Pathophysiology of Edema
Pathophysiology of Edema
Pathophysiology of Edema
EDEMA
60% of lean body weight is water, two third of which is intracellular and one third
is extra cellular mostly as interstitial fluid
Pathophysiology of edema
movement of fluid between vascular & interstitial spaces .The outflow of fluid
from arteriolar end is balanced by the inflow at the venular end and small amount
drain by lymphatics.
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Factors regulate edema:
exudate (1.020).
*Localized increase in venous pressure e.g (deep venous thrombosis DVT) with
edema of the affected limb.
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Reduced plasma osmotic pressure: (reduced plasma proteins)
Result from:
Causes:
Morphology of edema:
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Special forms of edema:
1. Pulmonary edema
Seen in:
The lung is 2-3 times their normal weight, cut section frothy, blood tinged fluid
represent mixture of air, edematous fluid & extravasated RBCs.
2. Edema of brain
a. Subcutaneous edema in cardiac failure & renal failure can impair wound healing or
clearance of infection.
b. Pulmonary edema can cause death by interfering with normal ventilatory function
by:
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(2)Edematous fluid in alveolar spaces is favorable environment for bacterial
infection.
c. Brain edema if severe causes death due to brain herniated through foramen magnum
which causes compression of vital centers & also due to compression of vascular
supply of brain.
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Hyperemia: is an active process in which arteriolar dilation (e.g., at sites of
inflammation or in skeletal muscle during exercise) leads to increased blood flow
Affected tissues turn red (erythema) because of the engorgement of vessels with
oxygenated blood.
Hyperemia could be :
1. Local or General
2. Physiological or Pathological
B.Pathological: e.g:
obstruction).
Congested tissues take on a dusky reddish-blue color (cyanosis) due to red cell
stasis and the accumulation of deoxygenated hemoglobin.
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In long-standing chronic passive congestion, the lack of blood flow causes
chronic hypoxia
Capillary rupture in chronic congestion can also cause small hemorrhagic foci;
subsequent catabolism of extravasated red cells can leave residual clusters of
hemosiderin-laden macrophages.
Clinically:
A- Dilated veins e.g increase JVP (jugular venous pressure)
B- Edema (limbs, ascites, hepatospleenomegaly) .
Liver: will show chronic venous congestion causing a grossly mottled appearance
similar to the nut meg hence the name Nut meg liver.
Mic.:
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