Peripheral Circulation Flashcards

1
Q

How are capillaries specialised for exchange?

A

Numerous - nearby to all tissues.
Thin-walled - small diffusion barrier.
Small diameter - big SA:Vol.

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2
Q

What are the different types of capillaries?

A

Continuous - no clefts or pores (brain), or only clefts (muscle). Most capillaries.
Fenestrated - clefts and pores (kidney, intestine).
Discontinuous - clefts and massive pores (liver).

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3
Q

What are the differences between clefts and pores?

A

Clefts - between epithelial cells.
Pores - across capillaries.

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4
Q

How does exchange occur in capillaries?

A

Diffusion - self-regulated and non-saturable.
Non-polar - PLBL.
Polar - through clefts and pores.
Carrier-mediated - glucose transporters (brain).

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5
Q

What determines bulk flow?

A

Starling’s forces - capillary hydrostatic pressure and plasma osmotic pressure.
Varies between capillary beds.
An overall loss of fluid occurs from the capillaries, with the excess becoming lymph.

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6
Q

What are the causes of oedema?

A

An accumulation of excess fluid. Caused by -
Raised CVP (ventricular failure).
Lymphatic obstruction (surgery).
Increased capillary permeability (inflammation).
Hypoproteinaemia (liver failure).

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7
Q

What is Poiseuille’s Law?

A

Varying the radius of resistance vessels controls flow and redirects blood. It also controls TPR and regulates MAP. MAP = CO x TPR.

Low TPR = high flow = low MAP.

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8
Q

Why is controlling arteriolar radius important?

A

Affects flow through individual vascular beds and MAP (both affected together).

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9
Q

What is active hyperaemia?

A

Local control of flow and MAP.
Increased metabolic activity increases [metabolites], triggering the release of NO - this causes arteriolar dilation.
Flow increases to decrease [metabolites].
Blood supply is matched with the metabolic needs of that tissue.

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10
Q

What is pressure autoregulation?

A

Local control of flow and MAP.
High MAP = low flow, metabolites accumulate.
Triggers NO release, causing arteriolar dilation.
Flow increases and is restored to normal.
Ensures that a tissue maintains its blood supply despite changes in MAP.

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11
Q

What is reactive hyperaemia?

A

Local control of flow and MAP.
Triggered by an occlusion of blood supply.
Causes an increase in blood flow.

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12
Q

What is the injury response?

A

Mast cells release histamines, with cause arteriolar dilation, increased flow and permeability (aids delivery of leukocytes to the site or injury).

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13
Q

What is the role of the SNS in the control of MAP and flow?

A

Sympathetic nerves release noradrenaline.
Adrenal medulla releases adrenaline.
Binds to A1 receptors.
Arteriolar constriction occurs.
Flow decreases through that tissue, and tends to increase TPR and MAP.

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14
Q

What is the role of the PNS in the control of MAP and flow?

A

No effect.
Genitalia and salivary glands increase flow.

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15
Q

What is the role of skeletal and cardiac muscle in the control of MAP and flow?

A

Activates B2 receptors.
Arteriolar dilation occurs.
Flow increased through that tissue, and tends to decrease TPR and MAP.
Significant during exercise.

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16
Q

How is coronary circulation controlled?

A

Systole interrupts blood supply; still has to cope with increased demand during exercise.
Shows excellent active hyperaemia.
Expresses many B2 receptors.
Swamps sympathetic arteriolar constriction.

17
Q

How is cerebral circulation controlled?

A

Needs to be kept stable.
Shows excellent pressure autoregulation.

18
Q

How is pulmonary circulation controlled?

A

Low O2 causes arteriolar constriction.
Ensures blood is directed to ventilated lungs.

19
Q

How is renal circulation controlled?

A

Filtration rate is kept relatively constant during normal fluctuations in MAP.
Excellent pressure autoregulation.

20
Q

What are precapillary sphincters?

A

Closes off capillaries in response to local signals.