Pathophysiology of congestion + oedema Flashcards

1
Q

What is congestion?

A
  • relative excess of blood in vessels of tissue/organ

- this is a passive process and can be acute or chronic

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2
Q

Examples of congestion

A

Local acute congestion
-deep vein thrombosis

Local chronic congestion
-hepatic cirrhosis

Generalised acute congestion
-congestive cardiac failure

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3
Q

How does deep vein thrombosis lead to congestion?

A
  • In DVT, there is cclusion of the vein which causes localised acute congestion.
  • Blood will back up from veins, venules + capillaries
  • This will decrease outflow of blood and decrease the pressure gradient.
  • It will also decrease venous return. In extreme cases, No O2 > ischaemia +infarction
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4
Q

What is hepatic cirrhosis?

A
  • When the liver does not function properly due to liver damage (HBV, alcohol)
  • regenerating liver forms nodules of hepatocytes with intervening fibrosis
  • there is a loss of normal structure due to altered hepatic BF
  • Portal BF can be blocked and congestion in the portal vein and its branches will occur. This eill increase portal venous pressure. An alternative circulation ( collateral circulation) is used which anastomoses with systemic circulation.
  • If local chronic congestion, haemorrhage risk
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5
Q

What is congestive cardiac failure?

A
  • When the heart is unable to clear blood in right and left ventricles ( ineffective pump,)
  • CO will decrease which decrease GFR, renin-angiotensin-aldesterone system will be activated and increases Na+ & H2O retention > increasing PV
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6
Q

Examples that may cause an ineffective heart pump

A
  • Ischaemic disease

- valve disease

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7
Q

Treatment of overload of fluid in system

A

diuretics

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8
Q

State the effects of congestive cardiac failure

A
  • heart cannot clear blood from ventricles
  • back flow of blood into veins

Pulmonary oedema

  • left heart failure; blood dams back into lungs
  • crepitations in lungs, tachycardia

Liver - central venous congestion

  • right heart failure
  • blood dams back to systemiccirculation
  • raised JVP, hepatomegaly, peripheral oedema
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9
Q

The effect of hepatic central venous congestion on liver

A
Pericentral hepatocytes  (red)
-stasis of poorly ocygenated blood
Periportal hepatocytes (pale)
- better due to oxygenated blood in close proximity of hepatic arterioles
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10
Q

What is an oedema?

A

-accumulation of fluid in the extravascular space ( body cavities, intracellular tissue compartment)

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11
Q

What is a peripheral oedema?

A

-increased ISF in tissues

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12
Q

What is a effusion?

A
  • fluid collection in body cavities

- pleural, pericardial, joint effusions, ascites ( abdnominal cavity)

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13
Q

What is a transudate oedema?

A
  • A filtrate of blood and can be caused due to increased pressure in veins/capillarie(changes in the haemodynamic forces)
  • can be due to cardiac failure, or fluid overload
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14
Q

What is found in a transudate oedema?

A
  • no protein(albumin) and has fewer cells
  • Rich in water and electrolytes
  • Low specific gravity
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15
Q

What is an exudate oedema?

A

-fluid rich in protein/cells
part of inflammatory process due to increase vascular permeability
-caused by tumour, inflammation and allergy
-higher protein/albumin content ( cells)
-Water an electrolytes
-high specific gravity

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16
Q

Describe the pathophysiology of a pulmonary oedema

A

-Hydrostatic pressure causes a transudate
Left ventricular failure
- pressure in left atrium to increase which causes backflow of bloos to pulmonary veins, capillaries and arteries.
-this caused raised pulmonary vascular pressure and increases pulmonary BV
-Increased capillary hydrostatic pressure increases filtration > Pul.oedema

In lungs

  • perivascular and intersitial transudate
  • progresssive oedematous widening of alveolar septa + accumulation of oedema fluid in alveolar spaces
17
Q

Describe the pathophysioogy of a peripheral oedema

A

Right heart failure

  • heart cannot enoty RV during systole so blood retained in systmic veins will increase pressure in capillaries + increase filtration.
  • This leads to a peripheral oedema and secondary portal venous congestion via liver.

Congestive cardiac failure causes:

  • R+L ventricles failure
  • pul oedema/peripheral at same time
18
Q

State the pathophysiology of lymphatic blockage

A

Lymphatic pobstruction will cause hydrostatic pressure upset

  • if this is blocked, lymphoedema
  • e.g. breast cancer may require radiotherapy to axilla > fibrosis which leads to a decrease in outflow > oedema of upper limb
19
Q

Describe the pathophysiology of oedema in abnormal renal function

A
  • results in salt and H2O retention
  • secondary in heart failure > reduced renal BF
  • primary > acute tubular damage ( eg hypotension)
  • both decreases renal function

-This increases salt and H20, Intravascular fluid volume, secondary capillary hydrostatic pressure > oedema

20
Q

Describe the pathophysiology of low protein oedema

A

Oncotic pressure - transudate

  • capillary oncotic pressure requires normal protein levels
  • Hypoalbuminaemia will lead to decreased capillary oncotic pressure increased fitratin
21
Q

Examples of hypoalbunaemiea

A

Nephrotic syndrome
-leaky renal glomerular basement membrane > lose protein > oedema

Hepatic cirrhosis
-diffuse nodules and fibrosis in liver > liver unable to synthesise sufficient protein

Malnutrition
- insufficient intake of protein

22
Q

Describe the pathophysiology of permeability oedema

A

Endothelial permeability

  • damage to endothelial lining leads to an increase in ‘pores’ of membrane.
  • This leads to osmotic reflection coefficient of endothelium to decrease towards 0
  • proteins and larger molecules can now leak out
  • caused by acute inflammation ( pneumonia, burns etc)