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MHD2/Pharm - Endocrine > Pharm - Calcium > Flashcards

Pharm - Calcium Flashcards

1
Q

What are the essential functions of calcium?

A 
Skeleton/Teeth structure
Neurological transmission
Muscle contraction
Second messenger signaling 
Vesicle fusion
Blood coagulation
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2
Q

What channels are responsible for intracellular regulation of calcium levels?

A

Plasma Membrane Ca Pump
Na/Ca exchanger
SERCA
these all act to keep intracellular calcium low

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3
Q

What are the general ways that serum calcium is tightly regulated?

A

Absorption
Excretion
Mobilization from the skeleton

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4
Q

Describe what happens to dietary calcium

A

~1000mg/day ingested via diet
300mg is absorbed, and 100mg is lost endogenously
800 mg is excreted in feces
200 mg is excreted in urine

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5
Q

Describe the endogenous process of osteoclast activation

A

Osteoblasts expressing RANKL activate immature osteoclast precursor cells with RANK receptor. This interaction in the presence of MCSF triggers osteoclast differentiation

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6
Q

Describe the endogenous process of osteoblast activation

A

As bone is resorbed by osteoclasts, TGF beta, IGF1, growth factors and cytokines are released that stimulate osteoblast differentiation and activity

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7
Q

What is the paradoxical role of PTH in calcium balance?

A

Endogenous chronic PTH stimulation increases serum Ca and decreases serum PO4. Exogenous, intermittent PTH stimulation has the opposite effect, causing bone deposition of Ca

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8
Q

What are the main functions of PTH?

A

Increasing renal Ca resorption, PO4 excretion, and synthesis of calcitrol

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9
Q

What is osteoprotegrin (OPG)?

A

Endogenous inhibitor of RANKL

Prevents osteoclast maturation and bone resorption

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10
Q

Describe the synthesis and activation of vitamin D3

A

Synthesized in the skin following exposure to UV light as a pro-hormone.
Metabolized by liver (25 hydroxylase) and then kidney (1 alpha hydroxylase) to form active Calcitrol

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11
Q

What is the function of Vitamin D3?

A

Augments Ca and PO4 absorption from the small intestine
Decreases excretion of Ca and PO4 by kidneys
Inhibits PTH production

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12
Q

What is the function of calcitonin?

A

Secreted by parafollicular cells of the parathyroid in response to high serum Ca
Acts to decrease serum calcium and phosphate levels (bone and kidney effect)

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13
Q

What disorders are treated with calcitonin?

A

Paget’s disease of bone
Hypercalcemia
Osteoporosis

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14
Q

What are the common causes of hypercalcemia?

A

Primary hyperparathyroidism: parathyroid adenoma

Malignancy associated: paraneoplastic PTHrP

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15
Q

What are the symptoms of hypercalcemia?

A

Fatigue, polyuria, polydipsia, anorexia, nausea, vomiting, abdominal pain, muscle weakness, altered mental status

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16
Q

What are the common causes of hypocalcemia?

A

Hypoparathyroidism (PTH deficiency)

Vitamin D deficiency

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17
Q

What are the common causes of hyperphosphatemia?

A

Chronic kidney disease

Secondary hyperparathyroidism

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18
Q

What are the symptoms of hypocalcemia?

A

Tremor, muscle spasm, tetany, seizures, prolonged QTc interval

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19
Q

What are the symptoms of hyperphosphatemia?

A

Hypocalcemia, decreased calcitriol, increased PTH

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20
Q

What are Rickets and Osteomalacia?

A

Deficiencies in vitamin D intake/synthesis presenting with bone pain and symptoms of hypocalcemia
Rickets is in children; Osteomalacia is in adults

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21
Q

What is the difference between Type I and Type II osteoporosis?

A

Type I involves loss of trabecular bone due to estrogen deficiency in postmenopausal women. Type II occurs in men and women and is related to age, increase in parathyroid axis function

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22
Q

What is Paget’s disease of the bone?

A

Disordered sites of bone remodeling from increased bone resorption and formation
May present with bone pain, deformities and fractures

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23
Q

Mechanism of action for vitamin D, calcitriol and vitamin D analogues

A

Agonists of vitamin D receptor causing increased Ca and PO4 intestinal absorption, renal reabsorption, and decreased PTH

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24
Q

What are the clinical uses of vitamin D, calcitriol and vitamin D analogues?

A

Rickets, Osteomalacia
Prevent/Treat osteoporosis
Hypoparathyroidism
Chronic kidney disease (secondary hypoparathyroidism)

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25
Q

What adverse effects are associated with vitamin D treatment?

A

Hypercalcemia due to potent effect on intestinal absorption of Ca

26
Q

What are the contraindications for vitamin D treatment?

A

In the presence of hyperphosphatemia, Vitamin D treatment can promote metastatic calcification, hypercoaguable state, tissue infarction, skin necrosis
Often fatal systemic bacterial infections due to non-healing ulcerations

27
Q

How is metastatic calcification prevented in the setting of vitamin D treatment?

A

Phosphate levels are reduced by restricting the diet or using phosphate binders like Sevelamer

28
Q

What is the mechanism of action of bisphosphonates?

A

Analogs of pyrophosphate that have strong affinity for bone surfaces undergoing remodeling. They bind and inhibit farnesyl pyrophosphate synthetase to inhibit osteoclast activity and function

29
Q

What are the bisphosphonate drugs?

A 
All end in "-dronate"
Alendronate
Pamidronate (IV)
Risedronate
Zoledronate (IV)
30
Q

What are the clinical uses of bisphosphonates?

A

Osteoporosis (first line therapy)
Hypercalcemia
Metastatic bone disease
Paget’s disease of the bone

31
Q

Describe the important pharmacokinetics of bisphosphonates

A

They are very poorly absorbed, so they must be taken on an empty stomach
Maximal effect is in 2-4 days, but drug may remain in bone for lifetime

32
Q

What are the adverse effects of bisphosphonate treatment?

A 
Upper GI: heartburn, esophageal irritation, esophagitis
Transient hypocalcemia
Renal impairment
Ocular side effects
Osteonecrosis of the jaw
33
Q

What is osteonecrosis of the jaw?

A

Painful swelling, exposed bone and infection of jaw related to bisphosphonate or denosumab treatment. Typically follows dental procedures.

34
Q

What are the contraindications for bisphosphonate treatment?

A

Upper GI disease

Chronic kidney disease

35
Q

What drugs are alternatives for bisphosphonates if they are contraindicated?

A

Teriparitide (PTHR agonist)
Denosumab (RANKL antagonist)
Raloxifene (SERM)

36
Q

What is the mechanism of action of denosumab?

A

RANKL antagonist, prevents osteoclast differentiation and excessive bone loss

37
Q

What are the clinical uses of denosumab?

A

Osteoporosis: reduces fracture occurence
Hypercalcemia
Giant cell tumor of the bone

38
Q

What are the adverse effects of denosumab?

A

Hypocalcemia
Osteonecrosis of the jaw
Joint/muscle pain

39
Q

What are the contraindications for denosumab treatment?

A

Hypocalcemia

40
Q

What is the mechanism of action of teriparitide?

A

PTH receptor agonist

Teriparitide is actually the 34 AA of the N-terminal of PTH

41
Q

What are the clinical uses of teriparitide?

A

Osteoporosis (paradoxical effect of intermittent PTH stimulation)

42
Q

What is unique about teriparitide compared to the other osteoporosis drugs?

A

It is the only anabolic agent on the market. The others all decrease catabolism.

43
Q

What are the adverse effects of teriparitide?

A

Transient hypercalcemia
Increased serum uric acid
Risk of osteosarcoma

44
Q

What are the contraindications for teriparitide treatment?

A

History of gout, renal stones
Children and adolescents
Patients with increased risk for osteosarcoma (active bone malignancy, Paget’s, increased Alk phos, prior radiation)

45
Q

What is the mechanism of action of raloxifene?

A

SERM: agonist in bone and liver, antagonist in breast and uterus
Inhibits bone loss via transcriptional regulation to decrease osteoclast function, increase osteoblast/osteocyte lifespan

46
Q

What are the clinical uses for raloxifene?

A

Treatment of osteoporosis in postmenopausal women

Osteoporosis in women with breast cancer, history of breast/endometrial cancer

47
Q

What are the adverse effects associated with raloxifene?

A

Venous thromboembolism

Worsened vasomotor symptoms (hot flashes/night sweats)

48
Q

What is the mechanism of action of calcitonin?

A

Binds to osteoclast receptors to prevent bone resorption and inhibits renal reabsorption of Ca. Results in a decrease in serum Ca

49
Q

What are the clinical uses of calcitonin?

A

Severe hypercalcemia
Paget’s disease
Postmenopausal osteoporosis

50
Q

What adverse effects are associated with calcitonin treatment?

A

Nausea, hand swelling, uticaria, intestinal cramping

Cancer with sustained use?

51
Q

What is the mechanism of action of cinacalcet?

A

Calcimimetic: allosterically enhances the sensitivity of the CaSR to Ca2+ levels. This causes lower Ca levels to trigger suppression of PTH, which decreases bone turnover, decreasing serum Ca and PO4

52
Q

What are the clinical uses of cinacalcet?

A

Secondary hyperparathyroidism due to CKD
Hypercalcemia due to parathyroid carcinoma
Primary hyperparathyroidism

53
Q

What adverse effects are associated with cinacalcet?

A

Hypocalcemia

Decreased seizure threshold

54
Q

What are the contraindications for cinacalcet treatment?

A

Hypocalcemia: Ca below 8.4 mg/dL

55
Q

What are the recommended treatment options for hypercalcemia?

A

Volume repletion with saline
Calcitonin
Bisphosphonates

56
Q

What are the recommended treatment options for hypocalcemia?

A

Vitamin D supplementation

Calcium supplementation

57
Q

What are the recommended treatment options for Rickets and osteomalacia?

A

Vitamin D supplementation

58
Q

What are the recommended treatment options for primary hyperparathyroidism?

A

Surgery
Cincacalcet
Bisphosphonates

59
Q

What are the recommended treatment options for CKD, hyperphosphatemia, secondary hyperparathyroidism?

A

Phosphate binder: Sevelamer
Cinacalcet
Calcitriol

60
Q

What are the recommended treatment options for osteoporosis?

A 
Calcium/Vitamin D supplements
Bisphosphonates
Denosumab
Raloxifene
Calcitonin
Teriparitide
61
Q

What are the recommended treatment options for Paget’s disease?

A

Bisphosphonates

Calcitonin

MHD2/Pharm - Endocrine (7 decks)

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