Exchange and the Lymphatic System Flashcards

1
Q

Describe continuous capillaries

A

no clefts or pores e.g in the brain

clefts only e.g in muscle

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2
Q

Describe fenestrated capillaries

A

clefts and pores e.g intestine

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3
Q

Describe discontinuous capillaries

A

clefts and massive pores e.g liver

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4
Q

how is diffusion self-regulating and non-saturable?

A

if a cell uses more O2 then there is a bigger conc gradient and more O2 moves across

it is non-saturable meaning there is no limit to how much O2 can move across

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5
Q

where is there specific glucose carrier-mediated transport?

A

in the brain - gets through blood brain barrier

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6
Q

What is bulk flow?

A

mass exchange of fluid

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7
Q

What does hydrostatic pressure do and how is it corrected?

A

pushes fluid out through the leaky capillaries and this moves into the lymph capillaries - this results in an osmotic (oncotic) pressure building up which draws fluid back in

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8
Q

what is the balance of hydrostatic and oncotic pressure known as?

A

starling’s forces - not the same as starling’s law

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9
Q

What is oedema?

A

accumulation of excess fluid

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10
Q

how can you get oedema? (4)

A

lymphatic obstruction - parasitic disease, surgery

raised CVP - venous pressures become elevated in legs and feet whilst standing but when lying down thoracic blood volume increases so CVP increases, in heart failure or with venous obstruction.

hypoproteinaemia - low protein due to liver failure or nephrosis

Increased capillary permeability - proinflammatory mediators ie histamine etc

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11
Q

how does low protein cause oedema?

A

decrease in oncotic gradient
meaning it doesn’t pull H20 back into the vessel because of the loss of the gradient

instead it pushes H20 out of the vessels down its conc gradient into the interstitial tissue space

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12
Q

what controls the blood flow in capillaries?

A

arterioles as there is no smooth muscle in capillaries to contract/dilate themselves

capillaries single layer of endothelium and associated connective tissue and connect arteries to veins

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13
Q

what has a major affect on resistance and therefore on flow?

A

radius of the arteriole.

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14
Q

what is varying the radius of resistance vessels is also used to control?

A

TPR and therefore regulates MAP

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15
Q

what are the 2 levels of control over smooth muscle around the arterioles that help keep blood flow to each vascular bed sufficient?

A

intrinsic and extrinsic control mechanisms

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16
Q

what is intrinsic control

A

control from within a particular bit of the body
it is concerned with meeting the selfish needs of each individual tissue - like ensuring it is getting enough O2 to carry out function

17
Q

what is extrinsic control?

A

it is concerned with ensuring that the TPR (and therefore MAP) of the whole body stays in the right ball park. There are neural and hormonal aspects.

18
Q

Neural aspect of extrinsic control of smooth muscle around arterioles

A

sympathetic nerves - release NA which binds to alpha 1 receptors causing arteriolar constriction therefore a decrease in flow through that tissue, and tends to increase TPR which subsequently increases MAP. This happens throughout the body.

parasympathetic nerves usually have no effect

19
Q

Hormonal aspect of extrinsic control of smooth muscle around arterioles

A

Adrenaline - released from adrenal medulla and binds to alpha 1 receptors causing arteriolar constriction which decreases flow through that tissue and increases TPR

BUT in some tissues e.g skeletal and cardiac muscle, it also activates beta 2 receptors which cause increase in flow through that tissue and tends to decrease TPR

20
Q

where do alpha 1 and beta 2 receptor effects tend to occur?

A

alpha 1 - most regions

beta 2 specific places eg skeletal or cardiac muscle

21
Q

Name the mechanisms involved in intrinsic control of smooth muscle around arterioles (4)

A

active (metabolic) hyperaemia
pressure (flow) autoregulation
reactive hyperaemia
injury response

22
Q

active (metabolic) hyperaemia

A

when skeletal muscle starts working from being at rest there is an increase in metabolites which is sensed by endothelial cells

these cells start producing chemical messenger EDRF - this makes smooth muscle relax and dilate

this reduces resistance to blood flow and so increases flow which washes the metabolites away

23
Q

Pressure (flow) autoregulation

A

reduction of arteriole pressure is the first thing triggering process here but otherwise it is the same mechanism as active hyperaemia

a decrease in MAP causes decreased flow so the metabolites accumulate which triggers release od EDRF by endothelial cells

flow is restored to normal - makes sure tissue maintains its blood supply despite changes in MAP

24
Q

Reactive hyperaemia

A

occlusion of blood supply causes a subsequent increase in blood flow. Extreme version of pressure autoregulation. Transient increase in organ blood flow following brief period of ischaemia

25
Q

Injury response

A

delivery of blood born leukocytes to injured area through blood

c-fibres (sensory receptors) detect damaging stimuli and mast cells release chemical messengers like histamine - this causes arteriolar dilation which increases blood flow and increases permeability

26
Q

how is the coronary circulation special

A

blood supply is interrupted by systole
shows excellent active (metabolic) hyperaemia - most sensitive to its own metabolites

expresses many Beta 2 receptors which trumps any sympathetic arteriolar constriction

27
Q

cerebral circulation

A

shows excellent pressure autoregulation (intrinsic)

28
Q

how is the pulmonary circulation unique

A

decrease in O2 cause arteriolar constriction which is different to the rest of the body
this ensures blood is redirected to the best ventilated parts of the lung

29
Q

renal circulation

A

main function is filtration which depends on pressure
changes in MAP would have big effects on blood volume

shows excellent pressure autoregulation - intrinsic control

30
Q

what are some other hormones involved with extrinsic control other than adrenaline?

A

angiotensin II
vasoprassin
atrial natriuretic factor