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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
What kinds of contraction speed is in a fascicles
There is at least one of each in east fascicle
26
Slow twitch vs fast twitch fibres
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
27
Motor units and fibres
Each type of fibre has its own motor units | ie fast do not share with slow
28
Cardiac muscle features
``` Central nuclei Striated Intercalated discs - gap junctions (electrical and mechanical coupling with neighbour cells) Form branches Glycogen around cell T tubules along Z line ```
29
ANP and BNP
Released from heart during failure ANP - atrial, congestive heart failure BNP - ventricular hypertrophy (cells get bigger) mitral valve disease
30
Explain ANP and BNP
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
31
Hypertrophy
Cells get bigger
32
Hyperplasia
Cells get multiplied
33
Atrophy
Smaller than normal heart
34
Describe conducting system of heart
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
35
Cardiac vs Skeletal
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,
36
Smooth muscle characteristics
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
37
Smooth muscle cell cave-like invaginations
Pinocytic caveolae
38
Ultra structure of smooth muscle cell
``` 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
Where is smooth muscle found
Contractile walls - vascular structures, respiratory tract, gut
40
Clinical disorders smooth muscle
``` Involuntary muscle High BP painful menstruation Lung disease Abnormal movements of gut (IBS) Incontinence ```
41
Gut smooth muscle example
Longitudinal and circular Peristalsis Mucosal
42
How are smooth muscles stimulated
Neurotransmitters from varicosities to wide synaptic cleft
43
What often happens to smooth muscles
Tear - mild, moderate, severe
44
Muscle repair for skeletal
Skeletal - cells themselves cannot, regenerated via mitosis of satellite cells (hyperplasia). Satellite cells can also merge together multiple cells - hypertrophy.
45
Muscle repair for cardiac
Incapable of regeneration | After damage, fibroblasts invade and lay scar tissue
46
Muscle repair for smooth and example
Repair themselves | Pregnant uterus
47
Purkinje fibres
``` Modified myocytes SPECIALISED Receive impulse from AV node transmit it to ventricle walls Lots of glycogen Lots of gap junctions ```
48
Cardiac vs smooth
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
Cardiac nerve supply and contraction
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
Cardiac contraction
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
Smooth muscle nerve supply
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
Skeletal muscle nerve supply
``` 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
Innervation ratio
More fibres per motor unit allow for more power, less allow for finer control
54
Kranocyte
Found at neuromuscular junction Covers Schwann cell Maybe anchors nerve to muscle cell
55
T tubules
Allow rapid transmission of action potential | Associated with sarcoplasmic reticulum and mitochondria
56
Skeletal muscle contraction (DETAIL IONS)
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
Myasthenia gravis
``` Skeletal muscle Autoimmune disease Antibodies block Ach receptor Smaller invaginations in synaptic cleft Reduced synaptic transmission Muscle weakness ```
58
Sliding filament theory outline
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
Muscle parts
Fibres, myofibrils, sarcomere
60
Sliding filament theory
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
Tropomyosin and troponin sliding filament theory
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
How is calcium release controlled
``` 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
Myosin structure
Rod like | 2 Heads protrude
64
Actin structure
2 protein F-actin fibres G actin fibres Tropomyosin-troponin complex sits over actin binding sites
65
M line
Centre Void of myosin heads Actin pulled towards it during contraction
66
Roles of troponin and creatine kinase
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
Lengths of sections during contraction
Actin and myosin DO NOT CHANGE - overlap more | sarcomeres shorten
68
Innervation and contraction explained skeletal
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
Origin vs insertion
Origin - Bone, proximal (close to midline), more stable, greater mass Insertion - muscle attaches, moved by contraction, distal, bone/tendon/connective tissue, more motion
70
Agonist
2 muscles working together, prime movers (main muscles responsible for movement)
71
Antagonist
Oppose prime movers (agonists)
72
Synergists
Assist prime movers (can’t act alone)
73
Neutralisers
Prevent unwanted movement that agonists can do
74
Fixators
Hold body part in place while another is moving
75
First class lever
``` See-saw Load on one end Effort downwards on other Fulcrum central Extension of head ```
76
Second class lever
``` Wheelbarrow Load ‘in wheelbarrow’ so central Effort one end Fulcrum at other end Standing on ball of foot ```
77
Third class lever
``` Fishing rod Effort in middle Load one end, fulcrum other Hard to perform Most common ```
78
How are skeletal muscles grouped together
In compartments Similar actions, thick dense fascia Location eg, anterior, posterior, lateral or medial
79
Compartment syndrome
Trauma to one compartment | Internal bleeding - exerts pressure on blood vessels and nerves
80
Compartment syndrome symptoms
``` 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
What are clinical markers of striated muscle death in blood
K ions, troponin (I, T and C), creatine kinase
82
Clinical markers for smooth muscle death
K ions
83
Name 5 muscular dysfunction
``` Duchene muscular dystrophy Rhabdomyolysis Myocardial infarction Botulism and organophosphate poisoning Malignant hypothermia ```
84
Duchene muscular dystrophy
X linked Recessive gene Most Common Mutation of dystrophin gene (joins sarcolemma to actin) Absence of dystrophin
85
Dystrophin absence causes…
Excess calcium to enter cell Calcium and water absorbed by mitochondria Mitochondria burst Muscle cell bursts (rhabdomyolysis) Creatine kinase and myoglobin levels HIGH
86
Creatine kinase
Diagnose heart attacks (lots of enzyme = lots of damage) Important in metabolically active tissues Released into blood by damaged skeletal muscle
87
What can cause a rise in creatine kinase
``` Myocardial infarction Vigorous exercise Vaccination A fall Rhabdomyolysis Kidney injury (myoglobin not removed) Muscle wastage ```
88
Troponin assays…
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
Botulism and Botox
``` Toxin produced by clostridium botulinum Blocks neurotransmitter release Causes paralysis of skeletal muscle Cosmetically for wrinkles Treat muscle spasm ```
90
Organophosphate poisoning
Pesticides Inhibits Ach esterase Ach activity stronger Effects somatic and autonomic signalling
91
Symptoms of poisoning organophosphate (muscarinic)
``` SLUDGE Salivation Lacrimation (crying) Urination Defecation GI cramps Emesis (vomitting) ```
92
Symptoms of organophosphate poisoning (nicotinic)
``` MTWTF Muscle cramps Tachycardia Weakness Twitching Fasciculations ```
93
Malignant hyperthermia
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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