Muscle Flashcards Preview

Body Logistics > Muscle > Flashcards

Flashcards in Muscle Deck (52):

What is myalgia?

Muscle pain


What is myasthenia?

Muscle weakness


What is the myocardium?

The muscular component of the heart


What is meant by the term 'myopathy'?

Any disease of the muscles


What is a myoclonus?

A sudden spasm of the muscles


What is the sarcolemma?

The outer membrane of a muscle cell


What is the sarcoplasm?

The cytoplasm of a muscle cell


What is the sarcoplasmic reticulum?

The smooth endoplasmic reticulum of a muscle cell


What are the three types of muscle

- Skeletal
- Cardiac
- Smooth


Which types of muscle are striated?

(Meaning streaked/striped)
- Skeletal
- Cardiac

But not smooth muscle


Describe the structure of skeletal muscle

- Long, parallel cylinders
- Multiple peripheral nuclei
- Striated


Describe the structure of cardiac muscle

- Striated
- Short branched cylinders
- Single central nucleus


Describe the structure of smooth muscle

- Non-striated
- Spindle shaped (tapering ends)
- Single central nucleus


How would you stain skeletal muscle?

- Colour differences not evident with H & E staining
- Specific stains
- E.g. Stain showing reaction to NADH in mitochondria


What are the three types of muscle fibres present in muscle?

Red, intermediate and white


Describe the properties of red muscle fibres

- Small diameter
- Rich vascularisation
- Rich in myoglobin
- Many mitochondria
- Contraction = slow, repetitive, relatively week
- Fatigue = slowly
- Enzymes = lots of oxidative enzymes, little ATPase
- Not many neuromuscular junctions
- Location = Limb muscles, postural muscles of back


Describe the properties of white muscle fibres

- Large diameter
- Poor vascularisation
- Poor myoglobin
- Few mitochondria
- Fast/ strong contraction
- Rapidly fatigued
- Lots of ATPase, poor in oxidative enzymes
- More neuromuscular junctions than red fibres
- Location = extraocular muscles and muscles controlling fingers


What is myoglobin?

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.


Is myoglobin present in all muscle?

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


How do muscles obtain oxygen? What is the effect of pH?

- Haemoglobin gives up oxygen to myoglobin
- Especially at low pH
- e.g. High levels of CO2/lactic acid = acidic pH


How are muscles remodelled?

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


What is disuse atrophy?

- E.g. Bed rest, limb immobilisation
- Loss of protein
- Reduced fibre diameter
- Loss of power


How can age lead to poor temperature regulation in relation to muscles?

- Muscle atrophy with age
- 50% muscle loss by 80
- Less muscle to respire and produce heat


What is denervation atrophy?

- Lower motor neurone lesions
- Muscle weakness
- Re-innervation within 3 months for recovery


What is hypertrophy?

- More contractile proteins and stored glycogen
- Fibres increase in diameter
- Increased enzyme activity for glycolysis, mitochondria, stored glycogen and blood flow


What is the explanation of increasing flexibility?

- Frequent stretching
- increasing length of sarcomeres


What are the M,H,A bands

MHAZI (M band in H in A in Z in I)

M line = centre of sarcomere (just myosin)
H zone = beginning of actin filaments with myosin
A band = end of myosin
Z = centre of I band (end of sarcomere)
I band = just actin


Describe the sliding filament mechanism

Thick filaments = myosin (anchored to M line)
Thin filaments = actin (anchored to Z line)

Myosin pulls actin along its length by forming cross bridges during contraction.

1. ATP is hydrolysed
2. Myosin head extends and attaches to actin
3. Power stroke pulls actin across myosin (shorted sarcomere)
4. ATP and phosphate released
5. New molecule of ATP binds to myosin = returns to position


What causes muscle contraction?

Muscle contraction controlled by calcium

When muscle is relaxed
- Tropomyosin blocks cross bridge binding sites on actin

- Calcium ions bind to troponin
- Displaces tropomyosin
- Exposes cross bridge binding site


What are skeletal muscles composed of?

Myofilaments (actin and myosin) form myofibrils
Muscle fibres/cells arranged in bundles
Endomyseium ensheaths each fibre
These bunch together to form fascicles
Wrapped by perimysium
Most outer layer connective tissue = epimysium (wraps many fascicles together)


What can troponin be used to measure?

- Cardiac ischaemia
- Released from ischaemic cardiac muscle within an hour
- Small change = cardiac muscle damage
- Not proportional to degree of damage


What is creatine kinase and what can it be measured for?

CK is an important enzyme in metabolically active tissues like muscle.

Creatine kinase 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.


What causes creatine kinase to be released into the blood?

• intramuscular injection,
• vigorous physical exercise,
• a fall (especially in the elderly),
• rhabdomyolysis (severe muscle breakdown),
• muscular dystrophy, and
• acute kidney injury.


What is the cause of rigor mortis in death?

Rigor configuration: myosin head tightly bound to actin molecule. In death, lack of ATP perpetuates this binding (rigor mortis).


What is a neuromuscular junction?

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.


How does a nerve impulse lead to the contraction of skeletal muscle?

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 (invagination for depolarization)
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.


How is the structure of cardiac muscle different to that of skeletal muscle?

- Distinct myofibrils are absent
- Myofilaments form continuous masses in the cytoplasm


What is the word used to describe tissue increasing in size by multiplication of their cells?



What are natriuretic peptides?

- 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 (stretching)
- Usually in response to heart failure.


What are the main physiological actions of natriuretic peptides?

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.


What is ANP?

- Atrial natriuretic peptide (ANP)
- 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).


What is BNP?

- Brain-type natriuretic peptide; BNP
- 32-amino acid peptide that is synthesized largely by the ventricles (as well as in the brain where it was first identified).


What test could you use in patients with heart failure?

- Both BNP and NT-pro-BNP are sensitive, diagnostic markers for heart failure in patients
- A rapid 15 minute immunoassay is possible.


Where are action potentials generated in the heart?

Sinoatrial node


How does an action potential travel through the heart?

- 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.


What are the key features of purkinje fibre cells?

Purkinje fibres are large cells with:
- abundant glycogen,
- sparse myofilaments,
- extensive gap junction sites.

All of the above allow them to conduct action potentials quickly


Describe the key features of smooth muscle

- 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.


What are myoepithelial cells and what are there functions?

– 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.


What are myofibroblasts?

Myofibroblasts, at sites of wound healing, produce collagenous matrix but also contract (abundant actin and myosin). Prominent in wound contraction and tooth eruption.


How does skeletal muscle repair itself?

- Can't divide
- Tissue regenerates by mitotic activity of satellite cells


How does cardiac muscle repair?

Incapable of regeneration. Following damage, fibroblasts invade, divide, and lay down scar tissue.


Can smooth muscle repair itself?

Cells retain their mitotic activity and can form new smooth muscle cells.
E.g. pregnant uterus where the muscle wall becomes thicker by hypertrophy (swelling) and by hyperplasia (mitosis) of individual cells.