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HSF Block 1 > Physio - Ca and P > Flashcards

Physio - Ca and P Flashcards

1
Q

What effects can hormones & local mediators have on bone function?

A

Local Mediators of Osteoblast Function

  • Part I : Osteoblast Differentiation
    • Mesenchymal Stem Cell –> Osteoprogenitors –> Osteoblasts
    • Wnt signaling:
      • increase beta-catenin/Runx2/Osterix
  • Part II: Osteogenesis - Bone Formation
    • Proliferation
      • high Runx/BSP
    • Osteoid Deposition
    • Mineralization
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2
Q

How does Ca Metabolism Occur?

What organs are involved?

A

Basics:

  • Blood Ca++ = tighly regulated!
  • Plays role in:
    • hormone secretion
    • muscle contraction
    • nerve conduction
    • protein exocytosis
    • 2nd messanger pathways

Organ systems:

  • Bone
  • GI
  • Kidneys

Key Factors/Hormones:

  • PTH
  • Vit-D (1,25-diOH)
  • Calcitonin

Calcium In/Out of Blood:

  • IN
    • intestinal adsorption = only way in
    • bone adsorption
  • OUT
    • renal excretion = only way out
    • bone formation
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3
Q

How do osteoblasts and osteoclasts regulate Ca++ homeostasis?

A

Osteoblasts:

  • Have receptor for PTH
    • PTH causes release of M-CSF
    • M-CSF binds to monocyte
    • Monocyte –> Macrophage –> expresses RANK
    • RANK binds to RANKL on osteoblast
      • forms a osteoclast
  • Build bone

Osteoclast:

  • Rely on osteoblast for regulation
  • Break down bone

Vitamin D3 Relationship:

  • Basics:
    • Critical for bone formation & promoting mineralization
  • Specific cell effects:
    • Osteoblasts + Osteoprogenitors = EXPRESS VDR
      • Osteoclasts do NOT
  1. Increases Osteoclast numbers:
    • stimulates RANKL expression
    • inhibits osteoprogerin (OPG)
      • antagonizes RANKL fxn
  2. Stimulates Osteoblast formation
    • regulates Runx2 expression
      • favors osteoblast formation
  3. Induces expression of osteocalcin & osteopontin
    • Ca++ binding proteins
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4
Q

How does Phosphate Metabolism Occur?

What organs are involved?

A

Basics:

  • Blood (P) regulation = tied to Ca++ regulation
    • Ca++ & (P) = components of hydroxyapatite
    • Regulated by same hormones
  • a little more than >1/2 adsorbed from diet
  • normally: bone resorbtion = bone remodeling = Ca++ 0mg

Organ systems:

  • Bone
  • GI
  • Kidneys = primary control mechanism

Key factors/hormones:

  • PTH
  • VitD (1,25-diOH-vitD)
  • Fibroblast Growth Factor - 23

Phosphate In/Out of Blood:

  • IN
    • intestinal adsorption (major)
    • bone adsorption (minor)
  • OUT
    • renal excreton (major)
    • bone formation (minor)
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5
Q

What are the Common pathogenesis of Hypo/Hypecalcemia?

A

HYPERTHYROIDISM

Parathyroid Hormone - Dependent

  • Primary Hyperparathyroidism
    • increase PTH
    • low Ca
  • Familiar hypocalciuric hypercalcemia

Parathyroid Hormone - Independent

  • Renal failure (acute or chronic)
  • Excess Vit-D
  • Drugs
    • Vit-A intoxication, etc

HYPOTHYROIDISM

Destruction of Parathyroid Tissue

  • Postsurgical
    • ​decrease in PTH
    • decrease in Ca
  • Post-radiation
  • Autoimmune
  • Metastatic infiltration
    • Gland infiltration

Reversible impairment in PTH secretion

Genetic Disorders of parathyroid synthesis

  • DiGeorge syndrome
    • congential; failure of 3rd & 4th gland pouches to dev.
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6
Q

What are common pathologies of Vitamin D deficiency?

A

Dysfunction of the following responsibilies of VitD (Calcitriol):

Genomic and non-genomic effects

  1. Regulation of gene expression
  2. Ligand for regulation of estrogen, progesterone, testosterone, corticosteroids, thyroid hormone
  3. Skin cell proliferation, hair growth, obesity, diabetees, cancer,
    • lead to pain & decrease QL

Skeletal Effects:

  1. Rickets
    • deficient mineralization at the growth plate
    • inadequate supply of Ca + P
    • long bone deformity
    • _young individual_s during growth (mostly)
      • Symptoms:
        • Decrease Vit D/Ca/PO
        • Increased PTH
      • Epiphyseal = widening
      • Metaphyseal = cupping
      • Short stature
  2. Osteomalacia
    • impaired mineralization of the bone matrix
    • inadequete supply/loss of Ca + P
    • Long (mature) bone deformity
    • Adults (mostly)

Notes:

  • Rickets & osteomalacia = occur together when growth plates are open
    • ONLY osteomalacia occurs after growth plates = fused
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7
Q

What is Primary Hyperparathyroidism?

A

Basics:

  • Excess secretion of PTH
    • benign parathyroid adenoma (80%)
    • thyroid gland hyperplasia (20%)
  • Incidental finds of serum electrolyte evaluation
    • low Ca++!

Risk Factors:

  • Hx neck radiation
  • Age >50 yrs
  • Female (2x more likely)

Symptoms:

  • Renal STONES (Hypercalicemia)
  • THRONES (Polyuris)
  • GROANS (weakness/constipation)
  • Psychiatric OVERTONES (depression)
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8
Q

How to we achieve Ca++ Homeostasis?

A

Hormones: Calcium Metabolism & Bone Turnover

Major Plasma Ca Regulators:

  • PTH
    • Key Fxn: promote Ca++ resorption in Kidney
      • Kidney = Ca+ resorption
      • Kidney/GI = + Renal Vit D3 synthesis
      • Bone = + Ca resorption
  • 1,25 Vit D3
    • Key Fxn: promote Ca++ resorption in Intestine
      • Kidney = + Renal Ca resorption
      • GI = + absorption of Ca
      • Bone = direct - Ca++ out / indirect - bone formation
        • inhibits PTH production

Other Ca Regulators:

  • Calcitonin**
    • Key fxn: inhibit bone resportion –> build bone
      • Low Ca++ = (-) calcitonin
      • Hight Ca++ = (+) calcitonin
  • Estrogens
    • (+) osteoblast function
    • (-) osteoclast function
  • Progesterone
    • (+) bone formation (prevents bone loss)
  • Glucocorticoids
    • (-) induce bone loss!
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9
Q

What are components of Cellular Calcium?

A

Basics:

  • Only 1% of Ca = Serum
  • Electrochemical charge across membrane = ~50
    • cell interior = neg, favoring Ca++ entry
  • Ca induced cell death = prevented via Ca+ pumps, channels, exchangers, and proteins to sequester Ca
  • Important in 2nd messasnger systems

Ca Effects:

  • Increase free radicals
  • Degrade membranes
  • Degrade proteins
  • Lead to cell death

3 Physiologic Forms:

  1. free ionized species
    • biologically active
    • regulates PTH
  2. protein associated species
    • albumin
  3. complexed species
    • citrate / bicarb
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10
Q

Calcium Metabolism Review

A
  • PTH: promotes resorption
    • (+) = hypocalcemia
      • Ca resorption/intake
    • (-) = hypercalcemia
      • Ca excretion/deposits
  • Vit D: promotes Ca resorption
  • Calcitonin: inhibit bone resorption
    • low Ca = (-) Calcitonin
    • high Ca = (+) Calcitonin
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11
Q

What is the Chronic & Acute relationship between PTH and Bone?

A

Basics:

  • Osteoblast express PTH receptor, osteoclasts lack it

Chronic PTH stimulation = bone loss

  1. promotes bone resportion
    • increases Ca++
  2. PTH induces M-CSF, RANKL, IL-6 expression
    • promotes osteoclastogenesis
  3. Inibits collagen synthesis
    • degrade osteoid –> more marrow accessible to osteoclast

Acute PTH stimulation = bone formation

  1. PTH induces osteocytic osteolysis
    • liberates local Ca++ that can be used for mineralization of osteoid
  2. Indirect stimulation of bone resorption
    • induces local release of bone growth factors
    • induce bone formation
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12
Q

What is CaSR?

A

CaSR

  • Ca++ sensing receptor (CaSR)
  • Hormones That Control Blood Ca++

Basics:

  • Ca++ levels directly regulate expression of PTH and calcitonin
  • Changes in extracellular Ca++ are sensed by a CaSR

Relevant CaSR Distribution:

  • Thyroid Gland:
    • _​_CaSR = secretion of calcitonin
  • Intestines
    • CaSR = uptake of nutrients (Ca++),
    • local release of Ca++ stores
    • rise in intracellular Ca++
  • Kidney:
    • CaSR is expressed in all nephron segments
    • increased Ca++ causes physiologically significant
      loss of Na, K, Cl, Ca++, and water (inhibits Ca++
      resorption)
  • Parathyroid gland: (highest CaSR levels expressed here)
    • PTH secretion = negative feedback loop
    • increased Ca++ activates PKC which prevents
      secretion of PTH
  • Osteoblast and chondrocytes:
    • _​_not well understood. CaSR -/- have deregulated
      endochondral bone formation
    • in-vitro Ca++ induces osteoblast proliferation and
      survival
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HSF Block 1 (19 decks)

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