Chapter 3 Hemodynamic Disorders
EDEMA
3 How is edema classified according to the distribution of the fluid?
Edema can be localized or generalized.
Localized edema: Typically, this involves one organ or part of the body. Clinically important examples of localized edema are brain edema, lung edema, or accumulation of fluid in the thoracic cavity (hydrothorax) or abdominal cavity (ascites).
5 What is hydrostatic edema?
Hydrostatic edema results from increased intravascular pressure owing to:
Impaired venous return: Increased central venous pressure caused by heart failure leads to generalized edema, which is, however, more pronounced in the lower extremities. Obstruction of veins by thrombi may lead to localized edema (e.g., edema of the calf as a result of thrombosis of popliteal veins).
6 What are the common causes of increased vascular permeability that lead to edema?
The most common cause of increased vascular permeability is inflammation. Inflammatory edema results from the action of mediators such as histamine, complement fragments (C3a and C5a), bradykinin, platelet-activating factor (PAF), and leukotrienes.
7 What is oncotic edema?
Oncotic pressure of the plasma is primarily maintained by albumin. Reduced concentration of albumin in plasma (hypoalbuminemia) may result from:
Decreased protein synthesis: Most plasma proteins are synthesized in the liver. Hypoalbuminemia, as seen in end-stage liver disease, is the most important cause of generalized edema caused by reduced protein synthesis in chronic liver disease.
Increased protein loss: Loss of proteins may occur through the kidneys in nephrotic syndrome or in the stool in protein-losing enteropathy.
8 How does sodium retention cause edema?
Retention of sodium plays a major role in the pathogenesis of cardiac edema. Heart failure is accompanied by reduced perfusion of the kidneys, which stimulates the juxtaglomerular apparatus to secrete renin. Renin activates the angiotensin system, resulting in an increased secretion of aldosterone from the adrenal cortex. Aldosterone acts on the distal convoluted tubules of the kidney, stimulating them to retain sodium. Retention of sodium is accompanied by water retention, which expands the intravascular volume, leading to increased hydrostatic pressure and hydrostatic edema.
9 What is lymphedema?
Lymphedema results from obstruction of lymphatics and an impaired clearance of lymph from the interstitial spaces. Typically, this is a localized form of edema involving parts of the body, as in:
Elephantiasis, a term used to denote massive leg edema caused by obstruction of inguinal lymph nodes by filarial worms in filariasis
10 What is the difference between transudate and exudate?
Transudate is an ultrafiltrate of plasma that contains few, if any, cells and does not contain large plasma proteins, such as fibrinogen. Transudate results from increased hydrostatic or reduced oncotic pressure. Exudate, on the other hand, is a sign of inflammation and is typically a consequence of increased vascular permeability. Vascular changes permit diapedesis of white blood cells and the passage of large-molecular-weight proteins of the plasma. Accordingly, transudate resembles serum, whereas exudate resembles cell-rich plasma. Transudates do not coagulate, whereas exudates do. The main differences between transudate and exudates are listed in Table 2-1
11 What is pitting edema?
Pitting edema is a clinical term used for subcutaneous leg edema typically found in patients suffering from heart failure. The name refers to the “pit” that can be induced by pressing the skin over the shin.
12 What is the pathogenesis of pulmonary edema?
Pulmonary edema is most often caused by increased pulmonary venous pressure secondary to left-heart failure. In adult respiratory distress syndrome, shock, or infections (pneumonia), pulmonary edema is caused by increased permeability of pulmonary capillaries. Pulmonary edema may also occur in generalized edema caused by hypoalbuminemia of end-stage liver disease or nephrotic syndrome.
13 What is the pathogenesis of ascites of cirrhosis?
Ascites, a common feature of cirrhosis (end-stage liver disease), represents a transudate that develops owing to:
Impaired lymph drainage: Normally a liter or more lymph flows through the liver, and in cirrhosis this lymph flow is diverted so that the lymph is not drained into the major lymphatics but enters the abdominal cavity.
Increased retention of sodium and water: Kidneys retain water and salt because of compensatory hyperaldosteronism. After the fluid begins accumulating in the abdominal cavity, the water in the intravascular compartment is reduced, providing a signal for the activation of the renin–angiotensin system. Ultimately, this will cause secondary hyperaldosteronism and retention of sodium and water in the kidney.
HYPEREMIA AND CONGESTION
15 What is the difference between active hyperemia and congestion?
In hyperemia, which is an active process, the increased blood influx into the tissues results from dilatation of arterioles. Typically this occurs in inflammation. Adrenergic stimuli cause dilatation of arterioles of the face during blushing. Increased blood flow through the muscles during exercise is another example of active hyperemia.
Congestion, also known as passive hyperemia, results from stagnation of blood in the capillaries caused by impeded outflow of blood on the venous end. Obstruction of veins with thrombi or backward pressure caused by heart failure is typically accompanied by congestion.
16 What is the color of hyperemic and congested tissues?
Hyperemic tissues contain increased amounts of oxygenated blood, and therefore such tissues appear bright red. In contrast, congested tissues contain increased amounts of deoxygenated venous blood and therefore appear dusky red or bluish. Hyperemic tissues are warm, whereas the congested tissues are clammy and cold.
17 How does acute congestion differ from chronic passive congestion?
In acute congestion, the blood is inside the dilated veins and capillaries. Such an accumulation of blood may pass without serious consequences, but if it occurs rapidly, the ensuing hypoxia and mechanical compression of tissue around the dilated blood vessels may cause necrosis. In chronic passive congestion, there is invariably ischemia accompanied by loss of parenchymal cells, which are usually replaced by fibrosis.
18 How does congestion affect the liver?
Acute congestion leads to centrilobular stasis of blood that fills the central vein and the sinusoids around it. If the congestion develops suddenly and a large amount of blood is retained in the liver, the centrilobular hepatocytes will undergo necrosis. In chronic passive congestion, the hepatocytes die off and are replaced by fibrous tissue. The cut surface of the liver in such cases has the appearance of a nutmeg. The fibrosis may progress, and the nutmeg liver may transform into cardiac cirrhosis.
19 How does chronic passive congestion affect the lungs?
Chronic passive congestion of the lungs is typically a consequence of left heart failure. It is accompanied by extravasation of red blood cells (RBCs) into the alveolar spaces. These RBCs fall apart and are taken up by macrophages, which can be expectorated as “heart failure cells.” Macrophages also enter the interstitial spaces, where they may die or stimulate fibroblasts to produce collagen. On gross examination at autopsy, such lungs appear brownish red, due to hemosiderin, and fibrotic, due to the deposition of collagen. The technical term for these changes is brown induration of the lungs.
20 How does chronic passive congestion affect the legs?
Prolonged stagnation of blood leads to dilatation of veins (varicose veins) and capillaries. RBCs leak out of the capillaries and die in the interstitial tissues of the subcutis. Hemosiderin formed from hemoglobin accounts for the brownish discoloration of the skin. Chronic ischemia of the skin impedes healing of minor traumatic injuries, and ulcers form. Such stasis ulcers tend to heal slowly or not at all.
HEMORRHAGE
21 What is hemorrhage?
Hemorrhage (bleeding) is escape of blood from blood vessels or the heart. Hemorrhages can be classified according to the site of origin:
Cardiac: These are usually caused by penetrating wounds or rupture of ventricle as a result of myocardial infarction.
Capillary: These are usually caused by trauma or surgery, but they may also occur in a variety of diseases characterized by weakness of vessel walls (e.g., Ehlers–Danlos syndrome and vitamin C deficiency) or platelet disorders (e.g., idiopathic thrombocytopenic purpura).
22 What are the differences between petechiae, purpura, and ecchymoses?
All three terms refer to hemorrhages into the skin and mucosae. Pinpoint hemorrhages smaller than 1 mm are called petechiae; those measuring 1 mm to 1 cm in diameter are called purpura; and those larger than 1 cm are called ecchymoses. This classification is arbitrary and has survived only by tradition. Note that petechiae often become confluent and become purpura or ecchymoses. To complicate matters, the term purpura is also used for several diseases characterized by widespread cutaneous hemorrhages (e.g., thrombotic thrombocytopenic purpura and Henoch–Schönlein purpura).
23 What is the color of a hematoma?
Hematoma is a grossly visible accumulation of extravasated blood in the tissue. First it is red, and then as the blood is deoxygenated, it becomes dusky and bluish red. As the RBCs fall apart, biliverdin forms, and the hematoma will appear greenish. Bilirubin formed from biliverdin will give it a yellow hue. After that, the remnants of the RBC may be resorbed and the tissue resumes its normal color, or the iron portion of heme pigment is taken up by macrophages and degraded into hemosiderin, which gives the tissues a brownish color.
24 How are hemorrhages into body cavities named?
Hemorrhage can occur into any of the preexisting body cavities. Such hemorrhages are named by combining the prefixes hem or hemato (from Greek haima, “blood”) and the anatomic site involved. Accordingly, most of these terms are self-explanatory. For example, terms such as hematopericardium, hematothorax, and hemarthrosis can be easily understood as denoting bleeding into the pericardial, pleural, or intraarticular space, respectively. Other terms are not so intuitively obvious. For example, hematocephalus denotes accumulation of blood in the ventricles of the brain. Hematocolpos signifies accumulation of blood in a vagina occluded by an imperforate hymen.
25 What is hematuria?
Hematuria is appearance of blood in urine. It may be classified as microscopic (i.e., detectable by microscopic examination of urine) or macroscopic if visible to the naked eye. Hematuria may be a sign of kidney or urinary tract disease.
26 What is hematemesis?
Hematemesis is vomiting of blood. Typically, it is a sign of esophageal and gastric hemorrhage. Common causes of hematemesis are ruptured esophageal varices and peptic ulcer of the stomach and duodenum.
27 What is hematochezia?
Hematochezia is bleeding through the rectum. It is typically caused by diseases of the large intestine.
28 What is melena?
Melena or black blood presenting as “coffee-ground” material in the stool is a sign of upper gastrointestinal bleeding. Such blood is partially digested by hydrochloric acid of the gastric juice and transformed into a black pigment called hematein. This pigment is not digested in the intestines and is passed in the feces.
29 What is the difference between epistaxis and hemoptysis?
Epistaxis is bleeding from the nose. Hemoptysis is bleeding from the lungs; literally it means “spitting of blood.”
HEMOSTASIS AND THROMBOSIS
31 How is hemostasis related to thrombosis?
Both processes are based on the coagulation of blood. Hemostasis (“stopping of hemorrhage”) is the physiologic process designed to stop the bleeding from ruptured blood vessels. Thrombosis is a pathologic form of coagulation of circulating blood inside intact vascular spaces.
32 What are the main components of the hemostatic process?
Both hemostasis and thrombosis depend on the interaction of numerous components, which can be grouped as related to the:
Key Points: Hemostasis and Thrombosis
33 How does endothelium of blood vessels act on the coagulation of blood?
Endothelial cells have both procoagulant and anticoagulant properties, and according to the needs of the body, they may either promote blood clotting or inhibit it.
34 How does endothelium prevent blood clotting?
Anticoagulant functions of endothelial cells include:
Inhibition of platelet aggregation: Endothelial cells secrete prostacyclin (PGI2) and nitric oxide (NO), which dilatate blood vessels, thus increasing the blood flow and reducing the chance of adhesion of platelets to the vessel wall. Prostacyclin also directly inhibits the aggregation of platelets.
Inhibition of platelet antithrombin activity: This is mostly accomplished by thrombomodulin, which captures thrombin and submits it for degradation by the anticoagulant protein C.
35 How does endothelium promote blood clotting?
Endothelial cells promote blood clotting through several mechanisms that are counterbalanced by the anticlotting forces. Procoagulant mechanisms include release of:
von Willebrand factor from Weibel–Palade granules in the cytoplasm of endothelial cells: This factor mediates the binding of platelets to surfaces and also serves as a carrier for the coagulation factor VIII.
Thromboplastin (tissue factor, F III): This promotes the extrinsic pathway of the coagulation cascade.
36 What are the essential components of platelets?
Platelets are derived from the fragmentation of the cytoplasm of megakaryocytes. Platelets have the following components that are essential for their participation in hemostasis and thrombosis:
Granules (alpha granules and delta granules or dense bodies): These granules contain a number of ready-made biologically active substances, including coagulation factors such as fibrinogen, mediators of inflammation such as histamine, and growth factors such as platelet-derived growth factor (PDGF).
Cytoskeleton: This is composed of tubulin, actin, and myosin filaments that allow the rapid extrusion of granules from the cytoplasm. Microfilaments and microtubules also mediate the change of the shape of platelets and account for the “clot retraction.”
Adhesion molecules and receptors: These glycoproteins are expressed on the cell membrane of activated platelets, allowing them to adhere to fibrinogen and von Willebrand factor and also each other.
37 What happens after activation of platelets?
Activation of platelets is followed by four phases of clot formation. These phases, which partially overlap one another, include:
38 What is the role of coagulation proteins in hemostasis and thrombosis?
Coagulation factors are a group of plasma proteins that are activated by acting upon each other in a sequence known as the extrinsic and intrinsic pathway. These proteins lead to activation of thrombin, which plays a crucial role in the polymerization of fibrinogen into fibrin. Fibrin formed at the end of the coagulation cascade represents the meshwork skeleton of the clot and also serves as the glue that holds together platelets and other components of the clot. Deficiency of coagulation factors results in bleeding disorders.
39 What is the difference between the intrinsic and the extrinsic coagulation pathway?
The intrinsic pathway is so called because it can be activated by pouring the blood into a test tube without adding any extrinsic material. The coagulation cascade is activated by the binding of Hageman factor (F XII) to negatively charged glass. The extrinsic pathway is activated by adding tissue factor, which activates factor VII.
The mnemonic TEEN helps in remembering that the activation of factor X through the intrinsic pathway involves factors twelve, eleven, eight, and nine.
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