertiary Hyperparathyroidism (4).

A
  1. Baseline of PTH increases dramatically.
  2. Even after cause is treated, PTH level remains inappropriately high.
  3. High PTH in absence of previous pathology leads to high absorption of Calcium in the intestines, kidneys and bones.
  4. Hypercalcaemia.
19
Q

Management of Tertiary Hyperparathyroidism.

A

Surgical Removal of Parathyroid Tissue.

20
Q

Aetiology of Tertiary Hyperparathyroidism.

A

Hyperplasia of all 4 Glands after Correction of Underlying Renal Disorder.

21
Q

Investigations of Tertiary Hyperparathyroidism.

A
  1. Calcium - Normal/High.
  2. PTH - High.
  3. Phosphate - Low/Normal.
  4. Vitamin D - Normal/Low.
  5. ALP - Elevated.