The document discusses edema, which is an increase in fluid volume in body tissues. It notes that 75% of body weight is water, with 50% being intracellular volume, 20% interstitial volume, and 5% intravascular volume. Edema can be local, such as pulmonary or cerebral edema, or disseminated, involving an increase in interstitial fluid volume. The pathogenesis of edema involves capillary permeability, hydrostatic pressure, oncotic pressure, tissue resistance, lymphatic drainage, and renal/hormonal factors.

1. A.Arputha Selvaraj
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75 % of total body weight is water
- 50 % - Intracellular volume
- 20 % - Interstitial volume
- 5 % - Intravascular volume

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EDEMA
Increasing of fluid volume in tissues.
-It is usually used to define the increasing of
extracellular and extravascular fluid volume

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EDEMA – Local (Pulmonary, cerebral, pharyngeal
- Disseminated (Increasing of interstitial
fluid volume)

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Intraperitoneal - Ascites
Intrapleural - Hydrothorax

6. PATHOGENESIS OF EDEMA
1) Capillary permeability
2) Hydrostatic pressure of intracapillary fluid
3) Oncotic pressure of intracapillary fluid
4) Oncotic pressure of interstitial fluid
5) Tissue resistance
6) Lymphatic drainnage
7) Renal hormonal factors
8) Atrial natriüretic peptide
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Capillary permeability
Water, electrolytes,gases – Diffusion
Proteins - Filtration
Chemical, bacterial, thermal, mechanical factors
may cause the increasing of permeability
– inflamatory edema / angioedema

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Hydrostatic pressure:
It forces the blood fluid pass into the tissues
through the capillary wall.
It is 32 mmHg at the arteriolar end of the
capillary, and 12 mmHg at the venule hand.

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Oncotic pressure:
Formed by plasma proteins (especially albumin)
It tries to keep the fluid in the capillary
The oncotic pressure of the capillary is 24 mmHg.

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Plasma protin content > İnterstitial protein content →
Plasma oncotic pressure > ınterstitial oncotic pressre
Effective oncotic pressure = Plasma oncotic pressure –
Interstitium oncotic pressure
Effective oncotic pressure decreases:
- As the decreasing of plasma oncotic pressure
( cirrhosis, malnutrition, nephrotic syndrome, protein
loosing ent.)
- As the increasing of interstitium oncotic pressure
(Increasing of permeability – inflamatory / allergy)

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Arteriolar end: Hydrostatic pressure > Oncotic pressure
⇒ Fluid passes into interstitium
Venule end: Oncotic pressure > Hydrostatic pressure
⇒ Fluid returns capillary bed
* The increase of pressure at the venule end ⇒Fluid
cannot return capillary and stay at the interstitium

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Oncotic pressure of the interstitium:
The amount of protein is nearly 0.3 % g / dl
and it is not so important

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Lymph drainege:
Some of the fluid in the interstitium and a few
amount of protein diffused into interstitium is carried
by lymph vessels. Obstruction of the vessels causes
edema.

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RENAL HORMONAL MECHANISM
Decreasing of stroke volume
Increasing of ADH Decreasing of kidney blood perfusion
Reabsorbtion of water Poor perfusion of juxta glomerular
in tubules of kidneys aparatus
Secretion of renin

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Renin
Angiotensinogen Angiotensin I
Converting enzyme
Angiotensin II

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Angiotensin II:
1) Causes vasoconstriction
2) Increases the secretion of aldosteron from adrenal
gland ( seconder hyperaldosteronism) – İncreases
sodium reabsorbtion in distal tubules

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-Secreted by the secretory granules in the atrium
-Secretion is stimulated by atrial enlargement ( plasma volume
increases)
-Increases diuresis and sodium output.
-Causes vasodilatation
-Inhibits renin and angiotensin release

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EDEMA
-Dısseminated edema
-Local edema

19. Disseminated Edema
Edema due to cardiac failure
Nephritic edema
Nephrotic edema
Edema caused by liver failure
Nutritional edema (inadequate intake)
Protein loss through gastrointestinal system
Edema due to endocrine pathologies
Edema during pregnancy
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20. Local edema
- Traumatic
- Inflammatory edema
- Obstriction of venous circulation
- Thrombophlebitis
- Compression of veins
-Lymphatic edema
-Angioneurotic edema
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- Blood volume per minute decreases ⇒ Water is
conserved by renal and hormonal mechanisms
- Hydrostatic pressure increases

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Mild and hard edema is seen in acute glomerulonephritis
Glomerular filtration decreases, but tubular reabsorbtion is
not disturbed. (glomerulotubular inbalance)
Capillaritis (generalized capillary disorder)

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-It is very soft and in anasarca type
-Low oncotic pressure due to protein loss
-Secondary hyperaldosteronism

24. Cirrhotic Edema
It is usually seen with ascites
Albumin synthesis in liver decreases
Some blood proteins are excreted in feces due to
portal hypertension
Aldosteron breakdown in liver decreases ;
secretion by adrenal gland increases (secondary
hyperaldosteronism)
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25. Nutritional edema
Kwashiworker
Malabsobtion Syndromes
Gastrectomy
 Cancer
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26. Edema due to endocrine
pathologies
Mixedema
Premenstrual edema
Pregnancy
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27. Iatrogenic Edema
Mineralocorticoid
Corticosteroid
Androgen
ADH
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Due tu increased permeability
- Microorganisms
- Connective tissue disorders

29. Venous Edema
Thrombophlebitis: Local inflamations cause
thrombus ⇒ venous obstriction
-Large and hard edema
- Erythema, hotness,pain
Compression of veins
-Ganglion, tumor,ascites
Edema related to varices
High hydrostatic pressure in veins
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30. Lymphatic Edema
Due to obstruction of lymph vessels,plasma proteins
cannot be taken from the interstitium
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Vessels insubcutaneous tissue enlarge due to local
histamine discharge and extravasation from
capillaries occurs
-Food allergy -Drug allergy
-Infections -Emotional

32. Thank You
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