BL Session 8 - Muscular System and Cardiovascular System Flashcards

1
Q

Define the following terms:

  • Myalgia
  • Myasthenia
  • Myocardium
  • Myopathy
  • Myoclonus
A
  • Myalgia: Muscle pain.
  • Myasthenia: Weakness of the muscles.
  • Myocardium: Muscular component of the heart.
  • Myopathy: Any disease of the muscles.
  • Myoclonus: A sudden spasm of the muscles.
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2
Q

Define the following terms:

  • Sarcolemma
  • Sarcoplasm
  • Sarcoplasmic reticulum
A
  • Sarcolemma: The outer membrane of a muscle cell.
  • Sarcoplasm: The cytoplasm of a muscle cell.
  • Sarcoplasmic reticulum: The smooth endoplasmic reticulum of a muscle cell.
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3
Q

Identify the three histological forms of muscle.

A
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4
Q

Characterise the three major categories of muscle in terms of:

  • Morphology
  • Connections
  • Control
  • Power
A

- Morphology:

I. Skeletal - striations, long parallel bundles, multiple peripheral nuclei

II. Cardiac - striations, short and branched, small central nucleus

III. Smooth - no striations, spindle shaped, small central nucleus

- Connections:

I. Skeletal - fascicles, tendons

II. Cardiac - junctions

III. Smooth - connective tissue

- Control:

I. Skeletal - somatic voluntary

II. Cardiac - autonomic involuntary

III. Smooth - autonomic involuntary

- Power:

I. Skeletal - rapid and forceful

II. Cardiac - lifelong variable rhythm

III. Smooth - slow and sustained

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5
Q

Outline the appearance of skeletal muscle.

A

Histologists have identified

  • Narrower red skeletal muscle fibres.
  • Wider white skeletal muscle fibres.
  • Intermediate skeletal muscle fibres.
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6
Q

Red, white and intermediate skeletal muscle fibres are present in any given muscle, but their proportions depend on the functional role of the muscle. Compare and contrast the different forms on the basis of:

  • Diameter
  • Vascularisation
  • Myoglobin
  • Mitochondria
  • Contraction
  • Fatigue
  • Enzymes
  • Innervation
  • Typical location
A
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7
Q

Describe the structure and function of myoglobin, as well as where it can be found.

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.
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8
Q

Outline the structure of skeletal muscle

A

A striated muscle cell is called a muscle fibre

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9
Q

Describe the appearance of skeletal muscle in an H&E stained light micrograph.

A
  • Peripheral nuclei can be observed (TS)
  • Nuclei in rows can be observed (LS)
  • Dashed line shows boundary of a fascicle
  • Each fasicle is surrounded by perimysium
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10
Q

Outline the remodeling of muscles.

A
  • Continual - Replacement of contractile proteins in 2 weeks
  • Destruction > replacement = atrophy
  • Replacement > destruction = hypertrophy
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11
Q

What are the types of muscle atrophy?

A
  • Denervation atrophy

I. Signs of lower motor neurone lesions: weakness, flaccidity, muscle atrophy

II. Re-innervation within 3 months for recovery

  • Disuse atrophy:

I. E.g. Bed rest, limb immobilisation, sedentary behaviour

II. Loss of protein - reduced fibre diameter - loss of power

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12
Q

Explain how muscle length may adjust.

A
  • Increases by frequent stretching (addition of sarcomeres)
  • Converse is true: consider limb in plaster
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13
Q

Describe the appearance of the skeletal muscle ultrastructure in transverse section in a TEM.

A
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14
Q

Describe the appearance of the skeletal muscle sarcomere bands in TEM.

A
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15
Q

Actin, troponin and tropomyosin molecules complex to form the thin filaments of skeletal and cardiac muscle. Outline the significance of Troponin.

A
  • Troponin Assays are a useful diagnostic tool
  • Troponin used as a marker for cardiac ischaemia
  • 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, the 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.
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16
Q

Briefly outline the composition of skeletal muscles.

A
  • Skeletal muscles are composed of fascicles
  • Fascicles are composed of muscle fibres (cells)
  • Muscle fibres are composed of myofibrils
  • Myofibrils are composed of myofilaments (actin & myosin)
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17
Q

Describe the structure of an individual myosin molecule.

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
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18
Q

Describe the structure of the actin filament and troponin complex.

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
  • 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.
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19
Q

Outline the role and significance of Creatine Kinase.

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.
  • 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:

I. Intramuscular injection

II. Vigorous physical exercise

III. A fall (especially in the elderly)

IV. Rhabdomyolysis (severe muscle breakdown)

V. muscular dystrophy

VI. Acute kidney injury

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20
Q

Outline the contraction mechanism in light of the following stages:

  • Attachment
  • Release
  • Bending
  • Force Generation
  • Reattachment
A

- Stage 1: Attachment – Myosin head tightly binds to actin molecule in regions of overlap.

- Stage 2: Release – ATP binds the myosin head causing it to uncouple from the actin filament.

- Stage 3: Bending – Hydrolysis of the ATP causes the uncoupled myosin head to bend and advance a short distance

- Stage 4: Force Generation – The myosin head binds weakly to the actin filament causing release of inorganic phosphate which strengthens binding, and causes the ‘power stroke’ in which the myosin head returns to its former position.

- Stage 5: Reattachment – ATP binds to the myosin head causing detachment from actin. The myosin head will bind tightly again and the cycle will repeat.

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21
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.
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22
Q

Describe the structure of a neuromuscular junction as well as its role.

A
  • Small terminal swellings of the axon that contain vesicles of acetylcholine.
  • A nerve impulse causes the release of acetylcholine which binds receptors on the sarcolemma to initiate an action potential propagated along the muscle
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23
Q

Outline the contraction of skeletal muscle.

A
  • Initiation: nerve impulse along motor neuron axon arrives at neuromuscular junction.
  • Impulse prompts release of acetylcholine (Ach) into synaptic cleft causing local depolarization of sarcolemma.
  • Voltage-gated Na+ channels open; Na+ enters cell.
  • General depolarization spreads over sarcolemma and into T tubules, causing them to change their conformation.
  • Ca2+ is rapidly released from the terminal cisternae into the sarcoplasm.
  • Ca2+ binds to the TnC subunit of troponin.
  • The contraction cycle is initiated and Ca2+ is returned to the terminal cisternae of sarcoplasmic reticulum.
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24
Q

The cardiac muscle fibres in LS show:

A
  • Striations
  • Centrally positioned nuclei (1 or 2 per cell)
  • Intercalated discs (for electrical & mechanical coupling with adjacent cells - see asterisks)
  • Branching (arrows)
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25
Q

The cardiac muscle fibres in TS show:

A
  • Central nuclei
  • Endomysium bearing a rich supply of capillaries
  • Some lobular profiles representing incipient branching of fibres
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26
Q

Describe the appearance of the ultrastructure of the cardiac muscle in TS in a TEM.

A
  • In contrast to skeletal muscle, the distinct myofibrils are absent; instead myofilaments of actin and myosin form continuous masses in the cytoplasm.
  • Mitochondria and sarcoplasmic reticulum penetrate through the cytoplasm between the myofilaments.
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27
Q

Outline the structure and location of T tubules and the sarcoplasmic reticulum of cardiac muscle.

A
  • In contrast to skeletal muscle, the T tubules of cardiac muscle lie in register with the Z bands and not with the A-I band junction.
  • The close association of the sarcoplasmic reticulum and the T tubules at the diads permits the release of ionic calcium into the sarcoplasm and subsequent muscle contraction.
28
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.
29
Q

What are the functions of natriuretic peptides?

A

Reduce arterial pressure by:

  • Decreasing blood volume
  • Decreasing systemic vascular resistance.
30
Q

Outline ANP.

A

- Atrial natriuretic peptide (ANP) is a 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).
31
Q

What is BNP?

A

- BNP (brain-type natriuretic peptide) is another natriuretic peptide that is synthesised largely by the ventricles (as well as the brain where it was first identified).

  • BNP is released by the same mechanisms that release ANP, and it has similar physiological actions.
32
Q

What is the significance of natriuretic peptides?

A
  • Both BNP and NT-pro-BNP are sensitive, diagnostic markers for heart failure in patients
  • A rapid 15 minute immunoassay is possible.
  • To summarize, natriuretic peptides serve as a counter-regulatory system for the renin-angiotensin-aldosterone system (RAAS).
33
Q

Describe the structure and function of purkinje fibres.

A
  • All cardiac muscle cells exhibit a spontaneous rhythmic contraction
  • In the heart, action potentials generated in the SAN, pass to the AVN 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.
34
Q

What are Purkinje fibres?

A
  • Purkinje fibres are large cells with:

I. Abundant glycogen

II. Sparse myofilaments

III. Extensive gap junction sites

  • The Purkinje fibres conduct action potentials more rapidly that cardiac muscle fibres
  • This rapid conduction enables the ventricles to contract in a synchronous manner.
35
Q

Outline the structure of smooth muscle.

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
  • Form sheets, bundles or layers containing thousands of cells.
36
Q

What is the role of smooth muscle?

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

I. E.g. of vascular structures.

II. E.g. Open cavities - gut, respiratory tract and genitourinary system

  • It is involuntary and therefore be of clinical significance in disorders such as:

I. High blood pressure (i.e. primary hypertension)

II. Asthma

III. Atherosclerosis

IV. Abnormal gut mobility (i.e. in Irritable Bowel Syndrome)

37
Q

Outline what is meant by modified smooth muscle cells.

A
  • 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).

I. Contraction assists secretion of sweat, saliva or milk into secretory ducts.

II. Myoepithelial cells in the ocular iris contract to dilate the pupil.

  • Myofibroblasts at sites of wound healing:

I. Produce collagenous matrix but also contract (abundant actin and myosin).

II. Prominent in wound contraction and tooth eruption.

38
Q

Describe the structure of smooth muscle.

A
  • Smooth muscle thick and thin filaments are arranged diagonally within the cell, spiralling down the long axis like stripes on a barbers pole, so the smooth muscle contracts in a twisting way.
  • Most smooth muscle cells are innervated by the ANS fibres that release their neurotransmitters from varicosities into a wide synaptic cleft.
39
Q

Discuss the limited nature of repair possible in mature muscle.

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).
  • Cardiac muscle is incapable of regeneration. Following damage, fibroblasts invade, divide, and lay down scar tissue.
  • 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.
40
Q

What is the role of the cardiovascular system?

A
  • Circulates and transports nutrients, oxygen, carbon dioxide, hormones, and blood cells to and from the cells of the body
  • Fights disease
  • Stabilizes temperature and pH, thus helping to maintain homeostasis.
41
Q

Outline the distribution of blood.

A

An average adult has 5.0 litres of circulating blood:

  • 3.25 litres will be in the veins
  • 1.0 litres will be in the heart and lungs
  • 0.5 litres will be in the peripheral arteries
  • 0.25 litres will be in the capillaries but have by far the greatest surface area for substance exchange
42
Q

What are end arteries?

A
  • An end arteries is a terminal artery supplying all or most of the blood to a body part without significant collateral circulation.
  • Such arteries undergo progressive branching without the development of channels connecting with other arteries, so that, if occluded, there is insufficient blood supply to the dependant tissue.
  • Examples of functional end arteries are the coronary arteries, splenic artery, cerebral arteries and renal arteries.
  • The best example of an absolute end artery (anatomically true end arteries) is the central artery to the retina.
43
Q

What is collateral circulation?

A
44
Q

Outline the structure of the aortic arch.

A
45
Q

What are the three layers of the walls of the arteries and veins?

A
  • Tunica intima (next to the lumen)
  • An intermediate tunica media
  • An outer tunica adventitia
46
Q

What is an aneurysm?

A

Aneurysm: dilatation of a blood vessel.

47
Q

Outline the structure of muscular arteries.

A

- Tunica intima: Endothelium. Subendothelial layer. Thick internal elastic lamina.

- Tunica media: Main feature: 40 layers of smooth muscle cells. (These cells are connected by gap junctions for coordinated contraction). Prominent external elastic lamina.

- Tunica adventitia: Thin layer of fibroelastic connective tissue containing vasa vasorum (not very prominent), lymphatic vessels and nerve fibres.

48
Q

What are arterioles?

A

Arterioles: Arteries with a diameter of less than 0.1 mm are considered to be arterioles. Arterioles have only one to three layers of smooth muscle in their tunica media.

49
Q

Describe the structure and function of metarterioles

A
  • Arteries that supply blood to capillary beds are called metarterioles.
  • The individual muscle cells are spaced apart and each encircles the endothelium of a capillary arising from the metarteriole. This is a precapillary sphincter.
  • Each smooth muscle cell is believed to function as a sphincter, upon contraction, controlling blood flow into the capillary bed.
50
Q

What are lymphatic and pre-capillary spincters?

A
51
Q

Outline the importance of the dilation and constriction of the arteries.

A
52
Q

Outline the properties of capillaries

A
  • Our capillaries hold only 5% of our total blood volume. However, they present by far the largest surface area for gas and nutrient exchange (estimated to be about 600 m2).
  • Passing red blood cells fill virtually the entire capillary lumen, minimizing the diffusion path to adjacent tissues.
  • It is during passage through the capillaries that blood velocity is at its lowest (0.03 cm/s = 0.3 mm/s), allowing time for gas and nutrient exchange with surrounding tissues.
  • A capillary is essentially a tube, just large enough to allow the passage of blood cells one at a time.
  • The capillary is made of a single layer of endothelium and its basement membrane.
53
Q

What are pericytes?

A
  • Pericytes form a branching network on the outer surface of the endothelium.
  • These cells can divide into muscle cells, or fibroblasts, during angiogenesis, tumour growth and wound healing.
54
Q

What is the structure and function of post-capillary venules?

A
  • The post-capillary venule wall is similar to that of capillaries (endothelial lining with associated pericytes)
  • Post-capillary venules receive blood from capillaries and are even more permeable than capillaries.
  • Because their pressure is lower than that of capillaries or the surrounding tissue, fluid tends to drain into them, except when an inflammatory response is operating, in which case fluid and leukocytes emigrate.
  • Post-capillary venules are the preferred location for emigration of leukocytes from the blood.
55
Q

Outline the properties of veins.

A
  • As a general rule, veins have a larger diameter than any accompanying artery, and a thinner wall that has more connective tissue and fewer elastic and muscle fibres
  • Small- and medium-sized veins have a well-developed adventitia. The tunica intima is thin, as is the tunica media (2 or 3 layers of smooth muscle)
  • Large veins have diameters > 10 mm. The tunica intima is thicker. Most large veins do not have a prominent tunica media, but have a well-developed tunica adventitia. An exception are the superficial veins of the legs, which have a well-defined muscular wall, possibly to resist distension caused by gravity.
  • Veins are also called capacitance vessels.
56
Q

What is capacitance?

A

- Capacitance: the ability of a blood vessel to increase the volume of blood it holds without a large increase in pressure.

  • It is inversely proportional to elasticity.
  • Because veins have thin, non-elastic walls, they can stretch a great deal.
57
Q

How does venous blood get from the legs back to the heart in a standing human?

A
  • There are valves in the veins of the lower limbs, the upper limbs and heart.
  • There are no valves in the intraabdominal, intrathoracic or neck veins.
  • Calf muscle pump failure leads to venous hypertension.
58
Q

What is pulmonary oedema?

A

- Pulmonary oedema: a medical emergency, is an accumulation of fluid in the lungs.

  • Most often a consequence of congestive heart failure, pulmonary oedema typically occurs when the heart is unable to pump blood out through the arteries as quickly as it is returned to the heart through the veins.
  • Failure of the left side of the heart (left ventricle) causes blood to accumulate in the veins of the lungs (pulmonary veins), producing a dangerous rise in blood pressure within these veins.
  • Sustained high pressure in the pulmonary veins eventually forces some fluid from the blood into the surrounding microscopic air sacs (alveoli), which transfer oxygen to the bloodstream.
59
Q

What is orthopnea?

A

Orthopnea: is shortness of breath (dyspnea) that occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair.

60
Q

What is paroxysmal nocturnal dyspnoea?

A

- Paroxysmal nocturnal dyspnoea (PND): refers to attacks of severe shortness of breath and coughing that generally occur at night.

  • It usually awakens the person from sleep, and may be quite frightening.
61
Q

What is muscle hypertrophy?

A

Muscle hypertrophy: Response to a requirement for increased muscle work, particularly that which increases muscle tension.

62
Q

What is muscle atrophy?

A
  • Reduction in number of cells and/or size of cells
  • Due to:

I. Muscle inactivity

II. Malnutrition

III. Cancer

IV. Congestive cardiac failure, chronic obstructive pulmonary disease (COPD), renal failure

V. Neurogenic – e.g motor neurone disease, spinal cord injury

63
Q

What are diseases caused by smooth muscle dysfunction?

A
  • Asthma
  • Irritable Bowel Syndrome
  • Primary hypertension
  • Detrusor instability
64
Q

What are indicators of muscle injury/necrosis?

A
  • Creatine kinase (all muscle)
  • Myoglobinuria (skeletal muscle)
  • Troponin I (cardiac)
65
Q

Describe the features of the Cardiovascular system.

A
  • The essential components of the human cardiovascular system are the heart, blood and blood vessels.
  • The pulmonary circulation, a “loop” through the lungs where blood is oxygenated.
  • The systemic circulation, a “loop” through the rest of the body to provide oxygenated blood and receive deoxygenated blood.
  • Humans, as well as other vertebrates, have a closed cardiovascular system (meaning that the blood never leaves the network of arteries, veins and capillaries).