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Yr 1 - Nerves & Muscle > Cardiac and Smooth Muscle > Flashcards

Cardiac and Smooth Muscle Flashcards

1
Q

What is skeletal muscle controlled by?

A

Somatic motor neurones (voluntary)

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2
Q

Describe cardiac muscle

A
  • Striated (like skeletal), branched, interconnected
  • Cardiac smaller than skeletal muscle cells
  • Rich in glycogen, myoglobin and mitochondria
  • Striated, with characteristic A and I-bands
  • Contains actin & myosin myofilaments
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3
Q

What is cardiac muscle controlled by?

A

Controlled involuntarily by endocrine and autonomic nervous systems

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4
Q

Describe mitochondria of cardiac compared to skeletal

A

Mitochondria comprise 30% of volume of the cell vs. only 2% in skeletal

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5
Q

What is function of intercalated discs in cardiac muscle?

A

Specialised cell-cell contacts as cell membranes interlock. 2 functions:

  • Mechanical coupling –> Desmosomes hold cells together
  • Electrical coupling –> Gap junctions allow action potentials to spread quickly to adjoining cells
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6
Q

What are intercalated discs?

A

Intercalated discs are unique structural formations found between the myocardial cells of the heart. They play vital roles in bonding cardiac muscle cells together and in transmitting signals between cells

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7
Q

What are the 3 types of cell junction that make up an intercalated disc?

A
  1. Fascia adherens
  2. Desmosomes
  3. Gap junctions
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8
Q

What are fascia adherens?

A
  • Anchoring sites for actin

* Connect to closest sarcomere

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9
Q

What are desmosomes?

A
  • Stop separation during contraction by binding intermediate filaments, joining the cells together
  • Also known as macula adherens
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10
Q

What are gap junctions?

A

Allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarisation of the heart muscle

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11
Q

What cells are autorhytmic?

A

Fibres spontaneously contract (sino atrial node) - Pacemaker cells)

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12
Q

What are arrythmias?

A

In the patient with coronary ischemia, areas of heart muscle can begin to randomly depolarise

Depolarisation of one irritable myocyte rapidly propagates via the all-or-none principle, which can lead to a fatal arrhythmia (ventricular fibrillation or ventricular tachycardia). Fatal arrhythmias are the most common cause of sudden death during a myocardial infarction.

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13
Q

What are the 2 cell types in cardiac muscle?

A
  1. Contractile cells

2. Autorhythmic cells

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14
Q

Describe contractile cells

A

• Myocytes contract the heart

- Don’t initiate their own AP

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15
Q

Describe autorhythmic cells

A
  • Initiate APs
  • No stable resting membrane potential (Neural input not necessary to initiate an AP)
  • Pacemaker activity instead ( Slow depolarization, drift to threshold, then firing)
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16
Q

Describe membrane potential of:

  1. Skeletal muscle
  2. Contractile myocardium
  3. Autorhythmic myocardium
A
  1. Stable at -70 mV
  2. Stable at -90 mV
  3. Unstable pacemaker potential (usually starts about -60 mV)
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17
Q

Describe events leading to threshold potential of:

  1. Skeletal muscle
  2. Contractile myocardium
  3. Autorhythmic myocardium
A
  1. Net Na+ entry through ACh operated channels
  2. Depolarisation enters via gap junctions
  3. Net Na+ entry through If channels, reinforced by Ca2+ entry
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18
Q

Describe rising phase of AP of:

  1. Skeletal muscle
  2. Contractile myocardium
  3. Autorhythmic myocardium
A
  1. Na+ entry
  2. Na+ entry
  3. Ca2+
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19
Q

Describe repolarisation phase of:

  1. Skeletal muscle
  2. Contractile myocardium
  3. Autorhythmic myocardium
A
  1. Rapid –> caused by K+ efflux
  2. Extended plateau caused by Ca2+ entry, rapid phase caused by K+ efflux
  3. Rapid, caused by K+ efflux
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20
Q

Describe hyperpolarisation of:

  1. Skeletal muscle
  2. Contractile myocardium
  3. Autorhythmic myocardium
A
  1. Due to excessive K+ efflux at K+ permeability when K+ channels close, leak of K+ and Na+ restores potential to resting state
  2. None (resting potential is -90mV, the equilibrium potential for K+)
  3. Normally none, when repolarisation hits -60mV, the If channels open again. ACh can hyperpolarise the cell
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21
Q

Describe AP of:

  1. Skeletal muscle
  2. Contractile myocardium
  3. Autorhythmic myocardium
A
  1. Short
  2. Extended
  3. Variable
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22
Q

Describe refractory period of:

  1. Skeletal muscle
  2. Contractile myocardium
  3. Autorhythmic myocardium
A
  1. Generally brief
  2. Long because resetting of Na+ channel gates delayed until end of AP
  3. None
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23
Q

How is pacemaker potential conducted from nodal tissue to adjacent contractile cells and beyond?

A

Through gap junctions in intercalated discs

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24
Q

What is Wolff-Parkinson-White (WPW) Syndrome?

A

Disorder of the conduction system of the heart, referred to as pre-excitation syndrome

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25
Q

What is WPW syndrome caused by?

A

Caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles

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26
Q

What does WPW lead to?

A

Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.

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27
Q

What is complete heart block caused by?

A

• No transmission through the AV node
o His-Purkinje fibres take over pacemaker (pace the heart between 20 and 40 beats/min)
o Slower pacemaker activity in distal parts of the conducting system allows the heart to continue beating if the SA node fails

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28
Q

What is heart rate and cardiac output like of patients with complete heart block?

A
  • Bradycardia

- Reduced cardiac output

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29
Q

What are the 4 main classes of anti arrhythmic agents?

A
  1. Class I –> Sodium channel blockers
  2. Class II – Beta blockers
  3. Class III –> Potassium channel blockers
  4. Class IV –> Calcium channel blockers
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30
Q

How do beta blockers work?

A
  • Block effects of catecholamines at the B-1 adrenergic receptors
  • Decreases sympathetic activity on heart
  • Decrease conduction in SA and AV nodes
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31
Q

What are beta-blockers used to treat?

A

Treatment of supraventricular tachycardias

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32
Q

How do K+ channel blockers work?

A

Block potassium channels, thereby prolonging repolarisation

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33
Q

What are K+ channel blockers used to treat?

A

Treat ventricular tachycardia & atrial fibrillation

34
Q

How do Ca2+ channel blockers work?

A
  • Decrease conduction through AV & SA nodes
  • Shorten phase II (plateau) of cardiac action potential
  • Reduce contractility of the heart, not appropriate in heart failure
35
Q

How do Ca2+ channel blockers contrast to beta-blockers?

A

They allow body to retain adrenergic control of heart rate and contractility

36
Q

What is SA and AV node AP upstroke dependent on?

A

Ca2+ dependent

37
Q

What is ventricular upstroke dependent on?

A

Na+ dependent

38
Q

Skeletal muscle has a short refractory period but a longer twitch. After the refractory period the muscle can re-stimulated, what does this allow?

A

During the muscle contraction allows summation of twitches

39
Q

How is cardiac muscle refractory period in relation to the twitch?

A
  • Cardiac muscle long refractory period as long as the muscle twitch
  • Can’t get summation
40
Q

Describe cardiac excitation-excitation coupling

A
  • Action potential invades the T-tubules (just as in skeletal muscle)
  • This opens voltage-gated L-type Ca2+ channels in the T-tubule membrane (there is an abundance of these channels, unlike the situation in skeletal muscle)
  • Ca2+ enters through L-type Ca2+ channels
  • This triggers further Ca2+ release from adjacent sarcoplasmic reticulum (SR) as Ca2+ influx from L-type channel is not sufficient for contraction
  • Amplifies Ca2+ (‘calcium induced calcium release’)
  • Ca2+ binds to troponin-C
  • Contraction proceeds in same way as in skeletal muscle
  • The channels in the SR remain open after the L-type close
  • Each L-type channel appears to control only one SR release channel due to the local structure, this means tight local control
41
Q

Where does AP invade in cardiac muscles? What does this cause?

A

T-tubules

This opens voltage-gated L-type Ca2+ channels in the T tubule membrane (there is an abundance of these channels, unlike the situation in skeletal muscle) and Ca2+ enters

42
Q

What does Ca2+ entering cardiac muscles result in?

A

This triggers further Ca2+ release from adjacent sarcoplasmic reticulum (SR)

Amplifies Ca2+ (‘calcium induced calcium release’)

43
Q

Why is further Ca2+ released from adjacent SR?

A

As Ca2+ influx from L-type channel is not sufficient for contraction

44
Q

What does Ca2+ bind to in cardiac cell?

A

Troponin-C

45
Q

What occurs after Ca2+ binds to troponin-C?

A
  • Contraction proceeds in same way as in skeletal muscle

* The channels in the SR remain open after the L-type close

46
Q

Why does each L-type channel appear to control only one SR release channel?

A

Due to the local structure, this means tight local control

47
Q

How does noradrenaine affect the heart?

A

increases the contractile force of the heart

48
Q

How does noradrenaline increase the contractile force of the heart?

A

It acts through the beta-type adrenergic receptor to increase cAMP, to activate PKA which phosphorylates the L-type channel, increasing passive Ca2+ influx.

49
Q

How does digitalis glycosides (e.g. digoxin) act to treat heart conditions?

A

Inhibits Na+/K+ ATPase pump (mainly in myocardium)

50
Q

What does inhibition of Na+/K+ ATPase result in?

A

This causes an increase in intracellular Na+ levels which results in reversal of the action of the sodium-calcium exchanger which normally imports 3 intracellular Na+ ions into cell and 1 intracellular Ca2+ ion out of cell

51
Q

What does reversal of this exchange (Na+/K+ ATPase) result in?

A

An increase in the intracellular calcium concentration that is available to the contractile proteins

52
Q

What does increase in the intracellular calcium concentration result in?

A
  • Lengthens phase 4 and phase 0 of the cardiac action potential which leads to a decrease in heart rate
  • Increased storage of Ca in SR
53
Q

What does increase in storage of Ca in SR lead to?

A

Causes corresponding increase in the release of calcium during each action potential
o This leads to increased contractility (force of contraction) of the heart without increasing heart energy expenditure

54
Q

What is effect of ACh from parasympathetic nerves on pacemaker function?

A

o Stimulates vagus nerve
o Decrease SA node rate
o Decrease heart rate

55
Q

What is effect of noradrenaline from sympathetic nerves on pacemaker function?

A

o Increases rate of depolarisation of pacemaker cells of SA node
o Develop action potentials at an increased rate
o Increase heart rate

56
Q

The resting length of cardiac muscle cells is set below its ‘optimal level’. What does this mean? What does this result in?

A

When the heart is in diastole, the degree of overlap between the thick and thin filaments in the ventricular muscle cells is less than optimal

This means that, up to a point, stretching the cells more will result in a greater degree of myosin–actin overlap and, therefore, in an increase in the amount of force generated when the cells contract

57
Q

What are smooth muscles controlled by?

A

• Involuntary muscles
o Controlled by endocrine and autonomic nervous systems
o Usually 2 sheets of closely opposed fibres that overlay one another (one is circular and one is longitudinal)

58
Q

What does alternating contraction and relaxation of 2 layers in smooth muscle cause?

A

Mixes substances in lumen of hollow organs (peristalsis)

59
Q

What can excessive smooth muscle contraction in the respiratory tract cause?

A

Difficulty breathing –> asthma attack

60
Q

What can inadequate tone in vascular smooth muscle cause?

A

Septic shock –> an overwhelming infection releases inflammatory mediators that cause dilation of systemic blood vessels, resulting in severe hypotension

61
Q

Describe fibres of smooth muscle compared to skeletal muscle?

A

Smaller fibres, more actin than myosin (16:1, 2:1 in skeletal), no sarcomeres, no striation, no troponin, no T-tubules

62
Q

What is contraction in smooth muscle regulated by?

A

By Ca2+ via a protein called calmodulin and an enzyme called myosin kinase

63
Q

What does contraction of smooth muscle depend on?

A

Increase in cystolic Ca2+

64
Q

What is contraction of smooth muscle regulated by?

A

Myosin molecules of the thick filament (not by the thin filament which lacks troponin, unlike skeletal and cardiac mscle)

65
Q

What must occur before cross bridges can form in smooth muscle contraction?

A

Myosin molecule must be phosphorylated at a specific site on the myosin ‘light chains’

66
Q

What does Ca2+ bind to in smooth muscle?

A

Calmodulin (not troponin) which interacts with enzyme myosin kinase to phosphorylate myosin

67
Q

Once myosin cross bridge is phosphorylated by myosin kinase in smooth muscle, what happens?

A

It is capable of attaching to actin filament and generating tension in a similar way as occurs in skeletal muscle

68
Q

What happens when cytoplasmic Ca2+ falls in smooth muscle?

A

The Ca2+-calmodulin complex dissociates, inactivating myosin kinase

69
Q

What are the cross bridges in smooth muscle dephosphorylated by?

A

By the enzyme myosin phosphatase

70
Q

What is an important feature of smooth muscle?

A

Its ability to maintain force over long periods of time (eg Sphincters)

71
Q

Why does contraction of smooth muscle occur more slowly?

A

Cross bridge cycling is much slower

The duration of the contraction in response to a stimulus is long

Reduced ATP consumption

72
Q

Why is cross bridge cycling in smooth muscle slower?

A
  1. Smooth muscle myosin has a slow ATPase rate so once attached, it takes a long time for each cross bridge to detach from the actin filament
  2. The rate of Ca2+removal from the cytoplasm is slow, so prolonging the duration of contraction
73
Q

What is single-unit (unitary) smooth muscle?

A

• Most common
• Gap junctions so act as single unit
• Electrical activity may arise spontaneously due to the presence of ‘pacemaker’ cells
–> Action potentials are developed
• Nervous regulation is via the autonomic nervous system

74
Q

What is multi-unit smooth muscle?

A
  • Lack gap junction –> cells innervated individually
  • Allows fine control, examples include ciliary muscle of the eye controlling size of pupil and piloerector muscles of hair follicles
  • Not spontaneously active
  • Innervation is autonomic
  • There is no inherent response to stretch
  • Contractions are slow and sustained
75
Q

What are varicosities?

A

Autonomic nerves make multiple contacts with the cell

No specialised postjunctional membrane, receptors spread across cell membrane.

76
Q

What is molecular basis for:

  1. Cardiac muscle
  2. Skeletal muscle
  3. Smooth muscle
A
  1. Ca2+-troponin C
  2. Ca2+-troponin C
  3. Ca2+-calmodulin
77
Q

What causes the end of contraction of:

  1. Cardiac muscle
  2. Skeletal muscle
  3. Smooth muscle
A
  1. Repolarisation of AP
  2. Breakdown of ACh in NMJ
  3. Myosin light chain phosphatase activity
78
Q

What is dilated cardiomyopathy?

A
  • Heart enlarges, functions poorly
  • Muscle becomes weak, inefficient causing fluid build-up in the lungs, → breathlessness → left heart failure
  • Right heart failure → fluid build-up in tissues & organs (legs, ankles, liver, abdomen)
79
Q

What is hypertrophic cardiomyopathy?

A

A disease of the myocardium in which a portion of the myocardium is hypertrophied (thickened) without any obvious cause

May thicken in normal individuals as a result of high blood pressure or prolonged athletic training

80
Q

What is leiomyoma (fibroids)?

A

A smooth muscle disorder

  • Benign growth
  • Female reproductive tract
  • Heavy uterine bleeding &/or pain

Yr 1 - Nerves & Muscle (11 decks)

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