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DEMS > Unit 4 week 3 > Flashcards

Unit 4 week 3 Flashcards

1
Q

Physiologic roles for calcium:

A

Structural role: major constituent of mineral matrix of bone

Biochemical role: essential regulator of excitation-contraction coupling, stimulus-secretion coupling, blood clotting, membrane excitability, cellular permeability, and other metabolic functions

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2
Q

_______ [Ca2+] out → cells are hyper-excitable

_________ [Ca2+] out → cells are hypo-exitable

A

Decreased [Ca2+] out → cells are hyper-excitable

Increased [Ca2+] out → cells are hypo-exitable

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3
Q

Physiologic roles for Phosphate: (5)

A

1) Structural role: part of mineral matrix of bone
2) High energy compounds
3) Membrane phospholipids
4) Regulation
5) DNA, RNA

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4
Q

Calcium Homeostasis Compartments:

Bone - two influx/efflux paths

A

99% of body calcium, in form of hydroxyapatite

10g in/out per day via osteolytic diffusion in and out of bone

250 mg in/out per day via osteoclastic bone breakdown and reformation

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5
Q

Calcium Homeostasis Compartments:

Intracellular compartment

A

contains 10g of calcium

Cytosolic Ca2+ maintain by intracellular Ca2+ buffers, compartmentalization into ER calcium stores by ATP-Ca2+ pump and Na/Ca antiporter

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6
Q

Calcium Homeostasis Compartments:

Extracellular compartment

A

blood and interstitial spaces (in equilibrium)

Contains 8-10 mg/dL

50% free

10% salts (bicarb, phosphate)

40% bound to albumin

Free Ca2+ levels are the regulated variable

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7
Q

Calcium Homeostasis Compartments:

Kidney

A

Kidney filters 10g of Ca2+/day with 98% reabsorbed

Ca2+ salts and free → filterable by kidney

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8
Q

Calcium Homeostasis Compartments:

Gut

dietary absorption, excretion in feces?

A

Dietary input = 1 g
Feces output = 825 mg

500 mg absorbed in gut
325 mg excreted from serum into feces

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9
Q

PTH actions in general

A

increases plasma calcium, decreased phosphate

**Responsible for short term regulation of blood calcium

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10
Q

PTH actions on Bone (2)

A

1) Rapid increased efflux of labile bone calcium via DIRECT upregulation of osteolytic bone actions

2) Slow effect of increased bone remodeling → increased calcium AND phosphate
- INDIRECT effect via osteoblasts and subsequent upregulation of osteoclasts

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11
Q

PTH actions on Kidney (3)

A

1) INCREASED calcium reabsorption (distal tubule)
2) DECREASED phosphate reabsorption
3) increased synthesis of 1,25 (OH)2 Vitamin D

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12
Q

PTH actions on GI tract (1)

A

indirect via vitamin D → enhance Ca2+ absorption

PTH increases 25-hydroxylase and 1-hydroxylase enzyme activity converting VitD to active form

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13
Q

Calcitonin

A

produced by parafollicular C cells of thyroid

Secreted in response to elevated Ca2+ and in response to gastrin, CCK, secretin, and glucagon

Decreases efflux of labile bone calcium

Used therapeutically to slow down high turnover bone disorders

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14
Q

Vitamin D Synthesis: (3)

A

1) 7-dehydrocholesterol in skin acted on by sunlight → Vitamin D (inert)
2) In liver add hydroxyl group → 25-OH Vitamin D
3) In kidney add hydroxyl group → 1, 25 (OH)2 Vitamin D = ACTIVE form

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15
Q

Types of Vitamin D generated by kidney

A

In kidney add hydroxyl group → 1, 25 (OH)2 Vitamin D = ACTIVE form

Kidney also has 24-hydroxylase activity → 24, 25 (OH)2 Vitamin D = inactive form

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16
Q

Vitamin D is transported in the blood bound to ___________

A

transcalciferin

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17
Q

Vitamin D is responsible for __________ regulation of blood calcium

A

**Responsible for long term regulation of blood calcium

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18
Q

Vitamin D Regulation:

__________ inhibits 1-hydroxylase

_________ increases 1-hydroxylase and 24-hydroxylase activity –> increased _______________ –> increased ________ absorption from the gut

A

1,25 (OH)2 Vitamin D inhibits 1-hydroxylase

PTH increases 1-hydroxylase and 25-hydroxylase activity → increased 1,25 (OH)2 Vitamin D → increased Ca2+ absorption from gut

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19
Q

Vitamin D Regulation:

Decreased phosphate –> increase actions of __________ and decrease actions of ___________ –> increased _________ –> increased _______ absorption from the gut

A

Decreased phosphate →

Increase actions of 1-hydroxylase, decrease actions of 24-hydroxylase

→ increased 1,25 (OH)2 Vitamin D → increased phosphate absorption from gut

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20
Q

Actions of (1,25 OH2) Vitamin D

2

A

1) Interact with nuclear receptors in GI tract to increase synthesis of Calcium binding proteins (CALBINDIN) expressed in the lumen of the intestine AND increase active transport of Ca2+ into enterocyte and out of enterocyte into blood
2) Mobilize bone by sensitizing bone to PTH

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21
Q

Calcium absorption -

Three steps:

A

1) Ca2+ active transport from gut lumen into enterocyte (mostly in duodenum)
2) Binds Calbindin in cell → Ca2+ carried to basolateral side
3) Ca2+ actively pumped out of enterocyte

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22
Q

Is there a limit to calcium absorption?

A

Limited “up-regulation” to compensate for low intake → chronically low intake associated with low bone mass, and high intake associated with high bone mass

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23
Q

5 things that enhance Ca2+ absorption in the gut?

A

1) Increased vitamin D → synthesis of Ca-transport proteins
2) Increased physiologic demand (pregnancy, adolescence)
3) Gastric acidity (release Ca2+ from food matrix)
4) Lactose (maintains solubility)
5) Increased dietary protein → high intake assoc. with high Ca absorbed

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24
Q

7 things that decrease Ca2+ absorption in the gut?

A

1) Vitamin D deficiency (northern latitudes, limited skin exposure, dark pigmentation, elderly)
2) Steatorrhea: unabsorbed fatty acids bind Ca2+ → “soaps”
3) Gastric alkalinity
4) Oxalic acid (spinach)
5) Phytic acid (legumes, soy, corn, wheat)
6) Caffeine (increases Ca2+ urinary excretion)
7) Dietary protein: increases Ca2+ urinary excretion (net neutral because increased absorption)

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25
Q

Key hormonal regulators of calcium homeostasis (3)

A

PTH
1,25 (OH)2D
Calcitonin

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26
Q

Metabolism and Homeostasis of Calcium

A

Serum Ca2+ is maintained in a very tight range at all cost

Development of deficiency is a long-term “silent” process because maintenance of serum [Ca] is at expense of bone

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27
Q

Most high risk groups for Ca2+ deficiency (4)

A

1) Premature infants
2) Adolescence
3) Peri-menopause
4) Post bariatric surgery

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28
Q

Premature infants and Ca2+:

A

Preterm infants at risk for “osteomalacia of prematurity”

80% of Ca2+ transfer in third trimester

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29
Q

School-Aged Children and Ca2+

A

higher requirements, and puts children at risk for Ca deficient rickets

Studied by Framingham Children’s Study → concluded there is beneficial effect of childhood dairy consumption on adolescent bone status

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30
Q

Adolescence and Ca2+

A

hormonal changes favor Ca absorption/bone deposition

50% of bone mineral mass accrued during adolescence

Highest in EARLY puberty

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31
Q

After skeletal maturity/”peri-menopause” and Ca2+

A

high requirements, increased losses, low intake

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32
Q

Pregnancy/lactation and Ca2+

A

physiologic increase in need, NOT dietary increase in need

Physiologic responses compensate for increased Ca demand, so no requirement for increased dietary intake

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33
Q

Physiologic compensation in Pregnancy vs. lactation

A

Ca absorption increases during pregnancy

During lactation, increased PTH (bone mass lost) and bone mass recovered with post-weaning

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34
Q

Dietary and lifestyle factors impacting bone health: (5)

A

1) **Primary determinant of bone mineral density (BMD) are genetic and intrinsic factors
2) Age - strongest empiric predictor of BMD
3) Nutritional/dietary factors
4) Behaviors/Lifestyle
5) Medications/Medical Conditions

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35
Q

Nutritional/dietary factors and bone health (9)

A

1) Lifetime Ca intake - limited ability to adapt to low Ca intake
2) Protein intake
3) Phosphate intake
4) Vitamin D
5) Vitamin K (cofactor with osteocalcin and other bone forming proteins
6) Sodium intake - high Na+ intake → increased urinary Ca2+ excretion
7) Vegetarian diet (high in fruits/veggies is positive for bone health)
8) Caffeine (increases urinary Ca excretion)
9) Whole diet pattern (e.g. DASH diet)

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36
Q

Behaviors/Lifestyle and bone health (3 factors)

A

1) Exercise (weight bearing): muscle mass directly related to bone mass
Mechanosensors in bone stimulate osteoblasts

2) Smoking
3) Alcohol - depresses osteoblasts

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37
Q

Medications/Medical Conditions and bone health (3)

A

Glucocorticoids

Chronic illness (associated with malabsorption, chronic systemic inflammation)

Hypogonadism (especially low estrogen)

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38
Q

Optimizing bone density: (7)

A

1) Achieve “peak bone mass” when you can (adolescence)
2) Weight bearing activity
3) Maintain good Ca intake over lifetime
4) Avoid excess alcohol and tobacco
5) Minimize practices that enhance calcium loss or bone resorption
6) Maintain healthy diet that supports bone health
7) Supplement when necessary

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39
Q

Ca-carbonate vs. Ca-citrate supplements

A

Ca-Carbonate (Tums): best absorbed WITH meals

Ca-Citrate: best absorbed BETWEEN meals

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40
Q

Can you over supplement Calcium?

A

Oversupplentation → increase MI, stroke and death risk

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41
Q

DASH diet and calcium

A

may have benefits to long term bone status

Increased dietary Ca intake + higher fruit/veg intake (Mg, VitC)

Na+ reduction → decreased urinary Ca2+

Decreased turnover of bone

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42
Q

Osteoporosis

A

compromised bone strength predisposing to risk of fragility fractures

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43
Q

Fragility fractures in osteoporosis: 3 common locations

A

total of 1.5 million/yr

Spine (700,000/yr in US)
Hip (300,000/yr in US)
Wrist (250,000/yr in US)

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44
Q

Increased risk of fragility fractures with (4)

A

age, falls, low bone mass, previous fractures

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45
Q

Non modifiable risk factors for osteoporosis (5)

A

age, race, gender, family history, early menopause

46
Q

Modifiable risk factors for osteoporosis (7)

A

low Ca or VitD intake, estrogen deficiency, sedentary lifestyle, smoking, excess alcohol, excess caffeine, medications

47
Q

Mechanism of osteoporosis

A

bone resorption > formation → lose bone mass

BUT low bone mass is NOT always osteoporosis

48
Q

Prevention of osteoporosis (4)

A
  1. Calcium: 1000-1500 mg/day
  2. Vitamin D: 1000 units/day
  3. Exercise: aerobic and resistance
  4. Falls: assessment and prevention
49
Q

Treatment of osteoporosis: 2 strategies

A

alter bone remodeling

  1. Decrease bone resorption
  2. Increase bone formation
50
Q

Osteoclasts

A

use enzymes and acid to break down old bone

51
Q

Activation of osteoclasts

A

RANK receptor on osteoclast binds RANK-L and stimulates OC

RANK = receptor activator of nuclear factor KB

52
Q

Decay receptor for RANK-L

A

Osteoprotegerin

53
Q

Osteoblasts

A

form new bone from osteoid

54
Q

New bone formation

A

Osteoid calcifies with addition of Ca and PO4

New bone has mechanoreceptors (OSTEOCYTES)

55
Q

Activation of osteoblasts

A

Wnt Frizzled / LRP-5 B-Catenin activates OBs

56
Q

Inhibition of osteoblasts

A

Sclerostin inhibits Wnt pathway → inhibit OBs

57
Q

_____ and ____ regulate bone formation and resorption

A

PTH and 1,25 (OH)- Vit D

58
Q

How does PTH regulate bone formation and resorption?

A

Stimulate preosteoblast proliferation and differentiation into osteoblasts

PTH → inhibit osteocyte production of Sclerostin

PTH → stimulate osteoblast expression of RANKL → bind RANK on osteoclast → promote formation of mature osteoclasts

59
Q

Sclerostin

A

glycoprotein that blocks osteoblast differentiation via inhibition of Wnt signaling pathway

60
Q

Osteoprotegerin (OPG):

A

“decoy” molecules released by osteoblasts that bind RANKL and prevent activation of RANK receptor

61
Q

Osteomalacia (adults) and Rickets (children):

A

impaired bone mineralization resulting in soft, weak bones

62
Q

Pathophysiology of osteomalacia/rickets

A

inadequate Ca x phosphate product for bone mineralization

63
Q

Causes of osteomalacia/rickets

A
  1. Vitamin D Disorders

2. Phosphate disorders:

64
Q

2 phosphate disorders that cause osteomalacia/rickets

A
  1. Acquired hypophosphatemia

2. Congenital hypophosphatemia rickets

65
Q

Acquired hypophosphatemia

A

poor oral intake, renal phosphate wasting

66
Q

Congenital hypophosphatemic rickets

A

“Vitamin D Resistance Rickets”

Renal phosphate wasting

Impaired 1,25 (OH)2 VitD Formation

67
Q

Symptoms of osteomalacia

A

pain, deformities, fractures

Pseudofractures (Milkman, Looser’s Lines)

68
Q

Symptoms of rickets

A

pain, deformities, muscle weakness, short stature

Bowing of long bones

Flaring ends of long bones

Delayed epiphyseal calcification

69
Q

Paget’s disease

A

idiopathic bone condition characterized by excessive/unregulated bone resorption and formation

70
Q

Causes of Paget’s disease

A

development of Paget’s disease requires

1) Genetic enhancement of osteoclast formation/reactivity
2) Chronic paramyxovirus infection that induces changes in osteoclast precursors

  • Possible link with dog ownership
  • See paramyxovirus-like inclusions in nuclei + cytoplasm of osteoclasts
71
Q

Clinical features of Paget’s: Skeletal

A

pain, deformity, fractures, osteoarthritis, hypervascularity, acetabular protrusion, osteogenic sarcoma

Common sites of involvement: pelvis, skull, vertebrae, femur, tibia

72
Q

Clinical features of Paget’s: Neurological

A

deafness (8th nerve, ossicles), cranial nerve compression by bone, spinal cord compression (vascular)

73
Q

Clinical features of Paget’s: Cardiovasclar

A

atherosclerosis, aortic stenosis, CHF (high output)

74
Q

Clinical course of Paget’s

A

phases of resorption and formation

  1. Osteoclastic
  2. Osteoclastic/Osteoblastic
  3. Osteoblastic
75
Q

Diagnosis of Paget’s

A
  1. Remodeling markers elevated
  2. Xray fractures very specific
  3. Bone scan very specific
  4. Bone biopsy occasionally needed
76
Q

X ray features of Paget’s

A
  • Osteolytic lesions: “blades of grass” sign in long bones, resorption front in flat bones
  • Osteosclerotic lesions near lytic areas
  • Thickened disorganized trabeculae
  • Thickened, expanded cortex
  • Expansion of bone size
77
Q

Bone scan finding Paget’s

A

Focal areas of intense uptake

78
Q

Histology of Paget’s

A

increased osteoclast numbers, increased osteoclast nuclei, increase osteoblasts in periphery, disorganized / mosaic / woven bone

79
Q

Actions of PTH (3)

A

1) Enhance renal reabsorption of Ca
2) Stimulate renal excretion of P
3) Increases bone formation AND reabsorption by stimulating osteoblasts AND osteoclasts
4) Stimulates activation of VitD in kidney

80
Q

Mechanism my which PTH increases bone formation and reabsorption

continuous vs. intermittent dosing?

A

Stimulates RANK with RANKL on osteoclasts to increase bone remodeling and eventually osteoblastic bone formation

Increase in bone resorption with CONTINUOUS dose BUT low and INTERMITTENT doses of PTH stimulate formation without increasing bone resorption

81
Q

Primary stimulus for PTH secretion is ___________

A

hypocalcemia

82
Q

Vitamin D vs. PTH vs. FGF23 vs. Calcitonin effects on Ca and P

A

PTH: increase Ca, decrease P
Vitamin D: increase Ca and P
FGF23: decrease P
Calcitonin: decrease Ca and P

83
Q

3 direct actions of Vitamin D

1 indirect feedback loop action of Vitamin D

A

Direct actions:
1) Increases gut absorption of Ca and P

2) Increases bone formation AND reabsorption by stimulating osteoblasts AND osteoclasts
3) Enhance renal reabsorption of Ca and P

Feedback loops: inhibit PTH synthesis/release from parathyroid glands

84
Q

Direct and indirect actions of FGF23

A

Direct actions: Stimulates renal excretion of P

Feedback loops: inhibits VitD activation in kidney

85
Q

Calcitonin actions

A

in pharmacologic concentrations can reduce serum Ca and P by inhibiting bone resorption by osteoclasts

1) Inhibit osteoclastic bone resorption → decreased Ca and P
2) Reduce reabsorption / increase excretion of Ca and P → decreased Ca and P

86
Q

Cholecalciferol vs. Ergocalciferol Vitamin D supplements

A

Cholecalciferol (VitD3) → less expensive

Ergocalciferol (VitD2) → less efficient than D3 in elevating serum 25-OHD3 - use D3 when possible

87
Q

Calcifediol

A

(25(OH) VitD3) → most useful in patients with liver disease

Onset more rapid than VitD3, but shorter half life

88
Q

Calcitriol

A

(1,25 (OH)2 VitD3) → most useful in patients with decreased synthesis of calcitriol (chronic renal failure, type 1 VitD-dependent rickets)

Rapid onset of action

Can cause hypercalcemia, kidney stones

89
Q

Dihydrotachysterol

A

functionally equivalent to 1a-OHD3, requires hepatic 25-hydroxylation to become active

Alternative for use in disorders that require calcitriol

Rapid onset of action, short duration of action

90
Q

Cinacalcet

mechanism?
use? (2)

A

binds allosterically to calcium sensing receptor in parathyroid gland

Increases sensitivity of CaSR to Ca2+ → reduced release of PTH

Complementary to Vit D and analogs that target VDR

Use: secondary hyperparathyroidism and non-surgical option in primary hyperparathyroidism

91
Q

Antiresorptive agents used in osteoporosis (3)

A

1) Raloxifene-Estrogen: increase production of OPG by osteoblasts
- Prevent RANK-RANKL interaction

2) Denosumab: binds RANKL → prevent RANK-RANKL interaction
3) Bisphosphonates and Calcitonin: inhibit bone resorption by osteoclasts

92
Q

Use of Calcitonin

A

approved for treatment (not prevention) of osteoporosis

Not as effective as bisphosphonates or teriparatide

Useful if back pain is a problem

93
Q

Estrogens - mechanism?

A

Increase bone mass as agonist at ERa receptors on osteoblasts and osteoclasts

94
Q

How does estrogen increase bone mass? (3)

A

1) Regulate osteoblasts: increase synthesis of Type I collagen, osteocalcin, osteopontin, osteonectin, alk phos
2) Decrease number and activity of osteoclasts by altering cytokine signals from osteoblasts
3) Increase osteoblast production of osteoprotegerin (OPG) “decoy” receptor for RANKL → prevent osteoclast activation

95
Q

Osteoprotegrin

A

“decoy” receptor for RANKL → prevent osteoclast activation

96
Q

Estrogen pharmacologic use

A

Mechanism: reduce bone resorption via inhibitory effects on osteoclasts

-Must give in first 5 years after menopause

Progestational agent reduces endometrial carcinoma risk

Use: no longer first line for osteoporosis, can be used for prevention in patients without heart disease

97
Q

How does pharmacologic doses of glucocorticoids decrease bone density (3)

A

1) Lower serum Ca2+ by blocking VitD-stimulated intestinal Ca2+ transport → increases PTH → stimulate osteoclasts
2) Increase production of RANKL by osteoblasts, decrease production of osteoprotegerin → more RANKL binding to RANK → increase bone resorption
3) Suppress osteoblasts

98
Q

Thiazide diuretics used to treat _________ by _____________

A

hypercalciuria

reducing calcium urinary excretion

99
Q

Aldronate, Risedronate, and Zoledronate (IV)

A

Bisphonphonates

100
Q

Mechanism of bisphosphonates?

A

Bind active sites of bone remodeling and inhibit osteoclasts

→ osteoclast apoptosis and inhibit osteoclast function

101
Q

Use of bisphosphonates

A

most effective drugs for PREVENTION and TREATMENT of osteoporosis

first line for hypercalcemia of malignancy

Potent inhibition of osteoclastic bone resorption

Can resolve hypercalcemia in 24-72 hrs, lasts for weeks

Can prevent postmenopausal vertebral/nonvertebral fractures

102
Q

Adverse reactions of bisphosphonates

A

GI effects: heartburn, abdominal pain, diarrhea
-Esophagitis (stay upright after dose)

Severe bone, joint, muscle pain - osteonecrosis of jaw (rare)

Contraindications: achalasia, scleroderma esophagus, esophageal strictures

103
Q

Raloxifene

A

Selective Estrogen Receptor Modulators (SERMs)

104
Q

Selective Estrogen Receptor Modulators (SERMs)

use?

A

reduce risk of vertebral fractures, but less effective than estrogen or bisphosphonates

105
Q

SERMs

advantages and disadvantages relative to estrogen

A

Advantages relative to estrogen: reduce risk of breast cancer and coronary events

Disadvantages relative to estrogen:
Worsening of vasomotor symptoms (hot flashes) and leg cramps
Increased risk of thromboembolic disorders

106
Q

Teriparatide

mechanism?

A

synthetic PTH fragment that stimulates bone FORMATION

Intermittent administration of PTH analog increases osteoblast activity and bone formation

107
Q

Teriparatide

use?

A

treatment of severe osteoporosis
Use for longer than 24 months NOT recommended

daily subcutaneous dose

108
Q

Denosumab

mechanism?

A

ab against RANKL → reduce osteoclast activation, improve bone mineral density

109
Q

Denosumab

use?

A

Dose adjustment in chronic renal disease

Use: treatment in patients with high fracture risk

110
Q

Treatment of hypercalcemia (5)

A

1) Saline diuretics (+/- furosemide)
2) Bisphosphonates
3) Calcitonin
4) Phosphates
5) Glucocorticoids

111
Q

Treatment of hypocalcemia (3)

A

1) Calcium replacement (acute)
2) Calcium supplementation (chronic)
3) Vitamin D supplementation (chronic)

DEMS (10 decks)

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