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Bodylog 2023 > Muscles > Flashcards

Muscles Flashcards

1
Q

Types of striated muscle

A

Skeletal, cardiac

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2
Q

Types of non striated muscle

A

Smooth

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3
Q

What is myoglobin? (4)

A

Structure similar to subunit of haemoglobin
Higher affinity for oxygen than Haemoglobin
especially in acidic conditions
Doesn’t bond to CO2

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4
Q

Muscle cell components (5)

A

Sarcolemma - outer membrane
Sarcoplasm - cytoplasm
Sarcoplasmic reticulum - endoplasmic reticulum
Sarcosome - mitochondria
Sarcomere - contraction unit ONLY IN STRIATED

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5
Q

What is Rhabdomyolysis?
What will be released into the blood stream?

A

Striated muscle death, myoglobin released into bloodstream

K ions will be released too - show lysis

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6
Q

Myoglobin present in urine is… (3)

A

Myoglobinuria
Tea coloured
Can damage kidneys

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7
Q

What is it called when myoglobin is released into bloodstream?

A

Myoglobinaemia

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8
Q

What does type of movement in muscle depend on?

A

The direction of muscle fibre contraction

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9
Q

Movement is always…

A

Along direction of fascicle

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10
Q

3 connective tissue layers in muscle

A

Epimysium - around whole muscle
Perimysium - around fascicles
Endomysium - between muscle fibres

Continuous to tendon

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11
Q

Where is tension created

A

Origin tendon point (rigid)

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12
Q

Where is movement created?

A

Insertion tendon point

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13
Q

What are extrinsic muscles?
Give examples of them in action

A
  • Insertions into Bone and cartilage
  • Extrinsic muscles protrude the tongue, retract it and move it from side to side
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14
Q

What are intrinsic muscles?
Give an example of them in action

A
  • Not attached to bone
  • Intrinsic muscles within tongue are not attached to bone. They allow the tongue to change shape but not position – these aid swallowing
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15
Q

What muscle allows us to stick out the tongue

A

Geniohyoid muscle (genio means chin)

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16
Q

What do perimysiums do?

A

Connective tissue surrounding fascicle, lubricate

Carry nerves and blood vessels

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17
Q

Why can skeletal muscle appear different in microscopic image

A

Some will be transverse and some longitudinal cross sections

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18
Q

Fibres and their requirement for blood

A

Thin fibres need less blood

Thick fibres need more

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19
Q

What is a striated muscle cell called

A

Fibre

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20
Q

What does a muscle fibres contain

A

Many myofibrils

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21
Q

Thin vs thick filaments and their bands/stain

A 
Actin - thin 
Myosin - thick
I band - just actin so stains lighter 
H zone - just myosin (stains darker) 
A band is overlap of myosin and actin so stains DARK
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22
Q

What length is a sarcomere

A

Z line to z line

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23
Q

Feature of skeletal muscle

A

Abundant mitochondria between myofibrils

Nuclei are peripheral

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24
Q

The 3 Muscle contraction speeds and staining

A

Fast - light/white (limited mitochondria)
Intermediate - light red/pink
Slow - red (abundant mitochondria)

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25
Q

What kinds of contraction speed is in a fascicles

A

There is at least one of each in east fascicle

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26
Q

Slow twitch vs fast twitch fibres

A

Slow- lots of mitochondria so many cytochromes, good blood supply, high myoglobin contracts slower and for longer periods of time, endurance activities, lots of ATP, CO2

Fast- low mitochondria so low cytochromes, poor blood supply, low myoglobin, contracts fast and for short periods of time, sprinting, lots of lactate, little ATP

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27
Q

Motor units and fibres

A

Each type of fibre has its own motor units

ie fast do not share with slow

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28
Q

Cardiac muscle features

A 
Central nuclei 
Striated 
Intercalated discs - gap junctions (electrical and mechanical coupling with neighbour cells)
Form branches
Glycogen around cell
T tubules along Z line
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29
Q

ANP and BNP

A

Released from heart during failure
ANP - atrial, congestive heart failure
BNP - ventricular hypertrophy (cells get bigger) mitral valve disease

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30
Q

Explain ANP and BNP

A

BNP - causes vasodilation, lowers BP
ANP - acts on kidney, increases GFR, increases fluid into bladder, more fluid released into urine, lowers blood volume

Both - lower renin

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31
Q

Hypertrophy

A

Cells get bigger

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32
Q

Hyperplasia

A

Cells get multiplied

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33
Q

Atrophy

A

Smaller than normal heart

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34
Q

Describe conducting system of heart

A

Action potential
Atria; Sinoatrial node
To atrial ventricular node - slowly give atria time to contract
Bundle of His
Pass across bundle branches rapidly
Distributed very QUICKLY by purkinkje fibres to ventricular walls
Ventricles contract in unison - strong

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35
Q

Cardiac vs Skeletal

A

Both - striated

Cardiac - nucleus are centre, sarcomere not as developed, one contract cell type - cardiomyocyte, intercalated discs, own isotopes of Troponin I and T

Skeletal - peripheral nucleus, sarcomere,

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36
Q

Smooth muscle characteristics

A

Single large nucleus
Not striated, no sarcomere, no T tubules
Stretch
Actin and myosin
Slower contraction, less ATP
Numerous stimuli can stimulate - nerves, hormones, drugs, blood gases
Sheets, bundles and layers

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37
Q

Smooth muscle cell cave-like invaginations

A

Pinocytic caveolae

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38
Q

Ultra structure of smooth muscle cell

A 
Actin connects to dense plaque 
Actin connects to myosin
Myosin connects to another actin
Actin connects to dense plaque 
Gap junctions 
2 actin vs 1 myosin
39
Q

Where is smooth muscle found

A

Contractile walls - vascular structures, respiratory tract, gut

40
Q

Clinical disorders smooth muscle

A 
Involuntary muscle 
High BP
painful menstruation 
Lung disease
Abnormal movements of gut (IBS)
Incontinence
41
Q

Gut smooth muscle example

A

Longitudinal and circular
Peristalsis
Mucosal

42
Q

How are smooth muscles stimulated

A

Neurotransmitters from varicosities to wide synaptic cleft

43
Q

What often happens to smooth muscles

A

Tear - mild, moderate, severe

44
Q

Muscle repair for skeletal

A

Skeletal - cells themselves cannot, regenerated via mitosis of satellite cells (hyperplasia). Satellite cells can also merge together multiple cells - hypertrophy.

45
Q

Muscle repair for cardiac

A

Incapable of regeneration

After damage, fibroblasts invade and lay scar tissue

46
Q

Muscle repair for smooth and example

A

Repair themselves

Pregnant uterus

47
Q

Purkinje fibres

A 
Modified myocytes SPECIALISED 
Receive impulse from AV node 
transmit it to ventricle walls 
Lots of glycogen 
Lots of gap junctions
48
Q

Cardiac vs smooth

A

Both - central nucleus, one contractile type (fast and slow in skeletal), syncytium (wave) gap junctions

Cardiac - specialised cells/routes (purkinje fibres for conduction), striated, intercalated discs

Smooth - no sarcomeres, not striated

49
Q

Cardiac nerve supply and contraction

A

Nerve sits far away to allow neurotransmitter to spread (wave like)

Parasympathetic - slows down, straight to heart only to SA node

Sympathetic - speeds up, via spinal cord, cardiac nerve, to whole heart

50
Q

Cardiac contraction

A

Receptor is activated by acetylcholine binding
Cause action potential
DHP voltage sensitive calcium channels open
Calcium flows through
Calcium binds to TN-C
Allows myosin-actin complex
Pulls actin towards M line

51
Q

Smooth muscle nerve supply

A

Varicosities supply - sits far away neurotransmitter spreads (same as cardiac, wave like)

Neurotransmitter causes depolarisation, opens Ca voltage gated channels, calcium in, contraction

Contraction doesn’t stop until Ca decreases

52
Q

Skeletal muscle nerve supply

A 
Neuromuscular junction - nerve meets muscle at motor end plate 
Swellings on axon contain acetylcholine
Nerve impulse releases it
Binds to receptors on sarcolemma 
Action potential along muscle
53
Q

Innervation ratio

A

More fibres per motor unit allow for more power, less allow for finer control

54
Q

Kranocyte

A

Found at neuromuscular junction
Covers Schwann cell
Maybe anchors nerve to muscle cell

55
Q

T tubules

A

Allow rapid transmission of action potential

Associated with sarcoplasmic reticulum and mitochondria

56
Q

Skeletal muscle contraction (DETAIL IONS)

A

Nerve impulse arrives at neuromuscular junction
Acetylcholine is released to synaptic cleft
Sarcolemma LOCALLY depolarised
Voltage gated Na channels open, Na ions enter
Depolarisation of whole sarcolemma to T tubules
Voltage sensitive T tubule proteins conformational change
Voltage gated Ca channels open
Ca into sarcoplasm
binds to TnC subunit of troponin
Contraction
Ca ions return to sarcoplasmic reticulum

57
Q

Myasthenia gravis

A 
Skeletal muscle 
Autoimmune disease
Antibodies block Ach receptor 
Smaller invaginations in synaptic cleft 
Reduced synaptic transmission 
Muscle weakness
58
Q

Sliding filament theory outline

A

Cardiac, Skeletal
Myosin anchored to M line
Actin anchored to Z line (moves from each end)
Myosin and actin form cross bridges, myosin pulls actin

59
Q

Muscle parts

A

Fibres, myofibrils, sarcomere

60
Q

Sliding filament theory

A

ATP hydrolysed and binds - causes myosin head to extend (attached as ADP and Pi)
Attaches to binding site on actin - cross bridge
ADP pi detach
Power stroke pulls actin filament towards M line
Shortens sarcomere
Myosin remains attached until more ATP

61
Q

Tropomyosin and troponin sliding filament theory

A

Controlled by calcium - stored in sarcoplasmic reticulum
Blocks cross bridge binding sites on actin
Calcium binds to troponin, displaces tropomyosin
Exposes binding sites
Cross bridge can be formed

62
Q

How is calcium release controlled

A 
Stored in sarcoplasmic reticulum 
Neurotransmitter released from neuron
Bind to receptor
Depolarisation - electrical impulse travels down T tubules 
Opens Ca channels
Ions float to troponin
63
Q

Myosin structure

A

Rod like

2 Heads protrude

64
Q

Actin structure

A

2 protein
F-actin fibres
G actin fibres
Tropomyosin-troponin complex sits over actin binding sites

65
Q

M line

A

Centre
Void of myosin heads
Actin pulled towards it during contraction

66
Q

Roles of troponin and creatine kinase

A

TnC - calcium binding site
TnI - inhibits, binds tropomyosin and TnT to actin over binding site, dissociates when Ca attaches
TnT - moves tropomyosin
Creatine Kinase - produce ATP

67
Q

Lengths of sections during contraction

A

Actin and myosin DO NOT CHANGE - overlap more

sarcomeres shorten

68
Q

Innervation and contraction explained skeletal

A

Nerve impulse causes nerve to release acetylcholine to synaptic cleft
Acetylcholine binds to receptors on motor end plate
Action potential generated, travels down T tubules
Ca are released by Sarcoplasmic reticulum
Ca ions bind to TnC on tropomyosin-troponin complex
Exposes binding sites
ATP hydrolysis causes myosin to cock head and bind to actin
Releases ADP and Pi
Pulls actin towards M line - power stroke
Ca is taken up by sarcoplasmic reticulum
Tropomyosin slips back, covers binding site

69
Q

Origin vs insertion

A

Origin - Bone, proximal (close to midline), more stable, greater mass

Insertion - muscle attaches, moved by contraction, distal, bone/tendon/connective tissue, more motion

70
Q

Agonist

A

2 muscles working together, prime movers (main muscles responsible for movement)

71
Q

Antagonist

A

Oppose prime movers (agonists)

72
Q

Synergists

A

Assist prime movers (can’t act alone)

73
Q

Neutralisers

A

Prevent unwanted movement that agonists can do

74
Q

Fixators

A

Hold body part in place while another is moving

75
Q

First class lever

A 
See-saw
Load on one end
Effort downwards on other 
Fulcrum central 
Extension of head
76
Q

Second class lever

A 
Wheelbarrow 
Load ‘in wheelbarrow’ so central 
Effort one end 
Fulcrum at other end
Standing on ball of foot
77
Q

Third class lever

A 
Fishing rod
Effort in middle 
Load one end, fulcrum other
Hard to perform 
Most common
78
Q

How are skeletal muscles grouped together

A

In compartments
Similar actions, thick dense fascia
Location eg, anterior, posterior, lateral or medial

79
Q

Compartment syndrome

A

Trauma to one compartment

Internal bleeding - exerts pressure on blood vessels and nerves

80
Q

Compartment syndrome symptoms

A 
Deep pain - not localised
Aggravated by stretch 
Pins and needles (parathesia)
Tense and firm compartment 
Swollen shiny skin
Long time for capillary to refill (white skin for long time when pressed)
81
Q

What are clinical markers of striated muscle death in blood

A

K ions, troponin (I, T and C), creatine kinase

82
Q

Clinical markers for smooth muscle death

A

K ions

83
Q

Name 5 muscular dysfunction

A 
Duchene muscular dystrophy 
Rhabdomyolysis
Myocardial infarction 
Botulism and organophosphate poisoning
Malignant hypothermia
84
Q

Duchene muscular dystrophy

A

X linked Recessive gene
Most Common
Mutation of dystrophin gene (joins sarcolemma to actin)
Absence of dystrophin

85
Q

Dystrophin absence causes…

A

Excess calcium to enter cell
Calcium and water absorbed by mitochondria
Mitochondria burst
Muscle cell bursts (rhabdomyolysis)
Creatine kinase and myoglobin levels HIGH

86
Q

Creatine kinase

A

Diagnose heart attacks (lots of enzyme = lots of damage)
Important in metabolically active tissues
Released into blood by damaged skeletal muscle

87
Q

What can cause a rise in creatine kinase

A 
Myocardial infarction 
Vigorous exercise
Vaccination 
A fall
Rhabdomyolysis 
Kidney injury (myoglobin not removed) 
Muscle wastage
88
Q

Troponin assays…

A

Assess myocardial damage - cardiac isachaemia
Measure troponin (I and T) - specific isoforms in cardiac muscle - levels not proportional to damage
Measure within 20 hours

89
Q

Botulism and Botox

A 
Toxin produced by clostridium botulinum 
Blocks neurotransmitter release
Causes paralysis of skeletal muscle 
Cosmetically for wrinkles 
Treat muscle spasm
90
Q

Organophosphate poisoning

A

Pesticides
Inhibits Ach esterase
Ach activity stronger
Effects somatic and autonomic signalling

91
Q

Symptoms of poisoning organophosphate (muscarinic)

A 
SLUDGE 
Salivation 
Lacrimation (crying)
Urination 
Defecation 
GI cramps 
Emesis (vomitting)
92
Q

Symptoms of organophosphate poisoning (nicotinic)

A 
MTWTF
Muscle cramps
Tachycardia 
Weakness
Twitching 
Fasciculations
93
Q

Malignant hyperthermia

A

Reaction to anaesthetics
Muscle rigidity lots of Ca
Hot and metabolic acidosis
Muscle breakdown (high k ions)

Bodylog 2023 (6 decks)

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