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28 Cards in this Set
- Front
- Back
Definition of "edema"
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the accumulation of abnormal amounts of fluid in the intercellular tissue spaces or body cavities; two main types are inflammatory edema (an exudate) and noninflammatory (hemodynamic) edema (a transudate)
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Definition of "anasarca"
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severe generalized edema, producing marked swelling of subcutaneous tissues
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Conditions under which noninflammatory edema may occur (4)
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1. increase in intravascular hydrostatic pressure
2. decrease in colloid osmotic pressure of plasma 3. impairment of lymph flow 4. renal retention of salt and water |
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Reasons for increase in intravascular hydrostatic pressure
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Local increases:
--impaired venous outflow, e.g from thrombosis General increases: --congestive heart failure affecting right ventricular function --constrictive pericarditis --cirrhosis of liver --arteriolar dilatation |
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Reasons for reduced plasma oncotic pressure
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1. Loss of albumin (i.e., nephrotic syndrome)
2. Reduced synthesis of serum proteins (e.g., cirrhosis of liver or malnutrition) |
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Reasons for lymphatic obstruction
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(usually localized)
--inflammatory (e.g. from rxn to parasite) --neoplasm or cancer metastasis --postsurgical/postirradiation |
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Reasons for renal retention of salt and water
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--acute renal failure
--post-streptococcal glomerulonephritis --secondary aldosteronism due to decreased blood volume |
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Definition of "dependent edema"
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subcutaneous edema of the lower extremities due to right heart failure, called "dependent" because of the effects of gravity
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Definition of "pitting edema"
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generalized edema (anasarca) caused by renal dysfunction where finger pressure squeezes edemetous fluid out of subcutaneous tissues, leaving depressions
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Morphological appearance of brain edema
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In generalized edema: brain heavier than normal; swollen and flattened gyri, narrowed sulci; gelatinous white matter; perivascular spaces are widened into halos around vessels
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Definition of "hyperemia"
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AKA "active hyperemia," when arterial and arteriolar dilatation, caused by sympathetic neurogenic mechanisms, produce an increased flow into capillary beds with opening of inactive capillaries; causes redness (e.g., blushing)
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Definition of "congestion"
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AKA "passive hyperemia," results from impaired venous drainage and causes a blue-red coloration because of the increase in deoxygenated hemoglobin in the dammed blood. It can be localized, as in portal hypertension secondary to cirrhosis, or systemic, with either lungs affected (left heart failure) or the entire body except the lungs (right heart failure)
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These 3 organs develop the most obvious signs of chronic passive congestion
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lungs, liver and spleen
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Definition of "heart-failure cells"
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Chronic passive congestion of the lungs causes alveolar capillaries to be engorged with blood. When one ruptures, blood hemorrhages into the alveolar space and is cleaned up by macrophages. The breakdown of the hemoglobin fills the macrophages with the brown-yellow pigment hemosiderin, which is indigestible. This happens most often because of left heart failure.
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Definition of "nutmeg liver"
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Red-blue speckled appearance of liver with chronic passive congestion due to the distension of the central vein and surrounding sinusoids with blood; the peripheral hepatocytes develop fatty change.
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Definition of "ecchymosis"
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A large (greater than 2cm) subcutaneous hematoma, e.g., a bruise
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Definition of "thrombosis"
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A pathologic process in which a clotted mass of blood forms within the non-interrupted vascular system
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Overview of sequence of events in formation of normal hemostatic plug (4 steps)
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1. Brief period of vasoconstriction
2. Platelet activation and aggregation (primary hemostasis) 3. Formation of thrombin and fibrin (secondary hemostasis) 4. Polymerized fibrin and aggregated platelets form solid mass |
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Agonists released by activated platelets
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--adenosine diphosphate (ADP)
--thromboxane A2 --serotonin |
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Anti-platelet effects of endothelium
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--insulation from collagen
--surface prostacyclin (PGI2) and nitric oxide (NO) that vasodilate and inhibit platelet aggregation |
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Anticoagulant properties of endothelium
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--membrane-associated heparin-like molecules that catalyze the inactivation of thrombin and other factors via antithrombin III
--membrane-associated thrombomodulin that binds thrombin, turning it into an anticoagulant and activating Protein C, which inhibits clotting --Produces Protein S, which is a cofactor for Protein C activity |
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Fibrinolytic properties of endothelium
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--synthesis of tissue-type plasminogen activators (t-PA) that promote fibrinolytic activity and help clear fibrin deposits
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Prothrombotic properties of endothelium
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--synthesize and secrete von Willebrand factor (vWF) which is essential for platelet adhesion
--can be induced to make tissue factor, which activates the intrinsic clotting pathway --express binding sites for activated factors IX and X --secrete t-PA inhibitor |
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alpha granules
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Granules in platelets that contain fibrinogen, fibronectin, factors V and VIII, platelet factor 4 and growth factors. Their membranes also contain P-selectin.
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electron-dense bodies
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Granules in platelets that store nonmetabolic ATP and ADP, ionized calcium, histamine, serotonin, and epinephrine.
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3 reactions of platelet activation
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1. adhesion/shape change
2. secretion/release reaction 3. aggregation |
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What happens during platelet adhesion?
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Platelets attach to exposed collagen via pseudopods and vWF, then spread out and adhere tightly.
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What occurs during the secretion (release reaction) of platelets?
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After adhesion, agonists bind to platelet surface receptors and activate phospholipase C and signal transduction pathways mediated by protein kinase A and C, which allow the alpha granules and electron-dense bodies (delta granules) to secrete their contents.
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