Exchange and the Lymphatic System Flashcards
Describe continuous capillaries
no clefts or pores e.g in the brain
clefts only e.g in muscle
Describe fenestrated capillaries
clefts and pores e.g intestine
Describe discontinuous capillaries
clefts and massive pores e.g liver
how is diffusion self-regulating and non-saturable?
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
where is there specific glucose carrier-mediated transport?
in the brain - gets through blood brain barrier
What is bulk flow?
mass exchange of fluid
What does hydrostatic pressure do and how is it corrected?
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
what is the balance of hydrostatic and oncotic pressure known as?
starling’s forces - not the same as starling’s law
What is oedema?
accumulation of excess fluid
how can you get oedema? (4)
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
how does low protein cause oedema?
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
what controls the blood flow in capillaries?
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
what has a major affect on resistance and therefore on flow?
radius of the arteriole.
what is varying the radius of resistance vessels is also used to control?
TPR and therefore regulates MAP
what are the 2 levels of control over smooth muscle around the arterioles that help keep blood flow to each vascular bed sufficient?
intrinsic and extrinsic control mechanisms
what is intrinsic control
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
what is extrinsic control?
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.
Neural aspect of extrinsic control of smooth muscle around arterioles
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
Hormonal aspect of extrinsic control of smooth muscle around arterioles
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
where do alpha 1 and beta 2 receptor effects tend to occur?
alpha 1 - most regions
beta 2 specific places eg skeletal or cardiac muscle
Name the mechanisms involved in intrinsic control of smooth muscle around arterioles (4)
active (metabolic) hyperaemia
pressure (flow) autoregulation
reactive hyperaemia
injury response
active (metabolic) hyperaemia
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
Pressure (flow) autoregulation
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
Reactive hyperaemia
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
Injury response
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
how is the coronary circulation special
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
cerebral circulation
shows excellent pressure autoregulation (intrinsic)
how is the pulmonary circulation unique
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
renal circulation
main function is filtration which depends on pressure
changes in MAP would have big effects on blood volume
shows excellent pressure autoregulation - intrinsic control
what are some other hormones involved with extrinsic control other than adrenaline?
angiotensin II
vasoprassin
atrial natriuretic factor
