Microcirculation Flashcards

1
Q

Microcirculation structure

A
Arteriole (smooth muscle)
Terminal arteriole (precapillary sphincter)
Capillaries
Pericytic venule
Venule
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2
Q

Blood flow rate (Q)

A

Volume of blood passing through a vessel per unit time

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3
Q

Pressure gradient equation (ΔP)

Increase pressure gradient=?

A

Pressure A- Pressure B
A= arterioles
B= capillaries/ other end of arteriole
Increase flow rate

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4
Q

Increase BP effect on
ΔP
R (Resistance)
Q (Flow rate)

A

Increase ΔP
Increase Q
No effect on R

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5
Q

Link between ΔP, R, Q (Darcy’s Law)

A

ΔP= Q x R

Pressure gradient= Flow rate x Resistance

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6
Q

Arteriolar vasoconstriction effect on
ΔP
R
Q

A

No direct effect on ΔP
Increase R (because decreased radius of vessel)
Decrease Q

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7
Q

What relates
flow into tissue
pressure gradient
resistance of organ?

Why is ΔP the same as MAP?
Without pressure difference what would happen?

A

F(organ)= ΔP (MAP)/ R (organ)

ΔP is basically same as MAP because pressure out of tissue is negligible

Without it blood wouldn’t reach tissue capillary beds

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8
Q

Effect of vasoconstriction on
radius
Resistance
flow

A

decrease r
increase R
decrease F

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9
Q

Effect of vasodilation on
radius
Resistance
flow

A

increase r
decrease R
increase F

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10
Q

Vascular tone definition

Importance?

A

When arteriolar smooth muscle displays a state of partial constriction
Allows for further constriction+ dilation when required

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11
Q
Why are radii of arterioles adjusted indpendently? (Arteriole functions)
Regulated by?
Stimulation?
Driven by?
Leads to?
Name for it?
A

To accomplish 2 functions of arterioles:

  1. Match blood flow to metabolic needs of specific tissues, regulated by local intrinsic controls+ independent of nervous/ endocrine stimulation
  2. Help regulate systemic arterial blood pressure, regulated by extrinsic controls, travel by nerves/ blood+ usually centrally coordinated
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12
Q

Arteriole vasodilation
Stimulated by?
Called?

Function 1 of arterioles

A

Chemically driven by increased metabolites/ increased O2 usage= arteriole vasodilation
Called active hyperaemia

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13
Q

Arteriole vasoconstriction

Function 1 of arterioles

A

Decreased blood temperature/ increased stretch (distension) due to increased BP= arteriole vasoconstriction
Increased stretch effect (only) called myogenic autoregulation
Leads to decreased inflammation in injury

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14
Q

Myogenic autoregulation

Function 1 of arterioles

A

Opposite from CVS control when pressure decreases
Only happens in tissues where blood flow not required as much at the time
Increased BP→ increased flow in tissues→ sensed by stretch receptors→ causes constriction by increased resistance→ blood diverted from area

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15
Q

Arteriolar response to skeletal muscle arterioles in response to exercise

A

Active hyperaemia

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16
Q

Arteriolar response to small intestine arterioles in response to exercise

A

Myogenic vasoconstriction

17
Q

Blood pressure
Cadiac output (Q)
Total peripheral resistance (TPR)

A

MAP= Q x TPR

18
Q
Function 2 of arterioles: Neural
Location?
Causes?
Leads to 
Blood loss?
A

Cardiovascular control centre in medulla
Vasoconstriction
Decreased TPR
Blood loss for long time= lots of tissues undergo this= very little blood flow for long time= bad

19
Q

Function 2 of arterioles: Hormonal
Hormones?
Cause vasoconstriction

A

Vasopressin/ ADH
Angiotensin II
Adrenaline/ noradrenaline
Cause vasoconstriction

20
Q

Purpose of capillaries

A

Delivery of metabolic substrates to cells of organism

21
Q

Why is capillary density important?

A

Suited to enhance diffusion (Fick’s Law)
Minimise diffusion distance
Maximise SA
Maxmise time for diffusion

22
Q

What has denser capillary networks?

A

Highly metabolically active tissues

Skeletal muscle= huge capacity but limited flow at rest

23
Q

Purpose of precapillary sphincter

A

smooth muscle around arterioles

Allows some capillary beds to be shut down

24
Q
Types of capillaries
Small+ water soluble substances?
Lipid soluble substances?
Large+ water soluble substances?
Examples?
A

Continuous: H20- filled gap junction= water+soluble + small can go in, lipid soluble can diffuse through membrane, large= mechanism/ protein channel required

Fenestrated: everything can enter (except very big like cells), eg. glomerulus

Discontinuous e.g. bone marrow (WBCs, large gaps for cells at points

25
Q

What type of capillaries is the blood brain barrier?

A

Continuous but instead of H20 filled gap junctions, there are tight junctions= more control of what can enter and exit
Lipid soluble can go in
Some parts are fenestrated

26
Q

Capillary fluid movement
Forces?
Increase BP= affect on forces?

A

Protein-free plasma filters out of capillary
Mixes with interstitial fluid
Reabsorbed
Hydrostatic force out of capillaries
Oncotic pulling force into capillaries balances by end of capillary bed because of water soluble proteins in blood
Increased BP= increase hydrostatic force but no change to oncotic pressure (because conc. of water soluble proteins doesn’t change)

27
Q

Ultrafiltration pressure requirement

A

If pressure in capillary> Interstitial fluid

28
Q

Reabsorption pressure requirement

Not as effective as ultrafiltration= consequence?

A

If inward driving pressures> outward pressures across capillary
Lymphatic system required for net loss of fluid from vessels

29
Q

Where are lymphatic capillaries found?

A

Wherever there’s a blood capillary present

30
Q

Difference between lymphatic capillaries+ normal capillaries

A

Lymphatic capillaries have a terminal point, blood capillaries are part of a circulation

31
Q

Features of lymphatic capillaries

A

Openings for interstitial fluid to enter

Flaps= allow fluid to only travel one way down towards major lymphatic vessels

32
Q

Infection effect on lymphatic system

A

Increased lymph node size

Site of activation of lymphocytes

33
Q

Major lymphatic vessels that IF drains to

Where does lymph connect to circulation?

A

Right lymphatic duct
Thoracic duct

Right+ left subclavian veins

34
Q

Lymph drainage: If rate of production> rate of drainage

A

Oedema

35
Q

Elephantisis

A

Parasitic blockage of lymph nodes