Capillary dynamics and Starling's law Flashcards

1
Q
  1. Describe the features of capillaries the allow for exchanges to occur.
  2. What specialist cells to capillaries and venules have around them and what do they do?
  3. What is the average diameter of capillaries (range) and the diameter of RBCs
A
  1. They have 3 features allowing for exchange:
  • Low velocity blood flow
  • Large area for diffusion
  • Thin cell walls
  1. PERICYTEs; they do the following:
  • Allow alteration of luminal diameter
  • Synthesise and release constituents of basement membrane and extracellular matrix
  • Release vasoactive agents
  • Regulate flow through the junction between endothelial cells
  1. 5-9µ m and RBCs are 7.8µ m
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2
Q
  1. What are the types of capillaries, describe them and their sub-divisions? Include how molecules pass into the ISF and IVF spaces as well as where these types can be found.
A

The two types of capillary are:

a) Continous

  • Classic
  • Those with tight junctions
  • Sinusoidal capillaries (like in liver and spleen)- also called discontinous capillaries

Present in all tissues except skin and cartilage which have no capillaries.

Exchanges occur via the epithelial cells

  • Macromolecules (proteins etc) are transported by transcytosis
  • Lipid soluble molecules such as O2 and Co2 diffuse passively across the plasma membrane

b) Fenestrated

  • these have endothelial cells with small pores.
  • Can be seen in glomeruli and endocrine glands

These have pores in the plasma membrane. These allow water and solutes (including peptides and hormones) to pass between plasma and interstitial fluid.

Examples include endocrine organs (pituitary, hypothalamus, pineal gland and thyroid), choroid plexus and glomeruli and ileum

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3
Q

Describe Discontinous capillaries

A

Discontinuous capillaries

Liver capilliaries are termed sinusoids and look like flattened irregularly shaped capillaries. They have gaps between adjacent cells and the basal laminae in thinner/absent to allow free exchange. Proteins can pass here.

Specialised macrophages called KUPFFER cells are attached to the endothelium and project into the lumen. They engulf damaged RBCs, pathogens and debris. They also secrete cytokines like EPO.

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4
Q

Describe cerebral capillaries

A

These have tight junctions forming the BLOOD BRAIN BARRIER in the CNS and thymus.

Only small lipid soluble molecules can pass freely (like CO2 and O2).

Multiple transport mechanisms are present (e.g. GLUT1)and carry water soluble molecules across the BBB. Such molecules must pass via active or passive transport.

Water and ions must pass via channels

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5
Q

Vasomotion

  1. What is the flow rate through a capillary?
  2. What is the capillary pressure?
  3. How often do pre-capillary sphincter contract and why?
  4. What is VASOMOTION?
A
  1. 0.5-2 s at rest and 0.25 s where the tissue supplied is metabolically active. Flow rate is 0-0.2 cm/s
  2. Capillary pressures are approx 32 mm Hg at the arteriolar end and 15 mm Hg at the venous end
  3. The precapillary sphincter contract approx 12x per min allowing pulsatile flow.
  4. VASOMOTION is the cycling of contractions and relaxation controlled by a myogenic response to local metabolites.
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6
Q

What causes changes in capillary volume?

A

Factors that alter capillary sphincter tone:

  • Nitric oxide (NO)
  • Decreased tissue PO2 or increased PCO2
  • Elevated temperature
  • Rising K+ or H+ concentration
  • Lactic acid, or rise in acid concentration
  • Prostocyclin, thromboxane and endothelins
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7
Q

STARLING’S FORCES

  1. What are the two major factors effecting fluid shift across a capillary?
  2. What determines hydrostatic pressure in the capillaries?
A
  1. The two major factors affecting fluid shift across the capillary wall is HYDROSTATIC PRESSURE and COLLOID ONCOTIC PRESSURE (pressure due to non-diffusible molecules).

Note, if COP falls, fluid will accumulate in the interstitial fluid (ISF), and if lymphatic capacity is exceeded, oedema will develop.

2.Capillary hydrostatic pressure is determined by capillary flow, arteriolar resistance, venous resistance and systemic pressure. It is about 32 mm Hg at the arteriolar end, and 15 mm Hg at the venular end

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8
Q

STARLING’S FORCES

  1. What is the STARLING equation?
A

Fluid movement Q = KA[(pc-pi) – s(pc -p i)]

K = permeability constant

A = area of membrane

Pi = interstitial hydrostatic pressure

Pc = capillary hydrostatic pressure

s= reflection coefficient for albumin(0.6-0.9 depending on capillary bed)

pI= interstitial oncotic pressure

pc = capillary oncotic pressure

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9
Q

FLUID MOVEMENT

  1. Changes in what cause fluid to move into the tissues?
  2. What compensates for increased capillary filtration?
A
  1. Fluid will move into the tissues whenever the hydrostatic gradient increases or the osmotic gradient decreases.
  2. Increased capillary filtration is compensated for by increasing lymphatic drainage which preserves the oncotic pressure gradient.
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10
Q

What things cause an increase in lymphatic drainage?

A

As the interstitial fluid volume increases the concentration of proteoglycans and glycoaminoglycans will fall, resulting in increased lymphatic drainage. However, once its capacity is exceeded tissue oedema will occur. Plasma protein deficiency will have the same effect on the balance of filtration and reabsorption.

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11
Q

Vasodilation and vasoconstriction

  1. What does arteriolar constriction do to filtration pressure?
  2. How long does this last?
  3. What prevents pulmonary oedema?
A
  1. Arteriorlar constriction causes filtration pressure to become negative. Allowing reabsorption into the capillary.
  2. The reabsorption will only last transiently, as the sphincter will relax, increasing hydrostatic pressure again. The interstitial hydrostatic pressure will also rise, reducing the net driving force for absorption to zero.
  3. In the lung the hydrostatic pressure is less than the colloid osmotic pressure, so only osmosis prevents the alveolus filling with water.
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12
Q

What are the causes of increased ISF volume?

A

ISF volume increases if salt is retained as water diffuses into this space.

The following situations can cause oedema:

  • Excess ultrafiltration
    • Arteriolar vasodilation
    • Neurogenic pulmonary oedema
    • Fluid overload
    • Renal failure
    • Loss of auto regulation
    • Venous obstruction (increases capillary pressure)
    • Thrombus or CCF
  • Protein deficiency
    • Liver disease
  • Decrease osmotic pressure gradient across capillary (similar to above)
    • Malnutrition
    • Chronic illness
    • Pre-eclampsia
    • Nephrtoic syndrome
    • Cirrhosis
  • Increase capillary permeability
    • Substance P
    • Histamine
    • Interleukines (sepsis or glomerulonephritis)
    • Kinins
    • Accumulation of osmotically active substances in interstistium
    • Burns
    • Acute Lung Injury
    • Reperfusion injury
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