Flashcards
Tendons & ligaments
Cards in this deck (52)
- 1Tendon functionsMuscle to bone
Transmits force with minimal elongation- allows muscle belly to be some distancee from site of action & eliminate need for unnecessary length of muscle between origin & insertion (high tensile strength)
-Allows muscle pull to be accurately focused
-Change direction of muscle pull
-Acts as spring- stores energy in locomotion
-Hold other tendons in position
-Will extend ~10% without injury
-Can partly injure & be okay because fascicle still intact - 2LigamentBone to bone
Supports joint - 3MeniscusShock absorber
- 4Articular cartilagepressure tolerant
- 5Connective tissue- what are the two cell types?1. Parenchymal cells- main function of tissue
2. Support cells- structural scaffolding
*Support cells and associated ECM (collagen, elastin, proteoglycans, glycoproteins) often termed connective tissue - 6What makes up the ECM?Glycoproteins (fibronectin), proteoglycans, collagen, elastin
- 7Fibrillar collagenType I, II, III, V, XI
Synthesised as procollagen- form quarter stagger arrangement
Provide mechanical support - 8Fibril- associated collagensLink fibrillar collagens to one another or to ECM components
- 9Transmembrane collagensAdhesion receptors
- 10Sheet forming and anchoring collagensForm 2D structure in basal laminae or connect basal laminae in skin to underlying connective tissue
- 11Structure of fibrillar collagen- Triple helix i.e. 3 polypeptide chains (~1000 AA) consisting of H bonds
-Assemble in array to form fibrils- quarter stagger arrangement (i.e. displaced by one quarter their length)
-Covalent cross links form between lysine & hydroxylysine side chains
-5 Molecules packed in pentafibril - 12Describe the structure of a tendonTropocollagen triple helix's pack together to form a fibril which group together to form a primary fibre --> secondary bundle (fascicle) --> tertiary bundle (secondary & tertiary surrounded by endotenon connective tissue layer) --> tendon (surrounded by epitenon & then paratenon (connective tissue layers)
- 13What components make up a tendon?-Fibroblasts/ tenocytes (elongated fibroblast cells)
-May have sheaths
-55% water
-Collagen (mainly type I)- provides tensile properties
-Elastin- store energy during movement
-Proteoglycans- bind water to resist compression & regulate collagen fibril size (during growth & development) - 14Histology of tendonCrimp pattern due to collagen fibre bundles
Elongated & flattened fibroblasts - 15What are fibroblasts?Cells that synthesise ECM & collagen
- 16Describe the enthesisWhere tendon inserts on bone
Bone--> mineralised fibrocartilage --> fibrocartilage --> tendon - 17Describe fibrocartilage at boney pulleys & the enthesis What is the main proteoglycan in fibrocartilage?Present where tendons & ligaments are subject to compression
-Has increased proteoglycan (aggregates) conc to prevent tendons splaying apart under compression
-Aggrecan - 18What are wrap around regions-Where tendons change direction by wrapping around bony pulleys
-Fibrocartilaginous - 19Describe the site of connection between the muscle & tendonmyotendinous junction
-Where force transmitted from muscle to tendon
-Where new sarcomeres added during muscle growth
-Splitting of muscle fibres
-Increased SA for anchorage
-Contributes to mechanical strength - 20Ligament functions-Bone to Bone
-Provides attachment for muscles
-Guy ropes- tie down other soft tissue to bone
-Sends signals to brain- proprioception & joint stability
-Form articular discs- shock absorbers
-Hold bone together- guide & limit joint movement
-Rich nerve supply- stretching activates muscle contraction- prevents over stretching
-Have pain fibres- stretching/ twisting is very painful - 21Structure of ligaments-Hypocellular with fibrocytes- cells primarily capsular (flat & broad)
-More cartilage
-Dense fibrous bundles of collagen fibres are spirally wound to resist internal & external rotation - 22Describe the biochemical composition of ligaments-90% type I collagen, 10% type III
-Elastin
-Proteoglycans
-Water - 23What is the difference between cruciate and collateral ligaments?-Cruciate- support, stabilisation (maintains geometry of joint throughout flexing procedure)
-Collateral- stops joint moving from side to side - 24Tendons & exerciseimmobilisation- decreased proteoglycan conc, decreased collagen fibril size= decreased mech strength
Exercise- increased collagen fibril size= increased strength - 25Where does injury of the tendon tend to occur?insertion into bone
- 26What happens to ligaments during exercise/ training?-Increased collagen
-Increased fibril no.
-Increased small fibril no. - 27What happens with a cruciate ligament tear?Bleeding into joint capsule (haemarthrosis) usually within 2h of injury --> swelling
e.g. ACL- poor repair capability
MCL better repairing (90% of injuries in sport due to MCL & ACL) - 28Structure of sarcomere-One unit of repeating pattern of actin & myosin
-Thick filament= myosin (A band)/ thin= actin (I band)
-Space between overlapping myosin & actin filaments are projections of two myosin heads which can form cross links- heads have binding sites for actin & ATP- contraction: cross bridges make contact with thin filaments- exert force on them which pulls them in towards sarcomere= shortening of skeletal muscle- overlapping filaments move past each other (no change in length of filaments just slide past each other) - 29Skeletal muscle contraction-Depolarisation of T tubules= [Ca2+] in SR rises- binds to sites on troponin= changes shape
-Tropomyosin dragged away from myosin binding site on actin
-Cross bridge formed between actin & myosin- actin & myosin move past eachother= muscle shortens
-ATP comes in and Ca2+ pumped into SR- Actin & myosin dissociate - 30Sources of ATP for muscle contraction1. Dephosphorylation of phosphocreatine
2. Oxidation of FFA (mainly in blood)
3. Aerobic metabolism of carbs (glucose)
4. Anaerobic metabolism of carbs (mainly muscle glycogen stores) - 31Muscle tensionForce exerted on an object by a contracting muscle
-Depends on amount of overlap between thick & thin filaments
-More stretched a muscle is= increased resting length (less overlap)= more myosin heads avaliable= muscle contracts with more force at this longer resting length
*However beyond certain point- force developed is less because myosin's & actins aren't touching anymore
(bell shaped curve) - 32Isometric contractionStatic
Constant length of muscle
Support load in constant position e.g. trying to lift an object that is too heavy to raise - 33Isotonic concentric contractionMuscle shortens whilst load on muscle remains constant
External force < force muscle generating - 34Isotonic eccentric contraction-muscle LENGTHENS whilst resisting external load
ie hamstring lengthens to lower thigh in flexion - 35Oxidative muscle fibresRed muscle fibres due to lots of myoglobin (increases diffusion capacity of o2 into muscles & small O2 store)
-Mitochondria for oxidative phosphorylation
-Surrounded by lots of blood vessels to transport O2 & nutrients - 36Glycolytic muscle fibresPale white fibres (little myoglobin)
Few mitochondria & vessels
Glycolytic enzymes & glycogen stores - 37Slow twitch muscle fibres type ILow myosin ATPase activity- use ATP slowly
-Oxidative fibres
-Very resistant to fatigue - 38Fast muscle twitch fibres Type IIaHigh ATPase activity
-Mitochondria for oxidative phosphorylation & glycolytic fibres & glycogen
-Resitant to fatigue - 39Fast muscle twitch fibres Type IIbglycolytic white fibres
High ATPase activity
Lots of glycogen stores & glycolytic enzymes
Fatigue very quickly - 40Effect of exercise on muscles-Low intensity, long duration= increase in mitochondria, increased capillaries surrounding muscle
-Short duration, high intensity- hypertrophy of glycolytic fibres and increased synthesis of glycolytic enzymes - 41Gradation of muscle contraction depends on1. Frequency at which motor units are activated
2. Number of motor units recruited - 42Order of recruitment of muscle fibres1. Slow oxidative (Small motor neurone generate AP first)
2. Fast oxidative (intermediate size)
3. Fast glycolytic (large size) - 43Muscle fatigueFailure to maintain the required force or power output
(electrical activity is norm at NMJ during fatigue- depends on muscle fibre composition, intensity & duration of activity & physical fitness) - 44Peripheral muscle fatigueBiochemical changes within muscle
e.g. contraction failure- APs failed to be conducted- Ca2+ not released from SR- lactic acid build-up - elevated H+ affects muscle proteins (ATP hydrolysis produces H+- build up of ADP & Pi in muscle)- cross bridge cycling inhibited - 45Central muscle fatigueFailure of cerebral cortex to send excitatory signals to motor neurons
Central governor theory- power output by muscles is continually adjusted in regard to calculations made by the brain in regard to a safe level of exertion - 46Muscle crampStrong muscular contractions in response to ischaemia/ metabolic disturbance- nerve APs fired at abnormally high rates
-Causes: electolyte imblance in ECF, decreased K+, Mg, Ca, absence of ATP (calcium can't be removed from system- actin & myosin link not broken)
-Over exercising, dehydration, tight clothing, lactic acid accumulation - 47Muscle strains & pullsTearing of one of muscle fibres due to overstretching/ stretching cold muscles etc
-Most occur at myotendinous junction
-Associated with explosive activities (sprinting) & eccentric contractions (more forceful due to elastic recoil)
-Associated with muscles with lots of fast twitch fibres - 48De Quervain syndromeRepetitive movement injury
Tenosynovitis of sheath surrounding two tendons controlling movement of the thumb - 49Fibrodysplasia ossificans progressiveMuscle turns into bone
Rare genetic (autosomal dominant) disorder- mutation in bone morphogenetic protein responsible for embryology of bone - 50EMG electromyographyNeedle like electrode into muscle- detects propagation of AP over that muscle fibre
-Can be used for diagnosis of NM disorders - 51Changes in EMG: Acute denervation (trauma)Nerve supply to muscle severed (paralysis)
-Individual muscle fibres become hyper excitable- discharge of APs spontaneous & irregular.
If nerve doesn't regenerate= denervation atrophy of muscle fibres, loss of excitability, loss of striations - 52Motor neuron diseaseProgressive degeneration of motor neurones
= fasciculations seen under the skin due to random discharge of motor units
= eventually motor units may fail altogether
-Some recovery possible is motor nerves that survive branch out to supply muscle fibres that lost supply
-Give rise to giant motor unit potentials in EMG
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- undergrad Medicine Flashcards on Tendons & ligaments, created by tanitia.dooley on 24/02/2015.
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