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
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