Saturday, March 26, 2011

Magnesium, Hypermagnesemia

DEFINITION
Dogs—serum magnesium >2.51 mg/dL
Cats—serum magnesium >2.3 mg/dL

PATHOPHYSIOLOGY
Magnesium—second only to potassium as the most abundant intracellular cation; most is found in bone and muscle; required for many metabolic functions
Magnesium is an important cofactor in the sodium-potassium ATPase pump that maintains an electrical gradient across membranes and thus plays an important role in the activity of electrically excitable tissues.
Interference with the electrical gradient can change resting membrane potentials; repolarization disturbances result in neuromuscular and cardiac abnormalities.
Magnesium homeostasis is largely controlled by renal elimination; any condition that severely lowers the glomerular filtration rate can elicit hypermagnesemia.
High magnesium concentration impairs transmission of nerve impulses and decreases the postsynaptic response at the neuromuscular junction.
Magnesium has been called nature's calcium blocker; the most serious complications of hypermagnesemia result from calcium antagonism in the cardiac conduction system.

Hypertension, Systemic

DEFINITION
Sustained elevation in systolic or diastolic (or both) arterial blood pressure

PATHOPHYSIOLOGY
Blood pressure is determined by cardiac output and systemic vascular resistance; cardiac output determined by heart rate and stroke volume; systemic arterial blood pressure regulation depends on integration of complex mechanisms within the central and peripheral nervous systems, renal and cardiac tissues, and humoral factors, which synergistically affect cardiac output and peripheral vascular resistance.
Baroreceptors in the carotid sinus and aortic arch respond to changes in blood pressure; a fall in blood pressure increases sympathetic discharge, causing vasoconstriction and increased cardiac contractility and heart rate to return blood pressure to normal, humoral substances that modulate blood pressure include catecholamines, vasopressin, kinins, renin, angiotensin, aldosterone, prostaglandins, and atrial natriuretic peptide; the renin-angiotensin-aldosterone system is probably the most important component.
Hypertension—primary (e.g., essential or idiopathic) or secondary to an underlying disease process; secondary hypertension is more common in veterinary medicine; cause of primary hypertension is not fully understood but some have a hereditary component.

Histoplasmosis

DEFINITION
A systemic fungal infection cause by Histoplasma capsulatum

PATHOPHYSIOLOGY
Mycelial form grows in bird manure or organically enriched soil.
Mycelium—produces infectious spores (microconidia); inhaled into the terminal airways
Spores—germinate in the lungs; develop into yeasts, which are phagocytized by macrophages
Macrophages—distribute the organisms throughout the body
Ingested organisms may directly infect the intestinal tract.
Immune response—determines whether disease develops; affected animals often develop transient, asymptomatic infection.

Hepatitis, Infectious Canine

OVERVIEW
Viral disease of dogs and other Canidae caused by canine adenovirus 1 (CAV-1), which is serologically homogeneous and antigenically distinct from CAV-2, the respiratory virus
Infection—targets parenchymal organs (especially liver), eyes, and endothelium
Oronasal exposure—leads to tonsillar localization and viremia within 4–8 days; saliva and feces infectious during initial viremia
Virus—initially localizes in Kupffer cells and endothelium; replicates in Kupffer cells; release and damage of adjacent hepatocytes and massive viremia; with adequate antibody response, cleared from most organs within 10–14 days; persists in the renal tubules where it may be excreted in urine for 6–9 months
Chronic hepatitis—may develop with only a partial neutralizing antibody response
Cytotoxic ocular injury—leads to anterior uveitis and the classic hepatitis blue eye

Hepatic Amyloid

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

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

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.”

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.

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).