OVERVIEW
Amyloidoses—disorders that share the common feature of pathologic deposition of an extracellular insoluble fibrillar proteinaceous matrix
Amyloid—accumulates secondary to inflammatory or lymphoproliferative disorders or as a familial tendency
Dogs and cats—usually reactive or secondary amyloidosis; underlying primary inflammatory disorder common
Associated familial disorders—certain kindreds of dogs and cats
Multiple organs commonly involved; clinical signs usually owing to renal or liver involvement
Liver involvement—may be insidious; may lead to high liver enzymes, severe hepatomegaly, coagulopathy, liver rupture leading to hemoabdomen, and/or liver failure
Saturday, March 26, 2011
Globulin
DEFINITION
Heterogenous group of proteins; includes immunoglobulins, clotting factors, acute-phase proteins, and complement proteins
Hyperglobulinemia—high serum globulin concentration
Hypoglobulinemia—low serum globulin concentration
Gammopathy—any abnormality in the concentration of immunoglobulins
PATHOPHYSIOLOGY
Hyperglobulinemia—from increased production of immunoglobulins and hepatic synthesis of acute-phase proteins; falsely increased by dehydration; classified as either polyclonal or monoclonal; may result in hyperviscosity syndrome and impaired immune function
Polyclonal gammopathies—from production of immunoglobulins by several different cell lines; usually in response to persistent antigenic stimulation
Monoclonal gammopathies—from synthesis of one type of immunoglobulin by a single clone of cells; proliferation may be associated with lymphoid hyperplasia or neoplasia.
Hypoglobulinemia—from either impaired synthesis or extracorporeal globulin loss
Impaired synthesis—results in immunodeficiency syndromes; characterized by chronic infection and unthrifty appearance
Extracorporeal loss—commonly from gastrointestinal disease; also secondary to blood loss; rarely from hepatic insufficiency and renal losses
Heterogenous group of proteins; includes immunoglobulins, clotting factors, acute-phase proteins, and complement proteins
Hyperglobulinemia—high serum globulin concentration
Hypoglobulinemia—low serum globulin concentration
Gammopathy—any abnormality in the concentration of immunoglobulins
PATHOPHYSIOLOGY
Hyperglobulinemia—from increased production of immunoglobulins and hepatic synthesis of acute-phase proteins; falsely increased by dehydration; classified as either polyclonal or monoclonal; may result in hyperviscosity syndrome and impaired immune function
Polyclonal gammopathies—from production of immunoglobulins by several different cell lines; usually in response to persistent antigenic stimulation
Monoclonal gammopathies—from synthesis of one type of immunoglobulin by a single clone of cells; proliferation may be associated with lymphoid hyperplasia or neoplasia.
Hypoglobulinemia—from either impaired synthesis or extracorporeal globulin loss
Impaired synthesis—results in immunodeficiency syndromes; characterized by chronic infection and unthrifty appearance
Extracorporeal loss—commonly from gastrointestinal disease; also secondary to blood loss; rarely from hepatic insufficiency and renal losses
Gastroduodenal Ulcer Disease
DEFINITION
Erosive lesions that extend through the mucosa and into the muscularis mucosa
PATHOPHYSIOLOGY
Gastroduodenal ulcers result from single or multiple factors altering, damaging, or over-whelming the normal defense and repair mechanisms of the “gastric mucosal barrier.”
Factors that make up the “gastric mucosal barrier” and protect the stomach from ulcer formation include the mucus-bicarbonate layer over the epithelial cells, the gastric epithelial cells, gastric mucosal blood flow, epithelial cell restitution and repair, and prostaglandins produced by the gastrointestinal tract.
Factors that cause mucosal barrier damage and predispose to gastroduodenal ulcer formation include inhibiting the epithelial cell's ability to repair, decreasing the mucosal blood supply, and/or increasing gastric acid secretion.
The risk of gastroduodenal ulcer formation increases with the number of insults to the “gastric mucosal barrier.”
Erosive lesions that extend through the mucosa and into the muscularis mucosa
PATHOPHYSIOLOGY
Gastroduodenal ulcers result from single or multiple factors altering, damaging, or over-whelming the normal defense and repair mechanisms of the “gastric mucosal barrier.”
Factors that make up the “gastric mucosal barrier” and protect the stomach from ulcer formation include the mucus-bicarbonate layer over the epithelial cells, the gastric epithelial cells, gastric mucosal blood flow, epithelial cell restitution and repair, and prostaglandins produced by the gastrointestinal tract.
Factors that cause mucosal barrier damage and predispose to gastroduodenal ulcer formation include inhibiting the epithelial cell's ability to repair, decreasing the mucosal blood supply, and/or increasing gastric acid secretion.
The risk of gastroduodenal ulcer formation increases with the number of insults to the “gastric mucosal barrier.”
Fever
DEFINITION
Higher than normal body temperature because of a changed thermoregulatory set point in the hypothalamus; normal body temperature in dogs and cats is 100.2–102.8°F (37.8–39.3°C) Fever of unknown origin (FUO)—at least 103.5°F (39.7°C) on at least four occasions over a 14-day period and illness of 14 days' duration without an obvious cause
PATHOPHYSIOLOGY
Exogenous or endogenous pyrogens cause release of endogenous substances (e.g., interleukin-1 and prostaglandins) that reset the hypothalamic thermoregulatory center to a higher temperature, activating appropriate physiologic responses to raise the body temperature to this new set point. Physiologic consequences include increased metabolic demands, muscle catabolism, bone marrow suppression, heightened fluid and caloric requirements, and possibly disseminated intravascular coagulation (DIC) and shock.
Higher than normal body temperature because of a changed thermoregulatory set point in the hypothalamus; normal body temperature in dogs and cats is 100.2–102.8°F (37.8–39.3°C) Fever of unknown origin (FUO)—at least 103.5°F (39.7°C) on at least four occasions over a 14-day period and illness of 14 days' duration without an obvious cause
PATHOPHYSIOLOGY
Exogenous or endogenous pyrogens cause release of endogenous substances (e.g., interleukin-1 and prostaglandins) that reset the hypothalamic thermoregulatory center to a higher temperature, activating appropriate physiologic responses to raise the body temperature to this new set point. Physiologic consequences include increased metabolic demands, muscle catabolism, bone marrow suppression, heightened fluid and caloric requirements, and possibly disseminated intravascular coagulation (DIC) and shock.
Esophageal Diverticula Basics
OVERVIEW
An abnormal, circumscribed enlargement or dilatation of the esophagus producing a region for accumulation of ingesta
Two types of esophageal diverticula exist.
Pulsion (true) diverticula are associated with high intraluminal pressure leading to mucosal herniation through the muscularis; histologically, the cellular remnants are epithelium and connective tissue.
Traction (false) diverticula are caused by the outward pull of connective tissue on the esophagus; all four cell layers (mucosa, submucosa,muscularis, and adventitia) remain intact.
Approximately 50–70% of diverticula (especially epiphrenic pulsion types) are associated with other lesions of the esophagus ordiaphragm.
Organ systems affected include the gastrointestinal (regurgitation), musculoskeletal (weight loss), and respiratory (aspiration pneumonia).
An abnormal, circumscribed enlargement or dilatation of the esophagus producing a region for accumulation of ingesta
Two types of esophageal diverticula exist.
Pulsion (true) diverticula are associated with high intraluminal pressure leading to mucosal herniation through the muscularis; histologically, the cellular remnants are epithelium and connective tissue.
Traction (false) diverticula are caused by the outward pull of connective tissue on the esophagus; all four cell layers (mucosa, submucosa,muscularis, and adventitia) remain intact.
Approximately 50–70% of diverticula (especially epiphrenic pulsion types) are associated with other lesions of the esophagus ordiaphragm.
Organ systems affected include the gastrointestinal (regurgitation), musculoskeletal (weight loss), and respiratory (aspiration pneumonia).
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