OVERVIEW
Respiratory enteric orphan virus (reovirus)—genus in the family Reovirus; nonenveloped, double-stranded RNA virus; isolated from respiratory and enteric tracts; not associated with any known disease (hence orphan)
Ubiquitous in geographic distribution and host range, virtually every species of mammal, including humans
Virus—infects mature epithelial cells on luminal tips of the intestinal villi; causes cellular destruction, resulting in villous atrophy (similar to rotavirus and coronavirus)
Loss of absorptive capability and loss of brush border enzymes (e.g., disaccharidases) leads to osmotic diarrhea.
Tuesday, March 29, 2011
Q Fever
OVERVIEW
Caused by the zoonotic rickettsia Coxiella burnetii
Infection—most commonly by inhalation or ingestion of organisms while feeding on infected body fluids (urine, feces, milk, or parturient discharges), tissues (especially placenta), or carcasses of infected animal reservoir hosts (cattle, sheep, goats); can occur after tick exposure (many species of ticks implicated)
Lungs—thought to be main portal of entry to systemic circulation
Organism replicates in vascular endothelium; causes widespread vasculitis; severity depends on the pathogenicity of the strain of organism; vasculitis results in necrosis and hemorrhage in lungs, liver, and CNS
An extended latent period exists after recovery until chronic immune-complex phenomena develop; organism reactivated out of the latent state during parturition, resulting in large numbers entering the placenta, parturient fluids, urine, feces, and milk
Endemic worldwide
Caused by the zoonotic rickettsia Coxiella burnetii
Infection—most commonly by inhalation or ingestion of organisms while feeding on infected body fluids (urine, feces, milk, or parturient discharges), tissues (especially placenta), or carcasses of infected animal reservoir hosts (cattle, sheep, goats); can occur after tick exposure (many species of ticks implicated)
Lungs—thought to be main portal of entry to systemic circulation
Organism replicates in vascular endothelium; causes widespread vasculitis; severity depends on the pathogenicity of the strain of organism; vasculitis results in necrosis and hemorrhage in lungs, liver, and CNS
An extended latent period exists after recovery until chronic immune-complex phenomena develop; organism reactivated out of the latent state during parturition, resulting in large numbers entering the placenta, parturient fluids, urine, feces, and milk
Endemic worldwide
Pulmonary Mineralizations
OVERVIEW
Both calcification and ossification and may be generalized or localized
Discrete—if individual mineral deposits can be identified
Diffuse—preclude identification of individual deposits
Calcification—dystrophic or metastatic; dystrophic: occurs secondary to tissue degeneration or inflammation; metastatic: occurs secondary to metabolic disease; may be normal (e.g., the pleura in old dogs or premature calcification of the tracheal and bronchial cartilages in chondrodystrophic breeds); often a sign of inactivity of a lesion, thus most focal calcifications are functionally unimportant
Ossification—also called heterotopic bone formation; calcification of a bony matrix; pulmonary ossification in the form of small, multiple nodules (osteomas) common in normal dogs
Generalized pulmonary mineralizations of unknown cause—reported in dogs and cats under descriptive terms: pulmonary alveolar microlithiasis or pumice stone lung, bronchiolar microlithiasis, idiopathic pulmonary calcification or ossification
Both calcification and ossification and may be generalized or localized
Discrete—if individual mineral deposits can be identified
Diffuse—preclude identification of individual deposits
Calcification—dystrophic or metastatic; dystrophic: occurs secondary to tissue degeneration or inflammation; metastatic: occurs secondary to metabolic disease; may be normal (e.g., the pleura in old dogs or premature calcification of the tracheal and bronchial cartilages in chondrodystrophic breeds); often a sign of inactivity of a lesion, thus most focal calcifications are functionally unimportant
Ossification—also called heterotopic bone formation; calcification of a bony matrix; pulmonary ossification in the form of small, multiple nodules (osteomas) common in normal dogs
Generalized pulmonary mineralizations of unknown cause—reported in dogs and cats under descriptive terms: pulmonary alveolar microlithiasis or pumice stone lung, bronchiolar microlithiasis, idiopathic pulmonary calcification or ossification
Proteinuria
DEFINITION
A subjective increase in urinary protein detected by dipstick analysis; objectively, a urinary protein:creatinine ratio > 1 or a 24-h urinary protein content > 20 mg/kg
PATHOPHYSIOLOGY
Greater than normal delivery of low-molecular-weight plasma proteins to the glomerulus
Excessive leakage of proteins across the glomerular basement membrane secondary to altered permselectivity of the glomerulus
Reduced tubular reabsorptive capacity for proteins, or exudation of blood or serum into the lower urinary tract
A subjective increase in urinary protein detected by dipstick analysis; objectively, a urinary protein:creatinine ratio > 1 or a 24-h urinary protein content > 20 mg/kg
PATHOPHYSIOLOGY
Greater than normal delivery of low-molecular-weight plasma proteins to the glomerulus
Excessive leakage of proteins across the glomerular basement membrane secondary to altered permselectivity of the glomerulus
Reduced tubular reabsorptive capacity for proteins, or exudation of blood or serum into the lower urinary tract
Potassium, Hypokalemia
DEFINITION
Serum potassium concentration < 3.5 mEq/L
PATHOPHYSIOLOGY
Potassium is the major intracellular cation and thereby largely responsible for maintenance of intracellular volume.
The ratio of intracellular to extracellular potassium concentration is important in determining the cellular membrane potential. Rapid alterations in extracellular potassium concentration alter this ratio and predispose an animal to arrhythmias and conduction disturbances in excitable tissues (e.g., heart, nerve, and muscle)
Hypokalemia can be caused by excessive potassium loss via the gastrointestinal tract or kidneys or movement of potassium from the extracellular fluid compartment into cells (i.e., translocation).
Serum potassium concentration < 3.5 mEq/L
PATHOPHYSIOLOGY
Potassium is the major intracellular cation and thereby largely responsible for maintenance of intracellular volume.
The ratio of intracellular to extracellular potassium concentration is important in determining the cellular membrane potential. Rapid alterations in extracellular potassium concentration alter this ratio and predispose an animal to arrhythmias and conduction disturbances in excitable tissues (e.g., heart, nerve, and muscle)
Hypokalemia can be caused by excessive potassium loss via the gastrointestinal tract or kidneys or movement of potassium from the extracellular fluid compartment into cells (i.e., translocation).
Polyphagia
DEFINITION
Increased food intake
PATHOPHYSIOLOGY
Failure to assimilate or loss of nutrients (e.g., maldigestion/malabsorption syndromes such as EPI)
Inability to use nutrients (e.g., diabetes mellitus, poor quality diets, GI parasites)
Hypoglycemia (e.g., insulinoma, insulin overdose)
Increased metabolic rate or demand (e.g., hyperthyroidism, cold environments, pregnancy, lactation)
Psychologic or learned behaviors (e.g., palatable diets, competition, drugs such as anticonvulsants or glucocorticoids)
Increased food intake
PATHOPHYSIOLOGY
Failure to assimilate or loss of nutrients (e.g., maldigestion/malabsorption syndromes such as EPI)
Inability to use nutrients (e.g., diabetes mellitus, poor quality diets, GI parasites)
Hypoglycemia (e.g., insulinoma, insulin overdose)
Increased metabolic rate or demand (e.g., hyperthyroidism, cold environments, pregnancy, lactation)
Psychologic or learned behaviors (e.g., palatable diets, competition, drugs such as anticonvulsants or glucocorticoids)
Poisoning (Intoxication)
DEFINITION
Acutely ill patients are often diagnosed as poisoned when no other diagnosis is obvious.
Direct efforts toward stabilizing the patient.
Make the diagnosis after determining preexisting conditions and initially controlling clinical signs.
Goals of treatment—providing emergency intervention; preventing further exposure; preventing further absorption; applying specific antidotes; hastening elimination; providing supportive measures; offering client education
Suspected intoxication—suspected toxic materials and specimens may be valuable from a medicolegal aspect; maintain a proper chain of physical evidence; keep good medical records.
Valuable time can be saved by applying the appropriate treatment for a suspected or known intoxicant.
Acutely ill patients are often diagnosed as poisoned when no other diagnosis is obvious.
Direct efforts toward stabilizing the patient.
Make the diagnosis after determining preexisting conditions and initially controlling clinical signs.
Goals of treatment—providing emergency intervention; preventing further exposure; preventing further absorption; applying specific antidotes; hastening elimination; providing supportive measures; offering client education
Suspected intoxication—suspected toxic materials and specimens may be valuable from a medicolegal aspect; maintain a proper chain of physical evidence; keep good medical records.
Valuable time can be saved by applying the appropriate treatment for a suspected or known intoxicant.
Pneumonia, Bacterial
DEFINITION
The fully developed inflammatory response to virulent bacteria in lung parenchyma characterized by exudation of cells and fluid into conduction airways and alveolar spaces
PATHOPHYSIOLOGY
Bacteria—enter the lower respiratory tract primarily by the inhalation or aspiration routes; enter less commonly by the hematogenous route; infections incite an overt inflammatory reaction.
Tracheobronchial tree and lungs—normally not continuously sterile
Oropharyngeal bacteria—frequently aspirated; may be present for an unknown interval in the normal tracheobronchial tree and lung; have the potential to cause or complicate respiratory infection; cloud interpretation of airway and lung cultures
Respiratory infection—development depends on the complex interplay of many factors: size, inoculation site, number of organisms and their virulence, and resistance of the host
Viral infections—alter bacterial colonization patterns; increase bacterial adherence to respiratory epithelium; reduce mucociliary clearance and phagocytosis; thus may allow resident bacteria to invade the lower respiratory tract
Exudative phase—inflammatory hyperemia; serous exudation of high protein fluid into interstitial and alveolar spaces
Leukocytic emigration phase—leukocytes infiltrate the airways and alveoli; consolidation, ischemia, tissue necrosis, and atelectasis owing to bronchial occlusion, obstructive bronchiolitis, and impaired collateral ventilation
Mortality—associated with severe hypoxemia (low arterial oxygen concentration) and sepsis
The fully developed inflammatory response to virulent bacteria in lung parenchyma characterized by exudation of cells and fluid into conduction airways and alveolar spaces
PATHOPHYSIOLOGY
Bacteria—enter the lower respiratory tract primarily by the inhalation or aspiration routes; enter less commonly by the hematogenous route; infections incite an overt inflammatory reaction.
Tracheobronchial tree and lungs—normally not continuously sterile
Oropharyngeal bacteria—frequently aspirated; may be present for an unknown interval in the normal tracheobronchial tree and lung; have the potential to cause or complicate respiratory infection; cloud interpretation of airway and lung cultures
Respiratory infection—development depends on the complex interplay of many factors: size, inoculation site, number of organisms and their virulence, and resistance of the host
Viral infections—alter bacterial colonization patterns; increase bacterial adherence to respiratory epithelium; reduce mucociliary clearance and phagocytosis; thus may allow resident bacteria to invade the lower respiratory tract
Exudative phase—inflammatory hyperemia; serous exudation of high protein fluid into interstitial and alveolar spaces
Leukocytic emigration phase—leukocytes infiltrate the airways and alveoli; consolidation, ischemia, tissue necrosis, and atelectasis owing to bronchial occlusion, obstructive bronchiolitis, and impaired collateral ventilation
Mortality—associated with severe hypoxemia (low arterial oxygen concentration) and sepsis
Pneumocystosis
OVERVIEW
Pneumocystis carinii—saprophyte of the mammalian respiratory tract is whose life cycle completed in the alveolar spaces; classified as an atypical fungal organism based on analysis of nucleic acids
Infections—dogs, clinical; cats, subclinical; usually confined to the respiratory tract; a reported case of disseminated disease in a dog
Transmission—infected to susceptible animal within a species; strain differences may account for the lack of interspecies transmission.
Pneumocystis carinii—saprophyte of the mammalian respiratory tract is whose life cycle completed in the alveolar spaces; classified as an atypical fungal organism based on analysis of nucleic acids
Infections—dogs, clinical; cats, subclinical; usually confined to the respiratory tract; a reported case of disseminated disease in a dog
Transmission—infected to susceptible animal within a species; strain differences may account for the lack of interspecies transmission.
Plague (Yersinia pestis)
OVERVIEW
Yersinia pestis—gram-negative, bipolar staining rod; an Enterobacteriaceae; reservoir includes wild rodents (sylvatic), ground squirrels, prairie dogs, rabbits, bobcats, coyotes
Occurs worldwide
U.S.—reported cases from New Mexico, Arizona, California, Colorado, Idaho, Nevada, Oregon, Texas, Utah, Washington, Wyoming, and Hawaii
Common from May to October
Infected vectors (fleas) transmit the bacterium in bite.
Bacteria—rapidly migrate from skin lymphatics to regional lymph nodes; survive phagocytosis (because of capsule protection) and multiply in lymph nodes; phagocytic cells rupture and organism is resistant to further phagocytosis.
Infection—fever and painful lymphadenopathy (bubo); intense local inflammation results in bubonic plague; intermittent bacteremia; lymph nodes may rupture; may become septicemic with or without lymph node involvement
Cats—highly susceptible to infection; severe fatal disease
Dogs—naturally resistant to infection
Yersinia pestis—gram-negative, bipolar staining rod; an Enterobacteriaceae; reservoir includes wild rodents (sylvatic), ground squirrels, prairie dogs, rabbits, bobcats, coyotes
Occurs worldwide
U.S.—reported cases from New Mexico, Arizona, California, Colorado, Idaho, Nevada, Oregon, Texas, Utah, Washington, Wyoming, and Hawaii
Common from May to October
Infected vectors (fleas) transmit the bacterium in bite.
Bacteria—rapidly migrate from skin lymphatics to regional lymph nodes; survive phagocytosis (because of capsule protection) and multiply in lymph nodes; phagocytic cells rupture and organism is resistant to further phagocytosis.
Infection—fever and painful lymphadenopathy (bubo); intense local inflammation results in bubonic plague; intermittent bacteremia; lymph nodes may rupture; may become septicemic with or without lymph node involvement
Cats—highly susceptible to infection; severe fatal disease
Dogs—naturally resistant to infection
Perineal Hernia
OVERVIEW
Results from a defect in the musculature of the pelvic diaphragm
Allows herniation of retroperitoneal fat or pelvic viscera through the pelvic diaphragm
Organ systems potentially involved—GI, musculoskeletal, urologic, reproductive
SIGNALMENT
Much more common in dogs than cats
Almost exclusively (95%) male dogs
Usually older than 5 years of age
Boston terriers, collies, boxers, Pekingese, and mongrels overrepresented
Results from a defect in the musculature of the pelvic diaphragm
Allows herniation of retroperitoneal fat or pelvic viscera through the pelvic diaphragm
Organ systems potentially involved—GI, musculoskeletal, urologic, reproductive
SIGNALMENT
Much more common in dogs than cats
Almost exclusively (95%) male dogs
Usually older than 5 years of age
Boston terriers, collies, boxers, Pekingese, and mongrels overrepresented
Pericarditis
OVERVIEW
Inflammatory condition of the parietal (pericardial sac) and/or visceral (epicardium) pericardium; clinical syndromes caused by pericardial effusion, constrictive pericarditis, inflammatory extension to surrounding tissues (pleural, myocardium), or the underlying cause of the pericarditis
In dogs—most commonly seen as idiopathic hemorrhagic pericarditis, is a mild inflammatory condition that can lead to life-threatening pericardial effusion and tamponade
SIGNALMENT
Dogs and cats
Idiopathic hemorrhagic pericarditis more common in young to middle-aged, medium to large-breed dogs (e.g., great Pyrenees, Great Dane, Saint Bernard, golden retriever); males predisposed
Others depend on the underlying disease.
Inflammatory condition of the parietal (pericardial sac) and/or visceral (epicardium) pericardium; clinical syndromes caused by pericardial effusion, constrictive pericarditis, inflammatory extension to surrounding tissues (pleural, myocardium), or the underlying cause of the pericarditis
In dogs—most commonly seen as idiopathic hemorrhagic pericarditis, is a mild inflammatory condition that can lead to life-threatening pericardial effusion and tamponade
SIGNALMENT
Dogs and cats
Idiopathic hemorrhagic pericarditis more common in young to middle-aged, medium to large-breed dogs (e.g., great Pyrenees, Great Dane, Saint Bernard, golden retriever); males predisposed
Others depend on the underlying disease.
Pelvic Bladder
OVERVIEW
Describes a condition in which the neck of the bladder is located extremely caudally in the pelvic canal and the urethra is shortened or displaced; most often associated with incontinence in young intact female dogs, but some dogs with pelvic bladder do not exhibit urinary incontinence
SIGNALMENT
Dogs and rarely cats; the difference in prevalence between species is presumably because the cat has a longer urethra than a dog of similar size.
May occur in dogs of both sexes, either intact or neutered, but primarily affects young intact female dogs (< 1 year of age); usually detected in male dogs after neutering
Describes a condition in which the neck of the bladder is located extremely caudally in the pelvic canal and the urethra is shortened or displaced; most often associated with incontinence in young intact female dogs, but some dogs with pelvic bladder do not exhibit urinary incontinence
SIGNALMENT
Dogs and rarely cats; the difference in prevalence between species is presumably because the cat has a longer urethra than a dog of similar size.
May occur in dogs of both sexes, either intact or neutered, but primarily affects young intact female dogs (< 1 year of age); usually detected in male dogs after neutering
Parvoviral Infection - Dogs
DEFINITION
CPV-2 infection is an acute systemic illness characterized by hemorrhagic enteritis.
Often fatal in pups, who may collapse in a “shock-like” state and die suddenly without enteric signs, after only a brief period of malaise.
The myocardial form, observed in pups during the early outbreaks when the dog population was fully susceptible, is now rare.
Most pups are now protected against neonatal infection by maternal antibodies.
Monoclonal antibodies have revealed antigenic changes in CPV-2 since its emergence in 1978.
The original virus is now virtually extinct in the domestic dog population.
The viruses currently circulating in dogs, designated CPV-2a and CPV-2b, have been genetically stable since 1984.
These viruses are more virulent than the original isolates, and case mortality rates appear to be higher than in the earliest outbreaks.
Most of the clinical literature is based on the response of dogs to CPV-2 and should be reevaluated in light of the emergence and dominance of the newer types in dogs.
As with rabies variants, the antigenic changes in CPV-2 do not affect the ability of various vaccines to protect dogs.
CPV-2 infection is an acute systemic illness characterized by hemorrhagic enteritis.
Often fatal in pups, who may collapse in a “shock-like” state and die suddenly without enteric signs, after only a brief period of malaise.
The myocardial form, observed in pups during the early outbreaks when the dog population was fully susceptible, is now rare.
Most pups are now protected against neonatal infection by maternal antibodies.
Monoclonal antibodies have revealed antigenic changes in CPV-2 since its emergence in 1978.
The original virus is now virtually extinct in the domestic dog population.
The viruses currently circulating in dogs, designated CPV-2a and CPV-2b, have been genetically stable since 1984.
These viruses are more virulent than the original isolates, and case mortality rates appear to be higher than in the earliest outbreaks.
Most of the clinical literature is based on the response of dogs to CPV-2 and should be reevaluated in light of the emergence and dominance of the newer types in dogs.
As with rabies variants, the antigenic changes in CPV-2 do not affect the ability of various vaccines to protect dogs.
paralysis
DEFINITION
Paresis—weakness of voluntary movement
Paralysis—lack of voluntary movement
Quadriparesis (tetraparesis)—weakness of voluntary movements in all limbs
Quadriplegia (tetraplegia)—absence of all voluntary limb movement
Paraparesis—weakness of voluntary movements in pelvic limbs
Paraplegia—absence of all voluntary pelvic limb movement
PATHOPHYSIOLOGY
Weakness—may be caused by lesions in the upper or lower motor neuron system
Cell bodies or nuclei for the upper motor neuron system—located within the brain; responsible for initiating voluntary movement
Axons from these cell bodies—form tracts (rubrospinal, corticospinal, vestibulospinal, reticulospinal) that descend from the brain to synapse on interneurons in the spinal cord
Interneuronal axons—then synapse on large (a) motor neurons in the ventral gray matter of the spinal cord
Large motor neurons—cell bodies of origin for the lower motor neuron system, which is responsible for spinal reflexes
Collections of lower motor neurons in the cervical and lumbar intumescences—give rise to axons that form the ventral nerve roots, the spinal nerves, and (ultimately) the peripheral nerves that innervate limb muscles
Evaluation of limb reflexes—determine which system (upper or lower motor neuron) is involved
Upper motor neurons and their axons—inhibitory influence on the large motor neurons of the lower motor neuron system; maintain normal muscle tone and normal spinal reflexes; if injured, spinal reflexes are no longer inhibited or controlled and reflexes become exaggerated or hyperreflexic.
Large a motor neurons or their processes (peripheral nerves)—if injured, spinal reflexes cannot be elicited (areflexic) or are reduced (hyporeflexic).
Paresis—weakness of voluntary movement
Paralysis—lack of voluntary movement
Quadriparesis (tetraparesis)—weakness of voluntary movements in all limbs
Quadriplegia (tetraplegia)—absence of all voluntary limb movement
Paraparesis—weakness of voluntary movements in pelvic limbs
Paraplegia—absence of all voluntary pelvic limb movement
PATHOPHYSIOLOGY
Weakness—may be caused by lesions in the upper or lower motor neuron system
Cell bodies or nuclei for the upper motor neuron system—located within the brain; responsible for initiating voluntary movement
Axons from these cell bodies—form tracts (rubrospinal, corticospinal, vestibulospinal, reticulospinal) that descend from the brain to synapse on interneurons in the spinal cord
Interneuronal axons—then synapse on large (a) motor neurons in the ventral gray matter of the spinal cord
Large motor neurons—cell bodies of origin for the lower motor neuron system, which is responsible for spinal reflexes
Collections of lower motor neurons in the cervical and lumbar intumescences—give rise to axons that form the ventral nerve roots, the spinal nerves, and (ultimately) the peripheral nerves that innervate limb muscles
Evaluation of limb reflexes—determine which system (upper or lower motor neuron) is involved
Upper motor neurons and their axons—inhibitory influence on the large motor neurons of the lower motor neuron system; maintain normal muscle tone and normal spinal reflexes; if injured, spinal reflexes are no longer inhibited or controlled and reflexes become exaggerated or hyperreflexic.
Large a motor neurons or their processes (peripheral nerves)—if injured, spinal reflexes cannot be elicited (areflexic) or are reduced (hyporeflexic).
Papillomatosis
OVERVIEW
Papillomaviruses (PVs)—group of nonenveloped, double-stranded DNA viruses that induce proliferative cutaneous tumors in cats and dogs and mucosal tumors in dogs; each is host and fairly site-specific, with characteristic clinical and microscopic changes in infected tissues.
Tumors—papillomas, warts, or verrucae; generally benign; spontaneously regress; rarely may undergo conversion to SCC
Lesions—often multiple, well demarcated, and exophytic; sometimes hyperkeratotic plaques or with papules; may be deeply pigmented (black or brown), pink, tan, or white
Infection—inoculation through breaks in the epidermis or mucosal epithelium; iatrogenic transmission through use of contaminated instruments possible
Papillomaviruses (PVs)—group of nonenveloped, double-stranded DNA viruses that induce proliferative cutaneous tumors in cats and dogs and mucosal tumors in dogs; each is host and fairly site-specific, with characteristic clinical and microscopic changes in infected tissues.
Tumors—papillomas, warts, or verrucae; generally benign; spontaneously regress; rarely may undergo conversion to SCC
Lesions—often multiple, well demarcated, and exophytic; sometimes hyperkeratotic plaques or with papules; may be deeply pigmented (black or brown), pink, tan, or white
Infection—inoculation through breaks in the epidermis or mucosal epithelium; iatrogenic transmission through use of contaminated instruments possible
Pancreatitis
DEFINITION
Inflammation of the pancreas
Acute pancreatitis—inflammation of the pancreas that occurs abruptly with little or no permanent pathologic change
Chronic pancreatitis—continuing inflammatory disease that is often accompanied by irreversible morphologic change
PATHOPHYSIOLOGY
Most defense mechanisms prevent pancreatic autodigestion by the enzymes it secretes.
Under select circumstances, these natural defenses fail; autodigestion occurs when these digestive enzymes are activated within acinar cells.
Local and systemic tissue injury is due to the activity of released pancreatic enzymes and a variety of inflammatory mediators such as kinins, free radicals, and complement factors.
Inflammation of the pancreas
Acute pancreatitis—inflammation of the pancreas that occurs abruptly with little or no permanent pathologic change
Chronic pancreatitis—continuing inflammatory disease that is often accompanied by irreversible morphologic change
PATHOPHYSIOLOGY
Most defense mechanisms prevent pancreatic autodigestion by the enzymes it secretes.
Under select circumstances, these natural defenses fail; autodigestion occurs when these digestive enzymes are activated within acinar cells.
Local and systemic tissue injury is due to the activity of released pancreatic enzymes and a variety of inflammatory mediators such as kinins, free radicals, and complement factors.
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