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Phys and Pharm - MT essays > Microcirculation > Flashcards

Microcirculation Flashcards

1
Q

INTRO
vessel structures and functions

artery

A

oxygenated blood

thick muscular wall to withstand high pressure

smaller lumen than veins

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2
Q

INTRO
vessel structures and functions

arteriole

A

oxygenated

thick, muscular wall to withstand high pressure and contract

RESISTANCE VESSEL

small lumen

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3
Q

INTRO
vessel structures and functions

capillary

A

where exchange occurs of gases and nutrients/waste metabolites

one cell thick wall = no muscle

low pressure

tiny lumen

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4
Q

INTRO
vessel structures and functions

venue

A

deoxygenated blood

low pressure

thin wall

compliant

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5
Q

INTRO
vessel structures and functions

veins

A

deoxygenated

low pressure like venue = valves prevent back flow and skeletal muscle aids pumping especially when stood upright

large lumen = CAPACITANCE VESSELS

compliant

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6
Q

INTRO
vessel structures and functions

what does microcirculation comprise of?

A

microcirculation = arterioles, met-arterioles, venues and capillaries
(although no control of microcirculation occurs at capillaries)

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7
Q

MODULATORS OF VASCULAR TONE

what is vascular tone (not sure ab this)

A

the degree of constriction experienced by a blood vessel in response to the resistance the blood has to overcome

high tone = more contraction = more vasoconstriction due to high resistance

low tone = less contraction = more vasodilation due to low resistance

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8
Q

MODULATION OF VASCULAR TONE

how can we modulate vascular tone?

A

extrinsic

  • hormones
  • neural

intrinsic
- vasoconstrictor and vasodilator chemicals

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9
Q

MODULATION OF VASCULAR TONE

how does the sympathetic nervous system extrinsically modulate tone?

A
  1. NA acts on A1 adrenoreceptors of smooth muscle
    ATP is a co-transmitter that prolonged its vasoconstriction effects
  2. A acts on B2 on arteries supplying skeletal muscle

= overall sympathetic effect is more towards skeletal muscles than internal organs

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10
Q

MODULATION OF VASCULAR TONE

what are the local vasoconstrictors?

A
  1. endothelins (ET-1 is most abundant) acting on ETa and ETb receptors of smooth muscle
  2. thromboxane in response to injury and thus platelet activation
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11
Q

MODULATION OF VASCULAR TONE

what are local vasodilators?

A
  1. Adenosine from ATP breakdown on A2 receptors
  2. NO from the endothelium when Ca2+ release is stimulated which binds to calmodulin to stimulate NO from endothelium
  3. prostacyclin from arachidonic acid metabolism
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12
Q

MODULATION OF VASCULAR TONE

how do vasoconstrictors and vasodilators work

A

dilators are opposite:

constrictors increase ca2+ in cytoplasm by opening stores in sarcoplasmic reticulum and opening voltage gates channels

calcium bind to calmodulin to stimulate MLCK

MLCK phosphorylates myosin so it can interact with actin

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13
Q

MECHANISM OF CONTROL

why does tone have to be regulated

A

tone is regulated to match metabolic needs

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14
Q

MECHANISM OF CONTROL

what 2 theories are there for the mechanism as to how blood flow increases to tissues that have an increased metabolic rate/low oxygen

A

vasodilatory theory

oxygen demand theory

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15
Q

MECHANISM OF CONTROL

explain the vasodilatory theory

A

less oxygen stimulates formation of vasodilator substances like adenosine and NO

e.g. in heart
when heart becomes more metabolically active and oxygen demand increases, this stimulates breakdown of ATP

adenosine then leaks out to cause coronary vasodilation

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16
Q

MECHANISM OF CONTROL

explain the oxygen demand theory

A

oxygen is needed to cause contraction

when there’s not enough, blood vessels relax and thus dilate

17
Q

MECHANISM OF CONTROL

what is reactive hyperaemia?

A

when blood flow increases much more than normal following a blockage to blood supply = can last for hours depending on how long the blockage was

this is to repay the oxygen debt

18
Q

MECHANISM OF CONTROL

what is active hyperaemia?

A

the increase in blood flow when tissue becomes highly active

increase metabolism means nutrients are used up and vasodilators are released rapidly = blood flow increases 20 fold

19
Q

MECHANISM OF CONTROL

what is the extrinsic mechanism in skin?

A

anterior hypothalamus detect temperature

high temp = sympathetic system decreased to cause vasodilation= heat is lost

low temp = sympathetic innervation increased = vasoconstriction = retain heat

20
Q

MECHANISM OF CONTROL

what is the local mechanism in skin?

A

increased temp reduces affinity of alpha 2 Receptors for NA
= less sympathetic effect
= less vasoconstriction
= vasodilation

21
Q

CLINICAL

what is Raynaud’s phenomenon?

A

when low temp causes excessive vasoconstriction that blood flow is reduced

discolouration, skin atrophy, ulcers

caused by hyperactive sympathetic system = use vasodilators or inhibit sympathetic system

22
Q

MECHANISM OF CONTROL

what is the difference with non-apical skin

A

in non-apical skin, sympathetic innervation causes vasodilation instead of vasoconstriction as EACh released instead of NA

23
Q

HAEMODYNAMICS

what monitors blood pressure

A

baroreceptors in the aortic arch, pulmonary artery and carotid arteries monitor high blood pressure

baroreceptors in the atria and large veins monitor lower blood pressure

24
Q

HAEMODYNAMICS

how do baroreceptors work

A

baroreceptor sends signal to upper medulla

medulla responds with sympathetic or parasympathetic response (whichever is appropriate)

25
Q

HAEMODYNAMICS

explain the factors contributing to blood pressure

A

BP = blood flow x resistance

blood vol = increase vol increases pressure as closed system

compliancy = reduces pressure as resistance decreases (BP increases with age as compliance reduces)

26
Q

HAEMODYNAMICS

what is cardiac output

A

blood leaving heart per unit time (usually per minute)

CO = stroke vol x heart rate
5L/min

27
Q

HAEMODYNAMICS

what is the postural control reflex response

A
  1. stand up
  2. blood pools in legs and so preload of heart goes down
  3. thus cardiac output goes down which decreases blood vol and thus pressure
  4. baroreceptors detect and sympathetic system is triggered to vasoconstrict and increase heart rate
  5. vasoconstriction increases preload and thus stroke vol, heart rate increases thus cardiac output increases
  6. sympathetic system also causes vascular resistance to increase which forces an increases blood pressure so flow is constant
28
Q

AUTOREGULATION

what is auto regulation?

A

when blood flow is maintained constant through negative feedback when there is a change in pressure that initially changes the flow

29
Q

AUTOREGULATION

what are the 2 auto regulation theories?

A
  1. metabolic = pressure increases and washes out vasodilators = constriction = normal flow
  2. myogenic = high pressure stretches vessels which causes reactive constriction
    = rapid entry of ca2+ from ECF into arteriole cells by stretch-induced vascular depolarisation

in low pressure the stretch is less so cells are polarised and no ca2+ enters = relaxation reduces vascular resistance and flow returns

30
Q

AUTOREGULATION

which mechanism overbids the other?

A

metabolic factors override myogenic mechanism when metabolic demands increase significantly

31
Q

EXPERIMENTAL

explain the experiment by McCarron and Crichton

A
  1. measures diameter of rat artery with changes in blood pressure
  2. increased then shortly decreased
  3. ca2+ influx caused constriction when the vessel stretched

Phys and Pharm - MT essays (7 decks)

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