Muscle Flashcards

1
Q

What is myalgia?

A

Muscle pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is myasthenia

A

Weakness of the muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is myocardium?

A

Muscular component of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is myopathy

A

Any disease of the muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is myoclonus?

A

A sudden spasm of the muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sarcolemma =?

A

The outer membrane of a muscle cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sarcoplasm=?

A

The cytoplasm of a muscle cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Sarcoplasmic reticulum=?

A

The smooth endoplasmic reticulum of a muscle cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the three types of muscle?

A

Striated-skeletal, cardiac

Non striated- smooth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Can you describe the morphology of skeletal muscle?

A

Long parallel cylinders , multiple peripheral nuclei, striations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What connections does skeletal muscle make?

A

Fascicles bundles- a bundle of skeletal muscle fibres surrounded by perimysium.
Tendons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Can you describe the morphology of cardiac muscle?

A

Short branched cylinders, single central nucleus, striations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are cardiac muscle cells connected to each other?

A

Junctions join cells end to end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Can you describe the morphology of smooth muscle?

A

Spindle shaped, tapering ends, single central nucleus, no striations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What connections does smooth muscle make?

A

With Connective tissue, gap and desmosome-type junctions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the three different types of muscle fibre?

A

Red-slow twitch
Intermediate
White-fast twitch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How are white muscle fibres different to red muscle fibres?

A

They have a larger diameter, worse vascularisation, less myoglobin, less mitochondria, stronger contraction, fatigue rapidly, low in oxidative enzymes
Rich in ATPase
More neuromuscular junctions
DVMMCFEI - Do Voles Make More Fluffy Iced Elegant Cakes?
Diameter, vascularisation, myoglobin, mitochondria, fatigue, innervation, enzymes, contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is myoglobin?

A

-red protein containing haem
-stores oxygen
-structurally similar to a subunit of haemoglobin
-present in skeletal and cardiac muscle but not in smooth
Diving mammals have high amounts in their muscles enabling them to remain submerged for longer
Haemoglobin gives up oxygen to myoglobin especially when pH is lowered (eg. If active muscles are producing CO2 or lactic acid.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the difference between epimysium, endomysium and perimysium?

A

Epimysium is a membrane which surrounds the whole muscle, endomysium is connective tissue found in between muscle fibres and perimysium is found surrounding fascicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Can you name some of the various arrangements of skeletal muscle?

A

Circular- orbicularis oris (around mouth)
Convergent- pectoralis major
Parallel-extensor digitorum longus (inside of thigh)
Unipennate-front of lower leg
Multipennate-deltoid
Fusiform-biceps brachii
Bipennate-rectus femoris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is the tongue so mobile?

A
  • plasticity and strength of connective tissues

- multidirectional orientation of muscle fibres (interdigitation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is another name for a striated muscle cell?

A

A muscle fibre

23
Q

What are the four major proteins needed in muscle contraction?

A

Actin, myosin, tropomyosin and troponin

24
Q

What is the condition called when destruction of muscle is greater than replacement?

A

Atrophy

25
Q

What is the condition called when replacement of muscle exceeds destruction?

A

Hypertrophy

26
Q

What can atrophy be caused by?

A

Disuse- bed rest, sedentary behaviour
Causes-loss of protein, reduced fibre diameter- loss of power
Age- above 30 years, 50% muscle loss by 80 yrs.- serious consequences in temperature regulation
Enervation- signs of motor neurone lesions- weakness, flaciddity, atrophy (reinnervation usually within 3 months )

27
Q

Hypertrophy-causes?

A

More contractile proteins so increase in fibre diameter

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

28
Q

How is muscle length adjusted?

A

Increased by frequent stretching- addition of sarcomeres, if limb is immobilised then less sarcomeres.

29
Q

What is the hierarchy of muscle ultra structure?

A

Myofilaments (actin and myosin)- make up myofibrils- which make up muscle fibres (cells), which make up fascicles, which make up skeletal muscle

30
Q

Which three molecules complex to form the thin filaments of skeletal and cardiac muscle?

A

Acting tropomyosin and troponin

31
Q

What are troponin assays used for?

A

When cardiac muscle dies it releases troponin within one hour so troponin assay is a marker for cardiac ischaemia.
However- must be measured within 20 hours. The smallest changes in Troponin levels in the blood are indicative of cardiac muscle damage, although this quantity is not necessarily proportional to degree of damage

32
Q

What is CK ?

A

Creatine Kinase- an important enzyme in metabolically active tissues like muscle.

Used to diagnose MI's, enzyme increase largely proportional to infarct size
Also released into blood by damaged skeletal muscle and brain- this can arise from:
-intramuscular injection
Vigorous physical exercise
A fall
Rhabdomyolysis (severe muscle breakdown)
Muscle dystrophy 
Acute kidney injury
33
Q

Can you describe the morphology of myosin

A

Each individual 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.

34
Q

How are actin, tropomyosin and troponin arranged? And where does myosin interact with this?

A

The actin filament forms a helix, tropomyosin molecules coil around the actin helix, reinforcing it. A troponin complex is then attached to each tropomyosin molecule. In the centre of the sarcomere the thick filaments are devoid of myosin heads.
The myosin heads extend towards the actin filaments in the regions of potential overlap.

35
Q

How do calcium ions induce contraction?

A

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

36
Q

What is the sliding filament theory?

A

Myosin cross bridge attaches who actin myofilament with ADP and P attached to myosin head
The myosin head pivots and pulls on the actin filament sliding it towards the M line- releases ADP and P
A new ATP attaches to myosin head as the cross bridge detaches
As the ATP is split into ADP and P the myosin head is cocked to bind to a new actin binding site

37
Q

What is the extension of the sarcoplasmic reticulum called which conveys the action potential throughout the muscle fibre?

A

The T tubule

38
Q

Which neurotransmitter it stored in terminal swellings of the axon in neuromuscular junctions?

A

Acetyl choline

39
Q

What happens at the neuromuscular junction to initiate contraction?

A

Nerve impulse arises at NMJ. Impulse prompts release of Ach into synaptic cleft causing local depolarisation of sarcolemma.

Voltage gated Na+ channels open and ligand gated Na+ channels open so Na+ enters cell. General depolarisation spreads over sarcolemma and T tubules.

Voltage sensor proteins of T tubule membrane change their conformation.

Gated Ca2+ release channels of adjacent terminal cisternae are activated - Ca2+ is rapidly released into sarcoplasm.

40
Q

How are actin and myosin arranged in the cytoplasm?

A

No myofibrils, they just form continuous masses.

Mitochondria and SR penetrate through the cytoplasm between the myofilaments

41
Q

What is an intercalated disc and what is it a substitute for?

A

They are a junction between adjacent cardiac muscle cells and substitute for Z bands. They have gap junctions here for electrical coupling and adherens type junctions to anchor cells and provide anchorage for actin filaments.

42
Q

Where do the T tubules lie in Skeletal muscle and cardiac muscle?

A

Skeletal- at the A-I junction

Cardiac- within the Z bands

43
Q

What is it about the arrangement of the SR and T tubules that allows muscle contraction

A

They are closely associated at Diads which permits release of ionic calcium into the sarcoplasm and hence causes muscle contraction

44
Q

What is hypertrophy?

A

Enlargement of individual cells

45
Q

What is hyperplasia?

A

Multiplication of their cells.

46
Q

What are natriuretic peptides?

A

Peptide hormones synthesised by the heart, brain and other organs.
Release is stimulated by atrial and ventricular distension in response to heart failure

47
Q

What is the main physiological action of NP’s?

A

Reduce arterial pressure by decreasing blood volume and systemic vascular resistance.

48
Q

What is the clinical relevance of NP’s?

A

Normal hearts secrete extremely small amounts of ANP, but elevated levels are found in patients with left ventricular hypertrophy and mitral valve disease.

49
Q

What is ANP?

A

Atrial natriuretic peptide- 28 amino acid peptide that is synthesised, stored and released by atrial myocytes in response to atrial distension. Elevated levels of ANP are found during hypervolaemic states which occur in congestive heart failure.

50
Q

WHat is BNP?

A

Brain-type natriuretic peptide
32 amino acid peptide synthesised by the ventricles and brain
Released by same mechanisms as ANP and has similar physiological actions.
Proteolysis of ProBNP (108 aa) results in BNP and the N terminal piece of pro-BNP (76 aa)
Both of these are sensitive diagnostic markers for heart failure in patients (eg increased LV filling pressures and dysfunction)

51
Q

Where are action potentials generated in the heart?

A

In the sinoatrial node

52
Q

Where does the signal travel after being created in the SAN?

A

Passes to atrial ventricular node and from there to the ventricles

53
Q

How are impulses carried in the heart?>

A

Specialised myocardial cells- the distal conducting cells carrying impulses to the ventricular muscle are called purkinje fibres.

54
Q

How are purkinje fibres adapted to their function?

A
  • abundant glycogen
  • sparse myofilaments
  • extensive gap junction sites
  • this allows rapid conduction which allows the ventricles to contract in a synchronous manner