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physiology and pharmacology > Circulation > Flashcards

Circulation Flashcards

1
Q

what are the physical laws that govern fluid flow through vessels?

A

Blood flow = Pressure difference/ resistance
Darcy’s law (“ohms law”)
impendance = resistance for pulsative flow
pouiseuilles law

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2
Q

flow =

A

PiXradius(power 4)Xdifference in pressure/8XviscosityXlength of the vessel

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3
Q

Resistance =

A

8XviscosityXlength of vessel/piXradius(power of 4)

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4
Q

what is the radius critically important in determining flow and resistance?

A

because it is to the power of 4, meaning small changes in r have a huge impact!

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5
Q

what are the resistance vessels and why are they called this?

A

small arteries and particularly arterioles, as these are where blood first meets high resistance.

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6
Q

what is a key function of vessel diameter?

A

it is a key control point

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7
Q

what is the critical closing pressure?

A

tissue pressure will collapse vessels if the BP falls below a certain point.

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8
Q

in vessels Transmeural pressure (p) =

A

Tension/ radius

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9
Q

in vessels Tension =

A

pressure X internal radius / wall width

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10
Q

what is transmeural pressure?

A

pressure across the vessel wall.

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11
Q

why is the relationship between Laplace and aneurysms important?

A

because in aneurysms, they swell, this meaning the internal radius increases, there’s a decreased wall thickness… this is leading to an increase in tension. it can reach a point where the vessel can no longer balance tension and pressure which can cause it to burst.

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12
Q

compliance (c) =

A

volume change / pressure change

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13
Q

why are veins capacitance vessels?

A

because veins are more compliant than arteries and store more blood

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14
Q

why are you able to tell if a body has been moved after death using a post mortem?

A

because there is blood pooling, so the pooling would be in a different area to where expected.

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15
Q

what is the windkessel effect?

A

the shape of arterial blood pressure waveform in terms of interaction between stroke volume and compliance of the aorta and other large elastic arteries.

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16
Q

what is pulsatile discontinuous flow? where does this occur?

A

this is a pulse like flow, sometimes there is no flow. this is in the aorta and the pulmanory artery.

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17
Q

what is pulsatile continuous flow? where is this seen?

A

this is where there is an organ is continuously supplied with blood.The flow level is always greater than 0. This occurs further away from the aorta such as in the renal artery.

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18
Q

what’s the difference between laminar and turbulant flow?

A

laminar flow has a steady and parallel flow where as turbulent as vortices and eddies.

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19
Q

when is the reynolds number used?

A

to see if a flow is laminar or turbulent.

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20
Q

using the reynolds number Nr =

A

fluid density X vessel diameter X mean velocity / viscocity

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21
Q

what’s the difference between flow and velocity?

A 
Flow = Vol / time
Velocity = Distance / time
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22
Q

what does a NR

A

laminar flow

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23
Q

what does a NR > 3000 mean?

A

turbulent

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24
Q

what happens to blood pressure over arterioles?

A

it decreases

- the mean pressure is 35mmHg; pulse pressure 5mmHg

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25
Q

what happens to blood velocity at the arteriole?

A

it decreases.

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26
Q

where is the greatest fraction of blood stored?

A

in the venous system

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27
Q

why do cappilaries have a large S.A?

A

because they have a large cross sectional area.

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28
Q

how much of the total blood volume is in capillaries?

A

5% of the total blood volume.

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29
Q

how long does it take for blood to pass through a capillary? why is this?

A

about 1-2 s

because there’s is a low velocity in the capillaries.

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30
Q

what’s the difference between active and inactive capillaries?

A

inactive are collapsed.

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31
Q

what do metarterioles do?

A

they regulate the flow of blood into the capillaries using there precapillary sphincters. this directs flow,

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32
Q

what is net fluid transfer from capillaries to tissues by?

A

it’s by a balance of filtration and absorption.

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33
Q

what are the different types of filtration?

A

transcellular - using aquaporins.

paracellular - between cells

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34
Q

what does the net fluid transfer form?

A

tissue fluid

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35
Q

what does fluid formation depend on?

A
  1. the hydrostatic pressure difference between capillary and intersticial fluid
  2. the difference in colloid osmotic pressure
  3. the capillary filtration coefficient.
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36
Q

what’s the difference between blood hydrostatic pressure and tissue fluid hydrostatic pressure?
what does this mean for the hydrostatic pressure difference between capillary and intersticial fluid?

A

blood is normally higher than TF

- it is usually out

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37
Q

what causes the difference in colloid osmotic pressure?

that’s the plasma COP like and the TF COP like?

A

impermeable proteins such as albumin

plasma is high and TF very low

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38
Q

how does haemmorrhage cause abnormal TF levels?

A

blood pressure decreases resulting in more reabsorption

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39
Q

how does capillary damage cause abnormal tissue fluid levels?

A

tissue fluid increases and colloid osmotic pressure increases.
reduced reabsorption into blood
there’s fluid efflux

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40
Q

what is oedema? what happens to venous blood pressure?

A

increased tissue fluid

increase in venous blood pressure.

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41
Q

what vessels have smooth muscle?

A

all vessels apart from capillaries

42
Q

where is the smooth muscle “on capillaries” located?

A

in the pre-capillary sphincters

43
Q

where’s targeted in order to control circulation?

A

arteriole resistance, blood storage in veins also target vascular smooth muscle.

44
Q

what is myogenic regulation?

A

this is where the muscles themselves contract without stimulation.
stretch evokes a contraction.

45
Q

what is metabolite regulation?

A

changes in the levels of PCo2, pH, PO2, lactate, potassium due to metabolism. if metabolising more = more of these so vasodilation occurs to remove these metabolites and bring more oxygen.

46
Q

if put a cuff on the top of the arm restricting flow of blood to the lower arm?

A

there’s an increased blood flow from before the cuff in order to remove metabolites.

47
Q

what do most vessels (excluding capillaries and venuoles) have that allows control from the autonomic NS?

A

they have tonic sympathetic, adrenaline constrictor input. meaning the have alpha-adrenergic receptors.

48
Q

what allows the pre-capillary vessels in skeletal muscle, heart, lungs, and kidney have that allows control from the ANS?

A

they have sympathetic ACh vasoldilators.

49
Q

that does erectile tissue and glands have that allows control from the ANS?

A

they have parasympathetic ACh vasodilators.

50
Q

what do lots of action potentials down a sympathetic nerve fibre cause vessels to do? How is this opposed?

A

causes vasoconstriction.
weaker sympathetic tone (less APs) causes relaxation.
it isn’t on and off.

51
Q

what is the cutaneous density innervation like? why is this?

A

it’s high. this is because it is involved in thermoregulation meaning very tight control of blood flow is needed. this helps to avoid heat loss.

52
Q

what is cerebral density innervation like? why is this?

A

there’s little sympathetic input, this is because flow to the brain doesn’t change.

53
Q

what are the adrenal medullary hormones?

A

adrenaline and noradrenaline

54
Q

where do chromafin cells originate from? what does it share this common origin from?

A

originate from the neural crest, this is a shared common origin with the nervous system.

55
Q

why does adrenaline act differently on different tissues?

A

this is because of the different receptors and signal transduction

56
Q

what does adrenaline do to vessels at the skin/viscera?

A

vasoconstriction

57
Q

what does adrenaline do to vessels to skeletal muscle and the liver?

A

causes vasodilation.

58
Q

how can extrinsic control be used in defense reduction (fight or flight)?

A

adrenaline gets blood to the heart, skeletal muscle and liver.

59
Q

what are kinins?

A

they are signalling molecules

60
Q

what is bradykinin?

A

it is a vasodilatory peptide

61
Q

what does Angiotensin II do?
what is it formed by?
what does it act on?

A

cause vasoconstriction in the arterioles, this increases blood pressure.
formed by enzymes such as renin in the kidney.
acts on precursers of angiotensin (Angiotensinogen)

62
Q

why are angiotensin inhibitors used?

A

for hypotension treatment

63
Q

what distance do local agents act over?

what kind of half life do they have?

A

they act over short distances and have a short half life.

64
Q

what are prostaglandins?

A

most of them are vasodilators, in a very local area which don’t tend to pass through circulation.

65
Q

what is serotonin found in? what does it do? where is it localised to?

A

it is found in platelets, it causes vasoconstriction and is localised to the site of the damage.

66
Q

where is histamine found? what does histamine do? what can this lead to?

A

found in mast cells.
causes vasodilation and also alters the capillary filtration coefficient, which alters the permeability of blood vessel walls.
this can lead to oedema if the CFC is increased which in turn increases permeability.

67
Q

where does endothelium- derived relaxing factor act on?
when is it released?
what do the endothelium cells release? what does this cause?

A 
doesn't directly act on muscle, it acts on endothelium.
released after stimulation by e.g ACh
NO is released from the endo cells
this stimulates cGMP in the muscle
this leads to relaxation of the muscle.
68
Q

what is sildenafil citrate? how does this act and what does it cause?

A

it is viagra.
it inhibits cGMP breakdown
results in more sustained vasodilation.

69
Q

what is angina?

A

it’s when chest pain is caused by flow to the heartis restricted.

70
Q

what is nitroglycerin?
when is it used?
how does it work?

A

it’s an explosive but it’s also used medically.
used to ease the symptoms of angina
spontaneously degrades to form NO.
increase NO leads to vasodilation and an increase in flow and oxygen supply.

71
Q

when are endothelium derived hyperpolarising factors released?

A

released after stimulation by e.g ACh.

72
Q

What CNS centres are in the brainstem?

A

the medulla oblangata neural clusters

73
Q

what kind of response can central control be involved in?

A

an emotional response, homeostatic control, communication with the heart and blood vessels

74
Q

what are the medullary centres involved in?

A

cardioexcitation/inhibition and vasomotor output regulated by clusterings of neurons in the medulla.

75
Q

what do medullary neurons respond to int he local envornment?

A

pH, pCO2, pO2 ( these are related to the metabolic state of the tissue which is related to blood supply) and increase in intercranial pressure.

76
Q

how is blood supply in the brain/medulla restored? why does this lead to bradycardia?

A

by vasoconstriction which increases blood pressure.

the heart rate is slowed because some where else is detecting the rise in blood pressure.

77
Q

what are the different types of peripheral proprioreceptors and where are they found?

A

Baroreceptors (pressure receptors) - these are in various parts of circulation.
Stretch receptors - carotoid sinus, aortic arch which detect high pressures.
- in the atria and left ventricle and pulmanory veins -lower pressures.
Buffer nerves - glossopharyngeal and vagus

78
Q

how do buffer nerves work?

A

when arterial pressure increases there’s an increase in firing.
a decrease in vasoconstrictors leads to an increase in cardioinhibition.
this causes vasodilation, bradycardia, decrease in output and a decrease in blood pressure.

79
Q

what kind of regulation are buffer nerves?

A

short term regulation.

80
Q

what is the valsalva manoeuvre?

A

the clinical testing of baroceptors.

records oesophageal and arterial pressure.

81
Q

what are the possible reasons for female blood pressure being lower than males until it’s then greater after 50 years of age?

A

could be due to menopause

or could be that the males with a higher blood pressure have died.

82
Q

what’s the difference between essential hypertension and secondary hypertension?

A

with essential hypertension there’s clear risk factors however there’s no clear clinical cause.
secondary hypertension is a consequence of a clinical condition.

83
Q

MABP =

A

CO X TPR (Cardiac output X total peripheral resistance)

84
Q

what happens to CO with age?

A

it decreases

85
Q

what is the relationship with TPR and CO?

A

TPR increases with output.

86
Q

what kind of cardiac output is a likely suspect with EH?

A

that there’s an increased response to stress and catecholamines.

87
Q

what vessel abnormalities are likely suspects when it comes to EH?

A

sympathetic NS abnormalities.

local factors - low EDRF (vasodilator)

88
Q

what smooth muscle ion channel defects are likely suspects with EH?

A

muscle hypertrophy/ rigidy

kidney dysfunction - volume induced hypertension

89
Q

what is there to say EH could be genetic?

A

it correlates with relatedness
- seen in twin studies etc.
it varies with race (could be cultural though)
- it is at a higher incidence among afro-caribean

90
Q

what are the environmental risk factors of EH?

A

diet and obesity
adoption of western lifestyle
salt intake
vitamin D deficiency

91
Q

what percentage of people with EH are estimated to have a genetic predisposition?

A

30-50%

92
Q

what is there best evidence for polymorphisms in? (for EH)

A

angiotensinogen and ENaC

93
Q

what did studies with the chimpanzee show about salt intake?

A

they fed the chimpanzee a normal diet, then an elevated salt diet, then a normal diet again. can see a correlation between blood pressure and salt intake.

94
Q

what did human studies show about salt intake?

A

if reduce salt by 3 grams a day then that reduced MABP by 5mmHg. this is the equivalent to as drug that reduces strokes.
the studies also showed it has to be a NACL reductions rather than a Na+ reduction.

95
Q

what are some of the cuases of secondary hypertension?

A

renal disease
- nephron function impaired
- blood volume and blood pressure increase
-more damage and kidney failure.
renal artery stenosis
- narrowing of the renal arteries
- renin production and blood pressure increases.
pheochromocytomas
- increase in chromaffin cells
- increase in adrenaline cells and blood pressure.
hormone imbalance
-aldosterone increase
- Na+ and BP inceases
- this can be caused by mini adrenal tumours.

96
Q

what are the consequences of hypertension?

A
  • flushing, sweating, blurred vision
  • arteriosclerosis/artherosclerosis
    -aneurysms
    aortic diameter can increase from ~2.5cm to 8 cm
    this would require grafts to be used to restore normal size and function
  • stroke (can be aneurysms in the brain)
    hi- systolic
    can have bleeding (post aneurysm) or thrombosis.
    bleeding on the brain
  • MI (myocardial infarction)
  • retinal damage
    hypertensive retinopathy.
97
Q

what are non-pharmacologic treatments for hypertension?

A 
weight loss
exercise
diet (decrease in salt, alcohol, caffeine)
smoking 
relaxation
98
Q

what are the pharmacologic treatments of hypertension?

A

Diuretics
- total blood volume efected
Thiazides
- increased Na and Cl excretion
sympatholytics
- reduces effect of symp NS and catecholamines
Alpha blockers (sympatholytic)
- clonidin = decrease CNA sympathetic output
- prozosim = relaxes smooth muscle and decreases TPR
Beta- blockers (sympatholytic)
- propanolol = decreases heart rate and contractility
- these are phasing out, only prescribed under certain conditions as there’s many side effects.
Ca2+ channel blockers (sympatholytic)
Broad spectrum = minoxidil = decrease cardiac contraction and vasc muscle
selective = manidipine= vascular smooth muscle.

99
Q

How can the RAA system be used to treat hypertension?

A

ACE inhibitors = reduce the formation of angiotensin II= meoxipril
AGII Receptors
= sartan family

100
Q

what is the dual approach to treating hypertension?

A

use more than one therapy to target BP
low doses of multiple drugs - may become better tolerant to individual drug.
usually a diuretic and something else.

physiology and pharmacology (7 decks)

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