Arterial and Venous system Flashcards

1
Q

function of elastin fibres in aorta

A

Elastin fibres provide elasticity

– as blood is ejected the aorta expands, the rebound in diastole propels the blood onward

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2
Q

important structure in arteries

A

Arteries have a thick layer of smooth muscle

– allows them to withstand high pressures

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3
Q

collagen fibres function

A

Collagen fibres provide strength

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4
Q

how does collagen and elastin change throughout arteries

A

this and elastin decrease in abundance as arteries get smaller

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5
Q

how does collagen and elastin change WITH AGE

A

As we get old vessels get stiffer and less compliant

– one of the reasons blood pressure increases

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6
Q

Important structure of arterioles

A

Arterioles have a thick layer of smooth muscle
– as a total amount it is less than the large arteries but it is greater proportional
of the total wall

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7
Q

difference between arteries and arterioles

A

• Less elastin and collagen fibres

– less compliant compared to larger arteries

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8
Q

arterioles are site of

A

These are the site of total peripheral resistance
– think back to the Poiseuille’s Law (1 / r
4)
• Tone on these vessels determines where blood flows
– it always takes the path of least resistance

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9
Q

vascular tone

A

the level of constriction applied across vessels

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10
Q

state of arteries at rest

A

are slightly constricted meaning they can both

constrict and dilate

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11
Q

arterial tone

A

the balance of constrictors and dilators that are acting on the vascular smooth muscle

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12
Q

arterial constriction leads to..

A

decrease radius
increase resistance
decrease flow

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13
Q

arterial dilation

A

increase radius
decrease resistance
increase flow

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14
Q

what does vascular tone respond to

A

responds to both intrinsic (local) and extrinsic (systemic) factors

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15
Q

2 types of intrinsic factors

A
  1. intrinsic: mechanical stimuli E.G. stretch and shear

2. intrinsic: endothelial regulation plus other metabolites and autocoids in response to local demand

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16
Q

extrinsic

A

extrinsic: systemic regulation (nerves & hormones)

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17
Q

organs involved in primary intrinsic regulation of vascular tone

A

brain, kidney and heart
– local control regulating flow -
brain does not require external stimuli

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18
Q

primarily extrinsic regulation of vascular tone

A

skin
– think hypothalamus and temperature regulation
– also think cool peripheries following BP crash

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19
Q

interactions of regulation of vascular tone

A

skeletal muscle
– at rest systemic regulation
– during exercise local metabolites dominate

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20
Q

when do smooth muscles constrict

A

constricts when stretched
– occurs in most smooth muscles including vascular
– due to opening of Ca2+ channels

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21
Q

where does constriction occur

A

• Occurs in a number of vascular beds

– such as cerebral, renal and coronary

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22
Q

what does myogenic response of constriction of smooth muscle contribute to

A

This contributes to the basal tone of arteries and stabilises flow and prevents excessive perfusion
– it is an important feature of autoregulation

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23
Q

role of vascular endothelium

A
– interface between blood and body tissues
– control of blood coagulation
– regulates vascular structure
– mediates inflammatory responses
– regulates vascular tone
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24
Q

endothelium performs thru the release of what factors

A

paracrine factors

acting nearby; either the smooth muscle or platelets

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25
endothelial mediators. - dilators
nitric oxide (NO) and prostacyclin (PGI2)
26
vasoconstrictors
such as endothelins (ET), Ang II and thromboxane (TxA2)
27
what does nitric oxide synthase enzyme produce
free radical nitric oxide
28
NO function
a vasodilator, relaxing vascular smooth muscle – production increased by shear stress – also agents such as ACh, histamine and bradykinin
29
NO is an anti-//
anti-thrombogenic and anti-atherogenic | – a healthy endothelium provides a non-thrombogenic surface
30
drugs interacting NO pathway -nitrates
– e.g. glyceryl trinitrate (GTN) – used in angina – assumed to act as NO is released via metabolism – also available from dietary sources
31
drugs interacting NO pathway - phosphodiesterase inhibitors
– e.g. sildenafil (Viagra) – erectile dysfunction and pulmonary hypertension – prevents the breakdown of cGMP
32
what promotes vasodilation
Increased CO2, K+ , H+ and adenosine as well as decreased O2 all promote vasodilatation – increased tissue metabolism increases perfusion
33
vasoactive substances
histamine, bradykinin, serotonin (5-HT) and | eicosanoids/prostanoids
34
metabolic hyperaemia
increased metabolic rate in tissue accumulation of metabolites CO2 H+ K+ adenosine local vasodilation increased blood flow accumulated metabolites flushed out appropriate blood flow match metabolic rate
35
what nervous system is responsible for maintenance of vascular tone
SympatheticNS
36
most arteries are innervated by what fibres
sympathetic fibres
37
constriction is due to what hormone and what receptor
noradrenaline acting at α1 | -adrenoceptors
38
increased sympathetic activity increases
will increase vasoconstriction | – cold, clammy peripheries
39
what receptors lead to dilation in arteries
β-adrenoceptors (mainly β2 | -)
40
arteries are a target for circulating what hormone and what do they prevent
mainly a target for circulating adrenaline (adrenal medulla) | – prevalent in the skeletal muscle vascular beds and heart
41
vasodilator innervated by
parasympathetic innervation
42
organs innervated by PNS
face gut penis
43
PNS innervated vessels mediated by what hormone
ACh & nonadrenergic non-cholinergic (NANC) | – NANC transmitters include NO, substance P, VIP
44
mechanism of action of vasoactive hormones
Adrenaline from adrenal medulla. – tends to act via β adrenoceptor – constriction or dilation is vascular bed dependent • Angiotensin II – acts on AT receptors potent vasoconstrictor • Vasopressin (anti-diuretic hormone, ADH) – vasoconstrictor • Insulin and oestrogens – dilators by various mechanisms
45
function of venules and veins
carry blood from capillaries back to the heart | right atrium
46
structural difference between veins and arteries
Structurally veins are similar to arteries but have much thinner walls – very little smooth muscle, small amounts of collagen/elastin
47
what gives veins their capacitance function
distensibility gives then a capacitance function – two thirds of the blood volume is held in the venous system – x20 compliance of arteries
48
what are the veins innervated by and what hormones and receptors mediate them
• Like arteries, veins are innervated by SNS fibres – noradrenaline acts at ɑ1 -adrenoceptors to constricts veins
49
are veins capable of constricting
yes
50
affect of SNS fibres and noradrenaline
The effect of this is to raise pressure and decrease venous capacitance – redistributing the blood
51
function of valve
prevent backflow, blood is moved towards the heart | – increasing cardiac output via Starling’s Law
52
venous return is altered by
Skeletal muscle and thoracic pumps – vary the pressure gradient during their activity • Venous pressure/venoconstriction gravity
53
how does gravity influence pressure
Hydrostatic pressure increases 0.74 mmHg for every 1 cm beneath the heart – venous pressure the foot 100 mmHg, yet -10 mmHg in brain
54
how does gravity influence venous return and veins
• This increased transmural pressure distends the veins and venous return temporarily decreases – this is venous pooling
55
how does gravity influence muscle, valves and thoracic pump
The valves and muscle and thoracic pump break up the column into smaller sections aiding return – lack of movement (and muscle pump) increases ankle oedema
56
impact of failure of of valves
• Failure of valves also decrease return and increase venous pooling/oedema – varicose veins
57
what is triggered when pressure falls
Baroreceptor reflex is triggered as cardiac output and pressure fall – increased vaso/venoconstriction, heart rate and contractility – this should be imperceptible
58
what happends when baroreceptors cannot respond
In states where the baroreceptors cannot respond then there is postural drop and possibly syncope – dehydration, already low pressure, old age (stiffer vessels)
59
affect of positive g force - pilot in a steep climb
– black out as venous pooling increases – venous return drops as does cerebral perfusion – in a suit pilots can tolerate ~9 G
60
affect of negative g force - pilot in a steep dive
“red out” and blood rushes to head (red eyes) | – even in suit can only tolerate about 3 G
61
what does central venous pressure measure -CVP
measures right atrial pressure via | catheter in central vein
62
what does CVP reflect and what is used to assess
it reflects the venous return and cardiac function | – can be used to assess fluid volume in fluid replacement
63
how does CVP change in heart failure
CVP increases in heart failure due to volume expansion
64
where is jugular venous pressure - JVP
seen in the internal jugular vein | of a person sitting
65
A,C,V waves of the jugular venous pulse in the ..
right atrium
66
how to measure jugular venous pressure
• Sit patient at 45 degrees • The internal jugular veins fills from above – where can you visualise is the filling point? • The sternal angle is the zero point, more than 3 cm above is abnorma
67
what does increased jugular venous pressure suggest
A raised JVP suggest increased right atrial pressure – fluid overload – RV failure – tricuspid valve stenosis/regurgitation
68
hepatic portal vein function
carries blood from the gastro-intestinal tract to the liver – from intestinal capillaries to liver capillaries via portal vein – two capillary beds in series
69
what type of capillaries are the capillaries in the liver
sinusoidal type | – large gaps allows large substances to be absorbed
70
how do diseases like cirrhosis impact hepatic portal circulation and how is it corrected
, resistance in the hepatic portal system increases – to maintain flow pressure must increase (Q = ΔP ÷ R) – pressure increases giving portal hypertension
71
how are nutrients absorbed in the hepatic portal circulation
All substances absorbed from the intestines pass through the liver – this includes orally taken drugs – first pass metabolism
72
high portal pressure leads to
``` shunt vessels (varices) that bypass the liver back into systemic venous system ```
73
what can shunt vessels lead to
this leads to morbidity – bleeding abnormalities and toxins damaging other organs – (hepatorenal syndrome and hepatopulmonary syndrome)