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M103 T3 > M103 T3 L18 > Flashcards

M103 T3 L18 Flashcards

1
Q

What are the different parts of the sarcomere?

A 
Z line
M line
A band
I band
H band
thick filaments
thin filaments
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2
Q

What are the two different ways of changing the contratile force in cardiac muscle?

A

intrinsic regulation

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3
Q

What does Starling’s law state?

A

if you put more blood into the heart, you cause stronger contractions so that you empty the heart of blood more

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4
Q

What is the effect of intrinsic regulation on the contratile force in cardiac muscle?

A

increased contractility, which is both longer and stronger than under normal circumstances

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5
Q

How does intrinsic regulation work?

A

as the cell is stretched out, it is more feasible for cross bridge formation to occur throughout the thick filament
AAR, more cross bridges interact within filaments, more myosin in acting
AAR, there is more power for longer

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6
Q

What is the difference between intrinsic and extrinsic regulation in terms of where the regulation occurs?

A

intrin - when regulation is occurring at the level of that particular cell due to activities happening exclusively in the cell
extrin - depends on activities due to release of compounds / hormones from other cells

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7
Q

Why is it called extrinsic regulation?

A

bc it’s extrinsic to the cardiac myocyte bc the noradrenaline is being released by the NS

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8
Q

What type of stimulation does extrinsic regulation use?

A

sympathetic stimulation

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9
Q

What is the effect of extrinsic regulation on the contratile force in cardiac muscle?

A

increased contractility of the same duration, which is both faster and stronger than under normal circumstances

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10
Q

How does extrinsic regulation work?

A

instead of more cross bridges, the extant crossbridges work more effectively

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11
Q

What is a result of increased end diastolic volume?

A

(more stretch leads to) increased contractile force of the heart

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12
Q

What causes increased end diastolic volume?

A

increased successful overlap of thin and thick filaments leads to increased force generation

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13
Q

What is the denervated heart rate?

A

about 100bpm

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14
Q

What is the normal resting heart rate?

A

about 60bpm

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15
Q

What keeps the normal resting heart rate at about 60bpm?

A

parotonic parasympathetic stimulation

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16
Q

What is the effect of noradrenaline and the adrenergic receptors?

A

lead to an increase in the funny current

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17
Q

How does noradrenaline work to increase the funny current?

A

noradrenaline affects the pacemaker channels
it therefore increases the slope of the pacemaker potential via the beta one receptor
the next actpt occurs sooner, so there’s an increase in the heart rate of the nodal cells

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18
Q

What does it mean if the slope of the pacemaker potential is increased?

A

it takes less time for the action potential to build up to the point where it overcomes the threshold potential so that another contraction can start in the heart

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19
Q

What is the effect of noradrenaline on nodal cells?

A

an increase in calcium current (increased contractile force)

an increase in potassium current

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20
Q

What is the effect of an increase in potassium current?

A

the delayed rectifier current increases
shortens the duration of the actpt
allows for faster heart rates

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21
Q

What does the HCN channel do?

A

conducts a net current inward by moving both Na in and K out

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22
Q

What is the reversal potential of the funny current?

A

-10 mV

if no other channel open in the cell except for the HCN channel, the cell would reach -10mV

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23
Q

When does the HCN channel open?

A

when the membrane becomes more negative than normal

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24
Q

What is the effect of the HCN channel?

A

it controls the slope of the pacemaker potential

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25
Q

What is pacemaker potential controlled by?

A

HCN channels

Na / Ca exchange

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26
Q

What is the effect of sympathetic stimulation on the funny current?

A

increases the funny current - increased upward pacemaker potential

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27
Q

What are the three different types of adrenergic receptors?

A

alpha1
alpha2
beta

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28
Q

What is the effect of alpha1 receptors?

A

cause vasoconstriction in most organs

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29
Q

How do alpha1 receptors work once stimulated by noradrenaline?

A

they activate GQ protein
stimulates the activity of phospholipase C
it breaks apart PIP2 into inositol triphosphate and diacylglycerol
IP3 will mobilise calcium
this causes vasoconstriction

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30
Q

What does phospholipase C do once activated?

A

it breaks apart PIP2

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31
Q

What does GQ protein do once activated?

A

stimulates the activity of phospholipase C

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32
Q

What does phospholipase C break apart PIP2 into?

A

inositol triphosphate

diacylglycerol

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33
Q

Where are beta1 adrenergic receptors located?

A

in heart cells

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34
Q

Where are beta2 adrenergic receptors located?

A

in the smooth muscle of skeletal muscle

in the lung

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35
Q

What does Gs protein do once activated?

A

activates adenyl cyclase which catalyses the change of ATP into cAMP
cAMP will affect downstream operators via protein kinase A, which it activates
affects the funny current

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36
Q

What is the effect of beta2 adrenergic receptors once activated?

A

increase in heart contraction
increase in heart rate d
increase funny current conduction
increase skeletal muscle perfusion

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37
Q

What does cAMP do once activated?

A

activates protein kinase A

affect downstreams operators via protein kinase A

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38
Q

What does adenyl cyclase do once activated?

A

catalyses the change of ATP into cAMP

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39
Q

How do beta2 adrenergic receptors increase skeletal muscle perfusion?

A

stimulates a potassium channel which hyperpolarizes the membranes
broncho dilation - causes relaxation of smooth muscles in the bronchial tree

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40
Q

What is the effect of parasympathetic stimulation on heart rate?

A

heart rate slows down

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41
Q

What hormone and nerve are involved in the parasympathetic stimulation on heart rate?

A

acetylcholine

vagus nerve

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42
Q

What is the effect of acetylcholine?

A

leads to an increase in potassium currents, particularly through the IK(ACh) channel

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43
Q

What is the effect of the opening of any K channel?

A

will make the membrane pt more negative
will hyperpolarize the membrane
leads to a decrease in the slope of the pacemaker potential

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44
Q

What are the three types of G protein coupled-receptors?

A

Gq (stimulatory receptor)
Gi (inhibitory receptor)
Gs (stimulatory receptor)

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45
Q

Which G protein coupled-receptor activates adenyl cyclase?

A

the Gs protein (by beta1&2)

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46
Q

Which G protein coupled-receptor inhibits adenyl cyclase?

A

the Gi protein (e.g by adenosine and the muscarinic receptor M2)

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47
Q

What is the effect of muscuranic receptors being activated?

A 
activates Gi
Inhibits adenyl cyclase
lower levels of cAMP
slower heart rate
decreased chronotropy 
decreased dromotropy
less strength and less contraction
heart rate slows down
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48
Q

What happens if muscuranic receptors are blocked with atropine?

A

Gi will not be activated, etc
cAMP levels increase
increased chronotropy
heart rate increases

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49
Q

What are delayed rectifier channels activated by?

A

positive voltages

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50
Q

When are inward rectifiers activated?

A

any time when the cells are mostly at a highly negative voltage

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51
Q

What are the three K+ channels in cardiomyocytes?

A

Delayed Rectifiers
Inward Rectifiers
ACh-sensitive K channels

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52
Q

What happens when the voltage goes below -60mV during a neural actpt?

A

the inward rectifier K channels tend to open

this causes the voltage to become more negative than at rest - goes towards -90mV

53
Q

What happens to the channels during after-hyperpolarisation?

A

the inward rectifiers briefly open at the same time as the delayed rectifiers

54
Q

What is the status of delayed rectifiers when there is a normal negative pt?

A

at rest, delayed rectifiers are closed

55
Q

What happens to the delayed rectifiers during repolarisation?

A

at rest, delayed rectifiers are closed
delayed rectifiers do everything slowly so they don’t actually close immediately
during repolarisation, the delayed rectifiers are still open bc they haven’t had time to close up again
AAR, both the delayed rectifier and the inward rectifier are open
leads to a more negative voltage than at rest until the delayed rectifiers finally catch up

56
Q

What is affected during after-hyperpolarisation?

A

delayed rectifiers

sodium permeability

57
Q

What happens to sodium channels during depolarisation?

A

they are temporarily inhibited due to inactivation
this takes time to recover from, so after a delay, the sodium channels disinhibit - they then are able to conduct a tiny amount of negative voltages

58
Q

How long does a neural act pt last?

A

2 ms

59
Q

How long does a cardiac act pt last?

A

300 - 400 ms

60
Q

What is the role fo T Tubules and Terminal Cisternae?

A

stores and releases calcium in response to membrane potential of cardiac myocytes

61
Q

What are ways of describing the location of t-tubules?

A

they are part of the plasma membrane, so the membrane currents they release are near the contractile machinery
these tubules are contiguous with extracellular fluid
they’re dive in deep into the cell
they’re adjacent to the sarcoplastic reticulum

62
Q

What are the two parts of the cell that the t-tubules are near to (summary)?

A

the outside bc they are a part of the plasma membrane

they also dive into parts of the cell deep, sort of like a crypt

63
Q

What happens when the T tubule depolarises?

A

the terminal cysternae to detect the change in voltage
communicates this to the sarcoplasmic reticulum
convinces the SR that it needs to release calcium into the cytosol

64
Q

What is the terminal cysternae specialised for?

A

for storing and releasing calcium

65
Q

How does E-C coupling work in skeletal muscle?

A

calcium channels open
the DHPR calcium channel triggers the ryanodine receptors to open
calcium pours into the terminal cysternae from the SR
increase in calcium concentration in the cytosol
allows contraction to occur

66
Q

What two structures are the DHPR calcium channels close to?

A

terminal cysternae

ryanodine receptor

67
Q

Where are ryanodine receptors found?

A

found in the sarcoplasmic reticulum in skeletal muscle cells

68
Q

What are the two types of proteins involved in EC coupling in cardiac myocytes?

A

ryanodine receptor

SERCA

69
Q

What happens when the ryanodine receptor 2 opens in the cardiac muscle cells?

A

it allows calcium to pour out of the SR into the cytoplasm

70
Q

How is the ryanodine receptor 2 opened?

A

(calcium induced calcium release)
the ryanodine receptors are right next to calcium channels in the membrane
the membrane depolarises
the calcium channels open slightly and allow a very small amount of calcium into the cell
but the ryanodine receptors are calcium sensitive - they detect the small amout of calcium and take that as a sign to open
they let out a huge amount of calcium out of the SR
this leads to a positive feedback loop

71
Q

What substance triggers the opening of ryanodine receptors (2)?

A

intracellular calcium release

72
Q

How is the positive feedback loop involving ryanodine receptor 2s stopped?

A

when the ryanodine receptor 2 channels automatically shut down

73
Q

How is calcium pumped back into the SR in cardiac muscle cells?

A

via SERCA pumps

movement is fuelled by ATP

74
Q

Where are SERCA pumps located?

A

in the cardiac muscle cell membrane

75
Q

What happens when the SERCA pumps are sympathetically stimulated?

A

it increases E-C coupling
can cause calcium overload
risk of arhythmia genesis

76
Q

What can cause calcium overload?

A

adrenergic activity (excessive sympathetic stimulation)

77
Q

What are the effects of a calcium overload?

A

can cause ectopic beats

78
Q

How do arrhythmias occur?

A

when ectopic beats cause the excess calcium (from calcium overload) to spill out into the cytosol
in pathological form
at inappropriate times
in the cardiac cycle

79
Q

What can make arrhythmias worse?

A

ectopic beats

arrhythmias

80
Q

What is the effect of calcium channel blockers on vessels?

A

they vasodilate

they oppose hypertension

81
Q

What are two examples of drugs that block calcium in the heart?

A

anti-anginal agents

antiarrhythmic agents

82
Q

What is the effect of calcium channel blocker agents in the heart?

A

reduces nodal rates
reduces conduction through the AV node
can makes heart failure worse

83
Q

What are examples of non-DHP calcium channels?

A

Verapamil

Diltiazem

84
Q

What are examples of non-DHP calcium channels?

A

Verapamil

Diltiazem

85
Q

Which calcium channels does verapamil target?

A

those in the heart

more than those in the vessels

86
Q

What happens when verapamil blocks the calcium channels in the heart?

A

it affects nodal cells
it slows down the nodal rate
it protects the ventricles from rapid atrial rhythms
it slows conduction going through AV node

87
Q

Which calcium channels does diltiazem target?

A

both heart and vessel channels

88
Q

What happens when diltiazem blocks the calcium channels?

A

Slows nodal rate
Vasodilates coronary arteries
Prevents angina

89
Q

How does diltiazem prevent angina?

A

reduces workload

increases perfusion

90
Q

What are the effects of inotropic agents?

A

they increase stroke volume

they increase contractile force in the heart

91
Q

What happens when the NA/K pump on the membrane is inhibited?

A

increased calcium in cytosol
stinumlates the vagus nerve
slows the heart rate, increases AV delay

92
Q

What happens if a small amount of the Na / K pumps are inhibited?

A

it leads to an increase in calcium in the cytosol

93
Q

What is the effect of digoxin on the heart rate?

A

it slows heart rate via the vagus nerve

it increases AV delay

94
Q

How does digoxin work?

A

by (slightly) inhibiting Na/K pump on membrane

by stimulating the vagus nerve

95
Q

What happens when the NA/K pump on the membrane is inhibited and there is increased calcium in cytosol?

A

it reverses the activity of the Na / Ca exchanger

so the extra sodium inside the cell can drive calcium into the cell by this exchanger

96
Q

What was digoxin used for?

A

to treat heart failure

97
Q

What was the effect of digoxin on heart failure?

A

improves the symptoms in heart failure patients so they feel much stronger
it doesn’t change the mortality at all

98
Q

What is used instead of digoxin to treat heart failure most commonly now, and why?

A

beta blockers

they reduce mortality

99
Q

How to beta blockers work to treat heart failure?

A

they lower the amount of calcium that’s going into the cardiac myocyte
so there is a less likely chance of calcium overload
therefore there is a lower risk of arrhythmias

100
Q

What is digoxin now used to treat?

A

atrial fibrillation

101
Q

How does myogenic control regulate unusually high pressure?

A

the endothelium detects stretching of the blood vessel due to unusually high pressure
makes local hormones that triggers the smooth muscle to squeeze harder so that the blood vessel can maintain its shape

102
Q

What structure is responsible for myogenic control?

A

the endothelium

103
Q

How does myogenic control regulate unusually high pressure?

A

the endothelium detects plasma factors
it produces a vasodilator, NO
NO diffuses from the endothelium into the smooth muscle cells
causes relaxation and vasodilation

104
Q

What is an example of a vasodilator made by the endothelium?

A

nitric oxide

105
Q

What does the endothelium control?

A

vascular tone

clotting

106
Q

How does the endothelium control clotting?

A

it produces lots of different substances related to clotting

107
Q

Which substances are made by the endothelium to control clotting?

A 
nitric oxide
bradykinin
Thromboxane A2
Angiotensin II
Angiotensin Converting Enzyme (ACE)
Fibrinolytic factors – t-PA
108
Q

What types of substances are made by the endothelium to control clotting?

A 
Hormones
Growth Factors
Blood factors (eg clotting)
Cytokines & Interleukins
Adhesion Molecules
Enzymes
109
Q

What is contraction initiated by in all vascular smooth muscle?

A

MLCK

110
Q

What is responsible for initiating contraction in brain, cardiac and skeletal muscle?

A

troponin

tropomyosin

111
Q

What is MLCK activated by?

A

calcium-calmodulin

112
Q

How does contraction occur in vascular smooth muscle?

A

calcium coming through the cell / released by the SR forms a complex with MLCK
to make calcium-calmodulin
binds to MLCK, turns it into an active kinase via phosphorylation
contraction is activated

113
Q

How does relaxation occur in vascular smooth muscle?

A

a phosphotase is activated by NO induced cascade

the dephosphorylation of myosin occurs via a phosphotase

114
Q

How does smooth muscle containing vasculature relax?

A

when there is beta2 stimulation

it phosphorylates K channels

115
Q

What is the effect of a1 adrenergic activity in core organs and the GI Tract?

A

it stimulates the phosphorylation of MLCK

leads to muscle contraction

116
Q

What happens if glycerol trinitrate is constantly administered to the patient?

A

they become tolerant to NO

so their vessels won’t vasodilate

117
Q

How is glycerol trinitrate administered to combat tolerance?

A

in a pulsed way - occasionally

118
Q

What is the effect of bradykinin in it’s role as a hormone?

A

it loosens capillaries and blood vessels

it constricts bronchi and GI tract smooth muscle

119
Q

What is the effect of bradykinin in it’s role as a vasodilator?

A

it stimulates NO production in endothelium

120
Q

What is the effect of bradykinin on saliva?

A

it increases capillary permeability

so it increases the production of saliva

121
Q

What causes the dry cough associated with ACE inhibitors?

A

ACE Inhibitors prevent the degradation of bradykinin
causes an accumulation of bradykinin that is not being degraded
causes the dry cough

122
Q

What are three examples of biomarkers in the plasma?

A

Troponin
Creatine Kinase
C reactive protein

123
Q

What does it mean if troponin is identified in the bloodstream?

A

bc it is an intracellular protein. if it is found outside of the cardiomyocytes in the bloodstream, it means that a cardiomyocytes somewhere has exploded

124
Q

What conditions can cause troponin to be released?

A

acute myocardial infarction
heart failure
etc

125
Q

Where and when is troponin released from?

A

troponin is released from cardiomyocytes during necrosis

126
Q

When are bloodstream troponin levels NOT elevated?

A

during unstable angina

127
Q

When do C reactive protein levels increase?

A

they increase in response to inflammation

128
Q

What substances are released from cardiomyocytes during necrosis?

A

Creatine Kinase

troponin

129
Q

What are high C reactive protein levels associated with?

A

the risk of cardiovascular disease and future events

M103 T3 (21 decks)

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