Muscles Flashcards

1
Q

Classify the different muscle types

A

Striated: skeletal, cardiac

Non-striated: smooth

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2
Q

What is myoglobin?

A

Myoglobin is a red protein containing haem, which functions as an oxygen-storing molecule, providing oxygen to the working muscles. It is structurally similar to a subunit of haemoglobin.

It is present in skeletal and cardiac muscle but is said not to be present in smooth muscle.

Diving mammals (i.e. seals and cetaceans) have particularly high amounts of myoglobin in their muscles, which allows them to remain submerged for longer than other air-breathing mammals.

Haemoglobin gives up oxygen to myoglobin, especially when pH is lowered.

When muscle dies (muscle necrosis) myoglobin is released into the bloodstream and can cause renal damage (myoglobinurea) because it is the kidneys that remove myoglobin from the blood into the urine.

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3
Q

What is a fascicle?

A

A muscle fascicle is a bundle of skeletal muscle fibers surrounded by perimysium, a type of connective tissue

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4
Q

What is endomysium?

A

The endomysium is a wispy layer of connective tissue that ensheaths each individual muscle fiber or muscle cell. It also contains capillaries and nerves. Endomysium is the deepest and smallest component of connective tissue in muscles

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5
Q

What is perimysium?

A

Perimysium is the name given to the fibrous sheath that surrounds (covers) each bundle of single muscle fibres, the bundle being known as a fascicle.

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6
Q

What is epimysium?

A

The epimysium is the fibrous tissue envelope that surrounds skeletal muscle. It is a layer of dense irregular connective tissue which ensheathes the entire muscle and protects muscles from friction against other muscles and bones.

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7
Q

Define fascia

A

A sheet of connective tissue (as an aponeurosis) covering or binding together body structures

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8
Q

Libs are divided into compartments delineated by fascia. What is compartment syndrome?

A

Trauma in one compartment could cause internal bleeding which exerts pressure on blood vessels and nerves
This can give rise to compartment syndrome
- deep constant poorly localised pain
- aggravated by passive stretch of muscle group
- parenthesis (altered sensation e.g. pins and needles)
- compartment may feel tense and firm
- swollen shiny skin, sometimes with obvious bruising
- prolonged capillary refill time

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9
Q

What ovens the tongue?

A

Extrinsic muscles protrude the tongue, retract it and move it from side to side.
Extrinsic muscles and suprahyoid muscles have insertions in bone or cartilage

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10
Q

What is the function of intrinsic muscles within the tongue?

A

Intrinsic muscles within tongue are not attached to bone. They allow the tongue to change shape but not position.

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11
Q

What is the geniohyoid muscle?

A

The prefix ‘genio-’ refers to the chin (hence genial). The geniohyoid muscle permits us to stick out the tongue. Hypoglossal nerve damage leads to deviation of the extended tongue.

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12
Q

Describe the muscle fibres and connective tissue of the tongue (SEE SLIDES FOR IMAGES)

A

Skeletal muscles of the tongue often terminate by interdigitation (arrows) with the collagen and extracellular matrix of their surrounding connective tissues.
The plasticity and strength of the connective tissues and the multidirectional orientation of the muscle fibres accounts for the mobility of the tongue.

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13
Q

What is a muscle fibre?

A

A striated muscle cell (very long)

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14
Q

What is the sarcolemma?

A

Plasma membrane of the muscle fibre

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15
Q

What are atrophy and hypertrophy?

A

Remodelling of muscles is
• Continual
• Replacement of contractile proteins in 2 weeks
• Destruction > replacement = atrophy
• Replacement > destruction = hypertrophy

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16
Q

Name and explain 3 types of atrophy?

A

Disuse Atrophy e.g., bed rest, limb immobilisation, sedentary behaviour

  • Loss of protein
  • Reduced fibre diameter
  • Loss of power

Muscle atrophy with age 30+ years old

  • 50% loss of muscle by 80 years
  • Muscles generate a lot of heat - loss of muscle mass leads to less heat generated

Denervation atrophy

  • signs of lower motor neurone lesions: weakness, flaccidity, muscle atrophy
  • Re-innervation within 3 months for recovery
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17
Q

What are the metabolic changes with hypertrophy?

A

More contractile proteins: hence, increase in fibre diameter

• Metabolic changes: increased - enzyme activity for glycolysis, mitochondria, stored glycogen, blood flow

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18
Q

What is a sarcomere?

A

The sarcomere is the fundamental unit of muscle structure. Its capacity for contraction is the essential trait that makes muscles work. It has two primary components

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19
Q

What is the A band?

A

The entire region where myosin is present

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20
Q

What is the H zone

A

The region where only myosin is present.

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21
Q

What are the I bands?

A

The regions where exclusively actin is present

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22
Q

What are Z lines?

A

The boundaries between adjacent sarcomeres

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23
Q

What is the M line?

A

The division halfway between the Z lines, lying in the A band
Strands of a protein called myomesin are found here

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24
Q

What is overstretching

A

Overstretching - the A and I filaments can no longer re-engage; thought to feature in some cardiac pathologies (i.e. enlarged ventricles)

25
Q

What are skeletal muscles composed of?

A

Fascicles composed of muscle fibres (cells) composed of myofibrils composed of myofilaments (actin and myosin)

26
Q

What makes up the thin filaments of skeletal and cardiac muscle?

A

Actin, tropomyosin and troponin

27
Q

What are troponin assays?

A

Troponin Assays are a Useful Diagnostic Tool Troponin (esp. I & T forms) used as a marker for cardiac ischaemia. NB: There are specific isoforms of cardiac I & T forms.
Released from ischaemic cardiac muscle within an hour. Must measure within 20 hours. The smallest changes in troponin levels in the blood are indicative of cardiac muscle damage.
However quantity of troponin is not necessarily proportional to the degree of damage.
Used by emergency units as the assay of choice, superseding muscle enzyme assays.

28
Q

What is Creatine Kinase and what can it be used to diagnose?

A

CK is an important enzyme in metabolically active tissues like muscle.
CK used to be measured to diagnose heart attacks (MIs), enzyme increase being largely proportional to infarct size, but has been largely superseded by troponin assay.

29
Q

What can lead to a rise in plasma creatine kinase?

A

CK is an enzyme that is also released into the blood by damaged skeletal muscle and brain. A rise in plasma CK can result from:
• intramuscular injection,
• vigorous physical exercise,
• a fall (especially in the elderly),
• rhabdomyolysis (severe muscle breakdown),
• muscular dystrophy, and
• acute kidney injury.

30
Q

Describe the structure of the thick filament

A

An individual myosin molecule has a rod-like structure from which two ‘heads’ protrude.
Each thick filament consists of many myosin molecules, whose heads protrude at opposite ends of the filament

31
Q

Describe the structure of the thin filament

A

The actin filament forms a helix. Tropomyosin molecules coil around the actin helix, reinforcing it. A troponin complex is attached to each tropomyosin molecule.

32
Q

How are actin and myosin connected?

A

In the centre of the sarcomere the thick filaments are devoid of myosin heads. The myosin heads extend towards the actin filaments in regions of potential overlap.

33
Q

What is the role of ionic calcium in the contraction mechanism?

A

When increased amounts of ionic calcium bind to TnC of troponin, a conformational change moves tropomyosin away from actin’s binding sites. This displacement allows myosin heads to bind actin, and contraction begins

34
Q

Describe and explain the sequence of events involved in the sliding of the thin filaments during contraction

A

1) Myosin head (in high energy configuration) attaches to the actin myofilament
2) ADP and Pi released, the myosin head pivots and bends as it pulls on the actin filament, sliding it towards the M line - this is the power stroke
3) ATP binds, cross bridge detaches, myosin head in low energy configuration
4) ATP splits into ADP and Pi - cocking of the myosin head occurs

35
Q

What is a neuromuscular junction?

A

A neuromuscular junction is a synapse between a motor neuron and skeletal muscle
Small terminal swellings of the axon contain vesicles of acetylcholine. A nerve impulse causes the release of acetylcholine which binds receptors on the sarcolemma to initiate an action potential propogated along the muscle.

36
Q

What are T-tubules?

A

Transverse tubules, formed by inward extensions of the sarcolema; main function is to allow electrical signals to move deeper into the cell.

37
Q

What are the events leading up to contraction of skeletal muscle?

A
  1. Initiation: nerve impulse along motor neuron
    axon arrives at neuromuscular junction.
  2. Impulse prompts release of acetylcholine (Ach) into synaptic cleft causing local depolarization of sarcolemma.
  3. Voltage-gated Na+ channels open; Na+ enters cell.
  4. General depolarization spreads over sarcolemma and into T tubules.
  5. Voltage sensor proteins of T tubule membrane change their conformation.
  6. Gated Ca2+ -release channels of adjacent terminal cisternae are activated by 5.
  7. Ca2+ is rapidly released from the terminal cisternae into the sarcoplasm.
  8. Ca2+ binds to the TnC subunit of troponin.
  9. The contraction cycle is initiated and Ca2+ is returned to the terminal cisternae of sarcoplasmic reticulum.
38
Q

What is a motor unit?

A

An alpha motor neurone and the muscle fibres it innervates
Each individual muscle fibre is innervated by one motor neurone
A single motor neurone can innervated many muscle fibres
The muscle fibres that make up a motor unit are all of the same contractile type, so each motor unit is fast or slow contracting

39
Q

Why would muscles need more or less average muscle fibres per motor unit?

A

Less - fine control e.g. inferior rectus which moves eyeball: 9
1st interosseus (hand): 108
Tibialis anterior (front of lower leg): 562
More - power e.g. gastrocnemius (calf muscle): 1934

40
Q

What is a muscle spindle?

A

A sensory end organ in a muscle that is sensitive to stretch in the muscle, consists of small striated muscle fibers richly supplied with nerve fibers, and is enclosed in a connective tissue sheath — called also stretch receptor.Innervated by 2 sensory and 1 motor axon
Gamma motor neurones keeps fibres taught
Type 1a sensory neurones relay rate of change in muscle length back to CNS
Type II sensory neurones provide position sense
Spindle walled off from rest of muscle by collagen sheath

41
Q

What is different about cardiac troponin?

A

Has 2 cardiac specific isoforms of troponin I and T

42
Q

What are 2 ways in which tissues can increase in size?

A

Tissues, including muscle, which increase in size may do so by - enlargement of their individual cells
(hypertrophy), or by - multiplication of their cells (hyperplasia)

Muscles usually grow by hypertrophy

43
Q

What are natriuretic peptides?

A

Natriuretic peptides are peptide hormones that are synthesized by the heart, brain and other organs. The release of these peptides by the heart is stimulated by atrial and ventricular distension, usually in response to heart failure.

44
Q

What are the main physiological actions of natriuretic peptides?

A

The main physiological actions of natriuretic peptides is to reduce arterial pressure by decreasing blood volume and systemic vascular resistance. Normal hearts secrete extremely small amounts of ANP, but elevated levels are found in patients with left ventricular (LV) hypertrophy and mitral valve disease.

45
Q

What is ANP?

A

Atrial natriuretic peptide (ANP) is a 28-amino acid peptide that is synthesized, stored, and released by atrial myocytes in response to atrial distension (amongst other stimulations). Therefore, elevated levels of ANP are found during hypervolemic states (elevated blood volume), which occur in congestive heart failure (CHF).

46
Q

What is BNP?

A

A second natriuretic peptide (brain-type natriuretic peptide; BNP) is a 32-amino acid peptide that is synthesized largely by the ventricles (as well as in the brain where it was first identified).
BNP is released by the same mechanisms that release ANP, and it has similar physiological actions. Proteolysis of pro-BNP (108 amino acids) results in BNP (32 amino acids) and the N-terminal piece of pro-BNP (NT-pro-BNP; 76 amino acids).
Both BNP and NT-pro-BNP are sensitive, diagnostic markers for heart failure in patients (for instance, of increased LV filling pressures and dysfunction).
A rapid 15 minute immunoassay is possible.

47
Q

Describe the contraction of cardiac muscle cells

A

All cardiac muscle cells exhibit a spontaneous rythmic contraction (evident in embryonic cardiac muscle and in isolated mature muscle cells in tissue culture).

In the heart, action potentials generated in the sinoatrial node, pass to the atrioventricular node and from there to the ventricles.

These impulses are carried by specialised myocardial cells, of which the distal conducting cells, carrying impulses to the ventricular muscle, are called Purkinje fibres.

48
Q

What is myocardium?

A

Cardiac muscle tissue

49
Q

What is endocardium?

A

The thin, smooth membrane which lines the inside of the chambers of the heart and forms the surface of the valves.

50
Q

What are Purkinje fibres?

A

Purkinje fibres are large cells with:

  • abundant glycogen,
  • sparse myofilaments,
  • extensive gap junction sites.

The Purkinje fibres conduct action potentials rapidly (3-4 m/s, compared to 0.5m/s for cardiac muscle fibres).
This rapid conduction enables the ventricles to contract in a synchronous manner

51
Q

Describe smooth muscle cells

A

Cells are spindle-shaped (fusiform) with a central nucleus.
Not striated, no sarcomeres, no T tubules Contraction still relies on actin-myosin interactions.
Contraction is slower, more sustained and requires less ATP.
May remain contracted for hours or days.
Capable of being stretched.
Responds to stimuli in form of nerve signals, hormones, drugs, or local concentrations of blood gases.
Form sheets, bundles or layers containing thousands of cells.

52
Q

Where is smooth muscle found?

A

Often forms contractile walls of passageways or cavities (modify volume)

  • e.g. in gut, respiratory tract and genitourinary system.
  • e.g. of vascular structures.
53
Q

Name some disorders in which smooth muscle has clinical significance

A

It is involuntary and can develop a “mind of its own” and therefore be of clinical significance in disorders such as:

  • high blood pressure (i.e. primary hypertension)
  • dysmenorrhea
  • asthma
  • atherosclerosis
  • abnormal gut mobility (i.e. in Irritable bowel syndrome)
  • detrusor muscle instability
54
Q

What are myoepithelial cells?

A

Modified smooth muscle cells: Can occur singly as myoepithelial, or myofibroblast cells.
Myoepithelial cells – stellate cells forming a basketwork around the secretory units of some exocrine glands (e.g sweat, salivary and mammary glands).
Contraction assists secretion of sweat, saliva or milk into secretory ducts. Myoepithelial cells in the ocular iris contract to dilate the pupil.

55
Q

What are myofibroblasts?

A

Modified smooth muscle cells: Can occur singly as myoepithelial, or myofibroblast cells.
Myofibroblasts, at sites of wound healing, produce collagenous matrix but also contract (abundant actin and myosin). Prominent in wound contraction and tooth eruption.

56
Q

How are smooth muscle cells innervated?

A

Most smooth muscle cells are innervated by autonomic nervous system fibres that release their neurotransmitters from varicosities into a wide synaptic cleft.

57
Q

Can skeletal muscle divide?

A

Skeletal muscle cells cannot divide but the tissue can regenerate by mitotic activity of satellite cells, so that hyperplasia follows muscle injury. Satellite cells can also fuse with existing muscle cells to increase mass (skeletal muscle hypertrophy).

58
Q

Can cardiac muscle regenerate?

A

Cardiac muscle is incapable of regeneration. Following damage, fibroblasts invade, divide, and lay down scar tissue.

59
Q

Can smooth muscle cells divide?

A

Smooth muscle cells retain their mitotic activity and can form new smooth muscle cells. This ability is particularly evident in the pregnant uterus where the muscle wall becomes thicker by hypertrophy (swelling) and by hyperplasia (mitosis) of individual cells.