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M103 T3 > M103 T3 L9 > Flashcards

M103 T3 L9 Flashcards

1
Q

What % of heart output does the heart receive?

A

20%

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2
Q

How does the Circle of Willis contribute to maintianing brain function?

A

if blood comes in through one artery and one bridge of the circle of Willis is blocked, it can be supplied by the other branch

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3
Q

What % of cardiac output do the kidneys receive?

A

20-25%

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4
Q

How do the kidneys contain a portal system?

A

bc the glomerular capillaries reformulate into peritubular capillaries
which then reabsorb / secrete water / electrolytes into either the loop of henle or the collection ducts

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5
Q

What two enzymes do the kidneys produce?

A

ACE

Renin

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6
Q

What are the two functions of ACE and renin?

A

they control blood volume and respond to renal bp

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7
Q

What can cause vasodilatation?

A

adrenergic activity into the blood vessels of skeletal muscles

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8
Q

What % of cardiac output do the muscles receive during strenuous exercise?

A

CO - 80%

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9
Q

Why are the muscles a major site of peripheral resistance?

A

bc they can regulate vasodilation / constriction at the arterial level

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10
Q

What amount of oxygen and perfusion does the skin receive?

A

surprisingly small amounts for the weight that it has

about 5%

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11
Q

How do Arterio–Venous Anastomoses differ from usual blood vessels?

A

don’t go through capillaries

they’re not primarily responsible for gas exchange

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12
Q

How do sweat glands produce sweat in thermoregulation?

A

blood passes near sweat gland
the water and electrolytes from which is used to produce a plasma ultrafiltrate
they are released on the skin

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13
Q

What is the skins’ response to trauma?

A

red reaction
flare
wheal

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14
Q

What is the primary function of Arterio–Venous Anastomoses?

A

allows for rapid cooling

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15
Q

What are the four sequential events of the cardiac cycle?

A

Ventricular filling
Isovolumic ventricular contraction
Ejection
Isovolumic ventricular relaxation

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16
Q

What are the different pressure volume loop shapes of the two stenosis valve pathologies?

A

aortic st- tall

mitral st - shifted right

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17
Q

What is the cause of murmurs?

A

an obstacle in the valve < turbulence < murmur

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18
Q

What causes a systolic murmur?

A

fluid leaving the ventricle through a somehow faulty valve

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19
Q

What causes a diastolic murmur?

A

fluid entering the ventricle through a somehow faulty valve

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20
Q

What are the two different types of K+ channels?

A

Delayed rectifier K+ channels

Inward rectifier K+ channels

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21
Q

What happens in delayed rectifier K+ channels?

A

they open when membrane depolarises

But all gating takes place with a delay - slowed down

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22
Q

What happens in inward rectifier K+ channels?

A

Open when Vm goes below -60 mV (becomes -ve inside)

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23
Q

Why are inward rectifier K+ channels unusual?

A

channels usually don’t open when cells are at rest but these do

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24
Q

What is the function of inward rectifier K+ channels?

A

to clamp membrane firmly at rest

to let K+ out of cell, repolarising

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25
Q

What is the potential of a resting cell and how is this maintained?

A

-70 mV
an inward rectifier K+ channels are open
K+ is flowing out is the dominant current
the resting membrane potential is near EK

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26
Q

How does initial depolarisation occur?

A

the cell becomes less negative
leads to a small depolarisation
inside the cell the voltage becomes less negative

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27
Q

What two things can trigger initial depolarisation?

A

a nearby cell depolarising

a synaptic transmission

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28
Q

How does sodium contribute to positive feedback when building up to an actpt?

A

the initial depolarisation causes a few of the Na+ channels to open
Na+ permeability increases
Na+ current flows through channels into cell
causes more depolarisation (the membrane potential moves closer to 0 mV)
this acts as a positive feedback loop

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29
Q

When will an “all-or-none” actpt occur?

A

when the voltage goes above the threshold voltage at -50 mV

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30
Q

What causes the membrane potential to reach over +30 mV?

A

the positive feedback of increased Na+ channel conductance

increased voltage

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31
Q

What range is considered overshoot?

A

Vm > 0

32
Q

What happens during repolarisation?

A

after actpt reaches max voltage, the Na channels naturally activate
the delayed rectifyer channels start to open
lets K+ out
leads to repolarisation
becomes less positive and more negative

33
Q

When do refractory periods mostly occur?

A

during-after hyperpolarisation

34
Q

What is the process behind what happens during after-hyperpolarisation?

A

the voltage goes below -60 mV
the inward rectifier K+ channels open again - they stay open until next depolarisation
the delayed rectifiers are strangely open, even though they delayed rectifiers like being closed when the voltage is negative
these normally clamp the voltage toward EK and are responsible for maintaining the resting membrane potential

35
Q

What are the three main events that happen during after-hyperpolarisation?

A

K+ permeability increases
Na+ permeability decreases
the membrane potential moves closer to EK

36
Q

What are the five phases by which an actpt generated in a ventricular myocyte in the heart?

A

Phase 0 - Depolarisation: Na+ gates open in response to wave of excitation from pacemaker
Phase 1 - Transient Outward Current: tiny amount of K+ leaves cell
Phase 2 - Plateau phase: Inflow of Ca2+ just about balances outflow of K+
Phase 3 - Rapid repolarisation phase: Vm falls as K+ leaves cell
Phase 4 - Back to resting potential

37
Q

What is the depolarisation time and size of the actpts in neural acpts?

A

depolarisation takes about 1 ms

actpts are always same size

38
Q

What are the three different types of actpts?

A

neural
skeletal muscle
cardiac

39
Q

What are two features of actpts in skeletal muscle acpts?

A

actpts are completed before contraction begins

has a short refractory period so repeated actpts leads to tetany

40
Q

What is the depolarisation time and size of the actpts in cardiac acpts?

A

depolarisation lasts up to 500 ms
actpts varies in duration and size
has a long refractory period, no tetany

41
Q

What happens in the plateau phase?

A

there is a Ca2+ current going in and a K+ current going out through a cell membrane
the voltage doesn’t change very much
there is a small decrease in Vm as time goes on
there is a decrease in calcium as time goes on

42
Q

What happens as a result of a decrease in calcium in the plateau phase?

A

K+ OUT vastly outnumbers Ca2+ IN
creates a positive feedback loop
lead to the rapid repolarisation phase

43
Q

What will vary cardiac actpts and how?

A

when the actpts occur in different regions of the heart - will cause variation in timing and shape
the timing of the different cardiac APs - will cause variation in the ECG
change in terms of slightly in terms of the ions being conducted

44
Q

What happens in AV conduction failure?

A

the AV node and Bundle of His are potential pacemakers and become pacemakers

45
Q

What does the QT interval align with?

A

ventricular depolarisation

ventricular repolarisation

46
Q

What order does a cardiac actpt occur in ventricular myocytes?

A

phases 4, 0, 1, 2, 3, 4

47
Q

What happens in phase 4 during a cardiac actpt in ventricular myocytes?

A

at rest, the inward rectifier K+ channel is open which leads to an outward current that stabilises membrane - clamps the membrane at a negative potential

48
Q

What causes phase 0 in a cardiac actpt in ventricular myocytes?

A

a sudden conduction of na channels

causes lots of na flows into the cell

49
Q

What happens to lead to phase 2 during a cardiac actpt in ventricular myocytes?

A

depolarization also leads to transient opening of time - and voltage-dependent Ca channels
rapid depolsarization

50
Q

What happens to the total K conductance upon depolarization during a cardiac actpt in ventricular myocytes?

A

it decreases rather than increases upon depolarization
it’s only over time that there is an increase in K current
Repolarization is greatly delayed due to phases 0 and 2

51
Q

What are features of actpts in SA and AV nodes?

A

at rest they spontaneously depolarise - they aren’t stable at rest

52
Q

Why aren’t SA and AV node actpts stable at rest?

A

bc there is no inward rectifier

53
Q

What are the differences in the upstroke of an actpt in SA / AV nodes compared to that in ventricular myocytes?

A

a transient increase in inward Ca (rather than na influx in ventricular myocytes)
nodal upstroke is slower than in ventricular myocytes - it doesn’t result in a sudden increase in voltage - ca takes its time during phase 0
there is no phase 1 or phase 2 in SA / AV node upstroke

54
Q

What causes the rapid repolarisation of actpts in SA and AV nodes?

A

the conductance of potassium K increasing shortly after depolarization due to delayed rectifiers

55
Q

What are two features of the resting potential that contribute to the autorhytmicity of SA node cells?

A

it’s unstable

it’s close to the voltage threshold

56
Q

At what rate will SA node cells independently beat at? What can this rate be affected by?

A

100 bpm
ics by symp activity
dcs by parasymp activity

57
Q

Why are the SA nodal cells usually the pacemaker?

A

bc they have fastest rate

so the SA (pacemaker) nodal cells are responsible for the initiation of a heart beat in the healthy heart

58
Q

In which myocytes is pacemaker potential present?

A

SA & AV node

conduction system only

59
Q

In which exceptional circumstances can pacemaker potential be seen in other cells?

A

injured cells in the main ventricular myocardium

contractile cells

60
Q

Why is the pacemaker potential is a replacement for resting potential?

A

bc pacemaker potential cells lack inward rectifier k channels
causes a slow drift upward of the pacemaker potential

61
Q

What determines the rate of actpt firing?

A

the slope of pacemaker potential

62
Q

What is If driven by and what is it responsible for?

A

driven by a HCN channel
responsible for autorhythmicity
is particularly active during the pacemaker potential

63
Q

What happens to If during hyperpolarization?

A

increases

not present during depolarization

64
Q

How does If lead to the net inward current?

A

there is a lot of Na+ current inward and a tiny K+ current outward
results in the cell depolarizing towards +30 mV not 0mV

65
Q

Why doesn’t drug therapy aim to block all of the Na+ channels?

A

it would kill the patient

66
Q

What is the effect of partial sodium blockers on patients?

A

slows down conduction velocity due to changes in the organisation of firing from the different regions of the heart
this can prevent (or cause) arrhythmias
It doesn’t prevent depolarisation or affect the heart rate

67
Q

What is the effect of calcium blockers on patients?

A

decrease heart rate - slows down the depolarisation of the SA node
decrease contractile force - lessens the amount of ca, which shortens the act pt of all cells affected by the plateau phase (lowered by ca reduction)

68
Q

What % of the body weight makes up the kidneys?

A

0.5 %

69
Q

How many times is the kidney over perfused for a standard organ of its weight?

A

50-fold over-perfused vol/weight

70
Q

What part of the kidneys form a portal system?

A

the renal capillary system

71
Q

What % of the body weight makes up the muscles?

A

mass - 40%

72
Q

How many times is the skin over perfused for a standard organ of its weight and why?

A

bc of the skin’s role in thermoregulation

73
Q

How does Arterio–Venous Anastomoses allow for rapid cooling?

A

by keeping the vessels at the level of arterials and the venules, the blood doesn’t really slow down a lot so the blood just goes fast, right through the skin and can cool off quite quickly

74
Q

What are the two types of systolic murmurs?

A

AV regurgitation or SL stenosis *E

75
Q

What are the different pressure volume loop shapes of the two regurgitation valve pathologies?

A

mitral rg- oval potato

aortic rg- lumpy potato shifted right

M103 T3 (21 decks)

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