Physiology Flashcards
(41 cards)
Connective tissue
1. Cells: A. Fibroblasts (resident) B. Macrophage (immigrant) C. Mast cells D. Plasma cells 2. Fibers: A. Collagen B. Elastic C. Reticular 3. ECM components
Hydroxyapatite
More Ca2+ and PO4 than needed
1. Inhibitors prevent xs precipitation
A. Pyrophosphate
Cleidocranial dysplasia
Birth defect
- Affects bone and teeth
- RUNX2 = runt related transcription factor 2
Osteogenesis imperfecta
Group of genetic disorders
- Brittle bone
- Osx (osterix) = transcription factor Sp7
Pages disease
Inc. osteoclasts activity
- Inc serum PO4 , urinary hydroxyapatite, and osteocalcin
- Mosaic pattern of lamellar bone
Bone resorption
- Integrins bind vitronectins on matrix surface -> seal w/ osteoclast
- Osteoclasts -> H+ and acid pro teases into lacunae
- V-type H+ pump and ClC7 mediate acid secretion at ruffled border mem
- Carbonic anhydrase (CA): in cytosol supplies H+
- Cl-HCO3 exchangers in mem opp ruffled border
- Clathrin: mediates vesicle formation
- TRAP (tartrate resistant acid phosphatase) = metalloenzyme
A. In osteoclasts and macrophages
Bone formation
- Intramembranous osteogenesis
A. Mesenchyme -> woven bone -> lamellar bone - Endochondral osteogenesis
A. Cartilage -> bone formation
Osteoclast signaling
- Inhibition
A. Calcitonin: dec plasma Ca2+
B. Adenlyl cyclase (AC) -> cAMP
C. Protein kinase A (PKA): P from ATP to ser or the on substrate - Stimulation
A. IL-6 -> RANKL expression on osteoblasts
B. Osteoprotegrin (OPG) from osteoblasts and osteogenic stromatolites cells- Bind RANKL -> prevent binding RANK
Signaling steps in resorption
- PTH binds osteoblast receptors
- Form RANKL and release M-CSF (macrophage-colony stimulating factor)
- RANKL binds RANK and M-CSF binds receptors on preosteoclasts
- PTH -> dec OPG inhibits preosteoclasts -> mature osteoclasts
A. OPG binds RANKL - Osteoclasts -> ruffled border and release lysozymes
- Osteocytes and blasts encased in bone matrix
WNT/Beta-catenin signaling pathway
- WNT from osteoprogenitors bind LRP5/LRP6 on osteoblasts -> Beta-catenin and inc OPG
A. Inc bone, dec osteoclasts - Sclerostin from osteocytes inhibits WNT/beta-catenin
- BMPs bind transmembrane ser/thr kinase receptors -> heterotopic bone formation
PTH
- Parathyroid chief cells
- Greater effect on [Ca2+] than calcitonin
- Inc [Ca2+] in blood by inc osteoclast activity
- Secretion regulated by [Ca2+] plasma
- Responses
A. Bone: inc osteoclasts -> inc Ca2+ blood
B. Intestine: calcitrol -> inc Ca2+ absorption -> inc Ca2+ blood
C. Kidney: calcitrol -> inc Ca2+ reabsorption -> inc Ca2+ blood
Calcitonin
- Thyroid c-cells
- Dec Ca2+ plasma
- Responses
A. Bones: dec osteoclast -> inc Ca2+ bone and dec Ca2+ blood
B. Intestines: dec PTH and calcitiol -> dec Ca2+ absorption -> dec Ca2+ blood
C. Kidney: dec calcitriol-> dec Ca2+ reabsorption -> dec Ca2+ blood
Phosphate homeostasis
- Regulators
A. PTH -> dec Pi reabsorption kidneys
B. Active vitamin D from renal tubule cells
C. FGF23 from osteocytes- [Pi]plasma feeds bask on osteocytes
- Distributed thru tissues
- Tissue damage -> hyperphosphatemia -> complex Ca2+ -> hypocalcemia
Costameres
Facilitate lateral transmission of force of contraction
1. Stabilize sarcolemma
2. Protein complexes
A. Dystrophin-glycoprotein complex (DGC)
B. Integrin-vinculin-talin complex
Isotonic contraction
- Shortens muscle
2. Enough force to move load
Isometric contraction
Muscles don’t shorten
1. Can’t move load
Isotonic eccentric contraction
Muscle lengthens
Transition from fast to slow twitch muscles
- Action potential
- Ca2+ -> CaN
- NFAT dephosphorylated -> into nucleus
- Slow-fiber gene expression
- Action potential
- Ca2+ into nucleus -> CaMK -> HDAC phosphorylated -> inhibits HDAC
- If not inhibited HDAC -> MEF2 -> slow fiber expression
Types of muscle fatigue
- Central -> CNS changes
- Peripheral
- High-frequency
- Low-frequency
- From ATP depletion, lactic acid accumulation, and glycogen depletion
Neuron action potential
1. Depolarization: Na+ -> inside cell A. [Na+] never higher inside than outside -gradient doesn’t change 2. Repolarization: K+ open A. K+ most permeable => resting membrane potential approaches Nearnst potential 3. Hyperpolarization: action potential approaches K+ potential 4. Two Na+ gates A. Activation B. Inactivation *open fast 5. K+ gate (only 1) A. Activated at same time as Na+ B. Slower 6. Hyperkalemia A. Inactivation gates close B. Can’t start new action potential C. Skeletal and cardiac muscl
Neuromuscular transmission at skeletal muscles
- Action potential
- Ca2+ voltage-gated channel open -> Ca2+ into presynaptic neuron
- ACh released from vesicles in presynaptic neuron
- ACh binds ligand-gated cholinergic receptor (nicotinic in skeletal muscle)
- Na+ into cell
A. Minimal K+ out of cell
B. Xs ACh broken down by AChesterase - Depolarization of motor end plate
Motor units
Nerve + fibers it innervates
- Only in skeletal muscles
- Precision depends on #fibers/neuron
Spinal cord fxns
- Major reflex center and conduction pathway between body and brain
- Basic steps
A. Receives sensory info
B. Transmits info -> higher centers in brain or remains local (ascending tracts)
C. Receives signal (descending tracts) from higher centers
D. Transmits signal -> targets - Several reflexes mediated by spinal cord
Gray matter organization
Laminae I-X