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Drug Action I > Block 4: Vitamin D and Potassium Binders > Flashcards

Block 4: Vitamin D and Potassium Binders Flashcards

1
Q

Describe the how calcium and phosphate maintain homeostasis?

A
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2
Q

Describe the dysregulation of mineral metabolism?

A
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3
Q

What is the pharmacological effects of vit D and analogues?

A

↑ serum (Ca2+) → suppress PTH secretion and ↑ intestinal absorption

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4
Q

What is the pharmacological effects of phosphate binding agents?

A

↓ intestinal absorption of phosphate by binding to dietary phosphate in the gut → lowering serum phosphate

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5
Q

What is the pharmacological effects of calcimimetics?

A

↑ sensitivity of Ca-SR (sensing receptor) in parathyroid glands to Ca2+ → ↓ PTH

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6
Q

Where is vitamin D obtained from?

A

Diet or sunlight-triggers synthesis in skin

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7
Q

Where does the production of vitamin D occur?

A

Liver, 25-hydroxylated → 25-OH vitamin D (Calcidiol): Prohormone → Calcifediol

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8
Q

How is vitamin D produced in organs other than the liver?

A

Kidney or other tissues: 1a-hydroxylated → 1, 25-OH2 Vit D (Calcitriol): Active

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9
Q

Too much or suprophysiological doses of Calcitriol → ___

A

Hypercalcemia

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10
Q

Unlike natural vitamin D, calcitriol analogs have _____ ____ effect?

A

Minimized hypercalcemic

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11
Q

What organs does vitamin d and analogs act on?

A

Intestine: ↑ both Ca2+ and phosphate absorption
Kidney: ↓ renal excretion of Ca2+ and ↑ tubular reabsorption of P
Bone: PTH, ↑ bone formation

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12
Q

What are the therapeutic uses of vitamin D and analogues?

A

Secondary hyperparathyroidism, psoriasis, osteoporosis

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13
Q

What is the MOA of vitamin D?

A
  1. Mediated by binding to membrane (mVDR) or nuclear (VDR) → slow genomic action
  2. Rapid nongenomic action
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14
Q

Where are vitamin D receptors found?

A
  1. PT gland
  2. Intestine
  3. Kidney
  4. Bone
  5. Other (prostate, endothelium, immune cells)
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15
Q

What are the non genomic action of Vit D and analogues?

A
  1. ↑ intestinal absorption of Ca and P
  2. ↓ renal excretion of Ca and ↑ tubular reabsorption of P
  3. ↓ PTH
  4. ↑ bone resorption/formation
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16
Q

Describe the analogs of vitamin D?

A
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17
Q

What are vitamin D products?

A
  1. Ergocalciferol: Vitamin D2 – lower affinity to Vit D binding protein
  2. Cholecalciferol: Vitamin D3
  3. Calcitriol: Active vitamin D (1,25-dihydroxy-Vitamin-D)
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18
Q

What are the ADRs of vitamin D products?

A
  1. Hypercalcemia
  2. w/ or w/o hyperphasphatemia
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19
Q

What are the vitamin D analogues? Differences?

A
  1. Doxercalciferol: Prodrug - activated by hepatic 25-hydroxylation to active 1α,25-(OH)2D2.
  2. Paricalcitol: ↓ serum PTH levels without producing hypercalcemia or altering serum phosphorus.
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20
Q

Indications for vitamin D analogs?

A

Secondary hyperparathyroidism

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21
Q

What are the types of phosphate binders?

A

Calcium-based and non-calcium

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22
Q

What are calcium based PB?

A

Calcium (carbonate, acetate, citrate)

23
Q

What are the non-calcium PB?

A
  1. Salts of Al, Mg, lanthanum, and Iron
  2. Sucroferric oxyhydroxide
  3. Sevelamer HCl or Carbonate
24
Q

What is the MOA of calcium-based PB?

A
  1. Bind to dietary phosphorus → form insoluble Ca-P complex → eliminated through feces, ↓ serum P
  2. Positive Ca2+ balance
25
Q

What is is the most common CB-PB? Why?

A

Calcium carbonate is inexpensive, effective, and readily available

26
Q

ADRs of calcium carbonate use?

A

High dose → hypercalcemia → risk to vascular calcifications and stiffness

27
Q

What is the MOA of lanthanum carbonate?

A

Bind to P → insoluble lanthunum phosphate complex → ↓ absorption of dietary P → ↓ serum P

28
Q

What is MOA of ferric citrate?

A

Ferric iron binds dietary phosphate in the GI tract → precipitates as ferric phosphate → not absorbed so excreted in the stool.

29
Q

What is the MOA of sucroferric oxyhydroxides?

A

The bound phosphate is eliminated with feces, insoluble, not absorbed and not metabolized

30
Q

Describe the phosphate binding of sucroferric oxyhydroxides?

A

Phosphate binding occurs by an exchange between hydroxyl groups in sucroferric oxyhydroxide and the phosphate in the GI environment

31
Q

What are the components of sucroferric oxyhydroxides?

A

Mixture of polynuclear iron (III)-oxyhydroxide, sucrose, and starches

32
Q

What are the salt forms of sevelamer?

A

Hydrochloride and carbonate (acid-base balance)

33
Q

MOA of sevelamer?

A

Nonabsorbable hydrogel → binds to P

34
Q

ADR and CI of Sevelamer?

A

ADR: less likely to induce hypercalcemia

CI: presense fo bowel obstruction or hypersensitivity

35
Q

What are calcimimetics?

A

Act as positive allosteric modifiers of calcium sensing receptors (Ca-SR)

36
Q

What is the primary role of Ca-SR?

A

Regulates PTH secretion to changes in extracellular Ca2+

37
Q

What is the MOA of calcimimetics?

A

Enhance sensitivity of Ca-SR to extracellular Ca2+ → Lowers Ca2+ due to PTH suppression

38
Q

What are the classes of calcimimetics?

A

Type 1: Direct agonist
Type 2: positive allosteric activator

39
Q

What is an example of a type 2 calcimimetic?

A

Cinacalcet

40
Q

What is MOA of Cinacalcet?

A

Enhances signal transduction by inducing conformational change in receptor and reducing receptor’s threshold for Ca2+

41
Q

What are the disadvantages of use aluminum PB?

A

Chronic use to Parkinsons, neurotoxic, hepatotoxic

42
Q

How is cinacalcet eliminated?

A

CYP3A4, CYP2D6, and CYP1A2 → eliminated renally

43
Q
A
44
Q

Does cinacalcet require a dosage adjustment?

A

Moderate to severe hepatic impairment but not in renal impairment

45
Q

DDI of cinacalet?

A

Strong CYP3A4 and CYP2D6 substrates

46
Q

Indications for cinacalet?

A
  1. Secondary hyperparathyroidism in CKD
  2. Hypercalcemia from PT carcinoma
  3. Primary hyperparathyroidism
47
Q

What is Sodium polystyrene sulfonate? MOA?

A

Cation-exchange resin

Swells → allows exchange of ions between Na+ on resin and K+

Bound-K+ moves through intestine → feces

Not absorbed into systemic circulation

48
Q

ADRs of SPS?

A

Hypernatremia, hypocalcemia, hypomagnesemia

49
Q

What is Patiromer? MOA?

A

Ca2+ containing non-absorbable K+ binding polymer

Distal colon (high free K+): Exchanges Ca2+ for K+, prevents K+ reabsorption → enhances excretion in the feces

50
Q

Indications for Patiromer use? Why

A

Approved for chronic but not emergency

Onset 7-48 hr (slow)

51
Q

What is Sodium zirconium cyclosilicate? MOA?

A

Non-absorbed, non-polymer inorganic powder with a micropore structure → captures K+ in exchange for H+ and Na+ cations

Very selective K+ in comparison to Ca and Mg → reduces free K+ in GI lumen → ↓ serum K+

52
Q

Onset of Sodium zirconium cyclosilicate?

A

1 h of admin

Normokalaemia → 24-48 hr

53
Q

What are the potassium binders?

A
  1. Sodium zirconium cyclosilicate
  2. Sodium polystyrene sulfonate
  3. Patiromer
54
Q
A

Drug Action I (32 decks)

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