deck_4805980 Flashcards
What is edema?
accumulation of fluid resulting from a net outward movement of water into extravascular spaces.
What is Hemostasis?
the process of blood clotting that prevents excessive bleeding after blood vessel damageInadequate hemostasis may result in hemorrhage, which can compromise regional tissue perfusion and, if massive and rapid, may lead to hypotension, shock, and death
What is the difference between thrombosis and embolism?
inappropriate clotting (thrombosis) or migration of clots (embolism) can obstruct blood vessels, potentially causing ischemic cell death (infarction).Indeed, thromboembolism lies at the heart of three major causes of morbidity and death in developed countries: myocardial infarction, pulmonary embolism, and cerebrovascular accident (stroke).
What do hyperemia and congestion mean?
both refer to an increase in blood volume within a tissue but they have different underlying mechanisms.
What is hyperemia caused by?
Hyperemia is an ACTIVE process resulting from arteriolar dilation and increased blood inflow, as occurs at sites of inflammation or in exercising skeletal muscle.Hyperemic tissues are redder than normal because of engorgement with oxygenated blood
What is congestion caused by?
Congestion is a PASSIVE process resulting from impaired outflow of venous blood from a tissue. It can occur systemically, as in cardiac failure, or locally as a consequence of an isolated venous obstruction.
What color are tissues experiencing congestion? Why?
Congested tissues have an abnormal blue-red color (cyanosis) that stems from the accumulation of deoxygenated hemoglobin in the affected area. In long-standing chronic congestion, inadequate tissue perfusion and persistent hypoxia may lead to parenchymal cell death and secondary tissue fibrosis, and the elevated intravascular pressures may cause edema or sometimes rupture capillaries, producing focal hemorrhages.
On microscopic examination, acute pulmonary congestion is marked by blood-engorged alveolar capillaries and variable degrees of alveolar septal edema and intra-alveolar hemorrhage. In chronic pulmonary congestion, the septa become thickened and fibrotic, and the alveolar spaces contain numerous macrophages laden with hemosiderin (“heart failure cells”) derived from phago- cytosed red cells.
On microscopic examination, acute pulmonary congestion is marked by blood-engorged alveolar capillaries and variable degrees of alveolar septal edema and intra-alveolar hemorrhage. In chronic pulmonary congestion, the septa become thickened and fibrotic, and the alveolar spaces contain numerous macrophages laden with hemosiderin (“heart failure cells”) derived from phago- cytosed red cells.
In acute hepatic congestion, the central vein and sinusoids are distended with blood, and there may even be central hepatocyte dropout due to necrosis. The periportal hepatocytes, better oxygenated because of their proximity to hepatic arterioles, experience less severe hypoxia and may develop only reversible fatty change. In chronic passive congestion of the liver, the central regions of the hepatic lobules, viewed on gross examination, are red-brown and slightly depressed (owing to cell loss) and are accentuated against the surrounding zones of uncon- gested tan, sometimes fatty, liver (nutmeg liver) Microscopic findings include centrilobular hepatocyte necrosis, hemorrhage, and hemosiderin-laden macrophages. In long-standing, severe hepatic congestion (most commonly associated with heart failure), hepatic fibro- sis (“cardiac cirrhosis”) can develop. Because the central portion of the hepatic lobule is the last to receive blood, centrilobular necrosis also can occur in any setting of reduced hepatic blood flow (including shock from any cause); there need not be previous hepatic congestion.
In acute hepatic congestion, the central vein and sinusoids are distended with blood, and there may even be central hepatocyte dropout due to necrosis. The periportal hepatocytes, better oxygenated because of their proximity to hepatic arterioles, experience less severe hypoxia and may develop only reversible fatty change. In chronic passive congestion of the liver, the central regions of the hepatic lobules, viewed on gross examination, are red-brown and slightly depressed (owing to cell loss) and are accentuated against the surrounding zones of uncon- gested tan, sometimes fatty, liver (nutmeg liver) Microscopic findings include centrilobular hepatocyte necrosis, hemorrhage, and hemosiderin-laden macrophages. In long-standing, severe hepatic congestion (most commonly associated with heart failure), hepatic fibro- sis (“cardiac cirrhosis”) can develop. Because the central portion of the hepatic lobule is the last to receive blood, centrilobular necrosis also can occur in any setting of reduced hepatic blood flow (including shock from any cause); there need not be previous hepatic congestion.
Where is the bulk of the body’s water held?
Approximately 60% of lean body weight is water, two thirds of which is intracellular. Most of the remaining water is found in extracellular compartments in the form of interstitial fluid; only 5% of the body’s water is in blood plasma.
Edema is an accumulation of interstitial fluid within tissues. Extravascular fluid can also collect in body cavities such as the pleural cavity (hydrotho- rax), the pericardial cavity (hydropericardium), or the perito- neal cavity (hydroperitoneum, or ascites).
Edema is an accumulation of interstitial fluid within tissues. Extravascular fluid can also collect in body cavities such as the pleural cavity (hydrothorax), the pericardial cavity (hydropericardium), or the peritoneal cavity (hydroperitoneum, or ascites).
What is Anasarca?
severe, generalized edema marked by profound swelling of subcutaneous tissues and accumulation of fluid in body cavities.
Fluid movement between the vascular and interstitial spaces is governed mainly by what two opposing forces?
the vascular hydrostatic pressure and the colloid osmotic pressure produced by plasma proteins.Normally, the outflow of fluid produced by hydrostatic pressure at the arteriolar end of the microcirculation is neatly balanced by inflow due to the slightly elevated osmotic pressure at the venular end; hence there is only a small net outflow of fluid into the interstitial space, which is drained by lymphatic vessels.
Generalized (as opposed to local) increases in venous pressure, with resultant systemic edema, occur most commonly in _____.
congestive heart failurecaused by increased arterial hydrostatic pressure. not colloid loss.
Several factors increase venous hydrostatic pressure in patients with congestive heart failure. Name some.
1) Increased hydrostatic pressureThe reduced cardiac output leads to hypoperfusion of the kidneys, triggering the renin-angiotensin-aldosterone axis and inducing sodium and water retention (secondary hyperaldosteronism). In patients with normal heart function, this adaptation increases cardiac filling and cardiac output, thereby improving renal perfusion. However, the failing heart often cannot increase its cardiac output in response to the compensatory increases in blood volume. Instead, a vicious circle of fluid retention, increased venous hydrostatic pressures, and worsening edema ensues. Unless cardiac output is restored or renal water retention is reduced (e.g., by salt restriction or treatment with diuretics or aldosterone antagonists) this downward spiral contin- ues. Because secondary hyperaldosteronism is a common feature of generalized edema, salt restriction, diuretics, and aldosterone antagonists also are of value in the manage- ment of generalized edema resulting from other causes.
Under normal circumstances ____ accounts for almost half of the total plasma protein
2) Reduced protein pressure (from last slide)albuminTherefore conditions in which albumin is either lost from the circulation or synthesized in inadequate amounts are common causes of reduced plasma osmotic pressure.
How does nephrotic syndrome affect plasma osmotic pressure?
damaged glomerular capillaries become leaky, leading to the loss of albumin (and other plasma proteins) in the urine and the development of generalized edema.
Reduced albumin synthesis occurs in the setting of severe liver disease (e.g., cirrhosis) and protein malnutrition. Regardless of cause, low albumin levels lead in a stepwise fashion to edema, reduced intravascular volume, renal hypoperfusion, and secondary hyperaldosteronism. Unfortunately, increased salt and water retention by the kidney not only fails to correct the plasma volume deficit but also exacerbates the edema, since the primary defect—low serum protein-persists.
Reduced albumin synthesis occurs in the setting of severe liver disease (e.g., cirrhosis) and protein malnutrition. Regardless of cause, low albumin levels lead in a stepwise fashion to edema, reduced intravascular volume, renal hypoperfusion, and secondary hyperaldosteronism. Unfortunately, increased salt and water retention by the kidney not only fails to correct the plasma volume deficit but also exacerbates the edema, since the primary defect—low serum protein-persists.
Impaired lymphatic drainage and consequent lymphedema usually result from what?
a localized obstruction caused by an inflammatory or neoplastic conditionFor example, the parasitic infection filariasis can cause massive edema of the lower extremity and external genitalia (so-called elephantiasis) by engendering inguinal lymphatic and lymph node fibrosis.Peau d’orange
How can salt retention cause edema?
Excessive retention of salt (and its obligate associated water) can lead to edema by increasing hydrostatic pres- sure (due to expansion of the intravascular volume) and reducing plasma osmotic pressure. Excessive salt and water retention are seen in a wide variety of diseases that compromise renal function, including poststreptococcal glo- merulonephritis and acute renal failure
Subcutaneous edema can be diffuse but usually accumulates preferentially in parts of the body positioned the greatest distance below the heart where hydrostatic pressures are highest. Thus, edema typically is most pronounced in the legs with standing and the sacrum with recumbency, a relationship termed dependent edema.
Subcutaneous edema can be diffuse but usually accumulates preferentially in parts of the body positioned the greatest distance below the heart where hydrostatic pressures are highest. Thus, edema typically is most pronounced in the legs with standing and the sacrum with recumbency, a relationship termed dependent edema.
How would you diagnose subcutaneous edema?
Finger pressure over edematous subcutaneous tissue displaces the interstitial fluid, leaving a finger-shaped depression; this appearance is called pitting edema.
Edema due to renal dysfunction or nephrotic syndrome often manifests first where?
loose connective tissues (e.g., the eyelids, causing periorbital edema).
Subcutaneous edema is important to recognize primarily because it signals what?
potential underlying cardiac or renal diseasehowever, when significant, it also can impair wound healing or the clearance of infections
Pulmonary edema is a common clinical problem that most frequently is seen in the setting of _______.
FROTHY MATERIALleft ventricular failure but also may occur in renal failure, acute respiratory distress syndrome, and inflammatory and infectious disorders of the lungIt can cause death by interfering with normal ventilatory function; besides impeding oxygen diffusion, alveolar edema fluid also creates a favorable environment for infectionsNOTE: Brain edema is life-threatening; if the swelling is severe, the brain can herniate (extrude) through the foramen magnum. With increased intracranial pressure, the brain stem vascular supply can be com- pressed.
What is a hemorrhage?
the extravasation of blood from vessels
