DEFINITION
Reversible vacuolar change in hepatocytes in dogs, associated with glucocorticoid treatment, hyperadrenocorticism (iatrogenic or spontaneous), or chronic illnesses in other organ systems; typified by high ALP activity without signs of hepatic insufficiency
PATHOPHYSIOLOGY
Glucocorticoids—cause reversible glycogen accumulation in hepatocytes within 2–3 days after administration; injectable and reposital forms usually induce more severe changes than do oral forms; topical, ocular, cutaneous, and aural administration may also produce an effect
Cell swelling—leads to parenchymal enlargement and hepatomegaly
Response (dogs)—marked individual variation related to the type, route, dosage, duration of treatment, and individual sensitivity; may develop even with low-dose, short-term oral medication
May develop with systemic diseases not related to glucocorticoid exposure or hyperadrenocorticism
Association with significant nonhepatobiliary health problems that involve inflammation—suggests a relationship with stress (endogenous glucocorticoid release) or acute phase reactants
Thursday, March 31, 2011
Squamous Cell Carcinoma, Tonsil
OVERVIEW
Rapid and progressive local invasion by cords of neoplastic squamous epithelium arising from the tonsillar fossa into tonsillar lymphoid tissue
Local extension common
Quick to metastasize to lymph nodes (> 98%), lungs (> 63%), and other distant organs (>20)
Composes 20%–25% of all oral tumors and 50% of all intraoral tumors in dogs and cats
Commonly unilateral, affecting the right more than the left tonsil
SIGNALMENT
Middle-aged or old (range, 2.5–17 years) dogs and cats
No known breed or sex predilection
Rapid and progressive local invasion by cords of neoplastic squamous epithelium arising from the tonsillar fossa into tonsillar lymphoid tissue
Local extension common
Quick to metastasize to lymph nodes (> 98%), lungs (> 63%), and other distant organs (>20)
Composes 20%–25% of all oral tumors and 50% of all intraoral tumors in dogs and cats
Commonly unilateral, affecting the right more than the left tonsil
SIGNALMENT
Middle-aged or old (range, 2.5–17 years) dogs and cats
No known breed or sex predilection
Splenomegaly
DEFINITION
Enlargement of the spleen; characterized as either diffuse or nodular
PATHOPHYSIOLOGY
Spleen—removal of senescent and abnormal erythrocytes; filtration and phagocytosis of antigenic particles; production of lymphocytes and plasma cells; reservoir for erythrocytes and platelets; hematopoiesis, as required
Many disorders are related to and reflect splenic functions.
Diffuse
Four general pathologic mechanisms
Inflammatory (splenitis)—associated with infectious agents; classified according to cell type (e.g., suppurative, necrotizing, eosinophilic, lymphoplasmacytic, and granulomatous-pyogranulomatous)
Lymphoreticular hyperplasia—hyperplasia of mononuclear phagocytes and lymphoid elements (in response to antigens); accelerated erythrocyte destruction
Congestion—associated with impaired venous drainage
Infiltration—involves cellular invasion of the spleen or deposition of abnormal substances
Enlargement of the spleen; characterized as either diffuse or nodular
PATHOPHYSIOLOGY
Spleen—removal of senescent and abnormal erythrocytes; filtration and phagocytosis of antigenic particles; production of lymphocytes and plasma cells; reservoir for erythrocytes and platelets; hematopoiesis, as required
Many disorders are related to and reflect splenic functions.
Diffuse
Four general pathologic mechanisms
Inflammatory (splenitis)—associated with infectious agents; classified according to cell type (e.g., suppurative, necrotizing, eosinophilic, lymphoplasmacytic, and granulomatous-pyogranulomatous)
Lymphoreticular hyperplasia—hyperplasia of mononuclear phagocytes and lymphoid elements (in response to antigens); accelerated erythrocyte destruction
Congestion—associated with impaired venous drainage
Infiltration—involves cellular invasion of the spleen or deposition of abnormal substances
Sinus Bradycardia
DEFINITION
Sinus rhythm in which impulses arise from the sinoatrial node at a slower than normal rate
ECG Features
Dogs—sinus rate < 70 bpm (< 60 bpm in giant breeds)
Cars—sinus rate < 120 bpm at home or < 150 bpm at the clinic
Rhythm regular, often with a slight variation in R-R interval; may be irregular if bradycardia due to high vagal tone
Normal P wave for each QRS complex
P-R interval constant
Sinus rhythm in which impulses arise from the sinoatrial node at a slower than normal rate
ECG Features
Dogs—sinus rate < 70 bpm (< 60 bpm in giant breeds)
Cars—sinus rate < 120 bpm at home or < 150 bpm at the clinic
Rhythm regular, often with a slight variation in R-R interval; may be irregular if bradycardia due to high vagal tone
Normal P wave for each QRS complex
P-R interval constant
Shock, Septic
DEFINITION
Develops as a complication of overwhelming systemic infection. Sepsis is defined as a systemic inflammatory response to infection. Occurs in severe sepsis and is associated with hypoperfusion or hypotension that may or may not respond to fluids or pharmacologic cardiovascular support to maintain arterial pressure.
PATHOPHYSIOLOGY
Results from cardiovascular and/or vasomotor failure caused by circulating endotoxin and inflammatory mediator release. Gram-positive or Gram-negative, aerobic or anaerobic, systemic bacterial infection is the most common underlying cause. The primary event is hypovolemia caused by pyrexia, dehydration, and vascular fluid leakage (because of increased microvascular permeability). Differential vasoconstriction and vasodilation of microvascular beds causes pooling of blood and differential tissue perfusion. Vasculitis and thromboembolic events further compromise tissue perfusion. The ultimate result is tissue hypoxemia and metabolic acidosis, leading to multiple organ failure. In Gram-negative bacterial sepsis, endotoxin (a lipopolysaccharide component of the outer bacterial membrane) plays a key role in the activation of the complement and fibrinolytic pathways. Endotoxin also stimulates macrophages to release cytokines, including tumor necrosis factor and interleukin-1, which in turn amplify the systemic response to endotoxin by stimulating neutrophils, endothelial cells, and platelets, and the release of other cellular mediators that are ultimately responsible for the cardiorespiratory and systemic manifestations of septic shock. Gram-positive bacteria produce other bacterial products capable of activating the same mediator responses.
SYSTEMS AFFECTED
Develops as a complication of overwhelming systemic infection. Sepsis is defined as a systemic inflammatory response to infection. Occurs in severe sepsis and is associated with hypoperfusion or hypotension that may or may not respond to fluids or pharmacologic cardiovascular support to maintain arterial pressure.
PATHOPHYSIOLOGY
Results from cardiovascular and/or vasomotor failure caused by circulating endotoxin and inflammatory mediator release. Gram-positive or Gram-negative, aerobic or anaerobic, systemic bacterial infection is the most common underlying cause. The primary event is hypovolemia caused by pyrexia, dehydration, and vascular fluid leakage (because of increased microvascular permeability). Differential vasoconstriction and vasodilation of microvascular beds causes pooling of blood and differential tissue perfusion. Vasculitis and thromboembolic events further compromise tissue perfusion. The ultimate result is tissue hypoxemia and metabolic acidosis, leading to multiple organ failure. In Gram-negative bacterial sepsis, endotoxin (a lipopolysaccharide component of the outer bacterial membrane) plays a key role in the activation of the complement and fibrinolytic pathways. Endotoxin also stimulates macrophages to release cytokines, including tumor necrosis factor and interleukin-1, which in turn amplify the systemic response to endotoxin by stimulating neutrophils, endothelial cells, and platelets, and the release of other cellular mediators that are ultimately responsible for the cardiorespiratory and systemic manifestations of septic shock. Gram-positive bacteria produce other bacterial products capable of activating the same mediator responses.
SYSTEMS AFFECTED
Shock, Cardiogenic
DEFINITION
Results from profound impairment of cardiac function leading to a decrease in stroke volume and cardiac output, venous congestion, and peripheral vasoconstriction.
Cardiac dysfunction may be caused by hypertrophic or dilated cardiomyopathies, pericardial tamponade, outflow obstructions, thrombosis, severe endocardiosis, heartworm disease, or severe arrhythmias.
Cardiac “pump” failure may also be secondary to systemic diseases causing myocardial dysfunction such as sepsis.
Results in hypotension and compromised tissue perfusion, with reduced tissue oxygen delivery
Results from profound impairment of cardiac function leading to a decrease in stroke volume and cardiac output, venous congestion, and peripheral vasoconstriction.
Cardiac dysfunction may be caused by hypertrophic or dilated cardiomyopathies, pericardial tamponade, outflow obstructions, thrombosis, severe endocardiosis, heartworm disease, or severe arrhythmias.
Cardiac “pump” failure may also be secondary to systemic diseases causing myocardial dysfunction such as sepsis.
Results in hypotension and compromised tissue perfusion, with reduced tissue oxygen delivery
Sepsis and Bacteremia
DEFINITION
Bacteremia—defined as the presence of bacterial organisms in the bloodstream
Sepsis—systemic response to bacterial infection (e.g., fever, hypotension)
Terms are not synonymous, although often used interchangeably
PATHOPHYSIOLOGY
Shedding of bacterial organisms into the bloodstream—may occur transiently, intermittently, or continually
The most critical host response for elimination of bacteremia—provided by mononuclear phagocyte system of the spleen and liver; activation leads to release of numerous cellular mediators (cytokines), some of which are beneficial and others detrimental; may lead to death of the host
Neutrophils—relatively more important for defense against extravascular infection
Bacteremia—transient, subclinical event or may escalate to overt sepsis when the immune system is overwhelmed; generally of more pathologic significance when the bloodstream is invaded from venous or lymphatic drainage sites
Bacteremia—defined as the presence of bacterial organisms in the bloodstream
Sepsis—systemic response to bacterial infection (e.g., fever, hypotension)
Terms are not synonymous, although often used interchangeably
PATHOPHYSIOLOGY
Shedding of bacterial organisms into the bloodstream—may occur transiently, intermittently, or continually
The most critical host response for elimination of bacteremia—provided by mononuclear phagocyte system of the spleen and liver; activation leads to release of numerous cellular mediators (cytokines), some of which are beneficial and others detrimental; may lead to death of the host
Neutrophils—relatively more important for defense against extravascular infection
Bacteremia—transient, subclinical event or may escalate to overt sepsis when the immune system is overwhelmed; generally of more pathologic significance when the bloodstream is invaded from venous or lymphatic drainage sites
Salmonellosis
DEFINITION
A bacterial disease that causes enteritis, septicemia, and abortions and is caused by many different serotypes of Salmonella
PATHOPHYSIOLOGY
Salmonella—a gram-negative bacterium; colonizes the small intestine (ileum); adheres to and invades the enterocytes; eventually enters and multiplies in the lamina propria and local mesenteric lymph nodes; cytotoxin (cell death) and enterotoxin (increases cAMP) are produced; inflammation occurs; and prostaglandin synthesis ensues; results in secretory diarrhea and mucosal sloughing
Uncomplicated gastroenteritis—organisms are stopped at the mesenteric lymph node stage; patient has only diarrhea, vomiting, and dehydration
Bacteremia and septicemia following gastroenteritis—more serious disease; focal extraintestinal infections (abortion, joint disease) or endotoxemia may result; may lead to organ infarction, generalized thrombosis, DIC, and death
Some patients recover from the septicemic form but suffer prolonged recovery as a result of their debilitated state.
A bacterial disease that causes enteritis, septicemia, and abortions and is caused by many different serotypes of Salmonella
PATHOPHYSIOLOGY
Salmonella—a gram-negative bacterium; colonizes the small intestine (ileum); adheres to and invades the enterocytes; eventually enters and multiplies in the lamina propria and local mesenteric lymph nodes; cytotoxin (cell death) and enterotoxin (increases cAMP) are produced; inflammation occurs; and prostaglandin synthesis ensues; results in secretory diarrhea and mucosal sloughing
Uncomplicated gastroenteritis—organisms are stopped at the mesenteric lymph node stage; patient has only diarrhea, vomiting, and dehydration
Bacteremia and septicemia following gastroenteritis—more serious disease; focal extraintestinal infections (abortion, joint disease) or endotoxemia may result; may lead to organ infarction, generalized thrombosis, DIC, and death
Some patients recover from the septicemic form but suffer prolonged recovery as a result of their debilitated state.
Rotavirus Infections
OVERVIEW
Nonenveloped, double-stranded RNA virus; rota (Latin; “wheel”) for shape of the capsid; genus within the family Reoviridae; relatively resistant to environmental destruction (acid and lipid solvents); unique double-capsid protects virus from inactivation in the upper gastrointestinal tract.
Wide host range, identified in almost every species investigated
Most significant cause of severe gastro-enteritis in young children (< 2 years) and animals throughout the world
Transmission—fecal–oral contamination
Infection—affects mature epithelial cells on luminal tips of the intestinal villi; causes swelling, degeneration, and desquamation; denuded villi contract; results in villous atrophy with loss of absorptive capability and loss of brush border enzymes (e.g., disaccharidases); leads to osmotic diarrhea
Nonenveloped, double-stranded RNA virus; rota (Latin; “wheel”) for shape of the capsid; genus within the family Reoviridae; relatively resistant to environmental destruction (acid and lipid solvents); unique double-capsid protects virus from inactivation in the upper gastrointestinal tract.
Wide host range, identified in almost every species investigated
Most significant cause of severe gastro-enteritis in young children (< 2 years) and animals throughout the world
Transmission—fecal–oral contamination
Infection—affects mature epithelial cells on luminal tips of the intestinal villi; causes swelling, degeneration, and desquamation; denuded villi contract; results in villous atrophy with loss of absorptive capability and loss of brush border enzymes (e.g., disaccharidases); leads to osmotic diarrhea
Rhinitis and Sinusitis
DEFINITION
Rhinitis—inflammation of the mucous membrane of the nose
Sinusitis—inflammation of the associated paranasal sinuses
Rhinosinusitis—coined term, because one rarely occurs without the other
PATHOPHYSIOLOGY
May be acute or chronic, noninfectious or infectious
Patients seen in clinics usually have chronic disease.
All causes are often complicated by opportunistic secondary microbial invasion.
Associated mucosal vascular congestion and friability, excessive mucus gland secretion, neutrophil chemotaxis, and nasolacrimal duct obstruction—lead to congestion, obstructed airflow, sneezing, epistaxis, nasal discharge (mucopurulent), and epiphora
Turbinate and facial bone destruction—may develop with neoplastic or fungal disease
Rhinitis—inflammation of the mucous membrane of the nose
Sinusitis—inflammation of the associated paranasal sinuses
Rhinosinusitis—coined term, because one rarely occurs without the other
PATHOPHYSIOLOGY
May be acute or chronic, noninfectious or infectious
Patients seen in clinics usually have chronic disease.
All causes are often complicated by opportunistic secondary microbial invasion.
Associated mucosal vascular congestion and friability, excessive mucus gland secretion, neutrophil chemotaxis, and nasolacrimal duct obstruction—lead to congestion, obstructed airflow, sneezing, epistaxis, nasal discharge (mucopurulent), and epiphora
Turbinate and facial bone destruction—may develop with neoplastic or fungal disease
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