Muscle tissue (cardiac/skeletal/smooth) Flashcards

1
Q

3 types of muscles and characteristics

A
  1. skeletal: striated, multinucleated, voluntary
  2. cardiac: striated, mononucleated, involuntary
  3. smooth: non striated, mononucleated, involuntary
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2
Q

general functions of muscle (5)

A
  1. procude movement
  2. stabilise body position
  3. regulate organ volume (sphincter)
  4. substance movement (peristalsis)
  5. heat production (involuntary shivering)
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3
Q

Properties of muscle tissue (5)

A
  1. CONTRACTILITY: shorten and generate force
  2. EXCITABILITY: respond to stimuli delivered by nerves or hormones
  3. CONDUCTIVITY: propagate stimuli over sarcolemma
  4. EXTENSIBILITY: ability to stretch without tissue damage
  5. ELASTICITY: return to original shape after being stretched
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4
Q

location of skeletal muscle tissue

A
  1. Muscles attached to bones of the axial/appendicular skelethon
  2. Soft tissue (tongue, pharinx, upper esophagus, lumbar diaphragm)
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5
Q

skeletal fibers organisation and composition

A

-long striated multinuc fibers (nuclei usually on cell periphery)
-sarcolemma = PM
-sarcoplasm = cytoplasm
-sarcoplasmic reticulum = SER
-sarcosomes = mitochondria

thick (myosin) and thin (actin) filaments arranged withing sarcomere units

!! contain satellite cells: provide small potential for regeneration

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6
Q

origin of skeletal muscle cells

A

myoblasts (mesenchymal)

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7
Q

what is the cause of the striations of the muscle

A

the thick and thin filaments of actin and myosin II

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8
Q

syncytium definition

A

A large cell-like structure formed by the joining together of two or more cells

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9
Q

Differentiation and development of skeletal muscle fibers

A
  1. myoblast origin
  2. active protein synthesis of proteins needed for myofibrils
  3. differentiation into mature fibers

!! some myoblasts dont differentiate and are present on the periphery of the myofibril –> differentiate into myofibrils to provide some regeneration potential upon injury (are not picked up with H&E)

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10
Q

levels of organisation of a muscle fiber bundle

A
  1. epimysium: dense CT sheath containing major vascular and nervous supply
  2. perimysium: thicker CT containing larger blood vessels
  3. fascicles: bundles of muscle fibers (2-10 fibers per fascicle)
  4. endomysium: reticular fiber layer containing smallest blood vessels
  5. muscle fiber
  6. myofibril (single cell)
  7. sarcomere (single unit)
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11
Q

3 types of skeletal muscle fibers

A
  1. RED: slow oxidative type 1 –> many mitochondria, capillaries, myoglobin and aerobic respiration, fatigue resistant, less tension is generated
  2. INTERMEDIATE: oxidative glycolytic type 2 –> many mitochondria, capillaries, myoglobin, large amounts of glycogen and can do anaerbobic glycolysis, short movement but fatigue resistant
  3. WHITE: fast glycolytic type 3 –> less myoglobin, fewer mitochondria/ capillaries, fast rapid movement, anaerobic resp (few oxidative enzymes), fatigue prone, highest muscle tension generated
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12
Q

muscle hypertophy vs muscle atrophy

A

HYPERTROPHY: increase in amount or thickness of myofibrils (either bcos of exercise or some treatments like testosterone/anabolics)

ATROPHY: decrease in amount or thickness of myofibrils (bcos of decreased movement)

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13
Q

Bands of the sarcomere (5)

A
  1. I band: only actin
  2. A band: both myosin and actin alternating
  3. H zone: only myosin
  4. M line: myosin and structural proteins that stabilise the sarcomere
  5. Z line: bisects the I band and is what defines the start/end boundary of a sarcomeric unit
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14
Q

dark vs light band of striated muscle properies

A

DARK: ANISOTROPIC (contain highly refractile protein molecules which refract polarized light in diff directions)

LIGHT: ISOTROPIC (refracts rays of polarised light at the same angle/direction)

!! Z line doesnt allow the passage of light

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15
Q

Structure of thick filament - myosin

A

TAIL: made of 2 heavy and 4 light chains

2 GLOBULAR HEADS:
-one has actin binding site
-one has ATP binding site for ATPase activity

-tail and heads are connected via hinge

!! DIMER –> tails attach together and the heads protrude

!! BARE ZONE: in the middle of the bundles - region that doesnt contain any protruding heads

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16
Q

Structure of thin filament - actin

A

G actin assembles to form F actin !! POSITIVE END AT THE Z LINES (polymerises)

-contains tropomyosin
-contains 3 troponin complexes:

  1. TNT: binds tropomyosin
  2. TNC: Ca2+ high affinity
  3. TNI: binds actin (to block actin-myosin interaction)
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17
Q

what protein is the Z line made up of

A

alpa actinin

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18
Q

Summary of the 3 types of proteins in sarcomere

A
  1. CONTRACTILE PROTEINS: myosin/actin
  2. REGULATORY PROTEINS: troponin/ tropomyosin
  3. STRUCTURAL PROTEINS: titin/ myomesin/ nebulin/ dystrophin/ desmin/ ankyrin
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19
Q

Roles of the structural muscle proteins

A
  1. nebulin: connects the +ve end of actin with Zline
  2. dystrophin, ankyrin and desmin: connect the sarcomere to the sarcolemma
  3. myomesin, Mprotein, obscurin: M line proteins
  4. titin: links myosin to Z lines
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20
Q

Process of skeletal muscle contraction (X STEPS)

A
  1. AP reaches sarcolemma at neuromuscular junction –> release of Ca2+ from SR
  2. Ca2+ binds to troponin causing conformational change in tropomyosin and exposing actin-myosin binding sites
  3. Myosin globular heads form cross bridges
  4. ATP binds to myosin head and changes conformation of binding site to cause uncoupling of globular head
  5. Hydrolysis of ATP causes bending of globular head to reach an actin binding site closer to the Z lines - recovery stroke
  6. Binding of myosin head to actin site and release of ADP + Pi which generates force and pulls actin towards the center of sarcomere - power stroke
21
Q

Pathology stemming from a defect in structural proteins of sarcomere

A

DUCHENNE MUSCULAR DYSTROPHY:
mutation to dystrophin protein which leads to muscle weakness (affects only males bcos dystrophin is encoded on X chromosome)

22
Q

Change in the length of different regions when a sarcomere is contracted

A

Z lines shorten
myosin is fixed
sarcomere overall shorten

23
Q

Organisation of the SER system in skeletal muscle

A

TRIAD ARRANGEMENT: 1 T tubule + 2 adjacent cisternae (repeating sections corresponding to the Z lines)

SR: tubular sacs which store Ca2+ in relaxed muscle and releases it in contracting muscle

T tubules: between 2 cisternae in line with Z lines, contain DHSRs (depolarisation sensitive receptors affecting Ca2+ release)

terminal cisternae: formed by ER and acts as a Ca2+ reservoir (membrane contains calcium channels, ryanodine receptors, and calsequestrin protein)

24
Q

Excitation contraction coupling function and process in SKELETAL muscle (5 STEPS)

A

ROLE: triggering muscle contraction from an action potential arriving at neuromuscular junction

PROCESS:
1. AP reaches sarcolemma at neuromuscular junction
2. Ach released at cleft and interacts with Ach sarcolemma receptors
3. Na+ influx depolarising sarcolemma
4. spread of AP across T tubule causes change in DHSR and triggers their opening
5. Release of Ca2+ that bind to troponin and trigger contraction process

25
Q

How do skeletal muscles achieve muscle relaxation? (3 steps)

A
  1. removal of Ach neurotransmitter at neuromuscular synaptic cleft (acetylcholinesterase enzyme degradation)
  2. removal of Ca2+ from troponin
  3. decrease of Ca2+ conc in cytplasm causes a reuptake into SER as the Ca2+ bind to calsequestrin protein
26
Q

significance of calsequestrin

A

highly acidic calcium binding protein on SR:

  1. allows the relaxation of muscle via Ca2+ reuptake
  2. allows a very high conc of Ca2+ to be readily available for release upon AP arrival (bcos lumen Ca2+ conc would be too low)
27
Q

Innervation of skeletal muscle fibers

A

-nerves originate at the level of the spinal cord or brainstem
-1 neuromuscular junction innervates 1 fiber
-main neurotransmitter used = ACh
-thin lamina layer of the non myelinated terminal SC
-spread of terminal into branches

28
Q

cardiac muscle location, function and characteristics

A

LOCATION: myoardium of the cardiac chambres

FUNCTION: coordinated contraction of the heart

CHARACTERISTICS:
-mononucleated
-striated
-myofibrils organised into sarcomeres
-nucleus is central and surrounded by organelles
-contain junctions

29
Q

what are the layers of the cardiac wall

A

EXTERNAL TO INTERNAL:

  1. epicardium
  2. pericardial cavity
  3. pericardium
  4. myocardium (contains cardiac muscle cells)
  5. endocardium
30
Q

organisation of cardiac muscle fibers

A

-long cardiac muscle cells
-connected at intercalated discs containing junctions
-each cell can be connected to more than one other cell causing the formation of branched fibers
-arranged in sarcomeres

31
Q

structure and characteristics of cadiac muscle CELLS

A

-long cylindrical cells
-connected with intercalated discs
-mononuclear (central nucleus) and surrounded by organelles (RER/Golgi)
-sacromeres formed
-high vascularisation found in the CT surrounding cells
-LARGE MITOCHONDRIA extending full length of the sarcomere sometimes
-diad formation of SER

JUXTANUCLEAR REGION: abundant glycogen granules which appear as white space bcos they are lost during stain prep

32
Q

structure of intercalated dicsc

A

made of transverse and longitudinal section

  1. FASCIA ADHERENS: transverse section -anchoring of actin filaments
  2. MACULAE ADHERENTES: transverse and longitudinal section - prevent pulling apart of cells under strain of contraction
  3. GAP JUNCTIONS: longitudinal section - provides ionic continuity between adjacent cells which permits them to behave as a syncytium
33
Q

Organisaton of the SER in cardiac mucle cells

A

DIAD ARRANGEMENT: 1 T tubule + small terminal cisternae

  • T tubule is at the level of the Z line
    -T tubule and SR network are in drect contact due to anastomosis
34
Q

what controls the contraction of cardiac muscle?

A

autonomic nervous system (involuntary) and the pacemaker cells

35
Q

Excitetion-coupling in CARDIAC muscle (4 STEPS)

A

STIMULUS: triggered by pacemaker cells and travels along purkinje fibers until it reaches cardiomyocytes

  1. AP arrives from adjacent cell/influx of Na+
  2. Voltage gated Ca2+ channels open and Ca2+ enters cell
  3. Calcium induced calcium release from SR via ryanodine receptors (RyR)
  4. Combination of SR Ca2+ and extraceullular fluid Ca2+ creates a Ca2+ spark that is sufficient to start the contraction
36
Q

Organisation of smooth muscle

A

-usually in bundles of sheets
-each cell surrounded by a basal lamina
-interconnected by gap junctions
-controled by autonomic nervous sytem - neuroendicrine contractio control

!! LOCATION: blood vessels, walls of hollow organs (GI/UT/dermis)

37
Q

specific arrangement of smooth muscle in certain organs like the intestine

A

present in 2 layers orthogonal to eachother
HENCE one looks like its coming out of the slide, and one looks like its running across the slide

38
Q

smooth muscle cells characteristics

A

-FUSIFORM (apex of one cell reaches the middle of the adjecent cell)
-central and elongated nucleus
-organelles mainly concentrated around the side of the nucleus (golgi/ mitochondria/glycogen granules/ ribosomes)
-caveole instead of SR

FILAMENTS:
-thin filaments with thick filament between them
-originate and end from dense bodies
-intermediate filaments conenct the dense bodies (dense bodies are made of alpha actinin)
-myosin scattered throughout cell in its inactive form (not seen without special staining)

39
Q

why do nuclei of smooth muscle cells appear long

A

due to muscle contraction that occurs during the preparation

40
Q

protein expression of the filaments in smooth muscle cells

A

ACTIN: calponin and caldesmon

INTERMEDIATE: desmin

MYOSIN: SMM singly oriented

41
Q

difference in the orientation of myosin of skeletal and smooth muscle cells

A

SKELETAL: BIPOLAR ORIENTATION:
-heads of myosin on each side are in diff orientations to maximise thin-thick filament interaction

SMOOTH: SIDE POLAR ORIENTATION:
-heads of myosin face different directions on each side of the filament
HENCE: has no bare zone in the center, but has tapered ends on the end

42
Q

what are the stimuli hat can trigger the contraction of smooth muscle cells (3)?

A
  1. MECHANICAL: stretching actions that trigger activation of mechanosensitive ion channels
  2. ELECTRICAL: neural stimulation via neurotransmitter release (causes opening of VDCC)
  3. CHEMICAL/HORMONAL: use of secondary messages WITHOUT the need for nervous stimulation (IP3/DAG)
43
Q

what are caveolae

A

invaginated microdomains of the PM

-contain caveolin proteins
-contain Ca2+ channels
-in close proximity to the SER

44
Q

Process of contraction in smooth muscle cells (5 STEPS)

A

STIMULUS: influx of Ca2+ from etracellular space via VDCC (voltage dependent Ca2+ channels)

  1. Ca2+ ions released from caveolae/SER and form Ca2+ calmodullin complexes
  2. Ca2+-calmodulling activates myosin light chain kinase (MLCK)
  3. MLCK phosphorylayes myosin light chain
  4. myoin unfolds and binds with actin (atp dependent cycle) -> contraction continues as long as myosin is phosphorylated
  5. LATCH STATE: myosin head attached to actin is dephosphorylayed and this causes a decrease in ATPase activity –> head is unable to detach from actin and this maintains strength of contraction over a long time

!! dense bodies are pulled together during the contraction

45
Q

What is the innervation of smooth muscle cells likes

A

Nerve terminals are observed only in CT adjacent to the muscle cells (synapses for neurotransmiter release)

46
Q

Repair and renewal potential of SKELETAL muscle

A

-limited regeneration capacity
-only via satellite cells bcos mitosis is not possible
-results in hypertrophy

47
Q

Repair and renewal potential of CARDIAC muscle

A

-thought to be non proliferative but evidence shows there is the capacity of renewal by vascular derived stem cells
-post myocardial infarction they undergo remodelling via fibroblasts which causes fibrous scarring
-results in hyperthrophy

48
Q

Repair and renewal potential of SMOOTH muscle

A

-proliferation via mitosis
-vascular pericytes can also produce smooth muscle
-results in hypertophy

49
Q
A