Exchange And The Lymphatic System Flashcards
How close is every tissue to a capillary
100um
Continuous capillaries
No clefts or pores eg the brain
Or only clefts eg muscle
Fenestrated capillaries
Clefts and pores eg intestine
Discontinuous capillaries
Clefts and massive pores eg liver
Facts about diffusion
Self regulating
Non saturable
Non polar can cross
Polar go through clefts or channels
Carrier mediated transport in capillaries example
Glucose transporter
What does hydrostatic pressure do
Forces fluid out of capillaries
What does osmotic (oncotic) pressure do
Forces fluid out of capillaries
How much fluid is lost and gained each day in capillaries
20L lost and 17L gained
The remainder is collected by lymph system
Causes of oedema
Lymphatic obstruction eg surgery
Raised CVP eg ventricular failure
Hypoproteinemia eg nephrosis, liver failure, nutrition
Increased capillary permeability eg inflammation
Equation for Mean Arterial Pressure
MAP=COxTPR
Difference in pressure = flow X resistance
And CVP is negligible
How is blood flow to each vascular bed kept sufficient and keep mean arterial pressure right
Two levels of control over smooth muscle surrounding arterioles
Intrinsic and extrinsic
Extrinsic (neural) control of smooth muscles on arterioles
Sympathetic releases noradrenaline which binds to a1 and causes arteriolar constriction, decreasing flow through that tissue and increasing TPR
parasympathetic does not much
Extrinsic (hormonal) control of smooth muscles around arterioles
Adrenaline is released from the adrenal medulla and binds to a1 receptors causing arteriolar constriction
BUT in skeletal and cardiac muscles it also activates b2 receptors causing vasodilation (redirection of blood in fight or flight)
Other hormones released in response to low blood volume
Angiotensin and vasopressin
Other hormones released in response to low blood volume
Angiotensin and vasopressin
Other hormone produced in response to high blood volume
Atrial natriuretic factor
Local (Intrinsic) controls of smooth muscle surrounding arterioles
Active hyperaemia
Pressure autoregulation
Reactive hyperaemia
Cause and response to active (metabolic) hyperaemia to control peripheral blood flow
More metabolic activity causes an increase in metabolite concentration (CO2, H+, K+) which causes a release of EDFR (NO)
This causes arteriolar dilation and the increased flow washes out metabolites
Pressure (flow) autoregulation
A decrease in MAP causes decreased flow
Metabolites accumulate and NO is released so the arterioles dilate and flow returns to normal
Reactive hyperaemia
Occlusion of blood supply causes a subsequent increase in blood flow (extreme version of pressure autoregulation)
Injury response
C fibre releases substance P and mast cells produce histamine
The increase in blood flow due to arteriolar dilation and the increase in permeability aids delivery of leukocytes etc to injured area
Coronary circulation flow characteristics
Blood supply is interrupted by systole but still has to cope with increased demand during exercise
Shows excellent hyperaemia (can dilate to have lots of blood)
n d lots of B2 receptors that swamp the sympathetic arteriolar constriction\\
Cerebral circulation
Needs to be kept very stable so shows excellent pressure autoregulation
Pulmonary circulation
Decrease in O2 causes arteriolar constriction (opposite to normal) so blood is directed to the best ventilated parts of the lung
Renal circulation
The main function is filtration which depends on pressure and so changes in MAP would have big effects
Therefore shows excellent pressure autoregulation
