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january exams > cardio > Flashcards

cardio Flashcards

1
Q

what level are the t tubules

A

z line

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2
Q

what are ryanodine receptors

A

calcium release channels on the sarcoplasmic reticulum

they move calcium

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3
Q

where are L type calcium channels located

A

on the wall of a t tubule

also known as DPHR

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4
Q

ryanodine receptors

A

they cluster and open in unison to activate to produce aa large signal

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5
Q

the events of cardiac excitation coupling

A

1- action potential arrives at t tubule
2-depolarises t-tubule
3- opens L type calcium channel
4- calcium released and binds to ryanodine receptor on SR
5-calcium released from SR
6- increase in calcium conc in cytoplasm
7- calcium can bind to troponin-C –> cross bridge formation

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6
Q

where are calcium release sites located

A

Z line

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7
Q

how does the heart ensure uniform contraction

A

1-calcium doesn’t have to move very far to get to middle of myofilament
2-all parts of the cell shorten at the same time

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8
Q

troponin complex

A

C- binds to calcium ions
I- binds to actin- inhibits the binding of myosin to actin
T- binds to tropomyosin

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9
Q

presence of Ca2+ to thin and thick filaments

A

1-Ca2+ binds to troponin C
2- troponin C binds more strongly to troponin I
3- troponin I no longer binds to actin
4- tropomyosin moves further into the groove of actin
5- the troponin complex swings out of the way
6- the actin-myosin binding site is uncovered, myosin cross-bridges can now bind to actin

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10
Q

removal of Ca2+

A

1- ATP dependent Ca2+ pump- back into SR
2-Na+/Ca2+ exchanger- uses Na+ chemical gradient
–>3 Na for 1 Ca2+- diff charge so may create current
3- sarcolemmal Ca2+ ATPase- uses energy to push Ca2+ up conc gradient

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11
Q

systole

A

contraction

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12
Q

diastole

A

relaxation

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13
Q

cardiac output

A

amount of blood pumped out of a ventricle in 1 minute

=HRxSV

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14
Q

stroke volume

A

volume ejected from 1 ejected in a single cardiac cycle

=EDV-ESV

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15
Q

End diastolic volume

A

volume of blood before contraction

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16
Q

End systolic volume

A

volume of blood left in ventricle after contraction

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17
Q

Ejection fraction

A

percentage of blood the ventricle can empty in 1 minute

=SV/EDV

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18
Q

heart failure

A

when the ejection fraction is below 40%

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19
Q

preload

A

the volume load on the ventricles before ventricular contraction
–>determined by EDV

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20
Q

after load

A

the pressure in the artery against which the ventricle is pumping
for the left ventricle it represents diastolic pressure- 80mmHg

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21
Q

Frank-Starling law of the heart

A

as the degree of stretch on the heart increases so does the force of contraction

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22
Q

Inotropic state

A

related to the degree of activation of the contractile proteins by Ca2+

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23
Q

factors that influence inotropic state

A

1- Action potential- increase in plateau length- increase Ca2+ influx
2- external ion concentration
a- increasing external Ca2+
b- lower external Na+- slows Na+/Ca2+ exchange- Ca2+ accumulates inside
3-force frequency relationship
increase stimulation frequency- more Ca2+ entry

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24
Q

sympathetic stimulation increase force of contraction

A

1- noradrenaline binds to B1 receptors in membrane
2-activated GTP binding protein Gs
3- the alpha subunit activated adenylate cyclase
4-increase cAMP production from ATP
5- activated protein kinase A
6- this affects function of different proteins

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25
Q

pKA phosphorylation

A

1- L type calcium channel- Increases calcium influx so more released from SR
2-ryanodine receptor- increases sensitivity to calcium- more released from SR
3-phosholamban- This interferes with the mechanism which takes away calcium
ATPase that sits on sarcoplasmic reticulum is normally inhibited
PKA can phosphorylate phospholamban so unleashes ATPase making it better at retaining calcium in calcium store—>more calcium in SR so more can be released
4- troponin– decreased sensitivity to Ca2+ so quicker relaxation- better filling of ventricles

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26
Q

catecholamines

A

increase the inotropic state- greater filling of ventricles so increased stroke volume

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27
Q

chronotropic effect

A

how it affects the heart

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28
Q

sympathetic on pacemaker potential

A

1- makes funny current stronger- slow depolarisation is faster- reaches threshold faster
2-decreases permeability to potassium- membrane potential doesn’t go as negative
3- increased L type Ca2+ current- faster upstroke

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29
Q

isovolumic contraction

A

volume doesn’t change but there is an increase in pressure due to mitral valve closing

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30
Q

isovolumic relaxation

A

no change in volume but there is a reduction in pressure

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31
Q

what circulatory tube regulates blood pressure

A

arterioles

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32
Q

echocardiography

A

maps the positions of the chambers of the ventricles

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33
Q

MRI

A

3D imaging- can track the change of the ventricular wall during the cardiac cycle

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34
Q

how does the ventricular wall change during contraction

A

1- isovolumetric contraction- myocytes shorten and swell sidewas
2- laminar- slide past each other and become more perpendicular to plane of ventricular wall

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35
Q

cellular basis of heart failure

A

1-increased stiffness- collagen and microtubules
2-changes in action potential
3-negative inotropic state

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36
Q

dysrhythmia/ arrhythmia

A

disturbance of cardiac rhythm

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37
Q

drug treatment for dysrhythmia

A 
class 1- sodium channel blockers- upstroke of non-pacemaker
class 2- beta blockers- L type calcium current- upstroke of pacemaker, plateau of non-pacemaker and funny current
class 3- potassium channel blockers- depolarisation
class 4- calcium channel blockers- upstroke of pacemaker and plateau in non-pacemaker
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38
Q

Sympathetic stimulation increases funny current and L type calcium current enhances:

A

early after depolarisation
Increased automaticity
Delayed after depolarisation

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39
Q

ischaemia

A

restriction in blood supply to tissues

40
Q

example of 1a drug

A

quinidine

41
Q

example of 1b drug

A

lidocaine

42
Q

example of 1c drug

A

flecainide

43
Q

class 1b drug

A

used to treat ischaemia as the channels are likely to be inactive
prevents a premature beat

44
Q

example of class 2 drug

A

propranolol and atenolol

45
Q

example of class 3 drug

A

sotalol and amiodarone

46
Q

example of class 4 drug

A

verapamil and dilitizaem

47
Q

aims for treating heart failure

A
  • relieve symptoms
  • improve exercise tolerance
  • reduce mortality
48
Q

in heart failure why do you feel breathless?

A

ventricular filling pressure is high for stroke volume

49
Q

in heart failure why do you feel fatigue and unable to exercise

A

as aortic pressure increases, stroke volume decreases

50
Q

how do beta blockers help heart failure

A

1- address the change in autonomic balance- reduce sympathetic
2- reduce hypertrophy
3-stimulates vasodilation
4-reduce dysrhythmia

51
Q

examples of ACE inhibitors

A

captopril and ramipril

52
Q

collaterals

A

connect systems derived from the major arteries

53
Q

stable angina

A
  • partial occlusion of a coronary artery
  • pain when exercising
  • intermittent symptoms with constant severity
54
Q

where is the heart located

A

2nd-5th rib

55
Q

papillary muscles

A

contract and pull on the chord terndinae to prevent the valves from exerting into the atria

56
Q

fibroblasts

A

contribute to extraceullar matrix

provide mechanical support

57
Q

endothelial cells

A

lining of blood vessels

58
Q

smooth muscle cells

A

in coronary arteries and cells

59
Q

conduction cells

A

generation and passing of electrical impulses

60
Q

cardiomyocytes

A

form the contractile apparatus of atria and ventricles

61
Q

roles of intercalated disc

A

mechanical coupling

electrical coupling

62
Q

net electrochemical driving force

A

difference between membrane potential of the cell and the equilibrium potential for a given ion

63
Q

what does high conc of KCl do?

A

sodium channels will be inactivated, paralyses muscles and stops cardiomyocytes from contracting

64
Q

where are the bipolar leads in an ECG placed

A

left leg, left arm, right arm

65
Q

what are the layers of a vessel

A

tunica adventitia- connective tissue
tunica media- smooth muscle and elastin
tunica intima- squamous endothelium

66
Q

what is darcys law?

A

the flow is proportional to the pressure difference between 2 points

67
Q

what is Bernoulli’s theory?

A

the pressure difference between points A and B is proportional to the difference in mechanical energy between A and B

68
Q

what is compliance?

A

change in volume per unit change in distending pressure

distending pressure= pressure inside-pressure outside

69
Q

autoregulation

A

intrinsic adjustment of flow to a tissue so that flow meets local requirements

70
Q

3 roles of lymphatic system

A

1- transports interstitial fluid back into the vascular system
2- transports fats from small intestine to the blood
3- lymphocytes play a role in immunological defences

71
Q

baroreceptors

A

monitor blood pressure
arterial- short term
cardiopulmonary- long term

72
Q

chemoreceptors

A

monitor the chemical composition of the blood

73
Q

2 hypotheses for exercise

A

1- central command- cerebral cortex

2- peripheral reflex- proprioceptor inputs from joints and muscles

74
Q

active hyperaemia

A

leads to increase in blood flow due to increase in metabolic demands

75
Q

role of cutaneous blood supply

A

1- heat exchanger for thermoregulation
2- supply of nutrients to cells
3- blood reservoir

76
Q

how the skin responds to heat

A

1- hypothalamus- reduced vasomotor tone- vasodilation

2- sweat- production of bradykinin- stimulates endothelial cells to release NO- vasodilation

77
Q

how the skin responds to cold

A

1- superficial vessels constrict strongly
2-blood bypasses capillaries, via AV shunts, to vital organs
3-skin may appear rosy- blood may be trapped in superficial vessels following rapid vasoconstriction

78
Q

minute ventilation

A

the total amount of air flowing into or out of the respiratory system per minute

79
Q

forced vital capacity

A

total volume of air expired after a maximal inspiration and forced exhale

80
Q

forced expiatory volume in 1 second

A

the volume of air expired in first second after maximum exhalation

81
Q

decreasing affinity for oxygen

A

goes to the right- favours unloading- capillaries

82
Q

increasing affinity for oxygen

A

goes to the left- favours loading- lungs

83
Q

how does increasing temperature affect O2 affinity

A

it decreases the affinity so the graph goes to the right and O2 is unloaded

84
Q

how does the decreasing the pH affect O2 affinity

A

it decreases the affinity so the graph goes to the right
aerobic- increase in CO2
anaerobic- increase in lactic acid

85
Q

how does increasing CO2 conc affect O2 affinity

A

increasing CO2 favours O2 unloading as CO2 has a lower affinity for Hb than O2 so will bind more and therefore unloading O2
bohr effect

86
Q

2,3 DPG

A

in hypoxia and anaemia promotes O2 unloading

87
Q

what happens to carbon dioxide in an erythrocyte?

A

1- converted into HCO3- and H+ by carbonic anhydrase
2- HCO3- leaves the cell and binds to Na and this is used to transport CO2 to the lungs
3- Cl- enters the cell to equal the charges–>chloride shift
4- the H+ is buffered by Hb- favours O2 unloading

88
Q

Haldane effect

A

increases the rate of CO2 elimination

O2 conc is increased and this favours unloading of CO2 from Hb

89
Q

what is hypoxemia

A

it is where PaO2 is abnormally low

90
Q

what is shunted blood?

A

when the blood enters the left ventricle without going through the ventilated areas of the lung so diluting the O2 conc in the left ventricle

91
Q

what are the chemoreceptors located on the ventral surface of the medulla called and what do they do?

A

central chemoreceptors

minute by minute control of ventilation

92
Q

how do central chemoreceptors work?

A

H+ cannot cross BBB
CO2 cross BBB, carbonic anhydrase converts it into H+ and HCO3-
the chemoreceptors then respond to the rise in H+
inputs then go to respiratory control centres in the pons and medulla

93
Q

where are peripheral chemoreceptors located

A

carotid and aortic bodies

94
Q

O2 sensing in carotid bodes

A

1- decrease in O2 inactivates membrane K+ channels, reducing K+ influx
2- depolarises the cell, activating Ca2+ channels
3- influx of Ca2+ and release of neurotransmitter (dopamine)
4- NT binds to receptors on afferent and causes a depolarisation and increase in action potential frequency

95
Q

causes of metabolic acidosis

A

diarrhoea
exercise
abnormal fat absorption
renal failure

96
Q

causes of metabolic alkalosis

A

vomiting

january exams (5 decks)

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