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CVS II > Capillaries > Flashcards

Capillaries Flashcards

1
Q

What does H2O solution contain in + out cells?

A

IN: O2, glucose, AA, hormones, immune response etc.
OUT: metabolic end products CO2, urea

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2
Q

Role of cell membranes + eg?

A

Support and protection
Cell-to-cell recognition eg immune system
Controls what enters or leaves the cell eg ion movement in nerves
Regulates cell function eg Insulin-mediated glucose uptake

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3
Q

What are the two layers of amphipathic phospholipids?

A

polar phosphate head (hydrophilic)

non-polar FA tails (hydrophobic)

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4
Q

eg of passive transport processes?

A

Diffusion: conc gradient, O2 uptake from lungs into blood
Convection: pressure gradient, circulation
Osmosis: osmotic pressure gradient, water uptake by cells
Electrochemical flux: electrical + conc gradient, ion flow during an AP in a nerve

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5
Q

Describe capillaries

A

Small diameter
Extension of inner lining of arterioles
Endothelium only – 1 cell thick
Semi-permeable

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6
Q

Role of capillaries?

A

Connect terminal arterioles to venules
Higher density in active tissue (muscles, liver, heart, kidneys, brain)
Solute exchange (passive diffusion, filtration): O2, glucose, AA, hormones, 💊
Fluid exchange (flow down pressure gradients): regulation of plasma + interstitial fluid volumes

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7
Q

What controls rate of solute transport?

A

Properties of passive diffusion
Properties of solutes + membranes (Fick’s law)
Properties of capillaries
Permeability

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8
Q

Properties of passive transport?

A

No ATP
Molecules move randomly
Move from high -> low conc
Transport of lipid-soluble solutes over short distances

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9
Q

Why does passive transport only work over short distances?

A

Time taken (t) for a randomly moving molecule to move net distance (x) in 1 specific direction increases when distance squared
t = x² / 2D
D : diffusion coefficient for molecule within medium
eg D for O2 in water vs air are diff

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10
Q

Properties of the solute?

A

Conc gradient
Size
Lipid solubility

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11
Q

Properties of the membrane?

A

Thickness/composition
Aq pores
Carrier-mediated transport
AT mechanisms

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12
Q

What’s Fick’s law?

A

Jₛ = - DA (ΔC/x)
D : Diffusion coefficient of solute-ease via solvent
A : Area
ΔC/x : Conc gradient (C1-C2) across distance x
Jₛ : Solute movement, mass per unit time m/t

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13
Q

Why’s Fick’s law negative?

A

flowing ‘down’ a conc gradient

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14
Q

3 types of capillaries?

A 
Continuous capillaries (least permeable)
Fenestrated capillaries
Discontinuous capillaries (most permeable)
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15
Q

Describe continuous capillaries

A

Moderate permeability
Tight gaps between neighbouring cells
Constant basement membrane

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16
Q

eg of continuous capillaries?

A

BBB

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17
Q

Describe fenestrated capillaries

A

High water permeability
Fenestration structures
Disrupts basement membrane

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18
Q

eg of fenestrated capillaries?

A

‘high water turnover’ tissues:

salivary glands, kidney, synovial joints, choroid plexus (CSF)

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19
Q

Describe discontinuous capillaries

A

Large fenestration structures

V disrupted basement membrane

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20
Q

eg of discontinuous capillaries?

A

When movement of cells is required:

🔴 in liver, spleen, bone marrow

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21
Q

What’s an intercellular cleft?

A

10-20 nm wide

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22
Q

What’s a glycocalyx?

A 
covers endothelium
-ve charged
blocks solute permeation+access to transport mechanisms
regulated
controls movement of molecules
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23
Q

What are caveolae + vesicles?

A

large pores system

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24
Q

Define permeability

A

rate of solute transfer by diffusion across unit area of membrane per unit conc diff
’how freely a solute crosses a membrane’

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25
Q

How does a porous membrane interfere with diffusion of lipid insoluble solute?

A

reduction in area for diffusion (A), increased path length through membrane (x), restricted diffusion in pore produces hydraulic issues (D)
ALL FACTORS = permeability (P)

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26
Q

What’s the modified Fick’s law for a porous membrane?

A 
Jₛ = -PAₘΔC
Jₛ : Rate of solute transport
P : Permeability [pore size, length (x), diffusion coefficient (D)]
Aₘ = SA of capillary
∆C = Conc gradient
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27
Q

How do large lipophobic proteins get transported?

A

big gaps in inflammation, trans-cellular channels, vesicles (endocytosis + exocytosis)

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28
Q

How do lipophilic O2, CO2 diffuse?

A

trans-cellular

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29
Q

How do small lipophobic glucose get transported?

A

filtration via inter-cellular, fenestral route

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30
Q

How does water get transported?

A

filtration via inter-cellular, fenestral route, water channels

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31
Q

How much of glucose is transported by diffusion?

A

98% of glucose transport into interstitial space

via passive diffusion – via GLUT transporter system

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32
Q

How much of glucose is transported by filtration?

A

2% glucose transport via fenestrations/intercellular gaps

33
Q

Why’s filtration of glucose much less than diffusion?

A

[glucose] in plasma is 1 g / L
Daily volume of plasma filtrate flowing into tissues = 8 L
Max filtration of glucose = 8 g / day
but glucose consumption of adult is 400 g / day

34
Q

What controls diffusion rate?

A

Increased blood flow
Fall in interstitial conc (more solute used, metabolism)
Recruitment of capillaries

35
Q

How increased blood flow controls diffusion rate?

A
  • increased conc of solutes in capillaries
  • more exchange along capillaries in lungs
  • less time for eq of O2/CO2 to occur between interstitial spaces + capillaries - reduces exchange
36
Q

How a fall in interstitial conc controls diffusion rate?

A
  • use more O2
  • increases conc diff for O2 to move in
  • metabolism increases blood flow - metabolic hyperaemia
  • more O2 delivery
37
Q

How a recruitment of capillaries controls diffusion rate?

A
  • dilation of arterioles
  • more capillaries perfused
  • increases SA for diffusion
  • shortens diffusion distance
  • faster diffusion
38
Q

Why does O2 transport from blood to muscle

increases over 40 times during exercise?

A
  • increase CO (blood flow)
  • use more O2 (fall in tissue concentration)
  • open up more capillaries (recruitment)
39
Q

Importance of fluid exchange?

A

Normal physiological function
H2O for chemical reactions
Abnormalities –> oedema/tissue swelling
Controlling blood, interstitial, cell volumes after drop in BP/poor end organ perfusion eg haemorrhage, sepsis, during surgery, dehydration

40
Q

What’s hydraulic pressure?

A

Pressure exerted when fluid moves across membrane into interstitial space due to blood flow
OUUUUUTTTTTTTT

41
Q

What’s oncotic pressure?

A

pressure exerted by plasma proteins that cannot pass through membrane, which creates suction force to move fluid from interstitial space into capillary
INNNNN

42
Q

What’s Starling’s principle of fluid exchange?

A

Fluid movement depends on balance between hydraulic + oncotic pressures across the capillary wall

43
Q

What are the Directions of Fluid Movements dominated by?

A

P꜀ and πₚ
P꜀: capillary BP
πₚ: plasma proteins

44
Q

Why does the hydraulic pressure mean easy movement across the membrane?

A

P꜀ > Pᵢ
P꜀: capillary BP
Pᵢ: interstitial fluid pressure

45
Q

Why does the osmotic pressure mean movement via intercellular gaps?

A

πₚ > πᵢ
πₚ: plasma proteins
πᵢ: interstitial proteins

46
Q

Equation of Starling’s principle of fluid exchange?

A 
Jᵥ = Lₚ A  [ (P꜀ - Pᵢ)  -  σ(πₚ - πᵢ) ]
Jᵥ ∝ (P꜀ - Pᵢ) - (πₚ - πᵢ)
Jᵥ: net filtration
Lₚ: Hydraulic conductance of endothelium, how Leaky endothelium is to fluid
A: wall area
σ: Reflection coefficient for intercellular gaps
(P꜀ - Pᵢ): hydraulic pressure diff
(πₚ - πᵢ): osmotic pressure diff
47
Q

What does it mean if σ for a plasma protein is 0.9?

A

10% plasma proteins are conducted across capillary wall into interstitial space

48
Q

What happens to σ if small gaps?

A

plasma proteins stay in lumen exerting osmotic pressure = 1

49
Q

Equation of effective osmotic pressure?

A

effective osmotic pressure = σ x potential osmotic pressure

50
Q

What does Starling’s principle tells us

A
  • constant osmotic p πₚ=25
  • first part of capillary P꜀=35mmHg so filtration
  • lose pressure down capillary
  • P꜀=πₚ both 25mmHg
  • more drop so P꜀=10mmHg so reabsorption
51
Q

Problems with Starling’s principle?

A
  • Fluid filtration throughout length of capillaries
  • No reabsorption - vital for fluid replacement
  • πᵢ not small, πₚ = πᵢ
  • Glycocalyx central to fluid exchange
  • Starling’s principle states that increasing πₚ + reabsorption with colloid fluids should increase blood volume but they don’t expand plasma volume
52
Q

What’s the revised equation of Starling’s principle of fluid exchange?

A

Jᵥ = Lₚ A [ (P꜀ - Pᵢ) - σ(πₚ - πg) ]
Jᵥ: net filtration
Lₚ: Hydraulic conductance of endothelium, how Leaky endothelium is to fluid
A: wall area
σ: Reflection coefficient for intercellular gaps
(P꜀ - Pᵢ): hydraulic pressure diff
(πₚ - πg): osmotic gradient

53
Q

Role of glycocalyx?

A

Glycocalyx acts as a barrier so plasma proteins move from lumen into interstitial space via vesicle system not via intercellular spaces as

54
Q

Why’s πₚ = πᵢ ?

A

Stream of fluid filtration from endothelium carries plasma proteins into interstitial space creating low πg (subglycocalyx region) - πₚ = πᵢ

55
Q

Why’s there filtration at venous end despite low P꜀?

A

Filtration occurs across length of capillaries

Less P꜀ at venous end means πᵢ moves into πg – less (πₚ - πg) osmotic gradient

56
Q

Why colloid fluid doesn’t expand blood volume in sick patient?

A

shedding of glycocalyx

57
Q

Why’s there brief reabsorption during haemorrhage?

A
  • less CO, less BP
  • sympathetic so vasoconstriction
  • low P꜀ (hypovolemia)
  • less blood volume
  • increased osmotic pressure>25mmHg
  • so fluid reabsorption to lower osmotic pressure
  • reabsorb 500ml over 0.5hr
  • stops when osmotic p normal
58
Q

Purpose of brief reabsorption during haemorrhage?

A 
Life-preserving
Supports CVP 
Increases CO
Rises BP
Greater end organ perfusion
59
Q

Role of lymphatic circulation?

A

returns excess tissue fluid/solutes back to the cardio-vascular system

60
Q

Features of lymph vessels?

A

valves + smooth muscle

61
Q

What contributes to lymph flow?

A

Spontaneous contractions of smooth muscle

Surrounding skeletal muscle contractions / relaxation

62
Q

Organization of lymphatic thoracic duct system?

A
  • initial lymphatic plexus
  • collecting lymphatic
  • afferent lymphatic
  • high endothelial venule
  • lymphocyte
  • lymph node
  • efferent lymphatic
  • cysterna chyli
  • lacteal
  • thoracic duct
63
Q

What does overall control of ECF balance depend on?

A

Capillary filtration
Capillary reabsorption
Lymphatic system

64
Q

What changes happen if imbalance of ECF?

A

Starling’s factors
Efficiency of lymphatic system
Influence fluid balance between intravascular + interstitial spaces

65
Q

What causes oedema?

A

Excess interstitial fluid by imbalance between

filtration, reabsorption, lymphatic function, glycocalyx function

66
Q

Factors that promote filtration?

A

increased P꜀
increased πg
increased Lₚ
decreased πₚ

67
Q

Factors that promote reabsorption?

A

decreased P꜀

increased πₚ

68
Q

Eg of clinical scenarios where there’s increased P꜀?

A

Dependent (gravitational) oedema – ‘standing up for long periods’
Deep venous thrombosis
Cardiac failure

69
Q

Describe DVT

A
  • prevention of venous return
  • increases venous pressure –> ‘back-up’ of pressure
  • increased P꜀ across capillaries
  • increased filtration
70
Q

What causes decreased πₚ?

A

Malnutrition/malabsorption, hepatic failure, nephrotic syndrome

71
Q

What’s Nephrotic syndrome?

A

protein lost in urine that isn’t replaced by liver production

72
Q

How does liver disease decrease πₚ

A

insufficient endogenous albumin produced

73
Q

Describe how kwashiorkor happens

A
  • reduced plasma protein conc
  • reduced oncotic pressure πₚ
  • greater P꜀
  • fluid from capillaries -> interstitial fluid
  • oedema
74
Q

eg of how inflammatory-mediated oedema occurs?

A

Insect bites/stings, infection, trauma, autoimmune disease

75
Q

Describe how inflammation causes oedema?

A
  • local chemical mediators of inflammation cause swelling
  • increase capillary permeabilty Lₚ
  • decreased σ
  • increased protein permeability
  • so πₚ = πg = πᵢ
  • increased P꜀
  • more filtration
76
Q

What’s filariasis/elephantitis?

A

nematode infestation, larvae migrate to lymphatic system grow/mate/form nests – block lympathetic drainage

77
Q

What’s lymphoedema?

A

from surgery to treat testicular cancer – removal of lymphatics

78
Q

eg of what causes dysfunctional glycocalyx

A

inflammation, sepsis, during surgery

79
Q

What happens if there’s dysfunctional glycocalyx?

A
  • giving fluids (crystalloids or colloids) causes movement of plasma proteins via intercellular gaps
  • so πₚ = πg = πᵢ
  • increased P꜀
  • more filtration
  • oedema

CVS II (19 decks)

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