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ERM > Endocrinology Part 4 > Flashcards

Endocrinology Part 4 Flashcards

1
Q

What does calcitonin do in the kidney?

A

Small decrease in Ca2+ and PO4 reabsorption

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2
Q

How is calcitonin controlled?

A

Stimulation of CSR increases calcitonin secretion

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3
Q

What stimulates the osteoclast?

A

PTH binds PTHR-1 on osteoblast which produces osteoid, OPG, and RANKL –> RANKL binds RANK on the osteoclast –> osteoclast releases H+ and proteases

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4
Q

Why is salmon calcitonin used over human calcitonin?

A

Salmon calcitonin is less likely to breakdown and has increased affinity for the receptor

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5
Q

What hormone can reduce RANKL production and increase OPG production?

A

Estrogen –> by directly increasing PTH

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6
Q

Starting with cholecalciferol how is Vitamin D activated?

A

Cholecalciferol –> 25 hydroxylase in the liver ==> calcifediol –> 1-alpha-hydroxylase in the kidney ==> calcitriol (active)

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7
Q

How does vitamin D affect Ca2+ and PO4?

A

Increase both Ca2+ and PO4 by increasing abosrption in the GI tract

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8
Q

What can excess vitamin D cause?

A

Hypercalcemia, increase RANKL expression = more resorption

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9
Q

What does vitamin D do in the kidney?

A

Small increase in Ca2+ and PO4 reabsorption

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10
Q

How is vitamin D synthesis controlled?

A

PTH increases activation of 1-alpha-hydroxylase which increase concentration of activated vitamin D

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11
Q

What is the MOA of teriparatide?

A

PTH analog –> leads to increased bone formation

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12
Q

How is teriparatid supplied?

A

Injectable

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13
Q

What are the adverse effects of teriparatid?

A

Muscle/bone pain

Osteosarcoma

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14
Q

What is the MOA of calcitonin?

A

MOA of calcitonin? How is it supplied? What are the adverse effects?
Decrease osteoclast function –> leads to decreased bone resorption, overactive remodeling, and Ca2+

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15
Q

How is calcitonin supplied?

A

Injectable and nasal spray

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16
Q

What are the AE of calcitonin

A

Low incidence of N/V

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17
Q

What is the MOA of bisphosphonates?

A

Decrease osteoclast function –> leads to decreased bone resorption and overactive remodeling

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18
Q

How are bisphosphonates supplied?

A

Oral and injectable

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19
Q

What are the AE of bisphosphonates?

A

Esophagitis
jaw necrosis,
atypical femur fractures

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20
Q

What is the MOA of raloxifene?

A

SERM –> agonist to ER in bone and liver (decrease resorption, increase formation, decrease LDL), antagonist to ER breast and uterus

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21
Q

How is raloxifene supplied?

A

Oral

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22
Q

What are the AE of raloxifene

A

Inc risk of thromboembolism & hot flashes

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23
Q

MOA of cinacalcet

A

Calcimimetic –> increases activation of the CSR to decrease PTH

24
Q

How is cinacalcet supplied?

A

Oral

25
Q

What are the adverse effects of cinacalcet?

A

HypOcalcemia

26
Q

How do loop diuretics affect calcium?

A

Decrease renal Ca2+ reabsorption

27
Q

How do thiazide diuretics affect calcium?

A

Increase renal Ca2+ reabsorption

28
Q

What can excess calcium supplementation cause?

A

HypERcalcemia
Constipation
Kidney stones

29
Q

What is the MOA of denosumab?

A

Monoclonal antibody to RANKL –> decrease bone resorption

30
Q

How is denosumab supplied?

A

Injectable

31
Q

What are the AE of denosumab?

A

Risk of infections/malginancies

32
Q

What are the symptoms of hypercalcemia?

A

Ion channel inhibition
Kidney
Cardiovascular
Soft tissue calcification Bone loss

33
Q

HypERcalcemia - ion channel inhibition sx

A 
Constipation
N/V
dec DTR's
Depression
Lethargy
Confusion
Memory loss
34
Q

HypERcalcemia - kidney sx

A

Polyuria
Polydipsia
Kidney stones

35
Q

HypERcalcemia - CV sx

A

BradyC
Sinus arrest
Dec QT

36
Q

HypERcalcemia - soft tissue calcification sx

A 
Pruritus
Crunchy skin
Pain/swelling joins
Inflammation
Risk of thromboembolism
37
Q

What can cause hypercalcemia?

A

Parathyroid tumor excreting excess PTH

Humoral hypercalcemia of malignancy releasing PTHrP

Bone tumor releasing RANKL

Excess vitamin D

Hyperthyroidism

Lithium

Thiazide diuretics

38
Q

How can hypercalcemia be treated?

A

Surgery of tumor, hydration, bisphosphonates, calcitonin, furosemide

Cinacalcet for PT tumor

High dose denosumab for bone tumor

39
Q

What are the symptoms of hypocalcemia?

A 
Muscle spasms
Tetany
Inc DTR's
Paresthesia
Hallucinations
Seizures
HF
Inc QT
Dry skin
Brittle nails
Hair loss
40
Q

What can cause hypocalcemia?

A

Hypoparathyroidism (low PTH)

Psuedohypoparathyroidsim (low PTHR-1)

Vitamin D deficiency

Ca2+ complex formation due to blood transfusion or muscle damage

41
Q

How can hypocalcemia be treated?

A

Treat the cause, give Ca2+/vitamin D supplementation, thiazide diuretics, off-label use of teriparatide

42
Q

What is rickets?

A

rickets?

Inadequate mineralization of bone in children (thin cortical bone)

43
Q

What are the symptoms of rickets?

A

the symptoms of rickets?

Short bones, deformities, fractures

44
Q

What is osteomalacia? symptoms?

A

Inadequate mineralization of bone in adults (thin cortical bone)

Causes bone pain and fractures

45
Q

What can cause inadequate mineralization of bone?

A

Vitamin D deficiency/activation problems,
low Ca2+,
low PO4-

46
Q

How can inadequate mineralization be treated?

A

Treat the cause (ie. if caused by dilantin , d/c the drug)

Ca2+/vitamin D supplementation

47
Q

What is Paget’s disease?

A

Localized hyperactive remodeling causing bone swelling, pain, fractures, and increased risk of sarcoma

48
Q

What can cause Paget’s disease?

A

Genetics or a virus

49
Q

How can Paget’s disease be treated?

A

Bisphosphonates and calcitonin

50
Q

What is renal osteodystrophy?

A

Chronic renal failure coupled with excessive bone resorption

51
Q

What can cause renal osteodystrophy?

A

Decreased activation of vitamin D –> decreases Ca2+ absorption in GI –> decreases fre e Ca2+ –> increases PTH –> increases resorption

Increased PO4 retention –> binds free Ca2+ –> increases PTH –> increases resorption

52
Q

How can renal osteodystrophy be treated?

A

Ca2+ and activated vitamin D supplementation

Cinacalcet

Sevelamer

53
Q

What is osteoporosis?

A

Loss of cortical bone resulting in thin/weak bone –> causes vertebral fractures, kyphosis, hip fractures, and wrist/forearm fractures

54
Q

What can cause primary osteoporosis?

A

Menopause and age

considered normal

55
Q

What can cause secondary osteoporosis?

A 
Excess PTH
Thyroid hormones
Glucocorticoids
Immobilization
Chronic phenytoin
Barbituates
Heparin use
56
Q

How can primary osteoporosis be diagnosed?

A

Measure BMD (Bone Mineral Density)

T > 2.5 sd below normal = osteoporosis

2.5 > T > 1 sd below normal = osteopenia

57
Q

How is primary osteoporosis treated?

A

Excercise, fall prevention, diet

Ca2+/vitamin D supplementation

Bisphosphonates

Estrogens, raloxifene

Calcitonin

Teriparatide

Low dose denosumab

ERM (27 decks)

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