DEFINITION
Ventricular preexcitation occurs when impulses originating in the sinoatrial node or atrium activate a portion of the ventricles prematurely through an accessory pathway without going through the AV node; the remainder of the ventricles is activated normally through the usual conduction system.
WPW syndrome consists of ventricular preexcitation with episodes of paroxysmal supraventricular tachycardia.
Monday, May 2, 2011
Monday, April 18, 2011
Weight Loss and Cachexia
DEFINITION
Weight loss is considered clinically important when it exceeds 10% of the normal body weight and is not associated with fluid loss.
Cachexia is defined as the state of extreme poor health and is associated with anorexia, weight loss, weakness, and mental depression.
PATHOPHYSIOLOGY
Weight loss can result from many different pathophysiologic mechanisms that share a common feature—insufficient caloric intake or availability to meet metabolic needs.
Insufficient caloric intake can be caused by (1) a high energy demand (e.g., that characteristic of a hypermetabolic state); (2) inadequate energy intake, including insufficient quantity or quality of food, or inadequate nutrient assimilation (e.g., with anorexia, dysphagia, regurgitation, or malabsorption–maldigestion disorders); (3) excessive loss of nutrients or fluid, which can occur in patients with gastrointestinal losses, glucosuria, proteinuria, or extensive skin lesions (burns, excoriations, etc.)
Weight loss is considered clinically important when it exceeds 10% of the normal body weight and is not associated with fluid loss.
Cachexia is defined as the state of extreme poor health and is associated with anorexia, weight loss, weakness, and mental depression.
PATHOPHYSIOLOGY
Weight loss can result from many different pathophysiologic mechanisms that share a common feature—insufficient caloric intake or availability to meet metabolic needs.
Insufficient caloric intake can be caused by (1) a high energy demand (e.g., that characteristic of a hypermetabolic state); (2) inadequate energy intake, including insufficient quantity or quality of food, or inadequate nutrient assimilation (e.g., with anorexia, dysphagia, regurgitation, or malabsorption–maldigestion disorders); (3) excessive loss of nutrients or fluid, which can occur in patients with gastrointestinal losses, glucosuria, proteinuria, or extensive skin lesions (burns, excoriations, etc.)
Vomiting, Acute
DEFINITION
Forceful, reflex expulsion of gastric contents from the oral cavity
Acute vomiting is defined as vomiting of short duration (<7 days) and variable frequency.
PATHOPHYSIOLOGY
A complex set of reflex activities under central neurologic control involving the coordination of GI, abdominal, and respiratory musculature
Often preceded by prodromal signs of nausea that can include depression, shivering, hiding or seeking comfort, hypersalivation, lip licking, frequent swallowing, and retching
Occurs when the VC in the medulla is stimulated by afferent activity from several sources
Stimulation can occur from stretch receptors, chemoreceptors, and osmoreceptors located throughout the GI tract, hepatobiliary system, genitourinary system, peritoneum, and pancreas.
The CTZ, when stimulated by a variety of drugs and toxins, can also stimulate the VC.
Higher centers can lead to psychogenic vomiting and input from the vestibular apparatus (e.g., motion sickness, vestibular disease) can stimulate the VC.
Forceful, reflex expulsion of gastric contents from the oral cavity
Acute vomiting is defined as vomiting of short duration (<7 days) and variable frequency.
PATHOPHYSIOLOGY
A complex set of reflex activities under central neurologic control involving the coordination of GI, abdominal, and respiratory musculature
Often preceded by prodromal signs of nausea that can include depression, shivering, hiding or seeking comfort, hypersalivation, lip licking, frequent swallowing, and retching
Occurs when the VC in the medulla is stimulated by afferent activity from several sources
Stimulation can occur from stretch receptors, chemoreceptors, and osmoreceptors located throughout the GI tract, hepatobiliary system, genitourinary system, peritoneum, and pancreas.
The CTZ, when stimulated by a variety of drugs and toxins, can also stimulate the VC.
Higher centers can lead to psychogenic vomiting and input from the vestibular apparatus (e.g., motion sickness, vestibular disease) can stimulate the VC.
Vitamin D Toxicity
DEFINITION
Abnormal accumulation of vitamin D in the body, most commonly from ingesting vitamin D–containing rodenticides or other preparation or oversupplementation
PATHOPHYSIOLOGY
Cholecalciferol—fat-soluble vitamin; absorbed through chylomicrons and transported to the liver, where it is metabolized to 25-hydroxycholecalciferol, the major circulating metabolite during vitamin D excess; further metabolism occurs in the kidney, where calcitriol is produced.
Cholecalciferol and 25-hydroxycholecalciferol—limited biological activity
Calcitriol—most potent cholecalciferol metabolite in terms of enhancing calcium resorption from bone and intestinal calcium uptake
Excessive ingestion—increased intestinal absorption of calcium; stimulated bone resorption; increased renal tubular reabsorption of calcium; results in hypercalcemia (serum calcium > 12 mg/dL) and associated dystrophic calcification
Abnormal accumulation of vitamin D in the body, most commonly from ingesting vitamin D–containing rodenticides or other preparation or oversupplementation
PATHOPHYSIOLOGY
Cholecalciferol—fat-soluble vitamin; absorbed through chylomicrons and transported to the liver, where it is metabolized to 25-hydroxycholecalciferol, the major circulating metabolite during vitamin D excess; further metabolism occurs in the kidney, where calcitriol is produced.
Cholecalciferol and 25-hydroxycholecalciferol—limited biological activity
Calcitriol—most potent cholecalciferol metabolite in terms of enhancing calcium resorption from bone and intestinal calcium uptake
Excessive ingestion—increased intestinal absorption of calcium; stimulated bone resorption; increased renal tubular reabsorption of calcium; results in hypercalcemia (serum calcium > 12 mg/dL) and associated dystrophic calcification
Vitamin A Toxicity
OVERVIEW
Skeletal disease that occurs after excessive intake of vitamin A
High concentrations of vitamin A—inhibits intramembranous and endochondral ossification, resulting in dystrophic calcification of the skeleton
SIGNALMENT
Cats aged 2–9 years
No breed or sex predilections recognized
Skeletal disease that occurs after excessive intake of vitamin A
High concentrations of vitamin A—inhibits intramembranous and endochondral ossification, resulting in dystrophic calcification of the skeleton
SIGNALMENT
Cats aged 2–9 years
No breed or sex predilections recognized
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