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Y1 LSS CVS > The Circulation > Flashcards

The Circulation Flashcards

CIrculation; Flow; Vascular starling forces; Lymphatic system; Law of LaPlace; Vascular endothelium; Vascular endothelium drugs (69 cards)

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1
Q

What are the two main physical principles of the circulatory system?

A

Double circulation - systemic and pulmonary, each with different pump
Pressure gradient - generated by heart, causes movement of blood

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2
Q

What is the function of the circulatory system?

A

Transport oxygen, CO2, nutrients, hormones, metabolites, cells and immunity related molecules around the body
Thermoregulation

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3
Q

What is the general order of the circulatory vessels?

A 
Arteries
-have a low sfa
-store little blood but at high fluctating pressure
Arterioles
-site of drop in BP
-can be constricted to control flow of blood
Capillaries
-highest total sfa
-form networks/beds for diffusion
Venules
-connect veins to capillary beds
Veins
-holds the most blood and at the lowest pressure
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4
Q

Define laminar flow

A

Velocity of fluid constant at any one point
Flows in layers
Fastest closest to centre of lumen (some friction with endothelial cell lining)
High level of shear stress - promotes endothelial cell survival and alignment in direction of flow to promote secretions to allow vasodilation and anticoagulation

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5
Q

Define turbulent flow

A

Associated with pathophysiological changes to endothelial lining
Erratic flow
Forms eddys
Prone to pooling
may lead to occlusion
Low shear stress promotes endothelial proliferation allows secretions to promote endothelial proliferation, apoptosis and shape change

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6
Q

What does the parabolic velocity profile show?

A

Shows how flow further from the wall = increased velocity
Tangent at any point on the parabolic profile = shear rate
shear rate x velocity = shear stress

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7
Q

What is shear stress?

A

Governs how well endothelial cells work

shear rate x viscosity

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8
Q

How is turbulent flow used in the measurement of blood pressure?

A

Release of BP cuff leads to turbulent flow

Can be heard with stethoscope

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9
Q

What is Poiseuille’s equation and its importance?

A

resistance = (8×length×viscosity)/(π×r^4)
length and viscosity are effectively constant so only radius changes rapidly
halving radius decreases flow 16 fold ∴ capillaries and arterioles have the most resistance to flow

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10
Q

What is vascular compliance?

A

The relationship between transmural pressure and vessel volume
change in volume/change in pressure
Dependent on vessel elasticity
Venous>arterial

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11
Q

Define elastance

A

Inverse of compliance
ΔPressure/Δvolume
Produced by elastin fibres in the vascular wall which leads to recoil upon stretching
Blood vessels with high compliance will have low elastance
arterial>venous
∴arteries recoil to maintain pressure whilst veins distend

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12
Q

What is the Windkessel effect?

A

Dampening effect of the change in pressure during ejection
Blood enters aorta faster than it is leaving ∴ 40% of stroke volume is stored by elastic arteries
when ejection ends and aortic valve closes, elastic arteries recoil and send off all stored blood
∴aortic pressure falls slowly and blood isnt lost all at once

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13
Q

How can compliance be modulated?

A

Externally - by stockings to reduce pooling in veins

Internally - by the Renin-angiotensin-aldosterone system, endogenous vasodilators/constrictors and vasoactive drugs

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14
Q

What is the effect of gravity on flow?

A

pulls blood towards ground
standing causes increased hydrostatic pressure ∴blood trasiently pools in veins due to high compliance
∴reduced venous return ∴ reduced CO and BP (starlings law)

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15
Q

Why do healthy individuals not faint when they stand up?

A

Standing activates SNS
constrict venous smooth muscle to stiffen veins
constrict arteries to increase resistance and maintain BP
increase HR and force of contraction to maintain CO

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16
Q

What is the relationship between the Law of LaPlace and blood flow?

A

increased radius increases flow but also leads to higher wall stress ∴ thicker wall is needed to produce higher tension as the radius increases for a given pressure

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17
Q

What is an aneurysm?

A

Balloon like distension increases radius of vessel
For same pressure, tension increases
If weakened fibres cannot supply needed force then will distend in negative feedback cycle until RUPTURE

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18
Q

What is the microcirculation?

A

Specific to each organ
1st order arterioles
Covered in smooth muscle
Branch to capillaries via terminal arterioles to enter tissues
Pre-capillary sphincters control blood flow to capillary bed
Venules leave tissue to collect blood and deliver to the heart

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19
Q

What is a fluid circuit?

A

Flow rate=pressure gradient/resistance

mainly affected by vessel radius - poiseuilles eqn

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20
Q

Where is the pressure gradient formed within the microcirculation?

A

Between arteriole and capillary

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21
Q

What would decrease the Windkessel effect?

A

decrease in arterial compliance

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22
Q

Where is the pressure gradient for a fluid circuit found?

A

between arteriole and capillary

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23
Q

Why do the radii of arterioles vary?

A

Local intrinsic control - matching blood flow to specific tissue needs
Extrinsic control - regulating BP

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24
Q

What is the formula for organ flow?

A

ΔP(MAP)/Resistance of organ

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25
What is active hyperemia?
Increase in organ blood flow associated with increased metabolic activity of an organ or tissue e.g. when activity of muscle increases, metabolism within that muscle increases ∴ so does oxygen consumpton, local tissues detect these increases and send a signal to the arterioles, arterioles vasodilate and increase oxygen reaching cells
26
What is myogenic vasoconstriction?
Local tissue responds to changes in physical environment like temperature changes ∴ if things get colder, this is sensed and sends signals that cause arterioles to vasoconstrict and reduce heat loss Also respond to changes in pressure e.g. if big increase in BP to organ that doesn't require extra flow, arterioles vasoconstrict to help direct greater blood flow to other organs
27
What is the general structure of a capillary?
Single endothelial cell wall Diameter big enough form 1 cell Extensive branching minimises diffusion distance, maximises diffusion time and maximises sfa
28
What are the 3 types of capillary?
Continuous Fenestrated Discontinuous
29
What are features of a continuous capillary?
junctions between endothelial cells are filled with water ∴allows water soluble and small molecules to diffuse over gap junctions Found in blood-brain barrier but these have no H2O gap junctions and only lipophilic molecules can leave and enter
30
What are features of a fenestrated capillary?
Circular fenestrae Slightly more leaky ∴allows larger molecules to leave blood Found in glomerulus kidney nephron
31
What are features of a discontinuous capillary?
Very large gap junctions Allows large molecules to leave blood Found in bone marrow
32
What is bulk flow?
Volume of protein free plasma that filters out of the capillary, mixes with surrounding interstitial fluild and is reabsorbed
33
What affects bulk flow?
2 Starling forces Hydrostatic pressure - from the heart, pushes fluid out Oncotic pressure - pulls fluid back into capillaries
34
What is ultrafiltration?
when pressure inside capillary>pressure in the interstitial fluid
35
What is reabsorption?
When inwards driving pressure>outwards driving pressure
36
Why is the lymphatic system needed?
Hydrostatic pressure at arteriolar end>venular end but oncotic pressure same throughout ∴net loss ∴lymphatic system needed
37
What is the structure of the lymphatic system?
Blind ended capillaries with a single layer of endothelial cells lie alongside blood capillaries Have a large water filled channel that reabsorbs excess interstitial fluid Has valves to ensure one way flow that depends on skeletal contraction/respiratory pumps Lymph nodes that have immune detection defence mechanisms Drainage into R lymphatic duct + thoracic duct then R and L subclavian veins for recirculation
38
What causes elephantitis?
Parasitic blockage of lymph nodes preventing fluid recirculation
39
What causes oedema?
Production rate of ISF>removal rate
40
What is the structure of the vascular endothelium and the functions of each layer?
Layer of cells that acts as a blood-vessel interface Lumen - hollow, where blood flows 3 layers: tunica intima - one cell thick, allows for exchange and haemostasis Internal elastic tissue tunica media - unconsciously controlled smooth muscle External elastic tissue tunica adventitia/externa - protects vessel and contains nerves and blood supply to vessel
41
What are the main functions of the vascular endothelium?
Vascular tone management -secrete and metabolise vasoactive substances Barrier -prevents atheroma development and impedes pathogens Growth - mediates cell proliferation Thrombostasis and haemostasis -prevents clots forming or molecules adhering to vessel wall Absorption and secretion -allows active/passive transport via diffusion/channels
42
What are prostaglandins?
group of compounds that can affect vascular tone
43
How are prostaglandins synthesised?
1) Phospholipids converted to arachidonic acid by phospholipase A₂ 2) Arachidonic acid converted to prostaglandin H₂ by COX1/2 3) converted to prostacyclin by prostacyclin synthase OR converted to thromboxane A₂ by thromboxane synthase OR converted to inflammatory mediators
44
What is thromboxane A₂?
Prostaglandin that is a : Vasoconstrictor Pro-atherogenic Pro-platelet
45
What is prostacyclin?
Prostaglandin that is a : Vasodilator Anti-atherogenic Anti-platelet
46
What are key vasodilators?
``` Endothelium derived: Nitric oxide Prostacyclin Non-endothelium derived: Kinins ANP ```
47
What are key vasoconstrictors?
``` Endothelium derived: Thromboxane A₂ Endothelin-1 Non endothelium derived: Angiotensin II ADH Noradrenaline adrenaline ```
48
What are the sources of nitric oxide?
Exogenous - diffuses from blood to vascular smooth muscle cells Endogenous - produced in response to Ach/bradykinin binding and shear stress
49
How is nitric oxide synthesised in the body?
1) ACh binds to G protein coupled receptor 2) Activates phospholipase C and moves along membrane 3) Phospholipase C catalyses PIP₂ -> IP₃ 4) this triggers Ca2+ release from ER 5) this upregulates endothelial nitric oxide synthase 6) eNOS converest L-arginine and oxygen to L citrulline and nitric oxide
50
How does nitric oxide cause vasodilation?
NO diffuses into vascular smooth muscle cells Activates guanylate cyclase to convert GTP to cGMP cGMP upregulates protein kinase G Protein kinase G activates K+ channels Causes hyperpolarisation and cell relaxation
51
How does prostacyclin cause vasodilation?
Prostacyclin diffuses into vascular smooth muscle cells Binds to membrane IP receptors This activates adenyl cyclase to convert ATP to cAMP cAMP inhibits myosin light chain kinases causing cell relaxation and vasodilation
52
How does Thromboxane A₂ cause vasoconstriction?
Binds to TPbeta receptors on VSMCs Activates phospholipase C to migrate along membrane and convert PIP₂ -> IP₃ and DAG IP₃ triggers Ca2+ influx from ER Ca2+ upregulates myosin light chain kinase causing VSMC contraction and vasoconstriction ALSO Binds to TPalpha receptors on platelets = activation Produce more Thromboxane A₂ in positive feedback response Platelets aggregate for haemostasis
53
How does endothelin-1 cause simultaneous vasoconstriction and vasodilation?
Endothelial cell produces big endothelin 1 Endothelin converting enzyme converts zymogen to ET-1 ET-1 binds to ETa and ETb receptors on VSMC Receptors release PLC PLC converts PIP₂ to IP₃ IP₃ triggers Ca2+ influx Cell contracts and vessel constricts ET-1 also binds to ETb on endothelial cell Upregulates eNOS Increased NO production NO diffuses into VSMC Cell relaxes Vessel dilates
54
How does angiotensin II cause vasoconstriction?
Renin cleaves angiotensinogen to Ang I ACE expressed on endothelial cells in renal/pulmonary circulation and cleaves Ang I to AngII Ang II diffuses across endothelium and binds to AT1 receptor Causes Phospholipase C to migrate along membrane and convert PIP₂ to IP₃ IP₃ triggers Ca2+ influx Ca2+ upregulates myosin light chain kinase Cell contracts ACE also metabolises bradykinin reducing NO mediated vasodilation Vessel constricts
55
What is the mechanism of action of ACE inhibitors?
Block ACE molecules from converting Ang I to Ang II This means Ang II doesnt bind to AT1 receptor and contraction does not take place Bradykinin is also not metabolised Instead bradykinin binds to B1 receptor and stimulates production of NO Causing vasodilation
56
What is the mechanism of action of aspirin?
Aspirin is an irreversible inhibitor of the COX enzyme (NSAIDS are reversible inhibitors) Inactivates COX-1 Switches function of COX-2 to generate protective lipids ∴SHOULD decrease thromboxane levels but also prostacyclin BUT in low doses prostacyclin falls slightly but is still quite high and thromboxane levels continue to fall This because thromboxane mainly made by platelets that have no nuclei to replace COX enzymes Prostacyclin made by endothelial cells and these are able to produce more COX enzymes and overcome the effects of aspirin This means aspirin has anti-platelet effects
57
What does the endothelium produce?
``` Adhesion molecules Matrix products Antithrombotic/procoagulant factors Vasodilating/vasoconstricting factors Growth factors ```
58
What is the difference between resting endothelium and activated endothelium?
``` Resting: -anti inflammatory -anti thrombotic -anti proliferative Activated: -Pro inflammatory -Pro thrombotic -pro angiogenic ```
59
What are activating factors that have an effect on the endothelium?
``` Viruses Smoking Mechanical stress Inflammation High blood pressure OxLDL High glucose ```
60
What are the main processes of endothelium activation?
Thrombosis Senescence Increased permeability Leukocyte recruitment
61
What is senescence?
Damaged/ageing cells undergo growth arrest to halt proliferation in response to stress/damage Stops damaged cells replicating but cells become pro-inflammatory and contribute to CVD
62
Why is increased permeability of activated endothelium bad?
Increased permeability allows plasma protein leakage and for lipoproteins to pass over and bind to proteoglycans where they are oxidised before macrophages engulf them to form foam cells These foam cells contain cholesterol and can lead to plaque formation = atherosclerosis
63
How is leukocyte recruitment altered when the endothelium is activated?
Normally they recruit and adhere to the endothelium of post-capillary venules and then migrate into tissues and use enzymes to leave vessels When endothelium activated leukocytes recruit and adhere to the endothelium of large arteries, migrate into the sub-endothelial space and then get stuck because arteries thick therefore leukocytes accumulate in large arteries
64
What is the mechanism of action of Ca2+ channel blockers?
Prevents IP₃ causing a Ca2+ influx to VSMCs | ∴prevents contraction and vasoconstriction
65
What is the mechanism of action of nitrovasodilators?
Found in GTN sprays Contains NO functional group which donates ready to use NO This is short acting and drops BP in the short term
66
What is autoregulation and its main theories?
Intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance Myogenic theory Metabolic theory Injury
67
What is the myogenic theory of autoregulation?
Smooth muscle fibres respond to tension in vessel wall | ∴increased pressure = contraction and reduced perfusion causes relaxation
68
What is the metabolic theory of autoregulation?
As blood flow decreases, metabolites accumulate | ∴causing dilation to increase flow and wash metabolites away
69
What is the injury related theory of autoregulation?
Serotonin release from platelets causes constriction

Y1 LSS CVS (8 decks)

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