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CVS Physiology > Gas exchange and the lymphatic system > Flashcards

Gas exchange and the lymphatic system Flashcards

1
Q

Features of capillaries

A
  • Thinwalled; presents a small diffusion barrier

- Small diameter; big SA:Volume ratio

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2
Q

Structure of capillaries (types)

A

Continous

  • no clefts/pores ( brain)
  • clefts only ( muscle)

Fenestrated
- clefts + pores ( intestine)

Discontinous
-clefts + massive pores ( liver)

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3
Q

Diffusion and carrier mediaed transport in Gas exchange

A

Diffusion

  • self regulating
  • non saturable
  • non polar substances acorss the membrane
  • polar substances via clefts/channels

Carrier mediated transport
-eg glucose transporter

Only few places (BBB) prevent diffusion of polar substances such as glucose = protein carrier

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4
Q

Bulk flow in capillaries - STarling forces

A
  • Bulk flow is the exchange of fluid
  • describes the balance between hydrostatic pressure and osmotic pressure.
  • hydrostaatic pressure pushing fluid out through leaky capillaries which builds up an osmotic pressure which draws fluid back in
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5
Q

Function of lymphatic system

A

-excess filtered fluid drains into lymphatic vessels > enters circulation

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6
Q

What is an oedema?

A

-accumulation of excess fluid in extravascular space

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7
Q

What can an oedema be caused by?

A 
Lymphatic obstruction (elephantiasis)
-due to filariasis, surgery
Raised CVP (high hydrostatic pressure)
-due to ventricular failure

Hypoproteinemia ( low osmotic pressure)
-due to nephrosis, liver failure, nutrition

Increased capillary permeability ( low osmotic pressure)
-inflammation ( rheumatism)

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8
Q

What vessels control BF

A
  • mainly by arterioles as they have smooth muscle + are resistance vessels
  • dilation/constrict
  • radius of arteriole has effect on resistance and hence flow
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9
Q

Thhe effect of dilation of arterioles on TPR

A
  • Reducing resistance of a vasucular bed will increase flow through the vascular bed but it will reduce TPR + also reducing mean arterial pressure
  • Hence, arteriolar radius affects flow through individual vascular beds and mean arterial pressure
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10
Q

Compensation

A

Control over smooth muscles surrounding arterioles:

Intrinsic + extrinsic mechanisms

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11
Q

Intrinsic + Extrinsic mechanisms

A

Intrinsic mechanisms
-meeting the selfish needs of each individual tissue

Extrinsic mechanisms
- ensures that the TPR ( MAP) of whole body stays in the right ball park

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12
Q

Neural extrinsic control

A

SYMP NERVES

  • releases noradrenaline
  • binds to A1 receptors
  • causes arteriolar constriction
  • thereflow, less flow to that tissue, and increases TRP

Parasympathetic nerves
-no effect

  • this is happening throughtout the body so main thing is to increase in TPR ( which increases MAP)
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13
Q

Extrinsic control ( hormonal)

A

Adrenaline

  • releases froma drenal medulla
  • binds to A1 receptors
  • causes arteriolar constriction
  • decreases BF tp tossue, and increases TPR

BUT

  • in some tissues (Skeletal/cardiac) it also activates B2 receptors which causes arteriolar dilation
  • therefore, increase BF through that tissue which decreases TPR
  • A1 is most important in increase TPR
  • B2 will help redirect blood flow to heart and SM during flight/fight reaction
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14
Q

Angiotensin 2

A
  • released by kidneys?
  • produced in response to Low BV
  • causes arteriolar constriction, therefore increase TPR
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15
Q

Vasopressin ( ADH )

A
  • released in repsonse to low BV

- causes arteriolar constriction, increasing TPR

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16
Q

Atrial natriuretic factor

A
  • released in response to high BV

- causes arteriolar dilation, hence decreases TPR

17
Q

Local intrinsic controls

A
  1. Active ( metabolic) hyperaemia
    - high metabolic activity causes increased concentration of metabolites which triggers release of EDRF/NO ( paracrines)
    - this causes arteriolar dilation
    - increased flow to wash out metabolites
    - adaptation to match blood supply to metabolic needs of that tissue
  2. Pressure ( flow) autorefulation
    - low MAP causes low BF
    - metabilites accumulates which triggers release of EDFR/NO
    - arterioles dilate + flow is restoe
18
Q

Local intrinsic controls

A
  1. Active ( metabolic) hyperaemia
    - high metabolic activity causes increased concentration of metabolites which triggers release of EDRF/NO ( paracrines)
    - this causes arteriolar dilation
    - increased flow to wash out metabolites
    - adaptation to match blood supply to metabolic needs of that tissue
  2. Pressure ( flow) autorefulation
    - low MAP causes low BF
    - metabilites accumulates which triggers release of EDFR/NO
    - arterioles dilate + flow is restored to normal ( or could be myogenic)
    - an adaptation to ensure that a tissue maintains its BS despite changes in MAP
  3. Reactive hyperaemia
    - occlusion of BS causes subsequent increase in BF
    - an extreme version of pressure autoregulation
  4. Injurty response
    - aids delivery of blood born leukocytes… to injured area
    - arteriolar dilation; inc BF/permeability
19
Q

Special areas

A
  • coronary circulation
  • BS is interupted by systole but still has to cope with increased demand during excercise
  • shows excellent active hyperaemia
  • expresses many B2 receptors
  • these swamp any sympathetic arteriolar constriciton

Cerebral circulation

  • needs to be stable
  • shows good pressure autoregulation
20
Q

Pulmonary circulation ( pul. shunt)

A
  • lows O2 causes arteriolar constriction
  • opposite response to most tissues
  • ensures that blood is directed to best ventilated parts o lung
21
Q

Renal circulation

A
  • main function is filtration which is dependent on pressure
  • changes in MAP affects BV
  • good pressure auto regulation

CVS Physiology (11 decks)

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