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Endocrine System > Disorders of Calcium and Parathyroid Gland > Flashcards

Disorders of Calcium and Parathyroid Gland Flashcards

1
Q

Mineral Metabolism Key players

Cellular level

A 
– Calcium
– Phosphorous
– PTH
– Vitamin D
– FGF23
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2
Q

Mineral Metabolism Key players

Tissue Level

A 
– Parathyroid glands
– Gut
– Kidney
– Bone
– Liver
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3
Q

Mineral Metabolism Minor players

Cellular level

A

– Calcitonin
– Magnesium
– Acid-­‐base state

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4
Q

Mineral Metabolism Minor players

Tissue Level

A

– Skin

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5
Q

Calcium distribution Total body calcium

A

~ 1 kg
– 99% in bone (hydroxyapatite)
– 1% extracellular and soft tissues
– 0.1% intracellular

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6
Q

Calcium distribution Serum calcium

A

– 40% protein bound
– 10% complexed (citrate or phosphate ions)
– 50% ionized – free calcium that is bioavailable

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7
Q

Low Calcium Stimulates release

A

PTH

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8
Q

Increase PTH

A

Increase calcium mobilizaIon from bone
Increase calcium reabsorpIon from DCT
Increase 1α-hydroxylase

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9
Q

Increase in 1α-hydroxylase

A

Increase calcium absorption from intestines from increase 1,25(OH)2D.

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10
Q

increase 1,25(OH)2D

A

stimulates reabsorption of Ca (distal nephron)

inactivates phosphate transporter (PCT)

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11
Q

Calcium-­‐sensing receptor (CaSR) senses

A

Ca++ level

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12
Q

CaSR found in & is a member of?

A

-parathyroid
-kidney
-C cells thyroid
-bone
Member of the GPCR family

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13
Q

Stimulating the calcium sensing receptor results in?

A

an Intra-cellular cascade to reduce PTH secretion

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14
Q

Work up of hypercalcemia (Differential Diagnosis)

Three thing?

A
  1. History and Physical
  2. Check albumin and total calcium x 2
  3. Check a PTH
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15
Q

PTH dependent hypercalcemia

A

− Hyperparathyroidism (primary/tertiary)
− Familial hypocalciuric hypercalcemia
− Medication-induced (Lithium or HCTZ-mediated)

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16
Q

PTH independent hypercalcemia

A
  • Tumor induced (PTHrP or bone metastases)
  • Granulomatous diseases (TB), sarcoidosis, lymphoma - ↑ 1,25 vit.D
  • Multiple myeloma
  • Hyperthyroidism/adrenal failure
  • Immobilization
  • Medication-induced: (vitamin D toxicity, vitamin A, milk-alkali)
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17
Q

Primary Hyperparathyroidism

A

80-85% adenoma
15% hyperplasia (MEN1, MEN2A, HPT-Jaw Tumor Syndrome, familial HPT)
<1% Parathyroid carcinoma

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18
Q

Sporadic Primary Hyperparathyroidism
Risk factors:
Etiology:
Buzz words:

A

age, race (AA>W>H), sex (F>M)
unknown
serendipity: stones, moans (abdominal), groans (psychic), & bones

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19
Q

Symptoms in Primary Hyperparathyroidism

A 
Fatigue/weakness
Musculoskeletal pain
Polydipsia/Polyuria
Constipation
Anorexia/nausea/Dyspepsia
Pruritus
Depression/Memory loss
Renal failure/Kidney stones
Osteoporosis/Fracture
Pancreatitis
Hypertension
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20
Q

Symptoms in Primary Hyperparathyroidism Most Common

A
  • Symptoms are non-­‐specific

* Majority of paIents are asymptomaIc

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21
Q

Primary HPT Work up Biochemical:

A
  • calcium, Albumin (ionized calcium),
  • PTH,
  • 25-OH vitamin D,
  • 24-hour urine calcium (to differentiate from FHH)
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22
Q

Primary HPT Work up Imaging:

A
  • Thyroid US (Localization study)
  • 99Tc-sestamibi scan (Localization study)
  • DXA
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23
Q

Management of Primary HPT ConservaIve management

A
  • Adequate hydraIon
  • Use of bisphosphonates in paIents with osteoporosis
  • Maintenance of vitamin D status (20-­‐30 ng/mL)
  • Cinacalcet has been approved by FDA for those who do not qualify for surgery and have moderate hypercalcemia (Ca >12.5 mg/dL)
  • Annual follow up: Ca/PTH, renal function, DXA
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24
Q

Familial Hypocalciuric Hypercalcemia Inactivating mutation causing?

A

Of CaSR, 100% penetrance
Mildly ↑ serum Ca, high-normal/mildly ↑ PTH, hypocalciuria.
Asymptomatic

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25
Q

Familial Hypocalciuric Hypercalcemia Work up:

A

Serum Ca, PTH, 24-hr urine calcium (<50-100 mg/

24 hr). Can also ask relatives to √ serum calcium. Genetic testing

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26
Q

Familial Hypocalciuric Hypercalcemia Treatment

A

No treatment is indicated

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27
Q

Tertiary Hyperparathyroidism Occurs in

A

The face of long standing secondary hyperparathyroidism
• At one point, these glands become
autonomous (recall Primary HPT)
– in the setting of end-stage renal disease
– Post-kidney transplant

28
Q

Parathyroid glands develop hyperplasia

A

Due to chronic low Calcium and/or high

Phosphorous levels

29
Q

Hypercalcemia of malignancy Clinical presentaIon

A

Consistent with signs & symptoms of hypercalcemia & potenIal diagnosis of malignancy

30
Q

Hypercalcemia of malignancy EIology:

A

breast, lung, lymphoma, thyroid, kidney, prostate, mulIple myeloma, pancreas…
Most common: breast & squamous cell carcinoma

31
Q

Hypercalcemia of malignancy

THE PTH LEVEL WILL BE

A

SUPPRESSED!!!

32
Q

Hypercalcemia can occur in malignancy without increase in PTHrP

A

− Bony metastases can increase calcium levels
− Humoral factors (cytokines, TNFa) can acIvate osteoclasts
− MulIple myeloma can cause significant bone destrucIon resulIng in hypercalcemia

33
Q

Granulomatous disorders causing hypercalcemia

A

Sarcoid

Lymphoma

34
Q

Granulomatous disorders causing hypercalcemia (sarcoid, lymphoma)

A 
Increased 25(OH)D3
 Increased1 25(OH)2D3
Decreased VDR (Vitamin D receptor)
 Increased 1α-hydroxylase
 Increased PTH
 Increased Ca
 Increased PO4
35
Q

Initial Treatment of Acute Hypercalcemia

A

Address Volume Status: Saline Diuresis ± Furosemide (only after volume status is corrected)
Calcitonin IM/SC (4-6 IU/kg q6-12 hours) – 3-4 days
Bisphosphonates (Pamidronate IV over 4 hrs- works for 2-3 wks or Zoledronic acid IV over 15 minutes works for 1-3 months)
Glucocorticoids (useful in myeloma, granulomatous disease, vitamin D toxicity)
Phosphate (*rarely used, caution elevated Ca x Phos product)
Dialysis

36
Q

Major Causes of Secondary PTH Elevation

A
  1. Hypocalcemia
  2. Hyperphosphatemia
  3. Vitamin D deficiency
37
Q

Renal Disease

A

Decrease 1a-hydroxylase
Decrease 1,25(OH)2D3
Increase PTH

38
Q

Approach to the patient with Secondary Hyperparathyroidism Symptoms:

A

Are non-specific and likely related to underlying disease causing elevated PTH but not due to PTH itself

39
Q

Approach to the patient with Secondary Hyperparathyroidism Evaluate key elements of the?

A

Calcium axis: serum PTH, Calcium (with albumin), Phosphorous, Creatinine, vitamin D. Do not collect 24-hour urine for calcium

40
Q

Approach to the patient with Secondary Hyperparathyroidism if calcium is normal

A

No indications for imaging studies

41
Q

Approach to the patient with Secondary Hyperparathyroidism Treatment

A

Treat underlying reason(s). Make sure vitamin D is always replete.

42
Q

Vitamin D Deficiency

A
  1. Severe vitamin D deficiency is rare
  2. Presenting complains in mild-to-moderate vit. D
    deficiency are very non-specific: musculoskeletal
    pains, fatigue
  3. 50% of patients with osteoporosis have vit. D
    deficiency
  4. Vitamin D replacement (>800 units/day) showed ~20% reduction in risk of fractures
43
Q

Hypocalcemia: Clinical signs

A 
agitation
hyperreflexia
convulsions
hypertension
long QT
44
Q

Hypocalcemia: DifferenIal Diagnosis of Hypoparathyroidsm (low PTH)

A

Primary process as low PTH decreases Calcium

  1. Post-thyroidectomy
  2. Idiopathic – antibodies to PTH
  3. Autoimmune
  4. Parathyroid agenesis – e.g. DiGeorge syndrome
  5. Hypomagnesaemia, hypermagnesemia, hyperphosphatemia
45
Q

Hypocalcemia: DifferenIal Diagnosis of Hyperparathyrodism (high PTH)

A

Secondary process or when PTH increases due to low calcium from other reasons.

  1. Renal Failure
  2. Vitamin D deficiency
  3. Vitamin D or PTH resistance syndromes
46
Q

Miscellaneous Causes of Hypocalcemia

A
  1. Acute pancreatitis: free fatty acids chelate calcium
  2. Massive transfusion: infusion of citrate will complex
    with calcium leading to decreased ionized calcium
  3. Tumor Lysis Syndrome or rhabdomyolysis:
    Phosphate release binds to ionized calcium
  4. Severe sepsis: Cytokines mediated?
  5. Medications: phosphate, bisphosphonates
  6. Hungry bone syndrome
47
Q

Work up of hypocalcemia

A
  1. History and Physical
  2. Check albumin and total calcium x 2
  3. Check PTH
48
Q

Work up of hypocalcemia PTH is low

A

Hypoparathyroidism
Magnesium deficiency
Phosphate excess

49
Q

Work up of hypocalcemia PTH is high

A

Severe vitamin D deficiency
Renal failure
Vitamin D resistance or PTH resistance

50
Q

Pseudohypoparathyroidism define:

A

The idiopathic inherited forms of PTH resistance.

51
Q

Pseudohypoparathyroidism PaIents

have

A

Elevated PTH (1000s), hypocalcaemia, hyperphosphatemia and/or specific morphological features including short stature, rounded face, foreshortened 4th and other metacarpals, obesity.

52
Q

Pseudohypoparathyroidism Molecular defect:

A

Inability of PTH sImulate intracellular signaling events (cAMP pathway) due to mutaIon in Gsα subunit or elements downstream to cAMP signaling

53
Q

Hypocalcaemia - Treatment Acute Hypocalcemic Crisis:

A

– Always correct Magnesium if low
– Calcium Gluconate (93 mg elemental Ca++/10 ml)
• 1 - 2 ampules over ~10 – 20 minutes
• 0.5-2.0 mg/kg/hr of elemental Calcium IV

54
Q

Hypocalcaemia - Treatment Long-term Management:

A

– Oral Calcium salts (up to 3 grams of elemental Ca/day)
– Vitamin D
• Ergocalciferol/Cholecalciferol (act in 10-14 days) -effective only if PTH is present
• Calcitriol - 0.5-1.0 mcg/day
– Hydrochlorothiazide – increases reabsorption of
Calcium in the distal tubule

55
Q

MEN – Multiple Endocrine Neoplasia

A

A syndrome in which 2 or more endocrine tumors occur in a single patient

56
Q

MEN Gentics & Tumor Type

A
  1. Autosomal dominant (e.g., DNA deletion)
    - germline or sporadic mutations (2nd hit hypothesis)
  2. Different penetrance (varying phenotype)
  3. Benign and malignant
  4. Functionally active and inactive
57
Q

MEN1- Affected gene

A

11q12-13

58
Q

MEN1 Presentation/penetrance

A

Prevalence up to 20/100,000; 2nd-3rd decade.
Remeber Three P’s
1.Parathyroid (Primary HPT) – 80-95%
2.Pancreas (insulinoma, gastrinoma, VIPoma) – 50%
3. Pituitary (prolactinoma, Cushing`s disease, acromegaly) - 25%

59
Q

MEN1 Signs/Symptoms

A

Kidney stones, hypercalcemia, recurrent peptic ulcers, fasting hypoglycemia, hypogonadism, galactorrhea, weight gain, diarrhea

60
Q

MEN1 Screening

A
  • Calcium, PTH
  • gastrin
  • insulin,glucose
  • prolactin
  • IGF-1
  • ACTH, cortisol
61
Q

Timeline of the MEN1 Phenotype

A

• Hypercalcemia due to Primary HPT manifests by age 40 (19-­‐40)
• Pituitary tumors diagnosed on average at age 38 (12-­‐83)
• PancreaIc tumors:
– Insulinoma at age 25
– Gastrinoma at age 35

62
Q

MEN2A Affected gene

A

RET 10q11.2

Mutation at codon Cys634

63
Q

MEN2A Presentation/ penetrance

A

1/30,000, any age, more in adults, 80% of all MEN2

  1. Medullary thyroid carcinoma – almost 100%
  2. Pheochromocytoma – 40%
  3. Primary HPT – 25%
64
Q

MEN2A Signs/ Symptoms

A

Thyroid nodule, hypertension, spells, diaphoresis, hypercalcemia,

65
Q

MEN2AB Affected gene

A

RET 10q11.2

Mutation at codon Met634

66
Q

MEN2AB Presentation/ penetrance

A

1/30,000, early onset, 5% of all MEN2

  1. Medullary thyroid carcinoma (more malignant) – 100%
  2. Mucosal neuromas – 100%
  3. Marfanoid habitus – 50%
  4. Pheochromocytoma – 50%
67
Q

MEN2AB Signs/Symptoms

A

Thyroid nodule, skin neuromas, Hirschsprung`s disease, hypertension, spells, diaphoresis,

Endocrine System (6 decks)

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