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Study Leave semester 2 year 1 > Cardio > Flashcards

Cardio Flashcards

1
Q

What are the two levels of control over smooth muscle, surrounding arteries?

A

Local/intrinsic mechanisms- selfish needs
Central/extrinsic mechanisms- for TPR and therefore MAP of whole body

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2
Q

Increase of metabolites in the blood perhaps due to exercise, leads to what

A

Local intrinsic control
Endothelial cells sense and release EDRF, so arteriolar dilate

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3
Q

What are the four local intrinsic controls

A

Active metabolic hyperaemia
Pressure flow auto regulation
Reactive hyperaemia
Injury

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4
Q

Difference between the
local/intrinsic controls?

A

Active/metabolic - trigger is increase in metabolites
Pressure/flow auto regulation - MAP decrease is the trigger, so metabolites washed away less, but same response
Reactive hyperaemia - trigger is occlusion of the blood supply: causes subsequent increase in blood flow (metabolites were not being washed away- and as such, arteriolar became very dilated).

Also injury response

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5
Q

What’s the injury response

A

When you injure yourself, your C-fibres get activated, they fire action potentials, to brain (ouch) but also collateral branches = release substance p, acts on mast cells, triggers histamine release, histamine = smooth muscle relaxes, arteriolar dilate, increase blood flow. Permeability increase.

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6
Q

Central control of blood pressure, what’s the difference between what the sympathetic and parasympathetic does.

A

Sympathetic = noradrenaline, binds to alpha 1 receptors, causes arteriolar constriction

Parasympathetic = no effect.

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7
Q

Parasympathetic nerves have no effect on blood pressure, what affect DOES it have

A

Genitalia and salivary glands have increased fliw

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8
Q

Normal hormonal central control of blood pressure

A

Adrenaline
A1 receptors
Arteriolar construction

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9
Q

adrenaline hormonal central control of blood pressure: adrenaline and alpha 1 vs adrenaline and beta 2

A

Well it’s alpha 1 receptors that the adrenaline binds to. But some tissues eg some muscle also activated beta 2 receptors. Which means opposite affect- arteriolar dilation, not construction.

Eg during exercise

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10
Q

What happens to coronary circulation during systole?

A

It’s interrupted
Because pressure in ventricles squishes blood vessels
Still has to cope with increased demand during exercise
So active/metabolic hyperaemia
Where the local paracrine signal like nitric oxide is released, = arteriolar dilation
Smooth muscles in the arterioles = beta 2 receptors = smooth muscle relaxation, and arteriolar dilation

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11
Q

What’s special about the cerebral circulation

A

Needs to be kept stable
So good pressure auto regulation, where MAP decrease is triggered, so EDRF

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12
Q

How is pulmonary circulation kept okay?

A

Decrease in O2 = arteriolar constriction , shynt

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13
Q

What’s the auto regulation like in the renal circulation?

A

Fantastic
Filtration rate kept relatively constant during normal fluctuations in MAP

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14
Q

What does MAP = equation

A

MAP = CO x TPR

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15
Q

What happens if MAP is too low/too high

A

Too low = fainting/syncope
Too high = hypertension

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16
Q

Why syncope

A

Because removes gravity, so less pooling, EDV restored, preload restored, stroke volume restored

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17
Q

Short term way of sensing blood pressure / MAP is what?

A

Arterial baroreflex

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18
Q

The arterial baroreflex is essentially an integrating centre that’s looks at the info, decides what to do with it etc

A

Yes

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19
Q

What are the two sensing sets of baroreceptors

A

The carotid sinus baroreceptors
The aortic arch baroreceptors

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20
Q

Where are the carotid sinus baroreceptors

A

In the common carotid arteries

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21
Q

Where’s the carotid sinus

A

It’s where the common carotid arteries become the internal carotid arteries

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22
Q

How do the baroreceptors (carotid sinus and aortic arch) actually work?

A

They detect changes in pressure by detecting stretch, and when they detect change in stretch, they increase the firing rate of action potentials

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23
Q

Less pressure = less firing rate of baroreceptors, true or false

A

True

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24
Q

When during the cardiac cycle do the baroreceptors have the highest firing rate?

A

when walls most stretched, so that’s early in systole.

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25
Q

Where do the aortic arch baroreceptors send their signals up?

A

Up the vagus nerve

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26
Q

Where do the carotid sinus baroreceptors send their signals up what nerve

A

The glossopharyngeal nerve

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27
Q

Where does the nerve signal from the baroreceptors ultimately go? (Both from vagus nerve and from the glossopharyngeal nerve)

A

The medullary cardiovascular centre

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28
Q

What are the responses of the medullary cardiovascular centre of MAP too high that’s via para Sympa?

A

Para Sympa is via the vagus nerve, this innervates the sinoatrial node in the heart,
So releases acetylcholine, binds to cholinergic muscarinic receptors on pacemakers, they hyperpolarise so take longer to get to threshold, Brady,

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29
Q

What affect does the parasympathetic nervous system have on the heart?

A

It causes the sinoatrial nerve to hyperpolarise, take longer to get to threshold, leads to Brady

Doesn’t innervate muscle of the ventricle, or change contractility

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30
Q

What affect does the sympathetic nervous system have on the heart? (HR and contractility)

A

Heart rate: Noradrenaline = beta 1 receptors, pacemaker depolarise faster to increase heart rate

Adrenaline = beta 1 receptors = up heart rate and increased contractility

Contractility: innervates ventricle, increase release of calcium, = more actin and myosin, increase ex-contraction coupling, so greater stroke volume

31
Q

What affect does Sympa on the blood vessels?

A

Cause smooth muscle to contract, you get vasoconstriction, via alpha 1 receptors on smooth muscle of blood vessels

32
Q

Venoconstricrion- vasoconstriction of the veins- specifically leads to what?

A

(Capacitance vessels) push more blood back to the heart- so up EDV, up preload, up contractility, up stroke volume, = up MAP

33
Q

Arteriolar construction- vasoconstriction of the arterioles- leads to what specifically?

A

Arterioles are resistance vessels- more difficult to push blood, so increase TPR, so increase MAP

34
Q

In the short term, what’s the most important input that the medullary cardiovascular centres receive?

A

From the medullary cardiovascular centres from arterial baroreceptors

35
Q

Are there other baroreceptors?

A

Yes
Chemoreceptors (for pCO2 and pO2)
Cardiopulmonary
Chemoreceptors for sensing metabolite concentrations

36
Q

What do chemoreceptors specifically detect?

A

Increase in CO2
Decrease in O2

They stimulate respiratory drive to breathe faster and deeper

37
Q

Why would joint receptors, sensing joint movement, say they need more blood?

A

If exercise, need more oxygen

38
Q

Could strong emotional stimuli trigger a cardiovascular response and how

A

Yes
It’s vasovagal syncope
Don’t know exactly how

39
Q

In the short term, how is MAP kept in range

A

Job of the arterial baroreflex

40
Q

What’s the bowman’s capsule

A

Place where blood comes in and is filtered under pressure

41
Q

Where does filtrate go after bowman’s capsule (where it’s filtered)

A

Filtrate comes into the proximal tubule
Through loop of henle
Onto the collecting duct
Off into bladder and is excreted

42
Q

The loop of henle is closely followed by what?

A

The efferent arteriole

43
Q

After bowman’s capsule, is filtrate ever reabsorbed?

A

Yes

44
Q

After bowman’s capsule and loop of henle etc, with filtrate coming in and out, what gradient is built up?

A

Big sodium gradient in the extra cellular fluid in the loop of henle

45
Q

Because the efferent arteriole follows the path of loop of henle, by controlling permeability, you control whether the water follows osmotic gradient, true or false

A

True

46
Q

True or false: by depending on whether you make the collecting duct (of water) permeability, you control how much water is reabsorbed

A

Trye

47
Q

How do you modulate how much water is reabsorbed from loop of henle / collecting duct, to arteriole

A

Basically water follows sodium. And if more sodium is retained, more water is retained, blood pressure higher

48
Q

If retaining lots of water, plasma volume will increase, and therefore your mean arterial pressure will increase. True or false

A

Yes

49
Q

What will happen if you make the collecting duct very impermeable?

A

Little reabsorption, lots of urine (= diuresis) and a reduction in plasma volume

50
Q

Diuresis =

A

Large amount of dilute urine

51
Q

Where is renin released from?

A

Released from granular cells of the renal juxtaglomerular apparatus

52
Q

Why is renin released from the juxtaglomerular apparatus? (3)

A

In response to one of three factors:

1) reduced sodium delivery through the tubule
2) sympathetic stimulation of the juxtaglomerular apparatus via beta 1 adrenroreceptors
3) decreased distension of afferent arterioles ‘renal baroreflex’

53
Q

Renin is inhibited by what

A

ANP, atrial natriuretic peptide (ANP)

54
Q

What’s ANP released by

A

A stretched Atria in response to increases in blood pressure

55
Q

If ANP is released by stretched Atria in response to increases in blood pressure, and it inhibits renin, what does that mean

A

That renin = up blood pressure somehow

56
Q

Relationship between sympathetic innervation and juxtaglomerular cells?

A

If juxtaglomerular cells are stimulated by sympathetic activation, then renin is released

57
Q

When blood pressure is low, sympathetic activation does what to JG cells?

A

Cause them to release renin

58
Q

Decreased blood pressure, = less filtration, = less delivery of sodium, yes or no

A

Yrs

59
Q

What does renin actually do?

A

Converts angiotensinogen to angiotensin 1
Angiotensin 1 is converted into angiotensin 2 by angiotensin converting enzyme

60
Q

How does angiotensinogen get to angiotensin 2?

A

Angiotensinogen > (via renin) angiotensin 1 > (via angiotensin converting enzyme) angiotensin 2

61
Q

What does angiotensin 2 do? (3)

A

1) stimulates release of aldosterone from the adrenal cortex
2) increases release of ADH from the pituitary
3) is a vasoconstrictor

62
Q

When angiotensin 2 stimulates the release of aldosterone, what happens?

A

Aldosterone increases Na+ reabsorption in the loop of henle,
Therefore reduces diuresis and increases plasma volume

63
Q

Angiotensin increases the release of anti-diuretic hormone (ADH), which does what

A

Increases water permeability of the collecting duct
So reduces diuresis and increases plasma volume
Increases sense of thirst

64
Q

Angiotensin 2 is a vasoconstrictor why is this okay

A

It increases TPR

65
Q

Where is the ADH produced?

A

Synthesised in the hypothalamus
Released from the posterior pituitary

66
Q

What triggers ADH production? (3)

A

Signs of low plasma volume =

Decrease in blood volume (senses by cardiopulmonary baroreceptors)
Increase in osmolarity of interstitial fluid
Circulating angiotensin 2 (triggered by RAAS)

67
Q

Antidiuretic works against low plasma volume and/or MAP

A
68
Q

What does ADH actually do? (2)

A

Increases permeability of collecting duct
Causes vasoconstriction therefore up MAP

69
Q

ADH is positive feedback system

A

False
Negative

70
Q

ANP and BNP is produced where?

A

Produced and released from myocardial cells in the atria and ventricles

71
Q

What triggers BNP and ANP release?

A

Increased distension of the atria and ventricles

72
Q

Increased distension of the atria and ventricles is a sign of what

A

Increased MAP

73
Q

What does ANP and BNP actually do?

A

Increase excretion of Na+
Inhibit the release of ANP
Act on medullary CV centres to reduce MAP

Study Leave semester 2 year 1 (9 decks)

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