Exchange and the Lymphatic System Flashcards
Describe the three possibles structures of capillaries
- Continuous: no pore or clefts e.g. brain, only pores e.g. muscle
- Fenestrated: clefts and pores e.g. intestine
- Discontinuous: clefts and massive pores e.g. liver
Explain the significance of Starling forces and the lymphatic system in relation to oedema
Obstruction of lymph vessels;
e.g. filariasis, surgery
Raised hydrostatic pressure;
- Raised CVP
e. g. ventricular failure
Low oncotic pressure;
- Hypoproteinuria
e. g. nephrosis, liver failure, malnutrition - Increased capillary permeability
e. g. inflammation –> rheumatism
What is Starlings Forces?
Hydrostatic pressure pushes fluid out of capillaries. This increases oncotic pressure, which pulls fluid back in. The balance between these pressures is referred to as Starlings Forces.
Describe extrinsic mechanisms of regulating MAP
Sympathetic;
- Release noradrenaline
- Acts on alpha-1 receptors
- Causes arteriolar constriction
Describe neural extrinsic mechanism of regulating MAP
Sympathetic;
- Release noradrenaline
- Acts on alpha-1 receptors
- Causes arteriolar constriction
- Decreases flow to that tissue, tends to increase TPR
Parasympathetic;
- Usually no effect
Describe hormonal extrinsic mechanism of regulating MAP
- Release adrenaline from adrenal medulla
- Acts on alpha-1 receptors
- Causes arteriolar constriction
- Decreases flow to that tissue, tends to increase TPR
HOWEVER
- It activates beta-2 receptors on some tissues e.g. skeletal and cardiac muscle
- Causes arteriolar DILATION
- Increases flow to that area, tends to decrease TPR
Describe the neural extrinsic mechanism of regulating MAP
Sympathetic;
- Release noradrenaline
- Acts on alpha-1 receptors
- Causes arteriolar constriction
- Decreases flow to that tissue, tends to increase TPR
Parasympathetic;
- Usually no effect
Describe the extrinsic mechanism of adrenaline in regulating MAP
- Release adrenaline from adrenal medulla
- Acts on alpha-1 receptors
- Causes arteriolar constriction
- Decreases flow to that tissue, tends to increase TPR
HOWEVER
- It activates beta-2 receptors on some tissues e.g. skeletal and cardiac muscle
- Causes arteriolar DILATION
- Increases flow to that area, tends to decrease TPR
Describe the extrinsic mechanism of angiotensin II and vasopressin (ADH) in regulating MAP
- Produced in response to low blood volume
- Causes arteriolar constriction
- Increases TPR
Describe the extrinsic mechanism of atrial natriuretic peptide in regulating MAP
- Produced in response to high blood volume
- Causes arteriolar dilation
- Decreases TPR
Describe the intrinsic mechanism of active (metabolic hyperaemia) hyperaemia in regulating MAP
- Increase in metabolic activity causes increase in metabolite conc.
- Triggers release of EDRF/NO
- Causes arteriolar dilation
- Increase in flow to wash out metabolites
Describe the intrinsic mechanism of pressure (flow) autoregulation in regulating MAP
- Decrease in MAP causes decreases in flow
- Metabolites accumulate
- Triggers release of EGRF/NO
- Causes arteriolar dilation
- Flow returns to normal
Describe the intrinsic mechanism of reactive hyperaemia in regulating MAP
- Occlusion of blood supply causes increase in flow
- Extreme version of pressure autoregulation
Describe the intrinsic mechanism of injury response in regulating MAP
- Mast cells release histamine in response to foreign substance
- Causes arteriolar dilation, increase in flow and permeability
- Aids delivery of blood-born leukocytes to injured area
Describe the basis of coronary circulation
- Blood supply is interrupted by systole
- Shows excellent active hyperaemia
- Expresses many beta-2 receptors
- These swamp any arteriolar constriction
