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Cardiovascular > 10. Biochemistry II - Contractility > Flashcards

10. Biochemistry II - Contractility Flashcards

1
Q

in the RESTING STATE are CARDIAC MUSCLE CELLS polarised or depolarised and why

A

POLARISED (about -90mv)

inside negative as POTASSIUM CHANNELS are OPEN
- K+ EFFLUX

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2
Q

how are MYOSIN and ACTIN BOUND in RELAXED STATE

A

WEAKLY BOUND

  • MYSOIN HEAD COCKED
  • TROPOMYOSIN PARTIALLY BLOCKS BINDING SITE on actin
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3
Q

how is MYOSIN enabled to BIND STRONGLY to ACTIN and cause actin filament to MOVE during CONTRACTION

A

CA2+ BINDS TROPONIN

TROPONIN-CA2+ COMPLEX PULLS TROPOMYOSIN away from binding site so it is exposed

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4
Q

during RELAXATION, CA2+ is PUMPED BACK INTO SR via a CALCIUM ATP-ASE. this transporter is CONTROLLED by a PROTEIN called…

A

PHOSPHOLAMBAN

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5
Q

ACTION POTENTIALS begin in SA NODE. what is the name of the CELLS in the SA node that SPONTANEOUSLY FIRE action potentials

A

AUTORHYTHMIC CELLS

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6
Q

ACTION POTENTIALS generated in AUTORHYTHMIC CELLS SPREAD from cells to cells through …. between adjacent cardiomyocytes

A

GAP JUNCTIONS and INTERCALATED DISCS

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7
Q

In SAN NA+ channels that cause DEPOLARISATION (unstable resting potential) are called If (FUNNY) CHANNELS. these belong to a family of …. channels

A

HCN CHANNELS

  • HYPERPOLARISATION-ACTIVATED CYCLIC NUCLEOTIDE-GATED Channels
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8
Q

If (FUNNY) CHANNELS are PERMEABLE to BOTH…

A

NA+ and K+

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9
Q

when SA NODE DEPOLARISES the signal TRAVELS to AV NODE via which PATHWAYS

A

INTERNODAL PATHWAYS

from AV node through AV bundles and bundle branches to the apex of the heart

  • purkinje fibres transmit impulses very rapidly so that cells in apex contract nearly simultaneously
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10
Q

P wave of ECG represents ATRIAL DEPOLARISATION. what does the LATTER PART of P WAVE represent which continues through the P-R / P-Q SEGMENT

A

START of ATRIAL CONTRACTION

Slows during P-R SEGMENT as passes through AV NODE

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11
Q

the SIGNALS TRAVEL through the BUNDLE BRANCHES to the APEX, takes place in which ECG WAVE

A

Q WAVE

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12
Q

which part of the BRAIN contains the CARDIOVASCULAR CENTRE

A

MEDULLA OBLONGATA

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13
Q

which AUTONOMIC NERVOUS SYSTEM causes DECREASE in HEART RATE

A

PARASYMPATHETIC

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14
Q

PARASYMPATHETIC NERVOUS SYSTEM DECREASES HEART RATE via which NERVE

A

VAGUS NERVE

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15
Q

SYMPATHETIC NERVOUS SYSTEM INCREASES HEART RATE via which NERVE

A

ACCELERATOR NERVE

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16
Q

which HIGHER BRAIN CENTRES input into CARDIOVASCULAR CENTRE (medulla oblongata)

A

CEREBRAL CORTEX, LIMBIC SYSTEM and HYPOTHALAMUS

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17
Q

input to CARDIOVASCULAR SYSTEM in medulla to moderate heart rate via which SENSORY RECEPTORS

A

PROPRIOCEPTORS - monitor movements
CHEMORECEPTORS - monitor blood chemistry
BARORECEPTORS - monitor blood pressure

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18
Q

PARASYMPATHETIC NERVES DECREASE HEART RATE via which HORMONE and which RECEPTORS does it act on

A

ACETYLCHOLINE

on MUSCARINIC RECEPTORS

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19
Q

SYMPATHETIC NERVES INCREASE HEART RATE via which HORMONR and which RECEPTORS does it act on

A

NORADRENALINE (norepinephrine)

on BETA-1 RECEPTORS

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20
Q

SYMPATHETIC NERVOUS SYSTEM CONTROLS which components of the HEART

A

ALL

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21
Q

PARASYMPATHETIC NERVOUS SYSTEM CONTROLS which components of the HEART

A

SA NODE & AV NODE

22
Q

SYMPATHETIC NERVOUS SYSTEM INCREASES HEART RATE meaning it is POSITIVELY ….

A

CHRONOTROPIC

23
Q

SYMPATHERIC NERVOUS SYSTEM INCREASES CONTRACTILITY meaning it is POSITIVELY ….

A

INOTROPIC

24
Q

PARASYMPATHETIC NERVOUS SYSTEM is NEGATIVELY …

A

CHRONOTROPIC

25
Q

PARASYMPATHETIC NERVOUS SYSTEM has what effect on CONTRACTILITY

A

LITTLE EFFECT

26
Q

PARASYMPATHETIC NERVOUS SYSTEM (using vagus nerve and releasing Ach) DECREASES HEART RATE by doing what to the IMPULSE

A

PROLONGS the DELAY at the AV NODE

27
Q

which NERVOUS SYSTEM controls the SA and AV NODES of the HEART

A

PARASYMPATHETIC

28
Q

PARASYMPATHETIC NS releases ACH which acts on MUSCARINIC RECEPTORS of the AUTORHYTMIC CELLS.

what does it cause in order to HYPERPOLARISE the cell (ion movement) (and DECREASE the RATE of DEPOLARISATION)

A

INCREASED K+ EFFLUX

DECREASED CA2+ INFLUX

29
Q

SYMPATHETIC NS releases NORADRENALINE which acts on BETA-1 RECEPTORS of AUTORHYTHMIC CELLS.

what does it cause in order to INCREASE RATE of DEPOLARISATION (ion movement)

A

INCREASES NA+ and CA2+ INFLUX

30
Q

Sympathetic ns

when NORADRENALINE BINDS to BETA-1 RECEPTORS what does it ACTIVATE

A

cAMP - SECOND MESSENGER system

-> ACTIVATION of PROTEIN KINASE A

31
Q

Sympathetic ns

NORADRENALINE BINDING to BETA-1 RECEPTORS ACTIVATES cAMP and PROTEIN KINASE A which PHOSPHORYLATES….

A

Voltage-Gated CA2+ CHANNELS and PHOSPHOLAMBAN

32
Q

Sympathetic nervous system releases noradrenaline -

PHOSPHORYLATION of Voltage-Gated CA2+ CHANNELS causes…. which leads to MORE FORCEFUL CONTRACTIONS

A

INCREASE in their OPEN TIME

INCREASE CA2+ ENTRY

INCREASES CA2+ STORES in SR
& INCREASES CA2+ RELEASED

therefore more forceful contractions

33
Q

what EFFECT does PHOSPHOLAMBAN have on CA2+-ATPase

A

INHIBITOR of it

34
Q

Sympathetic NS

Activated PROTEIN KINASE A also PHOSPHORYLATES PHOSPHOLAMBAN which does what in order to SHORTER DURATION of CONTRACTION

A

RELIEVES INHIBITION effect on ca2+-ATPase

INCREASES CA2+-ATPase on SR

REMOVES CA2+ from CYTOSOL FASTER
- SHORTENS CA-TROPONIN BINDING TIME

shortens contraction duration

35
Q

Sympathetic NS

Activated PROTEIN KINASE A also PHOSPHORYLATES PHOSPHOLAMBAN which does what in order to create MORE FORCEFUL CONTRACTIONS

A

INCREASES CA2+-ATPase on SR

INCREASES CALCIUM STORES in SR
and so INCREASES CALCIUM RELEASE

therefore more forceful contractions

36
Q

what are the 2 possible CALCIUM REGULATED CARDIAC SIGNALLING PATHWAYS

A
  1. by DEPOLARISATION
  2. by STIMULATION via ADRENERGIC RECEPTORS (BETA-1) (sympathetic nervous system)
37
Q

BETA-1 RECEPTORS that BIND NORADRENALINE are what type of RECEPTORS

A

ADRENERGIC RECEPTORS

  • G-PROTEIN COUPLED
38
Q

CO = SV X HR

at REST what is the AVERAGE CO in adults

A

4.9 litres per min

39
Q

what is the EQUATION for STROKE VOLUME (amount of blood transferred from left ventricle to arterial system during systole)

A

SV= EDV (END DIASTOLIC VOLUME) - ESV (END SYSTOLIC VOLUME)

EDV - total volume of blood in the ventricle at the end of diastole, dependent on PRELOAD

ESV - volume of blood remaining in ventricle at end of Systole, Dependent on AFTERLOAD

40
Q

STOKE VOLUME is DETERMINED by which 3 FACTORS

A
  • PRELOAD: the initial STRETCHING of cardiac myocytes before contraction, related to ventricular filling
  • CONTRACTILITY: force that the muscle can generate at any given length
  • AFTERLOAD: the ARTERIAL PRESSURE against which the muscle will contract
41
Q

what is EJECTION FRACTION (EF)

A

AMOUNT OF BLOOD PUMPED OUT OF VENTRICLE (SV)
/
TOTAL AMOUNT OF BLOOD IN VENTRICLE (EDV)

= SV / EDV x 100

42
Q

what is the NORMAL/HEALTHY EJECTION FRACTION range - what proportion of the blood in the ventricle should be pumped out

A

50-65%

43
Q

what is PRELOAD

A

the DEGREE of MYOCARDIAL STRETCH caused by END-DIASTOLIC VOLUME

this stretch represents the load placed on cardiac muscles before they contract

  • increased EDV stretches the heart
  • cardiac muscles stretch and contract MORE FORCEFULLY, ejecting MORE BLOOD (FRANK STARLING LAW)
44
Q

AFTERLOAD refers to the amount of ..

A

RESISTANCE / PRESSURE that the heart must PUMP AGAINST
during systole

determined by VASCULAR RESISTANCE

45
Q

VASOCONSTRICTION will have what effect on AFTERLOAD

A

INCREASE AFTERLOAD PRESSURE

46
Q

PRELOAD is influenced by which factors

A
  • VENTRICULAR FILLING
  • FILLING TIME
47
Q

CONTRACTILITY is influenced by which factors

A
  • AUTONOMIC INNERVATION
  • HORMONES
48
Q

AFTERLOAD is influenced by which factors

A
  • VASODILATION / VASOCONSTRICTION
49
Q

what does the FRANK-STARLING LAW state

A

that the STRENGTH of VASCULAR CONTRACTION is DEPENDENT of the LENGTH of the RESTING FIBRES (due to myocyte STRETCH)

  • INCREASE in LEFT VENTRICULAR PRELOAD causes STROKE VOLUME to INCREASE
    without the need for extrinsic neural or hormonal regulatory mechanisms
50
Q

the STARLING CURVE defines the …… RELATIONSHIP in the intact HEART

A

LENGTH-FORCE RELATIONSHIP

increase STRETCH (indicated by EDV), increases FORCE (indicated by SV)

as more stretch means MORE TENSION in muscle fibres

51
Q

besides STARLING LAW and STRETCH/PRELOAD, what also INCREASES CONTRACTILITY

A

SYMPATHETIC STIMULATION

  • ADRENALINE
52
Q

how is FRANK-STARLING RELATIONSHIP in HEART FAILURE

A

DAMAGED MYOCYTES - LESS STRETCH (stiffness)

  • REDUCTION in PRELOAD
    -> REDUCTION in STROKE VOLUME

molecular changes in cardiac cells cause decreased active (systolic) force and impaired (diastolic) relaxation together with a greater stiffness of the remodelled ventricular wall

Cardiovascular (16 decks)

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