This summary features chapter 4 of Robbins' Basic Pathology about hemodynamics, including the clotting system, thrombosis, hemostasis and disorders in this system. Written in high-level English with extensive explanations and in a story-like style flow.
Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
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Pathology 4
HC 3
The balance between protein retainment in the blood plasma and the net movement of
water and electrolytes to the tissues and back is often disturbed by pathologic conditions.
Any condition that alters endothelial function, increases vascular hydrostatic pressure, or
decrease plasma protein content promotes edema; the accumulation of fluid in tissues
because of net egress of water. Depending on the severity and location this may have
several consequences. Hemostasis is the regular mechanism of blood clotting that prevents
excess bleeding after damage. Inadequate hemostasis may result in hemorrhage, but
inappropriate clotting, thrombosis, or the subsequent migration of clots, embolism, may
cause an infarction.
Hyperemia and Congestion
Both are conditions that cause an increase in blood volume within a tissue. Hyperemia
(active) is the extra dilation of arterioles and increased blood inflow at sites of inflammation
or in exercising skeletal muscles. Congestion (passive) is the impaired outflow of venous
blood from a tissue – due to cardiac failure or venous obstruction. Tissues of the former are
redder, tissues of the latter bluer. Both are very local and tightly regulated conditions.
Edema
This is an accumulation of interstitial fluids in tissues or in body cavities, like the pleural and
pericardial cavities. Fluid exchange and the balance is maintained by two forces: the
vascular hydrostatic pressure forces water out; the colloid osmotic pressure lures water in.
Proteins tend to collect water around themselves as a cloak, to maintain their tertiary
structure. So, if water levels lower, they attract more water to restore the original situation.
Water is forced out because of the pressure, raising the protein concentration in the blood,
which leads to water entering the blood again. Net, there is little to no movement of water
in normal situations – there is equilibrium. In cases of edema, there either is an increased
hydrostatic pressure or a decreases colloid osmotic pressure. Inflammatory edema
nevertheless is rich in protein because of the increased vascular permeability. The causes of
edema in more detail:
- Increased hydrostatic pressure: mainly caused by, in turn, impaired venous return.
Deep venous thrombosis is a local cause of increases in intravenous pressure, while
systemic elevations are because of congestive heart failure. This besides lowers renal
blood flow, which activates the renin-angiotensin-aldosterone system that retains
water, which increases the blood volume; also leading to edema.
- A malnourished individual has lower plasma proteins (especially albumin), thus lower
osmotic pressures, which also results in edema as water will less likely move to the
blood. Also, in cases where plasma albumin is lost or not synthesized (liver disease)
may result in a decreased colloid osmotic pressure and general edema.
- Lymphatic obstruction compromises resorption of fluid from interstitial spaces,
mostly due to inflammatory or neoplastic conditions. Iatrogenic causes may also
constitute to lymphatic obstructions.
- Excessive retention of salt raises hydrostatic pressure and reduces plasma osmotic
pressure, which often occurs in compromised kidneys.
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