2155 (IC15) MBD

Question 1

Pathophysiology of MBD

Answer 1

1) When kidney failure occurs, dont synthesise 1 alpha hydroxylase enzyme that converts inactive Vit D to active Vit D
No vitamin D → no gut absorption of calcium → hypocalcemia
Impaired excretion of phosphorus causes Hyperphosphatemia (↑ Serum P)

2) Excess P also binds to Ca2+ in the blood, leading to hypocalcemia

3) Hyperphosphatemia, Vit D Deficiency and Hypocalcemia all stimulate parathyroid glands to ↑ production and secretion of parathyroid hormone (PTH) → Secondary Hyperthyroidism (SHPT)

4) SHPT causes bone diseases eg. erythropoietin resistance, marrow fibrosis, fractures and Systemic toxicity eg. Calcification, Hypertension

Question 2

Symptoms of MBD (3 points)

Answer 2

Bone fracture, pain
Muscle weakness, skeletal deformity, growth retardation
Pruritus (due to high serum P and uremic toxins)

Question 3

Conditions arising from SHPT (4 points)

Answer 3

Renal osteodystrophy

Calcification

Calcific uremic arteriolopathy (CUA)
Calcium deposits in arteries → Vascular thrombosis → Skin ischaemia and necrosis, ulceration → Develop sepsis

Metastatic calcification

Question 4

How to calculate adjusted Ca, and when should this formula be used?

Answer 4

corrected Ca = measured Ca + 0.02 (40 – albumin in g/L)
should be used when albumin is less than 40

Question 5

What is the PTH goal for CKD dialysis patients

Answer 5

2-9x ULN

Question 6

Food rich in phosphorus

Answer 6

Dark colas, canned tea and milk drinks
Dairy
Rich in protein
Wheat products, processed foods

Question 7

What are the 2 forms of calcium binders

Answer 7

Calcium Carbonate and Calcium Acetate

Question 8

Which is a better calcium binder?

Answer 8

Calcium acetate (despite having lower elemental calcium content)

Question 9

What are the other non Calcium binders (4 points)

Answer 9

Sevelamer
Lanthanum
Aluminium hydroxide
Sucroferric Oxyhydroxide

Question 10

Counselling points for phosphate binders (3 points)

Answer 10

Important to take with meals
Potential for drug interactions eg. quinolones (antibiotics), antiepileptics, digoxin, warfarin (drugs with narrow TI)
Chewed VS Whole

Question 11

Why does vitamin D deficiency occur in CKD?

Answer 11

Kidney failure → no 1 alpha hydroxylase enzyme to convert 25(OH) Vit D ⇒ to Calcitriol (Active Vit D)

Question 12

Optimal serum 25OH D level

Answer 12

> 30mcg/L

Question 13

What are the medications for vit d? Which are inactive, which are active?

Answer 13

Caltrate, Lynae (Cholecalciferol or Vit D3)
Calcitrol (active)
Alfacalcidol (partially active, need liver function)

Question 14

What does vit D do?

Answer 14

Enhance P and Ca absorption in the gut
(have other functions eg. endocrine, renal, immune and CV)

Question 15

What is the difference between Calcitrol and Alfacalcidol

Answer 15

Calcitriol is the fully active form of Vitamin D3.
Alfacalcidol is inactive, only requires hydroxylation by the liver to be active.

Question 16

What is the role of calcimimetics?

Answer 16

Bind to Calcium-sensing Receptors (CaSR) on parathyroid gland → fool gland into thinking that there is enough Ca2+ → Reduce PTH secretion
Also increases sensitivity of receptor and uptake of Ca2+ → Reduce Ca2+ concentrations

Question 17

MOA of Cinacalcet

Answer 17

MOA: Increase sensitivity of CaSR to extracellular Ca, resulting in reduced PTH and serum Ca concentrations
AKA makes CaSR take up more Ca2+ in the body → decreasing Ca2+ in the body

Question 18

Side effect of Cinacalcet and the symptoms

Answer 18

Hypocalcemia for pts with normal Ca2+ → Seizures, tetany, muscle cramps

Question 19

Monitoring for Cinacalcet

Answer 19

Monitor Ca once a week during initiation and titration, every 2 weeks for maintenance
Monitor PTH 2x a month during initiation and titration, once a month during maintenance

Question 20

What should you do when changing from Cinacelcet to Etelcalcetide

Answer 20

space apart 7 days