Pathophysiology of congestion and oedema Flashcards

1
Q

Critical relationship

A

Q = ChangeinP/R

Q = blood flow 
P = pressure 
R = resistance
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2
Q

What is Congestion?

A

Relative excess of blood in vessels of tissue or organ:

  • passive process
  • Not like acute inflammation: active hyperaemia
  • Acute or chronic
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3
Q

Clinical pathology examples

A

Local acute congestion
- Deep vein thrombosis

Local chronic congestion
- Hepatic cirrhosis

Generalised acute congestion
- Congestive cardiac failure

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4
Q

What is Deep vein thrombosis of the leg, and features?

A
  • Vein blocked causing localised acute congestion
  • Blood backs up in veins, venules, capillaries
  • Decreased outflow of blood
  • Local, acute congestion
  • Decreased pressure gradient
  • No O2 therefore ischaemia and infarction
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5
Q

What is Hepatic cirrhosis?

A
  • Results from serious liver damage e.g. HBV, alcohol
  • Regenerating liver forms nodules of hepatocytes with intervening fibrosis
  • Loss of normal architecture: altered hepatic blood flow
  • Portal blood flow blocked
  • Local chronic congestion: haemorrhage risk
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6
Q

What are consequences of portal-systemic shunts?

A
  • Caput medusae

- Oesophageal varices

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7
Q

Features of congestive cardiac failure

A

Heart unable to clear blood, right & left ventricles
- ineffective pump e.g. ischaemia, valve disease

Fluid (overload) in veins (Treatment: diuretics)

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8
Q

Pathophysiology of congestive cardiac failure

A

Decreased cardiac output (CO)

Decreased renal glomerular filtration rate (GFR)

  • Activation of renin-angiotensin-aldosterone system
  • Increased Na and H2O retention

Increased amount of fluid in body

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9
Q

What are effects of congestive cardiac failure?

A
  • Heart cannot clear blood from ventricles
  • Back pressure, blood dammed in veins
  • Lungs -pulmonary oedema
  • Liver: central venous congestion:
    Right heart failure
    Increased JVP, hepatomegaly, peripheral oedema
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10
Q

Pericentral hepatocytes and Periportal hepatocytes in hepatic central venous congestion

A

Pericentral hepatocytes (red) - Stasis of poorly oxygenated blood

Periportal hepatocytes (pale) - Relatively better oxygenated due to proximity of hepatic arterioles

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11
Q

What happens in normal microcirculation?

A
  • Constant movement of fluid through capillary beds; process of dynamic equilibrium
  • Driven by hydrostatic pressure from heart
  • Balanced by osmotic pressures and endothelial permeability
  • Filtration from capillary beds to interstitium
  • Capillaries-interstitium-capillaries and lymphatics
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12
Q

Which three components affect net flux and filtration?

A
  • Hydrostatic pressure
  • Oncotic pressure
  • Permeability characteristics and area of endothelium
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13
Q

What is Starling’s hypothesis?

A

Net filtration (Jv)= [(force favouring filtration/flow of fluid out of vessel) - endothelial permeability to proteins x (forces opposing filtration/keeping fluid in vessel)] x endothelial permeability to H2O x area of capillary bed

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14
Q

What is normal oedema?

A

Accumulation of abnormal amounts of fluid in the extravascular compartment

  • Intercellular tissue compartment (extracellular fluid)
  • Body cavities
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15
Q

What is peripheral oedema?

A

Increased interstitial fluid in tissues

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16
Q

What are oedema effusions?

A

Fluid collections in body cavities

  • Pleural, pericardial, joint effusions
  • Abdominal cavity: ascites
17
Q

What is Oedema: exudate?

A
  • Part of inflammatory process due to increased vascular permeability
  • Tumour, inflammation, allergy
  • Higher protein/albumin content (cells)
  • H2O & electrolytes
  • High specific gravity
18
Q

Pathophysiology of pulmonary oedema in left ventricular failure

A

Hydrostatic pressure - transudate

  • Increased left atrial pressure > passive retrograde flow to pulmonary veins, capillaries and arteries
  • Increased pulmonary vascular pressure
  • Increased pulmonary blood volume
  • Increased Pc > Increased filtration and pulmonary oedema
19
Q

Pathophysiology of pulmonary oedema in lungs

A
  • Perivascular and interstitial transudate
  • Progressive oedematous widening of alveolar septa
  • Accumulation of oedema fluid in alveolar spaces
20
Q

Pathophysiology of peripheral oedema

A

Right heart failure – cannot empty RV in systole
Blood retained in systemic veins > Increased pressure in capillaries > increased filtration > peripheral oedema
also, secondary portal venous congestion via liver

21
Q

Pathophysiology of peripheral oedema: Congestive cardiac failure

A
  • Right and left ventricles both fail
  • Pulmonary oedema and peripheral oedema at the same time
  • All about hydrostatic pressure (P)
22
Q

Pathophysiology of lymphatic blockage

A

Lymphatic obstruction - hydrostatic pressure upset

  • Lymphatic drainage is required for normal flow
  • If lymphatic system is blocked > lymphoedema
    e. g. breast cancer may require radiotherapy to axilla > fibrosis > decreased outflow > oedema of upper limb
23
Q

Pathophysiology of low protein oedema

A

Oncotic pressure - transudate

  • Oncotic pressurec requires normal protein levels
  • Hypoalbuminaemia > decreased oncotic pressurec > increases filtration
    e. g nephrotic syndrome
    e. g. hepatic cirrhosis
    e. g. malnutrition
24
Q

Pathophysiology of permeability oedema

A

Endothelial permeability - exudate

  • Damage to endothelial lining > Increases “pores” in membrane > osmotic reflection coefficient of endothelium decreases towards zero
  • Proteins and larger molecules can leak out (not just H2O)
    e. g. acute inflammation such as pneumonia
    e. g. burns