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Ortho > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the stages of intramembranous ossification?

A
  • ossification center appears in fibrous CT membrane
  • bone matrix is secreted w/in fibrous membrane
  • woven bone and periosteum form
  • bone collar of compact bone forms, and red marrow appears
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2
Q

Describe the first phase of intramembranous ossification?

A
  • an ossification center appears in fibrous CT membrane: selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an osssification center
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3
Q

Describe the 2nd phase of intramembranous ossification?

A
  • bone matrix (osteoid) is secreted w/in fibrous membrane:

osteoblasts begin to secrete osteoid which is mineralized w/in a few days, trapped osteoblasts become osteocytes

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4
Q

Describe the 3rd phase of intramembranous ossification?

A
  • woven bone and periosteum form:
    accumulating osteoid is laid down b/t embyronic blood vessels, which form a random network. The result is a network (instead of lamellae) of trabeculae, vascularized mesenchyme condenses on the external face of the woven bone and becomes the periosteum
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5
Q

Describe the 4th stage of intramembranous ossification?

A
  • bone collar of compact bone forms and red marrow appears:
    Trabeculae just deep to the periosteum thicken, forming a woven bone collar that is later replaced w/ mature lamellar bone, spongy bone, consisteing of distinct trabeculae, persists internally and its vascular tissue becomes red marrow.
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6
Q

When does endochondral ossification begin? Stages

A
  • begins in 2nd month of development, uses hyalien cartilage “bones” as models for bone construction
  • reqrs breakdown of hyaline cartilage prior to ossification

stages of endochondral ossification:

  • formation of bone collar
  • cavitation of hyaline cartilage
  • invasion of internal cavities by periosteal bud, and spongy bone formation
  • formation of medullary cavity, appearance of secondary ossification centers in the epiphyses
  • ossificaiton of epiphyses, w/ hyaline cartilage remaining only in epiphyseal plates
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7
Q

Describe postnatal bone growth?

A

in long bones:

  • cartilage on the side of epiphyseal plate closest to epiphyses is relatively inactive
  • cartilage abutting the shaft of the bone organizes into a pattern that allows fast, efficient growth
  • cells of epiphyseal plate proximal to resting cartilage form 3 fxnlly diff zones: growth, transformation, and osteogenic development
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8
Q

What are the fxnl zones in long bone growth?

A
  • growth zone: cartilage cells undergo mitosis, pushing epiphysis away from diaphysis
  • transformation zone: older cells enlarge, the matrix becomes calcified, cartilage cells die, and matrix begins to detiorate
  • osteogenic zone: new bone formation occurs
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9
Q

Remodeling of long bones?

A
  • growth in length: cartilage continually grows and is replaced by bone
  • remodeling: bone is resorbed and added by appositional growth
  • remodeling units: adjacent osteoblasts and osteoclasts deposit and resorb bone at periosteal and endosteal surfaces (this occurs throughout life, especially at stie of fractures)
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10
Q

Hormonal regulation of bone growth during youth?

A

during infancy and childhood, epiphyseal plate activity is stimulated by growth hormone

during puberty: testosterone and estrogens:

  • initially promote adolescent growth spurts
  • cause masculinization and feminization (hips) of specific parts of the skeleton
  • later induce epiphyseal plate closure, ending longitudinal bone growth
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11
Q

Where does bone deposition occur? What does this reqr?

A
  • occurs where bone is injured or added strength is needed
  • reqrs diet rich in protein, vit C, D, A, calcium, phosphorus, magnesium, and manganess
  • alkaline phosphatase is essential for mineralization of bone
  • sites of new matrix deposition are revealed by the:
    osteoid seam - unmineralized band of bone matrix
    calcification front - abrupt transition zone b/t the osteoid seam and the older mineralized bone
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12
Q

Describe bone resorption?

A
  • accomplished by osteoclasts
  • resorptin bays - grooves formed by osteoclasts as they break down bone matrix
  • resorption involves osteoclast secretion of:
    lysosomal enzymes that digest organic material, acids that convert Ca salts into soluble forms
  • dissolved matrix is transcytosed across the osteoclast’s cell where it is secreted into the interstitial fluid and then into the blood
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13
Q

Ca is necessary for what in the body?

A

in addition to healthy bone growth:

  • transmission of nerve impulses
  • muscle contraction
  • blood coagulation
  • secretion by glands and nerve cells
  • cell division
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14
Q

What are the 2 control loops that regulate bone remodeling?

A
  • hormonal mechanism maintains Ca homeostasis in the blood

- mechanical and gravitational forces acting on the skeleton

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15
Q

Hormonal mechanism of bone remodeling?

A
  • rising blood Ca levels trigger the thyroid to release calcitonin
  • calcitonin stimulates Ca salt deposit in the bone
  • falling blood Ca levels signal the parathyroid glands to release PTH
  • PTH signals osteoclasts to degrade bone matrix and release Ca into the blood
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16
Q

How do the bones respond to mechanical stress?

A
  • wolff’s law: a bone grows or remodels in response to forces or demands placed upon it
  • observations supporting wolff’s law include:
    long bones are thickest midway along shaft (where bending stress is greatest), curved bones are thickest where they are most likely to buckle
  • trabeculae form along lines of stress
  • large bony projections occur where heavy, active muscles attach (trochanter, tubercle)
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17
Q

How are bone fractures classified?

A

by:

  • position of bone ends after the fracture
  • completeness of the break
  • orientation of bone to long axis
  • whether or not the bone ends penetrate the skin
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18
Q

What is a nondisplaced fracture? Displaced?

A

nondisplaced- bone ends retain normal position

displaced: bone ends are out of normal alignment

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19
Q

What is a complete fracture? incomplete?

A
  • complete: bone is broken all the way through

- incomplete: bone isn’t broken all the way through

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20
Q

What is a linear fracture? Transverse?

A
  • linear: fracture is parallel to long axis of bone

- transverse: fracture is perpendicular to long axis of bone

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21
Q

What is a compound and simple fracture?

A
  • compound: (open) bone ends penetrate the skin

- simple: (closed) bone ends don’t penetrate the skin

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22
Q

What is a comminuted fracture? Spiral?

A
  • comminuted: bone fragments into 3 or more pieces, common in the elderly
  • spiral: ragged break when bone is excessively twisted, common sports injury, if seen in kids: think abuse
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23
Q

What is a depressed fracture? Compression?

A
  • depressed: broken bone pressed inward, typically skull fracture
  • compression: bone is crushed, common in porous bones (spinal fractures - osteoporosis )
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24
Q

What is an epiphyseal fracture? Greenstick?

A
  • epiphyseal: epiphysis separates from diaphysis along epiphyseal line; occurs where cartilage cells are dying
  • greenstick: incomplete fracture where one side of bone breaks and the other side bends, common in kids
25
Q

Stages of healing of a bone fracture?

A
  1. hematoma formation
  2. fibrocartilaginous callus formation
  3. bony callus formation
  4. bone remodeling
26
Q

Describe hematoma formation of healing of a bone fracture?

A
  • torn blood vessels hemorrhage
  • mass of clotted blood (hematoma) forms at fracture site
  • site becomes swollen, painful and inflammed
27
Q

Describe fibrocartilaginous callus formation of healing of a bone fracture?

A
  • fibrocartilaginous callus forms when:
  • osteoblasts and fibroblasts migrate to the fracture and begin reconstructing the bone, fibroblasts secrete collagen fibers that connect broken bone ends, osteoblasts begin forming spongy bone
  • osteoblasts furthest from capillaries secrete an externally bulging cartilaginous matrix that later calcifies
  • after fibrocartilaginous callus forms granulation tissue (soft callus) forms a few days after fracture
  • capillaries grow into tissue and phagocytic cells begin cleaning debris
28
Q

Describe bony callus formation of healing of a bone fracture?

A
  • new bone trabecular appear in fibrocartilaginous callus
  • and this converts into a bony hard callus
  • bone callus begins 3-4 wks after injury, and continues until firm union is formed 2-3 months later
29
Q

Describe bone remodeling of healing bone fracture?

A
  • excess material on bone shaft exterior and in the medullary canal is removed
  • compact bone is laid down to reconstruct shaft walls
30
Q

What is osteomalacia? Signs?

A
  • aka rickets
  • bones are inadequately mineralized causing softened, weakened deformed bones
  • main sx is pain when wt is put on affected bone
  • caused by insufficient Ca in the diet, or by vitamin D deficiency
  • signs of rickets:
    soft spot on baby’s head slow to close, bony necklace (ribs), curved bones, big lumpy jts, bowed legs
31
Q

What is osteoporosis?

A
  • group of diseases in which bone resorption outpaces bone deposit
  • spongy bone of spine is most vulnerable
  • occurs most often in postmenopausal women
  • bones become so fragile that sneezing or stepping off curb can cause fractures
32
Q

Tx of osteoporosis?

A
  • Ca and Vit D supplements
  • increased wt bearing exercise
  • hormone (estrogen) replacement therapy (HRT) slows bone loss
  • natural progesterone cream prompts new bone growth
  • statins increase bone mineral density
33
Q

What is Paget’s disease?

A
  • characterized by excessive bone formation and breakdown
  • pagetic bone w/ an excessively high ratio of woven to compact bone is formed
  • usually localized in spine, pelvis, femur and skull
  • unknown cause (possibly viral)
  • pagetic bone, along w/ reduced mineralization, causes spotty weakening of bone
  • osteoclast activity wanes, but osteoblast activity continues to work
  • may develop arthritis and deafness
  • tx: bisphosphonates (fosamax), didronate, calcitonin
34
Q

Development of bones (from fetus - old age)?

A
  • mesoderm gives rise to embryonic mesenchymal cells, which produce membranes and cartilages that form embryonic skeleton
  • the embryonic skeleton ossifies in a predictable timetable that allows fetal age to be easily determined by sonograms
  • at birth most long bones are well ossified (except for epiphyses)
  • by 25: nearly all bones are completely ossified
  • old age: bone resorption predominates
  • a single gene that codes for Vit D docking determines both tendency to accumulate bone mass early in life, and the risk for osteoporosis later in life
35
Q

Fxn of tendons and ligmanents?

A
  • ligaments: connect bone to bone, provide stability and limit motion in a jt
  • tendons: connect muscle to bone, allows for motion at a jt
  • comprised of parallel collagen fibers
36
Q

Tenditis and tendon ruptures tx?

A
  • overuse injuries: usually respond to rest

- if acute: may need surgery

37
Q

Tx of strains, sprains, and tears?

A
  • partial injuries will heal if protected

- complete injuries often need surgical repair

38
Q

What is bursitis? diff types?

A
  • inflammation from overuse
  • deep: greater trochanteric and rotator cuff
  • superficial: olecranon and pre-patellar
39
Q

Comparison of skeletal, cardiac and smooth muscle cells?

A
  • skeletal:
    elongated cell, mult peripheral nuclei, visible striations, voluntary
  • cardiac:
    branching cell, single central nucleus, visible striations, involuntary
  • smooth:
    spindle-shaped cell, single central nucleus, lack visible striations, involuntary
40
Q

Main fxns of skeletal muscle?

A
  1. movement of bones or fluids
  2. maintaining posture and body position
  3. stabilizing jts
  4. heat generation (shivering)
41
Q

Make up of skeletal muscle?

A
  • each muscle is served by one artery, nerve, and one or more veins
    CT sheaths of skeletal muscle:
  • epimysium: dense regulat CT surrounding entire muscle
  • perimysium: fibrous CT surrounding fascicles (groups of muscle fibers)
  • endomysium: fine areolar CT surrounding each muscle fiber
42
Q

What is the microscopic anatomy of a skeletal muscle fiber?

A
  • cylindrical cell 10-100
  • multiple peripheral nuclei
  • many mitochondria
  • glycosomes
  • contain myofibrils, sarcoplasmic reticulum and T tubules
43
Q

What are myofibrils? components?

A
  • densely packed, rodlike elements
  • 80% of cell volume
  • exhibit striations: dark A bands and light I bands
44
Q

What is a sarcomere?

A
  • smallest contractile unit (fxnl unit) of a muscle fiber
  • region of myofibril b/t 2 successive Z discs
  • composed of thick and thin myofilaments made of contractile proteins
  • optimal sarcomere operating length is (80-120% of resting length)
45
Q

What are the components of a sarcomere?

A
  • thick filaments: run the entire length of an A band
  • thin filaments: run length of I band and partway into A band
  • z disc: coin shaped sheet of proteins that anchors the thin filaments and connects myofibrils to one another
  • H zone: lighter midregion where filaments don’t overlap
  • M line: line of protein mymesin that hold adjacent thick filaments together
  • the fundamental until which allow contraction of muscle to take place
  • z discs are pulled toward each other
46
Q

Structure of thick and thin filament?

A
  • think filament:
    myosin tails, myosin heads
  • thin filament:
    G actin bears active sites for myosin head attachment during contraction, tropomyosin and troponin: regulatory proteins bound to actin
47
Q

What is the sarcoplasmic reticulum?

A
  • network of smooth endoplasmic reticulum
  • pairs of terminal cisternae form perpendicular cross channels
  • fxns in regulation of intracellular Ca levels
48
Q

What are the T tubules?

A
  • continuous w/ sarcolemma
  • penetrate the cell’s interior at each A band-I band jxn
  • paired terminal cisternae to form triads that encircle each sarcomere
49
Q

SLiding filament model of contraction?

A
  • in relaxed state, thin and thick filaments overlap only slightly
  • during contraction, myosin heads bind to actin, detach, and bind again, to propel the thin filaments towards the M line
  • as H zones shorten and disappear, sarcomeres shorten, and whole muscle shortens
50
Q

What are the requirements for skeletal muscle contraction?

A
  1. activation: neural stimulation at neuromuscular jxn

2. excitation-contraction coupling: generation and propagation of an action potential along sarcolemma

51
Q

Where is the neuromuscular jxn?

A
  • situated midway along length of muscle fiber
  • synaptic cleft
  • synaptic vesicles of axon terminal contain the neurotransmitter ACh
  • junctional folds of sarcolemma contain ACh receptors
52
Q

What happens at the neuromuscular junction?

A
  • skeletal muscles are stimulated by somatic motor neurons
  • axons of motor neurons travel from CNS via nerves to skeletal muscles
  • each axon forms several branches as it enters a muscle
  • each axon ending forms a neuromuscular junction w/ a single muscle fiber
  • nerve impulse arrives at axon terminal
  • ACh released (binds w/ receptors)
  • generation of AP
53
Q

Summary of events of an action potential?

A
  1. AP arrives at axon terminal of motor neuron
  2. voltage gated Ca channels open and Ca enters the axon terminal
  3. Ca entry causes some synaptic vesicles to release their contents (ACh) by exocytosis
  4. ACh diffuses across the synaptic cleft and binds to receptors in the sarcolemma
  5. ACh binding opens ion channels that allow simultaneous passage of Na into the muscle fiber and K out of muscle fiber
  6. ACh effects are terminated by its enzymatic breakdown in the synaptic cleft by acetylcholinesterase
54
Q

Where does Myasthenia gravis interupt the pathway of muscle contraction?

A
  • doesn’t allow ACh to bind to AChR so ion channel isn’t opened so muscle fibers don’t depolarize and there is no muscle contraction
55
Q

Where do neuromuscular blocekers interupt the pathway of muscle contraction?

A
  • also doesn’t allow ACh to bind to AChR so ion channel isn’t opened
56
Q

Where does botulinum toxin interupt muscle contraction pathway?

A
  • prevents Ca influx (no release of ACh)
57
Q

Where does MS interupt muscle contraction pathway?

A
  • in beginning: no action potential at nerve terminal
58
Q

What is summation and tetanus?

A
  • summation: rapid sequence of stimuli: muscle twitches fuse into each other, each subsequent one being stronger than its precedent (due to Ca++_
  • tetanus: very rapid sequence of stimuli: no relaxation
59
Q

Components of muscle fiber?

A
  • sarcolemma: muscle cell membrane
  • sarcoplasma: muscle cells cytoplasm
  • motor end plate: contact surface w/ axon terminal
  • T tubule: cell membrane extension into sarcoplasm (to reach myofibrils)
  • cisternae: areas of ER dedicated to Ca++ storage
  • myofibrils: organized into sarcomeres

Ortho (24 decks)

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