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Pharm Block 4 > Drugs on Calcium > Flashcards

Drugs on Calcium Flashcards

1
Q

Bone is made in 2 stages. What are these two stages?

A

Stage 1: Matrix– Type 1 collagen

Stage 2: Mineralization– Crystalline hydroxyapatite

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2
Q

Osteoblasts _____ bone while osteoclasts are involved in bone _____.

A

Formation, resorption (removes mineralized matrix)

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3
Q

Describe bone remodeling.

A

Continuous process of mature bone tissue removed from skeleton and new bone is formed. Occurs within
3-6 months. Maintains bone strength and mineral homeostasis.

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4
Q

What is a bone remodeling unit?

A

Tightly composed group of osteoblasts and osteoclasts

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5
Q

What are the steps of bone remodeling?

A
  1. Activation
  2. Reversal
  3. Bone Formation
  4. Mineralization
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6
Q

How long does activation of bone remodeling take?

A

~ 3 weeks

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7
Q

When does reversal of bone remodeling occur?

A

Between 3 wks. and 3 months.

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8
Q

When does formation of bone remodeling begin?

A

~ 3 mo.

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9
Q

What steps are osteoclasts and active osteoclasts involved with in bone remodeling respectively?

A

Activation and reversal

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10
Q

What steps are osteoblast precursors and osteoblasts involved with in bone remodeling respectively?

A

Reversal and bone formation

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11
Q

What step is the bone remodeling unit present during bone remodeling?

A

Mineralization

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12
Q

Why is vitamin D considered a hormone?

A

Because fits hormone definition of traveling in blood

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13
Q

What is the provitamin for Vit D3 and where is it synthesized?

A

7- dehydrocholestrol (Cholecalciferol), Synthesized in the skin under the influence of UV rays

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14
Q

What is the provitamin for Vit D2 and where is it synthesized?

A

Ergocalciferol, found in Plants, yeast, fungi

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15
Q

What is the source of provitamin Vit D1?

A

Food

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16
Q

What collectively makes up Vitamin D?

A

Vit D1, D2, and D3

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17
Q

What are the Vit D requirements for infants/children and adults?

A

400 IU, 200 IU

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18
Q

Where is Vit D absorbed and what is essential in the process?

A

Absorbed in small intestine, Bile essential

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19
Q

How is Vit D transported?

A

In plasma along with alpha globulin; then stored for prolonged periods.

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20
Q

How is Vit D excreted?

A

Mainly in bile

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21
Q

What are the three main actions of Vit D that ultimately causes the net effect of increased serum Ca2+?

A

Increase bone turn over, increase calcium absorption in DCT of kidney, and inhibits epidermal proliferation

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22
Q

What is the non-Vit D regulated action of increased bone turnover?

A

Recruits osteoclast precursor cells to resorption sites

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23
Q

What is the Vit D regulated (VDR) action of increased bone turnover?

A

Osteoblasts increases production of osteocalcin and IL-1

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24
Q

Where is calcitonin synthesized?

A

Thyroid parafollicular C cells

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25
Q

What is the MOA of calcitonin?

A

Hypocalcemic hormone
that is a Potent inhibitor of osteoclast mediated bone resorption. Calcitonin receptor is present on osteoclasts.
Decreased ruffled border surface.

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26
Q

What is the calcitonin effect?

A
  1. Decreased resorptive activity by inhibiting osteoclast bone resorption.
  2. Decreases renal excretion of Ca2+
  3. Plasma Phosphorus concentration lowered
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27
Q

What is Teriparatide?

A

Synthetic human 34 a.a terminal PTH fragment

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28
Q

When happens with continuous use of Teriparatide?

A

Bone demineralization and osteopenia

29
Q

When happens with intermittent use of Teriparatide?

A

Increases bone mineral density and decreases risk of vertebral and non-vertebral fractures

30
Q

What are the ADRs of Teriparatide?

A

Increased risk of osteosarcoma, Nephrolithiasis, Increased serum uric acid levels

31
Q

What is the MOA of Cinacalcet / Calcimimetic?

A

Increases sensitivity of CaSR to extracellular Ca2+ (lowers Ca2+ concentration at which PTH is suprressed)

32
Q

What do you give as treatment for parathyroid carcinoma?

A

Cinacalcet / Calcimimetic

33
Q

What are the ADRs of Cinacalcet / Calcimimetic?

A

Hypocalcemia,

Not to be used if <8.4mg/dl, Decreases seizure threshold

34
Q

What is the net effect of Vit D?

A

Prevent excretion of Ca2+ and phosphate

35
Q

What Vit D preparation is given orally and thru IV?

A

Cholecalciferol (D3)

36
Q

What Vit D preparation is given only orally?

A

Calcitriol (1, 25 (OH)2 vit D3)

37
Q

Which Vit D preparation is useful in patients with kidney dysfunction?

A

Alfacalcidol: 1-(OH) vit D3,

38
Q

What else do you give along with Vit D preparations so they work correctly?

39
Q

What are analogs of pyrophosphate?

A

Bisphosphonates

40
Q

What does pyrophosphate (-dronates) due in the body?

A

Increases bone resorption. It is a natural inhibitor of bone mineralization / formation.

41
Q

What is the MOA of bisphosphonates with bone mineralization?

A

The analogs have a strong affinity for bone and gets incorporated in matrix and remains until the bone is remodeled. Thus the bone does not get bigger, it just allows the bone to mineralize.

42
Q

What is the MOA of bisphosphonates with osteoclasts?

A

The analogs inhibit farnesyl pyrophosphate synthase (critical for osteoclast survival). This inhibits recruitment and promotes apoptosis of osteoclasts.

43
Q

What are the 2 most important ADRs of bisphosphonates?

A

Osteonecrosis of jaw (due to osteomylitis) and atypical subtrochanteric fracture (not shaft)

44
Q

Never give bisphosphonates after a fracture. Why?

A

Initial fracture healing requires osteoclastic overactivity

45
Q

What is Raloxifene?

A

Selective Estrogen Receptor Modulator (SERM)

46
Q

When is Raloxifene used?

A

Post-menopausal or pre-menopausal with increased risk of fractures

47
Q

What is the MOA of Raloxifene?

A

Increases bone mineral density (BMD). Shifts the balance to osteoblasts more than osteoclasts (does not inhibit osteoclast activity like bisphosphonates).

48
Q

What are the five drugs used in treating osteoporosis?

A 
Bisphosphonates
Teriparatide
Raloxifene
Denosumab
Calcitonin
49
Q

What are the four drugs used in treating Paget’s Disease?

A

Alendronate, Risedronate, Zoledronate (all bisphosphonates) and calcitonin subcutaneous injection (S.C. highlighted red) and nasal spray

50
Q

Vitamin D deficiency is seen in what adult condition?

A

Osteomalacia (bone pain, tenderness, muscle weakness)

51
Q

Vitamin D deficiency is seen in what child condition?

A

Rickets (failure to mineralize newly formed bone esp. weight-bearing bone and cartilage matrix, soft and bowing l of long bones)

52
Q

How does secondary hyperparathyroidism occur in renal failure?

A

Kidney excretes less phosphate. High blood phosphate precipitates calcium and forms calcium phosphate. This causes the blood calcium to decrease and stimulate PTH.

53
Q

What are the levels of PTH in secondary hyperparathyroidism occur in renal failure?

A

PTH > 88 pg/ml bone resorption is increased (normal 10 - 60 pg / ml)

54
Q

What are the three most important drugs used in treatment of Secondary hyperparathyroidism treatment?

A

aluminum hydroxide (phosphorus binders), cinacalcet, and calcitriol

55
Q

Which group of drugs is contradicted in renal failure because can cause hypocalcemia?

A

Bisphosphonates

56
Q

How do you treat hypercalcemia?

A

First, hydrate the patient with fluids (to flush out) plus furosemide. Then give calcitonin.

57
Q

How is hypocalcemia (< 8.5 mg) treated?

A

Calcium and Vit D

58
Q

What is the contraindication for calcitonin?

A

Conditions of hypocalcemia

59
Q

Patient was brought in with confused state and lethargy. Passing excess urine (polyuria) and constipation. Calcium level is high. What is the Dx?

A

Hypercalcemia

60
Q

Patient comes in with tetany (Trousseau’s Sign, hand drop spasm sign) and face spasm when provoked (Chvostek’s sign). Patient is at risk for seizures. What is the Dx?

A

Hypocalcemia

61
Q

What are the mechanisms of action of vit D?

A
  1. Bone: increases bone turnover
  2. Renal: increases Ca2+ absorption
  3. inhibites epidermal proliferation
  4. Intestines: absorption by TRPV6 Ca2+ channel in duodenum and proximal jejunum increases Ca2+
62
Q

What are the mechanisms of action of PTH?

A
  1. Bone: Net increase in resorption and increased Ca2+(stimulates osteoblasts which synthesize RANK ligand activating osteoclast)
  2. Kidney: Increases calcium by ↑reabsorption and ↓excretion in distal nephron
    ↓reabsorption of phosphate: Retrieval of Na-P cotransport
    Stimulates Vitamin D to active form
  3. Intestine: Indirectly increases Calcium and phosphate absorption by enhancing formation of 1, 25 –(OH)2 vit D3 in kidney
63
Q

Which organ produces 1-a hydroxylase?

64
Q

How do you diagnose osteoporosis?

A

To diagnose osteoporosis and assess your risk of fracture and determine your need for treatment, your doctor will most likely order a bone density scan. This exam is used to measure bone mineral density (BMD). It is most commonly performed using dual-energy x-ray absorptiometry (DXA or DEXA) or bone densitometry. Osteoporosis is a T-score of -2.5 or lower.

65
Q

Does extra-vit D cause toxicity?

A 
An excess of vitamin D causes abnormally high blood concentrations of calcium, which can cause overcalcification of the bones, soft tissues, heart and kidneys. In addition, hypertension can result.[2] Symptoms of vitamin D toxicity may include the following:
Dehydration
Vomiting
Decreased appetite
Irritability
Constipation
Fatigue
Muscle weakness
Metastatic calcification of the soft tissues
66
Q

What is the mechanism of action of denosumab?

A

mAb (monoclonal Ab) that blocks osteoclast formation and activation. Increases bone mineral density. Binds with high affinity to RANKL mimicking OPG and reduces binding of RANKL to RANK.

67
Q

Bone Metabolism

68
Q

Bone Mineral Disorders

Pharm Block 4 (21 decks)

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