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62 Cards in this Set
- Front
- Back
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Epimysium
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coats entire muscle
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Perimysium
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coats separate sections of muscle fibers
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Endomysium
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coats single muscle fibers
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A Band
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Myosin
never changes sides |
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Distance of sarcomere
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from z band to z band
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T tubules
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extracellular extensions into the muscle to pass calcium deep into the muscle to have a fast and more even muscle contraction
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motor unit
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a single motor axon and all the muscle fibers they innervate
all contract in unison when axon fires all fibers attached to a single axon will be the same type of fiber |
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3 components of the thin filament
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Actin
Tropomyosin Troponin |
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Troponin I
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part that binds to the actin and blocks where myosin wants to bind
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Troponin C
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binds with calcium when it enters and activates troponin to move the tropomyosin
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Troponin T
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grabs tropomyosin when activated by calcium
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describe the cycle of a muscle contraction
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1. A myosin head attaches to actin filament and causes a phosphate to release
2. the release of a phosphate triggers the myosin head to move and "flick" this releases ADP in the process 3. ATP binds to myosin head to cause release from actin 4. as ATP is hydrolyzed the head repositions. then ADP and phoshate remain with myosin head |
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DHP receptor
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Voltage dependent calcium channel in muscle cells that near the T tubles and opens when sodium has depoalized the muscle cell
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Ryanodine receptor
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calicum induced calcium channels on the SR that pen once the DHP receptors have introduced calcium into the muscle cell
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Slow oxidative muscle fibers
type I |
slow with contraction
high fatigue resistance high mitochondria content and oxidation lots of capillaries high myoglobin red in color small fibers |
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What color are slow oxidative muscle fibers
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red
because of the high myoglobin |
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Fast Glycolytic muscle fibers
type II |
large white fibers
fast in conduction fatigue easy high anarobic enzyme content low mitochindia and little capillaries high glycogen- energy for the fiber low myoglibin |
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what is the fiber distrubution like in normal muscle?
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its like a mosiac and a distrbutionof both types of fibers that are intermingled
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Describe muscle fibers after reinnervation
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when the axons are cut in denervation they no longer link to the fibers, the surrouding axons will reach out and link to it neighbors and they will become the type of muscle fiber that is linkd to that axon. the motor units will be fewwer so they willll become larger and the distrbution will be clusters or clumps or type 1 or type 2
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satellite cells
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respond to muscle injury and provide additional nuclei for the hypertrophied muscle
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Diaphysis
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neck/ middle of the bone
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Epiphysis
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head of bone
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what type of collagen is mostly in bone?
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90% type 1 collagen
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What type of collagen is cartilage?
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mostly type II
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dislocation
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detachment of bone from joint
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subluxation
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partial loss of connection of bone to joint
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Sprain
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tear in ligament
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Strain
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damage to tendon or muscle
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Avulsion
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complete seperation of ligament or tendon from the bone
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which is worst Compartment syndrome or crush syndrome?
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Chrush syndrome
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Crush syndrome
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myoglobinemia- renal failure
ECF shift Acisdosis and hyperkalemia shock Cardaic dysrhythmia |
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Compartment syndrome
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Edema within compartment
rising pressuer muscle ischemia and neural injury form compartment tamponade muscle infarction---> lead to crush syndrome and rhabodo |
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causes of Rhabdomyolysis/ myoglobinuria
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Crush injury/ crush syndrome
compartment syndrome maglinant hypothermia infection herbal medicines snake bite cocaine cowfish hypernatremia fire ants viral infection immobility |
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osteomalacia
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metabolic diasease from inadequate and delayed mineralization of osteoid
vid D deficiency ricketts in kids |
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Osteosarcoma
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maglignant tumor forund in bone marrow
has a moth eaten pattern of bone destruction |
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Osteoporosis
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rate of bone resorption greatly esceeds that of bone formation
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Pagets disease
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excessive resorption of bone due to gentic mutations invloving RANK pathways
excess breaking down and rebuilt at a excellerated rate common in people over 40 1-5% of people over 40 biphosphate is the treatment |
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Duchenne muscular dystrophy
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most common form of MD
x-linked caused by a DNA deletion defect in dystrophin tension on sarcolemma and micro tears are not fixed properly bc of protein defect fat and connective tissue replace muscel tissue in late stage |
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Hystology slide of DMD
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micro fibers thruout
abnormla size fibers- some small some large lack of dystrophin |
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Gower sign
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walk backwards from a crotch postion to a standing postion
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3 diagonstics needs to confirm DMD
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Muscle cell biopsy- degeneration of fibers, and fat and connective tissue
CPK level 10x greater then normal EMG |
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Myasthenia Gravis
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auto immune disease wheere antibodies attack ACH receptors at neuromuscluar junction
abnormal Tcell activity? usually will see muscles of eyes effects first life threating with effect respirtory muscles worse thruut day with escess use of muscles |
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MG treatment
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often a thymectomy to remove thymus
ACHase inhibitors to keep ACH in junction as long as possible |
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Myasthenic syndrome
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produces similar symptoms but antibodies attach different receptors
attact voltagated gated calcium channels in Lambert-Eaton syndrome |
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what does c. botulinum do to the NM junction
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causes botulism and prevent the release of ACH from viscles
half life 1 month |
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What doest C. Tetani do tot he NM junction?
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cause tetnus
escessive release of ACH into the junction causes over stimunlain of muscles and you get lock jaw |
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Osteoporosis
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loss of spongy and compact bone
women more than men leads to compression fractures |
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why does menopause affect osteoporosis
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decrease in estrogen- estrogen increases OPG activity with counteracts RANKL and stops osteoclasts
increases expression of RANKL and RANK increased osteoclast activity |
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what from aging affects osteoporosis
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decrease replicative activity of osteoprogentior cells
decrease ins osteoblasts lack of physical activity lack of groth factors |
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osteomyelitis
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infection of bone
steps leukocytes enter release lytic enzymes pus spreads and impairs blood flow--> forms sequestra then the involucrum is formed over top |
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sequestration
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the capsulse of dead infected bone in osteomylitis
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involucrum
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new bone that is formed over the sequestration in osteomyelitis
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endogenous osteomyelitis
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infection from within the body
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Exogenous osteomyelitis
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infection introduced from outside the body
after hip surgery, bone break, ect |
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osteoarthritis
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wear and tear
cartilage thins leading to bone to bone contact nodes at joints no ankylosis worst at night after working joints all day |
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Rheumatoid arthritis
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autoimmune disease that destryos the synovial joints (rheumatiod factor)
more inflammatory will have ulnar deflection- fingers and tow with invert out from damage joints worst in morning |
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Gout
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excess purine and uric acid in body
big toe urate crystals can not be broken down by macrohage and end up rupturing the macrohage which causes a imflammatory reaction |
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tophus
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gouty crystals
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Synovitis
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infection of the joint
rare infection to get but difficult to treat becaus there is no blood flow to the synovial capsule |
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talipes equinovarus
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twisted feet bc lack of room in uterois
normally with straghten out with, may need brace, worst cases may need surgery |
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osteogenesis imperfecta
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lack of type one collagen leads to weakness with tensoin, sitll stong uner compression but will snap with any turn or twist
place rods that extend as they grow pt will have blue sclera |
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rickets
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lack of vit d
strong bones with tension weak under comrpession so they bow, dont break bc very elastic wide hips from outward femors |
