Disorders Of Serum Minerals Flashcards

1
Q

Ca above………….. are symptomatic

A

13 mg/dL

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2
Q

Differential Diagnosis

A

Hyperproteinemia
• Parathyroid hormone–related hypercalcemia
– Primary hyperparathyroidism
– Tertiary hyperparathyroidism
– Familial hypocalciuric hypercalcemia
• Non parathyroid hormone–mediated hypercalcemia
– Malignancy-associated hypercalcemia (PTHrP)
– Granulomatous diseases
– Milk-Alkali syndrome
– Hyperthyroidism, Parenteral nutrition, Immobilization,meditations.

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3
Q

Renal impairment due to hypercalcemia

A

• Afferent arteriolar vasoconstriction&raquo_space; ↓GFR,
• Diabetes insipidus

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4
Q

Cardiac impairment due to hypercalcemia

A

Shortening of the QTc interval, widened QRS, bradycardia

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5
Q

Hyperparathyroidism
• Primary hyperparathyroidism:
• Secondary hyperparathyroidism:
• Tertiary hyperparathyroidism:

A

85% single parathyroid adenoma

vitamin D deficiency, calcium deficiency, or chronic kidney disease

chronic renal failure

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6
Q

Primary para hyperparathyroidism

A

• Asymptomatic
➢ Osteoporosis, bone pain, nephrolithiasis,
– BMD is relatively preserved at the spine, lower at the hip, particularly low at the
⅓ radius. (This is because the ⅓ radius is a predominantly cortical.)

• Classic skeletal manifestations: osteitis fibrosa cystica , brown tumors

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7
Q

Familial hypocalciuric hypercalcemia (FHH):

A

*Autosomal dominant
* inactivating mutations of the calcium sensing receptor (CaSR)at PTH

• Hypercalcemia is typically mild, in the range of 11 to 12 mg/dL

➢ Abnormal calcium receptors are also expressed in the kidney

• Asymptomatic, Do not develop adverse sequelae

homozygous patients usually develop severe hypercalcemia in infancy

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8
Q

Malignancy-associated hypercalcemia
=A Non-PTH-mediated hypercalcemia

A

Among hospitalized patients (in known advanced malignancy)

• Approximately 50% of patients die within 30 days of developing malignancy-
associated hypercalcemia
• Tumors that commonly cause hypercalcemia include breast, renal, squamous cell,
ovarian carcinomas, multiple myeloma, and lymphoma

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9
Q

Malignancy-associated hypercalcemia
=A Non-PTH-mediated hypercalcemia

A
  1. Humoral hypercalcemia of malignancy (HHM) (~ 80% )
  2. local tumor invasion of the skeleton
  3. 1α-hydroxylase enzyme
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10
Q

Humoral hypercalcemia of malignancy (HHM) (~ 80% )

A

Results from excessive secretion of parathyroid hormone–related protein (PTHrP)

• PTHrP acts on the same receptor as PTH and can induce similar systemic effects.

• Reductions in the levels of PTH, 1,25-dihydroxyvitamin D3, and serum phosphorus

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11
Q

local tumor invasion of the skeleton

A

Breast cancer or a hematologic neoplasm such as multiple myeloma, leukemia, or lymphoma.

• Local factors secreted: PTHrP, RANKL, interleukin-6, …

• Hypercalcemia, hyperphosphatemia, ↓ PTH, ↓ PTHrP and ↓ 1,25(OH)2D

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12
Q

1α-hydroxylase enzyme

A

Secretion of 1,25(OH)2D by lymphomas and dysgerminomas.

• The increased 1,25(OH)2D leads to intestinal calcium hyperabsorption as well as
bone resorption.

This condition is mechanistically similar to the hypercalcemia that occurs in
granulomatous disease

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13
Q

Granulommatous disease

A

including sarcoidosis, tuberculosis, and fungal infections
➢ 1α-hydroxylase enzyme
• hypercalcemia and hyperphosphatemia

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14
Q

Milk-Alkali syndrome

A

Ingestion of very large quantities of calcium carbonate or other calcium-containing
antacids
• Triad of hypercalcemia, metabolic alkalosis, and acute kidney injury
• Calcium intake in patients typically exceeds 4 g/day

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15
Q

• Drugs that may cause hypercalcemia include

A

Thiazide diuretics
lithium
Vitamins D

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16
Q

Treatment of hypercealcemia due to overproduction of 1,25-vitamin D
related to granulomatous disease or lymphomas or dysgerminomas

A

Glucocorticoids

17
Q

Indications for Symptomatic primary HPT parathyroidectomy

A

kidney stones, reduced renal function.

serum calcium concentration greater than 1 mg/dL above normal.

18
Q

The initial treatment of hypercalceamia

A
  1. intravenous hydration with isotonic solution
  2. calcitonin SC /has a rapid onset of action, cause tachyphylaxis, should be discontinued after 24 to 48 hours.
  3. antiresorptive agents like bisphosphonates or denosumab.

Loop diuretics should be avoided unless patients have volume overload or heart failure.

19
Q

Hypoparathyroidism due to autoimmune polyglandular syndrome, where it can be
associated with

A

primary adrenal insufficiency (Addison’s disease)
mucocutaneous candidiasis
type 1 diabetes
autoimmune thyroid disease
vitiligo

20
Q

Hypocalceamia caused by hypoparathyroidism

A

Low serumPTH, hypocalcemia, phosphorus high normal or frankly elevated, reduced 1,25(OH)2D

• Asymptomatic basal ganglia calcification

• Treatment: large doses of calcium+active vitamin D (1,25[OH]2D)

• Adjunctive treatment; Thiazide diuretic
• Recombinant PTH 1-84

21
Q

Pseudo hypoparathyroidism
مستويات الپاراثورمون طبيعية أو عالية ولكن يتم مقاومة وظيفتها

Most common type?

A

end-organ resistance to PTH at the proximal tubules

Albright hereditary osteodystrophy or Pseudohypoparathyroidism Type Ia, is associated with resistance to multiple hormones.

Classic phenotype: short stature, shortened fourth and fifth
metacarpals and metatarsals, obesity, mental retardation,
subcutaneous calcifications, and café au lait spots

Action of PTH is preserved at DCT

22
Q

Long-term, high-dose treatment with older antiseizure medications such as
……………may lead to hypocalcemia and osteomalacia

A

phenytoin or phenobarbital

23
Q

Hypocalcemia can result from low magnesium levels which is related to

A

Alcoholism
cisplatin-based chemotherapy
Decreased PTH secretion and resistance to PTH Paradoxically

In rare instances, hypermagnesemia (divalent cation) can cause hypocalcemia

24
Q

Hyperphosphatemia that may cause hypocalceamia

A

Phosphate binds calcium

•Due to Rhabdomyolysis (e.g., crush injuries), renal failure, and tumor lysis syndrome, IATROGENIC

• Treatment involves reducing the serum phosphorus level
• Seizures can occur as the earliest manifestation

• **Intravenous calcium should not be given to hyper-phosphatemic patients because calcium-
phosphate salts can precipitate into soft tissues.g*

25
Q

Pancreatitis causing hypocalceamia

A

• The lipases autodigest omental and retroperitoneal fat into negatively charged ions that
tightly bind calcium in the ECF, resulting in hypocalcemia.

• Poor prognostic sign

26
Q

Chronic hyperphosphatemia can lead to

A

Soft tissue calcifications

27
Q

Pseudo-hyperphosphatemia

A

• Artifactually as a result of hemolysis

28
Q

Autosomal dominant hypophosphatemic rickets (ADHR)

A

Mutations in FGF23 that disrupt its breakdown