MUSCULATORY SYSTEM.pdf

 MUSCULATORY SYSTEM E 650 Skeletal Muscle in the human body TYPES OF MUSCLE TISSUE Smooth Muscle non-stricted and · involuntary Involuntary...

 MUSCULATORY SYSTEM E 650 Skeletal Muscle in the human body TYPES OF MUSCLE TISSUE Smooth Muscle non-stricted and · involuntary Involuntary - contract who conscious control Autonomic Nervous System control this Muscles spindle shape · voluntary - Muscles that contract a relax under conscious control Attached to Bone I regulates movements Mitosis · happened here (but limited) Skeletal Muscle Attached · in Bone · Nucleus is located at the periphery · A single muscle Fiber - Multinucleated contains multiple nucleus - cannotmultiply cannotundergo Mitosis - Stricted and · Voluntary Cardiac Muscle Stricted and Involuntary · - => - I Branches serves to communicate to other · Hx:Branches cardiac muscle cell simultaneously Borders OfBranches INTERCALATED DISCS point - OF - * ↳ connections ofcardiac muscle has desmosomes, gap junctions - cell junctions CONNECTIVE TISSUE LAYER OF MUSCLE MICROSCOP MACROSCOPIC to Epimysium - outermost; covers muscle belly ⑧ Perimysium - middle layer; covers fasicle ⑧ Endomysium - innermost; covers muscle cells or muscle fiber Ex: BICEPS - 2 belly Epimperium Belperingin - Musche - Fasicle MUSCLE BELLY covered by EPIMYSIUM FASICLE made up of (strands;"hair strand-like"Kapag naghihimayng meat) C - is covered by PERIMYSIUM SARCOLEMMA FASICLE I madeubFier SARCOPLASMIC RETICULUM covereau F -I ENDOMYSIUM - MUSCLE CELL/FIBER Muscle Bell-Epimysium /Fasicle perimysium - made up ofMYOFIBRILS I Muscle Cell Fiber Endomysium MYEEMENTS - RED LMyFibrils BLUE ↳Red) madea tents Troponin,too pomyosin THIN FILAMENTS protein Actin - · ① Thin Filament - Actin smallest I mostn umerous 8 Thick FilamentM yosin I read protein in our Muscles (tail -new "golfclub " Golf Club" · THICKFILAMENTS - protein Myosin has tail head 0 - MUSCLE HISTOLOGY ⑧ Myofibril I MYREEMENTS RED BLUE THIN FILAMENTS protein Actin - smallest I mostn umerous protein in our Muscles "golfclub " THICKFILAMENTS - protein Myosin has tail head ⑧ Sarcolemma - Cell membrane/Plasma Membrane ofthe Muscle · Transverse tubules or tubules perpendicular - sarcolemma Sarcoplasmic Reticulum r ⑧ - - Endoplasmic Storage For CAICIUM reticulum ofmuscle - most Fiber imp.ION for contraction ofMuscle Primary site ofCatin Body:BONE M castin cell S.R. site of Primary = Terminal Cisters - DILATED END saCSER · Sarcoplasm cytoplasm ofa muscle Fiber (muscle cell) GLYCOGEN- stored chains ofglucose Mainly stored in LIVER; Skeletal muscle Clb consumed win 24 his MYOGLOBIN-protein that binds oxygen in Muscle - in muscle muscle causes red color of · IT myoglobin ·TITIN largest protein in the body; - Found in muscle zdis-Myofibril - segments ,arcomere 3 5sarwomenene -  ④ Sarcomere M-LINE I - Functional/contractive unit of muscle; O 0 - From I discs to another 7-disc (2-line) 0 0 2 discs - separates one sarcomere to another SARCOMERE - attachment site for thin filaments - e A zone - contains thick but no thin filaments M line - passes in the middle ofAzone attachment For THICK FILAMENTS Thick 1 Thin Filaments #band-aka "dark band" S appearance in electron microscope "light band Il Eband-aka Thin Filaments ON! Alternate and dark bands creates tions light BOTH IN ACTIN: ⑧ Tropomyosin - e - Blocks the Myosin-binding sites in Actin (Relax muscle) ⑧ Troponin gre Holds the tropomyosin in place; H-zone binding the site for Ca ions to allow movement of tropomyosin  PRINCIPLES OF NERVE CONDUCTION CELL BODY AXON AXON TERMINAL at ⑦ - cation 1. 8 - Anion Pewr, I 8 8 - - Nat most numerous cation in k mostnumerous cation in I.F E.F. 0 - Anion chlorine, phosphate, etc. NEURON iiiiiiiiii T EXTRACELLULAR & FLUIDS ·8 W C · - C C C, w I - CNS - / Polarized state of Neuron =- 70m difference called Resting Potential During Resting state (constant) Membrane ↳ Difference of charges OFECF A ICF Intracellular Fluid is ALWAYS MORE - 70 to Extracellular F. There is a 70m difference between the Extracellular Fluid - Intra cellular fluid exiiiiiiiii iiiiiiiiiiiiiiiiiiiiii EXTRACELLULAR iii itawareaadka 0 v H - Mechanically Gated Nat channel G need no mechanical stimulus open to C, of:touch, pressure, pain I andGenesee EXTRACELLULAR EXTRACELLULAR mini : FLUIDS... FLUIDS o W - # ① once may mechanical stimulus - mag-open Mechanical Gated Nat channel ② Process OF DIFFUSION (T concentration to concentration - Nat from ECF will enter ICF ③ As Nat From ECF enter cell, Nat carries & voltage the 70m in ICF will become more I positive (69,48,etc.) QRIZATION: process where Nat enter call - - naging more O cell  & Nat that carries & carries electrical potential into the cell->-55mv called Nerve threshold -- Once this threshold is meet - voltage-gated Nat channel will open Bakit need bumukas ng Voltage - Gated channel? ximumsi W Ift he stimulus is weak I did not meet the -55mv, voltage gated channel will not open and the signal will not be.. pass to other segment ng axon and diadbotsa CNS-7 C - tusok' pain- therefore NO PERCEPTION. ⑧onvragecutedvanopenamoreatwinterthethechargeoralwinds to (masma-depolarized) +30m-peak electrical called ACTION POTENTIAL ASOM - a will create discharge more a very strong imumis sens FLUIDS tusok' pain- * A After ma-pass yung signal sa other segment ofA xon, Mechanically gated & Voltage gated Nat channel closed. ⑦ After Action Potential, the charge is Neuron after working wants to be at its Resting state Voltage-gated opened, itfrom ICFwill move out. Dahil sobrang na ni ICF lalabas si ktsa V-GKT channel to maintain O sa ICF From DICFwill become more O-called REPOLARIZATION (0 state) State will be O viiiiiiiii FLUIDS 0 ⑧ v kt cell, sometimes theres too much itare As moves outfrom the coming out. ~ mannes putation (instead of to mar REPOLARIZATION PROCESS also cared HYPERPOLARIZATION (sobrang Polarized) ⑨ After ECFaura,Polaria to estateamis the repolarization process, All the channel were closed BUT IS NOT O N ITS RESTINGMEMBRANE POTENTIAL bos more Nat in ICF a more kt in iii. ⑱ FLUIDS SODIUM-POTASSIUM PUMP-restores the Resting Membrane Potential 1. -repositions the Nat 1kt its ↳ on original places Pumps Nat Out of the cell Ramps toone cell Earlie 0 8 NOTE:For every 2kt that goes INSIDE theres 3 Nat that ques OUT 2 3 (2 Piso 3 candy) BOARDS Nakpump From the inside to outside Na yung pinump->palabas sancy:a After Nat K+ Pump the cell will restore it's RESTING STATE :  SKELETAL MUSCLE muscle under voluntary control Mu,netin * RPM OF SKELETAL 1 CARDIAC=-90mV they fire action towards potential RMP OF NEURONS: -70mV muscle THRESHOLD=-55 mV Peak V=130mV (action potential) Sliding filament mechanism: - “Theory of muscle contraction” - myosin heads “walk” along thin filaments, - pulling the THIN filaments towards the M line; discs come closer -I- Pre-Contraction Phase: Sarcolemma (cell membrane M uscle) of Receptors in Memberhere RMP OF NEURONS: -70mV "a" voltage-gated cat channel in e easi) iii. Ach Ach - RPM OF SKELETAL 1 CARDIAC=-90mV Ach Ach THRESHOLD=-55 mV Peak V=130mV (action potential) NICOTINIC RECEPTOR I L receptor in sarcolema Iligand-gated Nat channels) Axon Terminals synaptic Cleft-space in the synapse SNAPSE area where neurons NEUROTRANSMITTERS 4 other cells communicates chemical messenger Neuromuscular junction molecules used by neurons synapse specific to Neurons & Muscle - communicate to w/ other cells/tissues Found w/in Axon terminals Action potential from nerve fiber stimulates v-G cat channels to OPEN (need voltage to open the V-G ca channel Kaya need Action Potential) Cat will enter the Axon terminal that will result to the mon't ofNeurotransmitter towards synaptic cleft-CALCIUM INFLUX Calcium Influx releases Ach in Neuromuscular Junction Ach will bind to Achreceptors (Nicotinic receptors) and it will OPEN After opening Nicotinic receptors, Nat will enter of Muscle RPM-90 mV will be more -->DEPOLARIZATION When threshold is reached, Voltage - Gated Channels will open--more Nat will enter Nat enters, creating strong Electrical Charge:+30mV (action potentiall It was not Action Potential will flow to Sarcolemma - and Flow to t-tubules Relationship ofI-tubules / Sarcoplasmic Reticulum: As Action potential travels down along the i-tubules, the electricity carries by 5-Tubules will stimulate the Sarcoplasmic Reticulum to release the stored cat in the Sarcoplasm coupen) Whatis the stimulus for the Sancoplasmic Reticulum to release cat?MUSCLE ACTION POTENTIAL BOARDS The released Catw ill binds to troponin-> Troponin blocking the Myosin head moves Tropomyosin away from ------- - BOARDS Contraction Cycle: Important Regulator of Muscle contraction?(ALCIUM Myosin head will attach to Actin- *Dross-Bridging" who are the regulatory activ Myosin proteins for muscular Troponin contraction? Trupomyosin Callow muscle contraction) t ATP in the myosin head is broken down by ATPase (enzyme) into ADP#P To breakdown ATP:ATPase 1 H2O Phosphate will be released producing high amounts ofenergy Need ma-breakdown ng ATP to extract energy Once the energy is extracted, energy will be passed to Myosin head power stroke occurs - Actin moves towards Mline;I discs moves towards each other--Sareomere shortens  Detachment ofMyosin from Actin occurs when ATP binds Myosin head again to Whatw ill make Myosin detach from actin?When another ATP binds into Myosin head BOARDS As long as there are High amounts ofCat and ATP available in the sarcoplasm -> Contraction cycle continues Cholding contraction -> CNS tuloytuloy lang and Action Ach--repeatedly bind to Nicotinicr. potential & release of --Depolarization) Ca+ Active Transport Pumps pumps in the Sarcoplasmic Reticulum (Binabalik Moves Cat back to Sarcoplasmic Reticulum when muscle is relaxed calcium is inside the Sarcoplasmic Reticulum. · continuously happening · During contraction, catrelease is Higher than cat returning SR Breaking Down of Acetylcholine CRUMPS - prob m/ electrolytes Acetylcholinesterase breaks down Ach after itbinds to Nicotinic Receptors Ift he signals from the CNs stopped, there should be NO Ach left in synaptic cleft. WHY? Because ift here is no Action Potential 1 Ach is still 8 the synaptic cleft--it may reactivate continuously the Nicotinic receptors ->INVOLUNTART movement REMEMBER: PATHOLOGY BOARDS A. Rigor mortis CAUSE: enzymes breaks S.R. leakage ofCat ① I Cat - phenomenon seen in dead body in the cytoplasm & LOSS OFATP muscle contracts - Muscles are in state of RIGIDITY due to CROSS BIDGING B. Botulinum toxin (Botox) From microorganism:Clostridium botulinum Grant spore Forming Bacteria - Prevents release of Ach in the neuromuscular junction (NMJ) may barrier - Results in Muscle Paralysis (Muscle Relaxation) C. Curare - Poisonous plant - Block Ach Receptors - Results in Muscle Paralysis (Muscle Relaxation) Example of Drugs:curonium suffix Non-Depolarizing Neuromuscular Tubocurare Pancuronium lethal injection (death sentence) (paralyzed) 3 - common component reversal agent:Neostigmine Mivacuronium - (Mivacure( Pyridostigmine D. Succinylcholine aka suxamethonium For laryngospasm - - Binds to Ach receptors - Results in Muscle Paralysis (Muscle Relaxation) Depolarizing Neuromuscular classification:Ach Antagonist NicotinicAgonist Skeletal Muscle Fibers (Types) Slow Oxidative Fibers - aka “Red muscle fibers” (red meat) TMyoglobin Capillaries - slow twitch, fatigue-resistant fibers only produce weak contraction;mabagal map god a - contains many large mitochondria - Generates ATP mainly by oxidative I can produce huge amount ofATP mechanisms USED TO:Maintain posture and endurance BOARDS Whata re the 2 color of the muscle? Fast Oxidative-Glycolytic Fibers REDI WHITE - intermediate Fast Glycolytic Fibers - aka “White muscle fibers” (white meat) Myoglobin (protein ↓ in muscle) - fast twitch fibers that fatigue quickly - generates ATP mainly by glycolysis ATP of Muscle cardiac depends on AEROBICRESPIRATION Cardiac Muscle Intercalated discs - connect ends of cardiac muscle to one another - contains desmosomes and gap junctions Smooth Muscle Tissue - Spindle shape - Irregularly arranged thin and thick filaments - Calmodulin - binding of Ca+ (Tropinin in Skeletal and Cardiac m.) - Myosin Light Chain Kinase - blocks Myosin from binding to actin (Tropomyosin in Skeletal and Cardiac m.) Muscle Groups Scalp Muscles (CN VII) MOTOR A. Occipitofrontalis > occipitalis - moves scalp posteriorly > Frontalis - moves scalp anteriorly; raises eyebrow; SURPRISE! B. Galea Aponeurotica - aponeurosis in the head; connects Occipitalis and Frontalis Mouth Muscle (CN VII) 10 Muscle of Facial Expressions A. Orbicularis oris - closes lips; kissing; pouting (major) B. Zygomaticus major - elevates upper lip C. Zygomaticus minor - elevates upper lip D. Levator anguli oris - “caninus muscle” Elevates angle of the Elevates the upper lip mouth 223 E. Levator labii superioris ala que nasi - elevates upper lip; ILSAQN longest name F. Levator labii superioris - elevates upper lip G. Depressor labii inferioris - depresses lower lip Depresses lower lip H. Depressor anguli oris - depresses angle of the mouth I. Buccinator - presses cheeks, whistling, blowing, sucking, Tissue in Frankel Functional Appliance kissing (major) Trumpeter's Muscle Orbicularis Oris Buccinator - keeps food away from vestibular area J. Risorius - moves angle of mouth laterally; fake or sardonic smile K. Mentalis - protrudes lower lip; causes wrinkling of skin; pouting Neck Muscle (CN VII) Platysma - depresses lower lip and mandible; GRIMACE (major) Orbit and Eyebrow Muscles (CN VII) q A. Orbicularis oculi - closes eye B. Corrugator supercilii - moves eyebrow inferiorly; wrinkles forehead; FROWNING Extrinsic Muscles of the Eye (SO4 LR6 R3) IO, LPS A. Superior oblique - moves eyeballs INFERIORLY and LATERALLY B. Lateral rectus - moves eyeballs LATERALLY C. Superior rectus - moves eyeballs SUPERIORLY D. Inferior rectus - moves eyeballs INFERIORLY E. Medial rectus - moves eyeballs MEDIALLY F. Inferior oblique - moves eyeballs SUPERIORLY and LATERALLY G. Levator palpebrae superioris - elevates EYELIDS OPEN EYES Ni-1. *  Muscles of Mastication (CN V3) TIME! Temporalis (Fan shape) O: Temporal bone * I: Coronoid process and Ramus (lateral side) C A: Anterior fibers: elevates mandible L Posterior fibers: retrude mandible 0 Internal Pterygoid (aka Medial Pterygoid) Muscle S O: Medial surface of the lateral pterygoid plate of sphenoid bone E I: Angle and Ramus (medial side) A: elevates mandible; side to side Masseter strongest Muscle ofMastication O: Maxilla and Zygomatic arch I: Angle and Ramus (lateral side) A: elevates mandible OPEN External Pterygoid (aka Lateral Pterygoid) Muscle O: Lateral surface of the lateral pterygoid plate of sphenoid bone I: Condyle/TMJ A: Protrudes mandible; Depresses mandible; moves mandible SIDE TO SIDE MATOR REMEMBER: A. What is the major muscle for mouth OPENING? ANTERIOR BELLY OF DIGASTRIC MUSCLE (CN V3) B. What innervates posterior belly of digastric muscle? CN VII elevates hyoid Temporalis Masseter Medial pterygoid 6/14/22 SIDE NOTES: Extrinsic Tongue Muscle TONGUE:MOTOR: CNXl1 4 PHARYNGEALPLEXYS IX9X Word before glossus' thats the origin I Genioglossus 0:Genial Tubercle 1:Tongue A:moves tongue inferiorly anteriorly (towards opposite sidel - superiorly posteriorly process T (opposite and 0: I:Tongue A:moves xT Genioglossus I styloglossus Styloid - tongue a CN PS stylogloss us) Ayoglossus 0:Hyoid 1:Tongue A:moves d tongue inferiorly - 0:Palate 1: (NIX, I Palatoglossus Tongue A:moves tongue superiorly towards palate I palate inferiorly towards tongue palate towards - moves - tongue Ytowards Palate REMEMBER: Pharyngeal S Extrinsic muscles: ↳) nerve network of O: first word before glossus ① CNIX, X I: Tongue Action: MOVES the tongue ⑫X, X1 Intrinsic Tongue Muscles (VITS) shapes the tongue vertical - Flattens/ broadens tongue - Inferior Longitudinal - shortens a thickens tongue CNXII - Transverse - elongates and narrows tongue Superior longitudinal - shortens thickens tongue REMEMBER: Intrinsic muscles: O & I : Tongue A: CHANGES the SHAPE of the tongue Suprahyoid Muscles DEPRESSES MANDIBLE and ELEVATES HOID Digastric Anteriorbelly (NV3 depress mandible;MAJOR muscle for MOUTHOPENING!!! r - Posteriorbelly - CNVII elevates hyoid Mylohyoid CNVs Floor of the mouth muscle of - (Mylohyoid-diFF. in Rx on Mand. posteriors teeth) stylohyoid - CNVI - Geniohyoid  Infrahyoid Muscles (TOSS) DEPRESSES HYOID Thyrohoid Omohyoid Sternohyoid Sternothyroid Rotator Cuff Muscle (SITS) control the mon't of shoulders Supraspinatus - medial rotation G Infraspinatus - lateral rotation & Teres minor - lateral rotation & Subscapularis - medial rotation G Hamstring Muscle (Hams3ngs - Bi semi semi) Biceps femoris I Flex the muscle Semimembranous Semitendinosus REMEMBER: 0:TaaS I: Baba "iinline ene Hamstring muscle - aka “Running muscle” Innvervated by SCIATIC NERVE - longest nerve in human body Arises at CRANIAL PLEXUS it Longest Cranial Nerve:Vagus Nerve (CNX) initial Largest Cranial Nerve:Trigeminal Nerve (CNV) LongestIntracranial Nerve: I (w/in cranium) Smallest Cranial Nerve: largest Cranial Nerve that - Trochnar were supplies the head neck:CNV 3 largest Cranial Nerve that supplies the Body:CNX * COVID-19 receptors:ACF2 receptor - Found in diff. parts ofthe body like: Brains lungs  Quadriceps Muscles (sa Recto may 3 Vastus) 3 Rectus femoris Vastus lateralis Frontedne Vastus intermedius a 4 Vastus medialis REMEMBER: Qudriceps muscles: EXTENDS the legs Innervated by FEMORAL NERVE INTRAMUSCULAR ADMINISTRATION FOR DRUGS: Vastus lateralis:Mostcommon used muscle for Drug administration esp. in Infants (pedo) Triceps likod(14), Deltoid safer part is Gluteal muscle:ventroglyteal side - anterior part corsogluteal side - superolateral corner Some muscle Pathologies: Porticolis - aka Wry Neck sternocleidomastoid Due to contraction of (mastoid bone-sternum-clavicle) BOARDS QUESTION:When Right sternocleidomastoid contract, chin will point to left side Muscular dystrophy - has muscle degeneration (genetics) Muscle after stroke:Atrophy (?) Once magalaw no muscle, mag stop and muscle Atrophy Most Common: Duchenne Muscle Dsystrophy (DMD) Fibrilation:may abnormal signal sa heart.Abnormal, random, spontaneous muscle contractions ↳ May lead to Cardiac arrest Pacemaker of2:Sinatrial node - gives proper signals/rhythm I terminalis found on,Crista p superior portion ofRight Atrium postero-superior * Ix: Defibrilation - electrical shock tries to restart SA node CPR Cardiac Arrest abrupt cessation cardiac pump function which may be reversible by - of a prompt intervention but will lead to death in its absence Ventricular Fibrilation - Fibrilation sa ventricles; most common mechanisms ofcardiac arrest Asystole - Flat line in ECG MANAGEMENT:CPR rightaway no need to Defibrilate (like computer) good Asystole:SA node shut downs->CPR (Manually pumping the heart ( in the heartstarts to circulate in the body -> goes to SA node -> Ifthe px still alive:SA node will function again -> But the signals are abnormal (Heart from Flatline, after CPR will send abnormal signals to heart)->DEFIBRILATION Conce may signal or reading na Si heart Kahit abnormal, DeFrib nal CPR-compression ratio - 30:2 /I compression oxygen/rescue breathes Rate:100 compression/min