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Adele Cardiovascular > Physiology - Part 1 > Flashcards

Physiology - Part 1 Flashcards

1
Q

what is the muscle membrane called?

A

sarcolemma

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2
Q

what is the name for the invaginations made by the sarcolemma?

A

T-tubules

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3
Q

what do the T-tubules interact with?

A

sarcoplasmic reticulum

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4
Q

what is a syncitium?

A

a single cell containing several nuclei, formed by fusion of cells

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5
Q

do cardiac cells form a true syncitium?

A

no, only functionally

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6
Q

what is an intercalated disc?

A

an arrangement of a desmosome and a gap junction

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7
Q

which of desmosomes or gap junctions provides the electrical connection?

A

gap junctions

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8
Q

which of desmosomes or gap junctions provides the physical connection?

A

desmosomes

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9
Q

roughly how long does a cardiac action potential last?

A

200-250 ms

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10
Q

can cardiac muscles exhibit tetanus?

A

no

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11
Q

is the refractory period in cardiac muscle long or short?

A

long

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12
Q

why can’t cardiac muscle exhibit tetanus?

A

due to the long refractory period

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13
Q

how long is the action potential in skeletal muscle?

A

2 ms

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14
Q

aside from preventing tetanus, why does cardiac muscle have a long action potential?

A

Ca entry from outside the cell can regulate contraction as it does not saturate the troponin

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15
Q

in non-pacemaker cardiac cells, what causes the resting membrane potential?

A

high resting permeability to K+

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16
Q

in non-pacemaker cardiac cells, what causes high resting permeability to K+?

A

leaky K+ channels

17
Q

in non-pacemaker cardiac cells, what causes the initial depolarisation?

A

increase in permeability to Na+

18
Q

in non-pacemaker cardiac cells, is the part of the action potential attributed to Na+ influx short or long?

A

short

19
Q

in non-pacemaker cardiac cells, what causes the action potential to plateau?

A

increase in PCa2+ (L-type) and decrease in PK+

20
Q

in non-pacemaker cardiac cells, what causes repolarisation of the cell?

A

decrease in PCa2+ (L-type) and increase in PK+

21
Q

in cardiac pacemaker cells, what causes the majority of the action potential?

A

increase in PCa2+ (L-type)

22
Q

in cardiac pacemaker cells, which three other events cause the pre potential?

A

decrease in PK+
increase in PNa+ (PF)
increase in PCa2+ (T-type)

23
Q

in cardiac pacemaker cells, what causes an increase in PF (funny sodium channels)?

A

previous action potential repolarising and coming back to baseline

24
Q

do calcium channel blockers increase or decrease the force of contraction of the cardiac muscles?

A

decrease

25
Q

do cardiac glycosides increase or decrease the force of contraction of the cardiac muscles?

A

increase

26
Q

does an increase in temperature affect the heart?

A

yes

27
Q

what happens to the heart when the temperature increases by 1°C?

A

increase by ~10 beats per minute

28
Q

what can happen to the heart in hyperkalemia?

A

fibrillation and heart block

29
Q

what can happen to the heart in hypokalemia?

A

fibrillation and heart block

30
Q

what can happen to the heart in hypercalcemia?

A

increased heart rate and increased force of contraction

31
Q

what can happen to the heart in hypocalcemia?

A

decreased heart rate and force of contraction

32
Q

how fast does depolarisation travel over the atria?

A

~0.5m/s

33
Q

why doesn’t depolarisation immediately spread straight down through the atria into the ventricles?

A

it hits the annulus fibrosus, non conducting part

34
Q

how does depolarisation travel from the atria to the ventricles?

A

through the atrioventricular node

35
Q

how fast does depolarisation travel through the atrioventricular node?

A

~0.05m/s

36
Q

how fast does depolarisation travel through the bundle of His and Purkinje fibres?

A

~5m/s

Adele Cardiovascular (14 decks)

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