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Respiratory/Musculoskeletal > CM- Disorders of Ca and Bone Metabolism > Flashcards

CM- Disorders of Ca and Bone Metabolism Flashcards

1
Q

If there is decreased calcium, what happens to PTH?

What are the 3 major effects?

A

PTH increases and:

  1. bone resorption
  2. increases 1,25 (OH)2 D –> gut absorption of Ca
  3. increase renal Ca resabsorption via CaSR
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2
Q

What are the 2 main causes of hypercalcemia?

A
  1. primary hyperparathyroidism (outpatient)

2. cancer (hopsital)

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3
Q

What are the 5 possible pathologies for hyperparathyroidism?

What is the most common?

A
  1. single, enlarged parathyroid gland (adenoma) - most common
  2. hyperplasia - enlargement of all 4 glands
  3. multiple parathyroid adenomas
  4. parathyroid carcinoma (PTH and Ca will be high)
  5. ectopic PTH production by tumors (or PTHrP)
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4
Q

What is the effect of PTH on bone?

A

It stimulates osteoclasts resulting in net bone resorption which releases Ca and P from the bone

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5
Q

What is the effect of PTH on the kidney?

A
  1. increases Ca resorption

2. decreases phosphorus resorption so you will have more free Ca (as a result- urinary phosphate increases)

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6
Q

What is the effect of PTH on the gut?

What is synthesized? What is the net effects on Ca and P?

A

PTH increases 1,25 (OH)2 D synthesis by activationg renal cytochrome p450 enzyme 1a-hydroxylase.

1,25(OH)2-D stimulates intestinal absorption of calcium and to a lesser extent phosphorus

the resultant hypercalcemia causes an increased filtered Ca load that causes hypercalciuria DESPITE increased renal reabsorption due to PTH.

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7
Q

What are the 2 familial syndromes associated with parathyroid hyperplasia (all 4 glands are overactive)

A
  1. MEN1 - defect in menin (tumor supressor) that causes:
    - primary hyperparathyroidism
    - pancreatic tumors
    - pituitary tumors
  2. MEN2a- activating RET proto-oncogene causing:
    - medullary thyroid carcinoma
    - pheo
    - primary hyperparathyroidism
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8
Q

A patient with primary hyperparathyroidism is usually asymptomatic. However, if they do present with symptoms, what 3 main things are you looking for?

A

“stones, bones, and abdominal groans”

  1. kidney stones
  2. bone disease (pain/fracture)
  3. pancreatitis and/or peptic ulcers
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9
Q

What symptoms are associated with hypercalcemia?

A 
fatigue
confusion
lethargy
depression 
coma 
polyuria, nocturia, constipation
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10
Q

A patients labs come back and they have high blood Ca, low blood phosphorus, high PTH and high Ca in the urine. What is the most likely cause of the problem?

A

Primary hyperparathyroidism

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11
Q

A patient presents with high blood Ca, low blood phosphorus, high PTH and low Ca in the urine. What is the likely problem?

A

Familial hypocalciuric hypercalcemia

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12
Q

What do labs show for primary hyperparathyroidism?

blood Ca, P, PTH and urinary Ca

A
  1. high blood Ca
  2. low blood P
  3. high PTH
  4. 24hr urinary Ca is high/high-normal (>250mg)
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13
Q

What do lab show for familial hypocalciuric hypercalcemia?

blood Ca, P, PTH, and urinary Ca

A
  1. high blood Ca
  2. low blood P
  3. high blood PTH
  4. low urinary Ca
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14
Q

How do you differentiate primary hyperparathyroidism from hypercalcemia of malignancy?

A

Primary:

  • longer duration of hypercalcemia, elevated PTH
  • tend to be asymptomatic
  • diagnosed outpatient

Malignancy:

  • weight loss, anorexia
  • more severe, acute
  • diagnosed in the hospital setting
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15
Q

What is the treatment for primary hyperparathyroidism?

A
  1. Surgical removal of the overactive parathyroid gland if the patient is symptomatic
  2. follow up without treatment for asymptomatic
  3. if not a candidate for surgery:
    - cinacacet which decreases blood Ca and PTH by activating CaSR
    - bisphosphonates which protect against bone loss
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16
Q

What are the 3 usual pathways of malignancies that cause hypercalcemia?

A
  1. PTHrP - humoral hypercalcemia of malignancy
  2. cytokines- local osteolytic hypercalcemia
  3. 1,25 (OH)2-D - increased gut absorption of Ca
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17
Q

What malignancies tend to have excess production of PTHrP?
What is this called?
What are the effects?

A
  1. Squamous cell carcinoma
  2. renal and breast carcinomas
  3. lymphomas

This is called humoral hypercalcemia of malignancy

PTHrP activates PTH receptor which leads to:

  • hypercalcemia
  • decreased blood phosphate
  • appropriately suppressed PTH
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18
Q

Describe local osteolytic hypercalcemia.
What is a classic example?
What are the effects?

A

Mets to the bone stimulate osteoclastic bone resorption via:
IL1, IL6, TNF, PGs

The classic example is multiple myeloma.

Ca is high because of the release from bone
PTH is suppressed bc of the high Ca
P is high because PTH is suppressed
1,25 OH2-D is low because PTH is suppressed

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19
Q

What are the blood levels of Ca, P, PTH for vitamin D toxicity?

A

Vitamin D will absorb more Ca from the gut. This leads to:

  1. increased Ca

The increased calcium will suppress the PTH so

  1. decreased PTH

The suppressed PTH allows for:

  1. increased blood phosphate
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20
Q

What are the 2 main causes of vitamin D toxicity?

A
  1. granulomatous diseases (sarcoid, TB, fungal) cause extra-renal production of 1,25 OH2-D
  2. Ingestion from:
    - fortified milk
    - excessive prescribed dose
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21
Q

What is the best marker for nutritional vitamin D status?

A

25 OH-D because it will be highly elevated in hypercalcemia due to dietary ingestion or vitamin D supplements (before kidney converts to 1,25 OH2-D)

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22
Q

What gene is mutated in familial hypocalciuric hypercalcemia?
Describe the disease effects on the kidney and parathyroid gland.

A

The CaSR gene is inactivated

Parathyroid gland: the CaSR requires inappropriately high levels of Ca to shut off synthesis and release of PTH

Kidney: defective CaSR requires inappropriately high Ca to inhibit renal reabsorption, therefore Ca in the urine is low

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23
Q

Why is it crucial to differentiate between primary parathyroidism and familial hypocalciuric hypercalcemia?

A

Primary parathyroidism can benefit from parathyroidectomy.

FHH should NOT get parathyroid surgery because you would have to remove all the glands, and the patients generally suffer no complications from the hypercalcemia

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24
Q

Why does immobilization cause hypercalcemia?

A

There is increased bone resorption caused by the decrease in weight bearing

25
Q

What are the 3 main steps for diagnosis of hypercalcemia?

A
  1. History
    - weight loss/anemia = cancer
    - cough/fever = granulamatous disease
    - too much intake
  2. Blood PTH
    - increase = FHH or primary
    - decreased = malignancy, vit D toxicity
  3. Blood phosphprus
    - increase = vit D excess or bone resorption
    - decrease = PTHrP
26
Q

What is the treatment of severe hypercalcemia?

A

Treated acutely if they have severe symptoms:
Ca>14mg/dl

  1. volume repletion with IV fluids to improve excretion
  2. medicine to decrease osteoclastic bone resorption –bisphosphonates
27
Q

What are the 2 most common causes of hypocalcemia?

A
  1. insufficient or ineffective PTH

2. insufficient or ineffective vitamin D

28
Q

A patient has low Ca and high P in the blood. What is your major concern?

A

Insufficient or ineffective PTH

29
Q

A patient has low Ca and low P in the blood. What is your major concern?

A

Insufficient or ineffective vitamin D

30
Q

What are the 3 major causes of insufficient PTH?

A
  1. hypoparathyroidism
  2. diGeorge syndrome
  3. severe hypomagnisium
31
Q

What is pseudohypoparathyroidism?

What are syptoms/signs that this is present?

A

When the patient produces enough PTH, but the patient is resistant to the effects.
(Blood PTH is high, but Ca is low and P is high)

The patient will have:

  • short fingers/toes (brachydactyly)
  • short stature
  • MR
  • cataracts
32
Q

What are the 4 major causes of insufficient/ineffective PTH?

A
  1. hypoparathyroidism
  2. pseudohypoparathyroidism
  3. hypomagnesemia
  4. activating mutation of CaSR
33
Q

What are the 4 ways vitamin D can be insufficient or ineffective?

A
  1. lack of vitamin D (poor sunlight, dietary lack)
  2. decreased 25OHD
  3. decreased 1,25 (OH)2-D
  4. inactivating mutation of VDR
34
Q

What are the 3 things that can decrease 25 OH-D?

A
  1. excess loss (malabsorption in gut, nephrotic)
  2. decreased production (liver disease, 25ahydroxylase deficiency)
  3. increased catabolism (anticonvulsants)
35
Q

What are the 2 major ways 1,25 (OH)2-D are decreased?

A
  1. kidney disease

2. 1ahydroxylase deficiency

36
Q

A patient presents with neuromuscular excitability, muscle cramps, paresthesia, laryngospasm, bronchospasm, seizures and arrhythmia. What is the likely problem?

A

Hypocalcemia

37
Q

What are the 2 tests to check for neuromuscular excitability in suspected hypocalcemia?

A
  1. Chvostek’s facial nerves - tap in front of ear and look for mouth/face twitch
  2. Trousseau’s - hold BP cuff on the arm for a few minutes then look for spasms
38
Q

What is treatment for hypocalcemia?

A

Calcium and Vit D supplementation.

If blood phosphate is high, decrease dairy intake.

39
Q

What are the most common locations for osteoporotic fractures?

A
  1. spine (thoracic, lumbar)
  2. hip (femoral neck, trochanter)
  3. distal forearm
40
Q

What is the best predictor for if someone is going to have a bone fracture?

A

Densitometry to measure bone mass

41
Q

What are the 4 main causes/risks for osteoporosis?

A
  1. Endocrine
    - estrogen/androgen deficiency
    - hyperparathyroidism
    - thyroid hormone excess
    - glucocorticoid excess
  2. Neoplasms
    - multiple myeloma, mets, mastocytosis
  3. Hereditary
    - genetic component inherited as polygenic train
  4. “other”
    - alcohol, smoking
    - exercise, diet
    - age
    - drugs
    - previous fracture
42
Q

Which drugs specifically increase the risk of osteoporisis?

A
  1. glucocorticoids
  2. aromatase inhibitors
  3. heparin
  4. anticonvulsants
43
Q

What happens in postmenopausal osteoporosis?

A

Lack of estrogen causes rapid/transient (up to 10 years) loss of bone

Lack of estrogen increases IL6,IL1, TNF which leads to excessive resorption

44
Q

Describe the pathogenesis of senile osteoporosis.

A

Calcium homeostasis is disrupted

  • decreased intestinal absorption
  • increased renal excretion
  • compensatory PTH increase

This leads to bone resorption.

45
Q

What are the major effects of glucocorticoids that cause osteoporosis?

A
  1. decreased bone formation
    - reduce blast replication
    - apoptosis of blasts and cytes
  2. increased bone resorption
    - inhibit intestinal absorption
    - increase renal excretion
  3. decreased sex hormone production (less estrogen)
  4. increase fall risk by reducing proximal muscle strength
46
Q

What are the 3 main contributing factors to osteoporosis in men?

A
  1. alcohol use
  2. hypogonadism
  3. glucocorticoids
47
Q

How is osteoporosis diagnosed?

A
  1. low bone mineral density to obtain a T score
  2. fracture on X-ray
  3. secondary causes are ruled out (labs should be normal with osteoporosis)
48
Q

What T score denotes osteopenia?

Osteoporosis?

A

BMD of 30 year old white women is used. If you are -1 to -2.5 SD below average, you are osteopenic
If you are below 2.5 SD below average, you have osteoporosis

49
Q

What is treatment for osteoporosis?

A
  1. education and evaluation of bone strength
  2. occupational therapy
  3. walking 30min/3days a week
  4. hip protectors/padded underwear
  5. Ca and vit D supplements to maintain bone mass
  6. Teriparatide- recombinant PTH to increase bone formation
  7. bisphosphonates to decrease bone resorption
50
Q

What is the difference between Rickets and osteomalacia?

A

Rickets occurs before the closure of the growth plates, and osteomalacia occurs in adulthood.

51
Q

What are the 3 major causes of rickets/osteomalacia?

A
  1. vitamin D deficiency/resistance
  2. hypophosphatemia
  3. drug-induced
52
Q

What are the 3 causes of hypophosphatemia that can lead to Rickets?

A
  1. decreased intestinal absorption
    - reduced intake
    - phosphate binders
  2. increased renal loss (X-linked hypophos. Rickets)
  3. FGF23 - increases renal loss of phosphate and suppresses 1,25 (OH)2-D
53
Q

What are the 3 drug-induced causes of rickets?

A
  1. enhanced 25OH-D catabolism
  2. blocked mineralization
  3. phosphate binders (aluminum)
54
Q

What are the major signs and symptoms of Rickets AND osteomalacia?

A
  1. bone pain
  2. muscle tenderness, weakness, waddling
  3. fractures/pseudofractures in unusual locations (ribs, sternum, scapula, metatarsals)
55
Q

What differentiates rickets from osteomalacia in terms of presentation?

A

Rickets has:

  1. decreased growth
  2. widened epiphysis (swollen wrists/ankles, richaitic rosary)
  3. deformed bones (bowing)
  4. tooth enamel defects (decreased vit. D)
56
Q

What are the lab abnormalities associated with Rickets/Osteomalacia?

A
  1. PTH increased
  2. Ca and phosphate decreased
  3. alkaline phosphatase increased
57
Q

What is the treatment for rickets/osteomalacia?

A
  1. calcium supplements
  2. vit d treatment
  3. phosphate supplements NOT at the same time as Ca
58
Q

Why do you have to give calcium supplements apart from phosphate?

A

To avoid phosphate binding

Respiratory/Musculoskeletal (36 decks)

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