GI, Liver, Pancreas, Gallblader Diseases Flashcards
Palatoschisis
cleft palate resulting in starvation (cant make negative pressure while nursing) or aspiration pneumonia
genetic (brachycephalic) or toxic (steroids, antifungals, antiseizures, Veratrum, lupine,) viral (canine distemper intrauterine infection or nutritional (excessive vitamin A or D)
occurs in dogs, horses, and cows
Cheiloschisis
cleft lip/ hair lip
What time frame does Veratrum californicum ingestion result in palatoschisis
on day 14 of gestation
What time frame of gestation does Lupine ingestion result in palatoschisis?
between days 40-50 of gestation
What is the cause of cleft palate (palatoschisis)
-Genetic (brachycephalic)
-Nutritional (excessive vit A or D)
-Drugs (Steroids, antifungals, antiseizure medications)
-Viruses (intrauterine infection of canine distemper)
-Toxic plants (Veratrum californicum- d14 or lupine d40-50)
Prognathism
developmental anomaly where extension or bulging out (protrusion) of the lower jaw (mandible). It occurs when the teeth are not properly aligned due to the shape of the face bones
Brachygnathia inferior
developmental anomaly where abnormal shortening of the mandible occurs
Agnathia
developmental anomaly where there is an absence of the mandible
Stomatitis
inflammation of the oral cavity
gingivitis
inflammation of the gingiva
glossitis
inflammation of the tongue
Pulpitis
inflammation of the tooth
Cheilitis
inflammation of the lip
pharyngitis
inflammation of the pharynx
What are the three infectious agents resulting in vesicular stomatitides?
1) Foot and Mouth Disease (picornavirus)
2) Vesicular stomatitis (Rhabdovirus)
3) Vesicular exanthema (Calicivirus)
What are the five infectious agents resulting in erosive/ulcerative stomatitides?
- Bovine viral diarrhea (pestivirus)
- Rinderpest (morbillivirus)
- Malignant catarrhal fever (herpes)
- Feline calicivirus
- Bluetongue (orbivirus)
Vesicular stomatitides
caused by virus-induced epithelial cytolysis leading to vesicles/bullae that rupture and erode leading to an ulcer/scab in the oral cavity
How do we sample oral lesions
-Punch/Wedge biopsies
What species is not susceptible to foot and mouth disease?
-Pigs
-Horses
-Cows
-Sheep
Horses
Can horses get foot and mouth disease?
No
What are causes of bacterial stomatitis?
-Actinomycosis: “Lumpy jaw”
-Actinobacillosis: “Wooden tongue”
-Necrobacillosis: ‘Calf diphtheria”
-Infectious stomatitis “mouth rot in reptiles’
What causes lumpy jaw
Actinomyces bovis
Lumpy Jaw
caused by actinomyces bovis
deep stomatitis and disfigured mandible
Pathogenesis: normal oral bacteria, invade through penetrating wounds, destroy bone (pyogranulomatous osteomyelitis)
What causes wooden tongue
Actinobacillus lingnieressi
Wooden Tongue
Caused by Actinobacillus lingnieressi
Tongue is very firm
Yellow granules exude from the ulcerated tongue surface (sulfur granules)
Necrobacillosis
focal or multifocial areas of oral necrosis
caused by fusobacerium necrophorum
Pathogenesis:
Trauma to oral cavity via mechanical trauma or primary viral infection leading colonization of F. necrophorum and coagulative necrosis
Mouth Rot
Infectious stomatitis of lizards, snakes, and turtles caused by stress leading to immunosuppression and normal bacterial overgrowth
Feline Lymphocytic Plasmacytic Stomatitis
Chronic gingivostomatitis with severe lymphoplasmacytic inflammation
affecting premolar/molar teeth (caudal oral mucosa lateral to palatoglossal folds
idiopathic (antigenic overstimulation +/- calicivirus)
tx: teeth extraction
How do you treat Feline Lymphocytic Plasmacytic Stomatitis
teeth extraction
What is the cause of Feline Lymphocytic Plasmacytic Stomatitis
idiopathic (antigenic overstimulation overstimulation +/- calicivirus)
Eosinophilic Stomatitis
Oral granulomas “rodent ulcers”
common in cats
occurs on lips, anywhere in the mouth
grouped into the eosinophilic granulomas complex
idiopathic, autoimmune cause
Neoplasms of the oral cavity in the dog
Melanoma (most common)
squamous cell carcinoma
fibrosarcoma
papilloma
Neoplasms of the oral cavity in the cat
Squamous cell carcinoma (most common)
fibrosarcoma
lymphoma
melanoma
Canine papilloma
generally papilloma virus induced
most common in younger dogs
may regress spontaneously
can look similar to papillary squamous cell carcinoma but would have evidence of histologic and/or radiographic evidence of invasion
Peripheral odontogenic fibroma
a neoplastic-like lesion of odontogenic mesenchyme
common in dogs and infrequent in cats
benign
Local excision is curative
Acanthomatous Ameloblastoma
a neoplastic like lesion
tumor of periodontal ligament
occurs in dogs
locally invasive- aggressive
Wide surgical excision is needed as recurrence is common
Does not metastasize
Gingival hyperplasia
very common in dogs, especially brachycephalic breeds
benign lesion
caused by trauma and irritation
Causes of trauma to the oral cavity
Physical (chewing, carrying heavy items, or trauma such as hit by vehicle or blunt force trauma)
Chemical (acid or alkali chemical burns)
Traumatic (electrocution)
Hypsodont teeth
teeth that continuously grow
horses, cheek teeth of ruminants, tusks of boars
Brachydont teeth
teeth that do not grow after eruption
Is enamel capable of regeneration and repair?
NO
Anodontia
a primary dysplasia where failure of development / agenesis of the teeth
Oligodontia
a primary dysplasia where too few teeth
Polyodontia
a primary dysplasia where supernumerary teeth
Enamel hypoplasia
a secondary dysplasia where the enamel is underdeveloped typically due to bovine viral diarrhea virus intrauterine infection, puppies of canine distemper virus, malnutrition, and vitamin/mineral deficits (Calcium, Vit A, C, D, phosphorus)
What can result due to abnormal wearing of the teeth
1) Wave mouth
2) Infection, loss, damage
3) Dental fractures
4) Surrounding soft tissue damage
What can result in the teeth being yellow?
Tetracyclines
What can result in the teeth being orange red
Porphyrins (heme components)
What can result in the teeth being brown
Fluorosis
Periodontal disease
common in dogs and sheep
Damage of gingiva and periodontal disease
Dental plaque (bacterial mass mixed with organic matrix and food)
Dental calculi or tarter - mineralized bacterial mass
Mineralized bacterial mass of periodontal disease
Dental calculi or tartar
Bacterial mass mixed with organic matrix and food
dental plaque
What is the result of periodontal disease?
-Tooth loss due to destruction of periodontal ligament
-Pulpitis
-Tooth root abscess
-Bacteremia leading to heart disease (endocarditis)
Ranula
a salivary gland disease where there is mucus extravasation
cyst involving the sublingual or submaxillary gland
Salivary cyst
distention of the salivary duct
Mucocele
pseudocyst in the glandular tissue (mucus extravasation)
Sialadenitis
inflammation of the salivary glands
Infectious causes of sialadenitis
1) Rabies
2) Canine distemper virus
3) Sialodacryoadenitis virus (Rats)
4) Salmonella typhisuis leading to suppurative parotid sialoadenitis (pigs)
Diseases of Salivary Glands
1) Sialadenitis due to infection or foreign body (grass awn)
2) Infarction
3) Sialolithiasis
4) Neoplasia
5) Mucocele
Sialolithiasis
when hardened mineral deposits formed in the salivary glands.
What are common neoplasms of a salivary gland?
-Adenoma
-Adenocarcinoma
-Mixed tumor
Lethal glossopharyngeal defect
“bird tongue”
congenital defect where the tongue is not as wide and rostral half of the tongue is folded medially where the papilla margins are
Choristoma of the tongue
a developmental tumor-like growth of microscopically normal tissue in an abnormal location.
hair on the tongue
Thrush
Candidiasis of the tongue
caused by canidida albicans
Infectious causes of glossitis
1) Candidiasis
2) Wooden Tongue (Actinobacillus linguieresii)
Uremic glossitis of carnivores
High Blood BUN (uremia) causes vascular damage/vasculitis leading to thrombosis and infarction +/- the caustic effect from ammonia due to urease-producing bacteria
Uremic glossitis of herbivores
High blood and salivary urea leading to GI bacteria split urea and ammonia causing local caustic effect
What is the most common cause of neoplasia of the tongue?
Squamous cell carcinoma
What type of cells make up the carnivore esophagus?
nonkeratinizing stratified squamous epithelium
What type of cells make up the ruminant, pig, and horse esophagus?
keratinizing stratified squamous epithelium
What species have an esophagus with nonkeratinizing stratified squamous epithelium
Carnivores
What animals have striated muscle in their esophagus?
Dogs and ruminants
What part of the esophagus has serosa?
only the abdominal portion
What portion of the horse esophagus is smooth muscle
aborad third distal 2/3
horses cannot vomit
Megaesophagus
primarily dogs and can be either
-Congenital: Persistent right 4th aortic arch (vascular ring) or idiopathic denervation
-Acquired: Neuromuscular (Myasthenia gravis or polymyositis), Chagas disease, Hypothyroidism, or lead poisoning
Chagas disease
a parasitic disease that can lead to acquired megaesophagus
Choke
esophageal obstruction
commonly over larynx, thoracic inlet, base of heart, and diaphragmatic hiatus
more common in large animals
Leads to: Perforation leading to pneumonia/pleuritis, cellulitis, stenosis, periesophageal adhesions
What are the 4 common sites for choke
-Over the larynx
-Thoracic inlet
-Base of heart
-Diaphragmatic hiatus
Bloat
increased intraabdominal pressure
prevents blood from returning to the heart
cervical part of esophagus becomes congested while the caudal part becomes blanched by blood being driven away
leading to a bloat line
Bloat line
a line in the esophagus caused by the cervical part becoming congested with blood from blood being prevented from returning to the heart and the caudal part having blood driven away (blanched)
Ulcerative esophagitis
full thickness mucosa destruction that can result in perforation
caused by:
1. Reflux (monogastric animals- aborad third linear ulcers)
2. Toxins (Cantharidin- blister beetles and spanish flies) or chemical burns
3. Viruses: papular stomatitis, BVDV, MCF
4. Trauma (foreign body or iatrogenic)
5. Parasitic: Gongylonema (ruminants and primates w intermediate host of cockroaches and dung beetles) or Gastrophilus nasalis (equids) or Spirocerca lupi (canids, intermediate host of dung beetles)
Spirocerca lupi
a parasite of dogs and canids that has an intermediate host of dung beetles
Produce nodules in the distal esophagus that then penetrate the aorta leading to rupture
granulomatous inflammation and fibrosis leading to neoplasia (fibrosarcoma and osteosarcoma)
Rarely hypertrophic osteopathy
What can cause esophageal sarcoma?
Spirocerca lupi
What can cause esophageal papilloma
bovine papilloma virus
What can cause esophageal squamous cell carcinoma
cows consuming bracken fern
cows with papilloma virus
Forestomach vs Stomachs
Forestomachs: House digestive flora for breaking down cellulose
Abomasum/C3/Stomach: Enzymatic and hydrolytic digestion of food. Non-glandular stomach- horses
Ruminal tympany
Bloat of the forestomach due to over-distention of the rumen due to accumulation of fermentation gases
Can be primary (frothy) or secondary (gaseous bloat)
Primary Ruminal tympany
Frothy bloat due to a change in diet to some types of legumes (alfalfa or grain concentrate) leading to a lower rumen pH and stable foam that mixes with rumen contents to block the cardia and failure to eructate and bloat
distended left paralumbar fossa
bloat line
Secondary Ruminal tympany
Bloat that is gaseous due to physical or functional obstruction (hairballs, plant fiber balls, lead substances, or sharp metal)
Stenosis of the esophagus
*Gases cant escape
Trichobezoar
a ruminal foreign body of hair (hairballs)
Phytobezoars
a ruminal foreign body of plant fiber balls
How can lead substances lead to secondary ruminal tympany
lead poisoning interferes with motility
What can lead to inflammation of the forestomachs?
1) Grain overload, rumen overload, lactic acidosis (Chemical rumenitis)
2) Sudden feed change
*Sequella of bacterial ruminitis (Fusobacteria necrophorum and Trueperella pyogenes) and mycotic ruminitis
What bacteria result in ruminitis after grain overload. lactic acidosis, or a sudden feed change?
Fusobacteria necrophroum
Trueperella pyogenes
Ruminitis-Liver Abscess
Result from rapidly fermentable grain leading to acidosis (low pH) and subsequent damage to mucosa from Fusobacterium necrophorum overgrowth leading to rumen wall abscess
Bacteria access and travel to the liver via the portal vein, causing liver abscesses
Result of Ruminitis-Liver Abscess complex
-Rumen wall abscess
-Multifocal hepatic abscesses
-Caudal vena caval pyemia (fatal septic embolism)
-Pulmonary embolic pneumonia and hemorrhage (rupture of pulmonary artery)
-Vegetative valvular endocarditis (tricuspid valve)
-Jugular thrombosis
Hemoptysis
coughing up blood, a result of rupture of the pulmonary artery due to septic embolism of ruminitis-liver abscess complex
What are the causative agents of mycotic ruminits
Aspergillus and Zygomyecetes (mucor)
Mycotic Ruminitis
caused by lactic acidosis, mechanical injury, or antibiotics (calves)
can be angioinvasive, resulting in infarction of the vessels
presents as circular well delineated lesions on the stomach wall
caused by aspergillus and Zygomycetes (mucor)
Vagal indigestion
function outflow problem from the forestomaches due to vagus nerve damage
Clinical signs: ruminoreticular distention
Can be type I-IV
I: lesions around vagus nerve (failure of eructation)
II: anatomical conditions resulting in failure of omasal transport
III: physical impaction of abomasum
IV: pregnancy related shifting of abomasum and partial forestomach obstruction
Type I vagal indigestion
lesions around the vagus nerve resulting in failure of eructation
Type II vagal indigestion
functional or anatomic conditions that result in failure of omasal transport
Type III vagal indigestion
Physical impaction of the abomasum leading to function outflow problem
Type IV vagal indigestion
Pregnancy related shifting of the abomasum and partial forestomach obstruction leading to a functional outflow problem of the forestomachs
Gastric Dilation and Volvulus
occur in large “barrel” chested dogs, rarely pigs, and guinea pigs
Causes: large means, postprandial exercise, hereditary
The dilated stomach and displacement (twisted) compresses on the diaphragm, vena cava and portal vein leading to decreased venous return and decreased cardiac output leading to shock
What causes gastric dilation and volvulus
Idiopathic but potentially large meals, postprandial exercise, hereditary
Gastric Dilation and Rupture
Horses with fermentable carbohydrates, lush pasture, excessive water intake
Aborad impaction (closer to stomach)
Grass sickness/dysautonomia
horses dropping really fast
Antemortem: hemorrhage, fibrin
PostMortem: clean tear
What species is gastric dilation and rupture common in?
Horses
How can you tell a gastric rupture in a horse is antemortem vs postmortem?
hemorrhage and fibrin in antemortem while clean tear in postmortem
LDA
Left displaced abomasum
mostly in dairy cows- seldom fatal but requires surgery, older high producers, post-calving period
leads to abomasal ulcers and fibrous adhesions due to HCl secretion from obstructions
How does LDA occur
left displaced abomasum occurs when animal is on a high grain diet and hypocalcemia leads to fermentation, atony, and production of gas, recent parturition, and displacement of abomasum to the cranial left abdomen leading to obstruction, HCl secretion, chloride sequestration, hypochloremia and metabolic alkalosis
What is a result of LDA?
abomasal ulcers and fibrous adhesions to the abdominal wall
short termL hypochloremia and metabolic alkalosis
What side of the body is the abomasum normally on?
the caudad right side
What is RDA
Right Displacement of the abomasum
Displaced to the right and dorsal with rotation (20% have volvulus) leading to vagus nerve trauma and vagal indgiestion
can be fatal
Is LDA or RDA more fatal?
RDA
What can result in gastric/abomasal impaction?
1) Low quality roughage - low water intake, poor mastication
2) Vagal nerve damage (vagal indigestion, pyloric stenosis)
3) Hypochloremia, hypokalemia, metabolic alkalosis
4) Abomasal empyting defect of Suffolk Sheep
Gastric ulcers
mucosal defect (partial thickness damage is erosion)
caused by foreign body, chemical, drugs (steroids or NSAIDS), stress, hepatic disease, vasculitis, gastritis, gastrinomas, mast cell tumors, Addison’s disease, equine ulceration syndrome, finely ground feed (pigs), idiopathic
Projectile vomiting
vomiting that is not accompanied by retching movements
True vomiting
accompanied with retching movements like contraction of abdominal wall and neck muscles and extension of the neck
What are the two main infectious causes of abomasitis in ruminants?
1) Clostridium septicum (Braxy) -hemorrhagic
2) Clostridium perfringens type A - ulcerative emphysematous
How does gastritis in pigs typically occur
hemorrhagic gastritis secondary to sepsis
What is the likely cause of hemorrhagic abomasitis and death due to endotoxemia
Clostridium septicum (Braxy)
What is the likely cause of ulcerative emphysematous abomasitis?
Clostridium perfingens type A
What oral tumor would have positive IHC labeling for melan A and PNL2?
melanoma
What three syndromes make up feline triaditis?
Inflammatory bowel disease (enteritis)
Cholangiohepatitis
Pancreatitis
Which hepatotoxic agent classically causes megalocytosis?
Pyrrolizidine alkaloid
What clostridial disease is associated with foci of necrosis, surrounding neutrophils and intrahepatic bacilli?
Clostridium piliforme
With cirrhosis of the liver what changes do you expect?
Parenchymal loss with fibrosis and nodular regeneration
Ruminant Haemonchosis
Caused by haemonchus contortus (sheep and goats) and haemonchus placei (cattle)
leading to blood loss
in heavy burden and lead to protein losing gastropathy leading to anemia and bottle jaw (submandibular edema)
Ruminant Ostertagiosis
Caused by O. Ostertagi (cattle) and teladorsagia circumcincta (sheep and goats)
*Lead to mucosal metaplasia/hyperplasia
Type I and II
Clinical signs: achlorhydria, diarrhea, hypoproteinemia, wasting
Type I Ostertagiosis
during July-September, typically in calves in their first grazing season
ingested larvae develop with arresting
Type II Ostertagiosis
during March to May, from the emergence of L4 stages ingested the previous autumn. from gastric glands within the abomasum
occurs months after larval ingestion
What gastric bot lives in the squamous portion of the horses gastric mucosa?
Gasterophilus intestinalis
What gastric bot lives in the glandular portion of the equine stomach and esophagus?
Gasterophilus nasalis
Draschia megastoma
equine stomach nematode that causes tumor like nodules and ulcers in the glandular mucosa
What can cause equine parasitic gastritis?
- gastric bots (gasterophilus intestinalus and nasalis)
- Draschia megastoma
- Trichostrongylosis
What neoplasms of the stomach are benign
Adenoma and Leiomyomas
What neoplasms do horses typically get in the stomach and are malignant?
Squamous cell carcinoma
What neoplasms do dogs typically get in the stomach and are malignant?
Adenocarcinomas
What neoplasms of the stomach are malignant?
- Squamous cell carcinoma (horses)
- Adenocarcinoma (Canine)
- Leiomyosarcoma
- Lymphoma (Abomasum)
Clinical signs of intestinal disease
- Anorexia
- Weight loss
- Poor hair coat
- Vomiting
- Belching/Flatulence
- Abdominal pain
- Changes in stool color and consistency (diarrhea)
Patterns of intestinal disease
-Normal
-Diffuse
-Regionally/locally extensive
-Multifocal
-Multifocal to coalescing
-Disseminated
Diarrhea
Secretion of abnormally fluid feces accompanied by an increased volume of feces and an increased frequency of defecation
can be inflammatory or non-inflammatory
1. Induce intestinal secretion
2. Induce inflammation
3. Invasion
Maldigestive/Malabsorptive Diarrhea
defective digestion/absorption leading to stools with increased osmolarity
-Dysfunction of intestinal loops, bacterial overgrowth, reduced gastric acidity
Osmotic diarrhea
Diarrhea exerted by luminal solutes such as undigested carbohydrates and proteins
Hypersecretive Diarrhea
Diarrhea where excessive intestinal fluid secretion induced by enterotoxins
Exudative Diarrhea
diarrhea from increased capillary or epithelial permeability
Deranged motility diarrhea
Diarrhea from either:
1) intestinal hypermotility leading to decreased intestinal transit time and malabsorption.
2) Decreased motility leading to increased intestinal transit time and subsequent bacterial overgrowth and malabsorption
Invasive and cytotoxin Mediated Diarrhea
diarrhea where bacteria ingestion results in cytotoxin release and acute inflammation results in diarrhea
Small Bowel Diarrhea
-Normal to mildly increased defecation frequency
-fecal volume is normal to increased
-no fecal mucus
-Melena present
-No tenesmus
-No urgency
-no dyschezia (difficulty pooping)
-Vomitting may be present
-Steatorrhea may be present (fat excretion)
Hematochezia
fresh blood passed in stool, often seen in large bowel diarrhea
What type of diarrhea had melena present
Small bowel diarrhea
What type of diarrhea often has mucus present?
Large bowel diarrhea
What type of diarrhea has a markedly increased frequency of defecation
Large bowel diarrhea
What type of diarrhea has a decreased fecal volume
large bowel diarrhea
Result of intestinal disease
1) Dehydration leading to hypoperfusion and shock
2) Metabolic acidosis
3) electrolyte imbalance
4) Hypoproteinemia leading to ascites
Broad causes of enteritis
1) Viruses- common in very young animals
2) Bacteria- primary or secondary to viral infections
3) Parasites - heavy burden
4) Dietary toxins (accidental or iatrogenic)
5) Allergies (food hypersensitivity)
6) Idiopathic (unknown causes)
7 Agents of bacterial enteritis
1) Clostridium
2) Mycobacterium avium spp. Paratuberculosis
3) Lawsonia intracellularis
4) Brachyspira hyodysenteriae
5) E Coli
6) Salmonella spp
7) Rhodococcus equi
What Clostridium enteritis results in enterotoxemia
Clostridium perfringens
What agent causes sudden death in well-nourished animals by necrotizing/hemorragic enterocolitis and toxemia. Growth favored by sudden feed changes, antibiotics, and fermentable feeds
Clostridium perfringes
What factors favor clostridial growth in the intestines?
Sudden feed changes, antibiotic, and fermentable feeds
C. perfringens type A
alpha toxin that causes necrohemorrhagic enteritis and abomasitis, hemorrhagic bowel syndrome
also antibiotic enteritis (horse and rabbits) and colitis X in horses
What causes antibiotic enteritis in horses and rabbits
Clostridium perfringens Type A
What is a cause of colitis X in horses
Clostridium perfringens Type A
What causes lamb dysentery?
Clostridium perfringens Type B (a, B, e toxins)
What does Clostridium perfringes Type C cause?
bloody diarrhea in neonates (esp piglets)
What can cause pulpy kidney disease and encephalomalacia in lambs?
Clostridium perfringes Type D (a, e toxins)
What Clostridium perfringens exotoxins can cause enteritis in lagomorphs and enterotoxemia in ruminants?
Clostridium perfringes Type E (a, l toxins)
How does pulp kidney (overeating) disease occur (type D)?
Rapid Diet Change (high in CHO)
Favors rapid growth of clostridial organisms massive toxin production
angiotoxin leads to endothelial damage
hemorrhages, encephalomalacia (symmetrical necrosis and hemorrhage and nephrosis
rapid death and decomposition of kidneys at a faster rate than that of the rest of the carcass
What is Clostridium difficile associated with
oral antibiotic use leading to colitis in horse (mucosal edema, congestion and hemorrhage)
What disease is caused by Clostridium piliforme
Tyzzer’s disease
What clostridium species causes enterocolitis and hepatitis in rodents, foals, dogs, and cats typically less than 1 month of age
Clostridium piliforme (Tyzzer’s disease)
What bacteria has a criss-crossed/haystack appearance and causes enterocolitis and hepatitis?
Clostridium piliforme (Tyzzer’s Disease)
What is a common agent that causes mycobacterial enteritis?
Mycobacterium avium spp. Paratuberculosis (Johne’s Disease)
How is Mycobacterium avium spp. Paratuberculosis transmitted
oral and transplacentally
What does Mycobacterium avium spp. Paratuberculosis infection lead to?
Johne’s Disease characterized by chronic wasting disease, diarrhea. malabsorption and cytokine effects
diffuse granulmatous enteritis with prominent mucosal folds due to expansion of lamina propria by macrophages
Granulomatous lymphangitis and lymphadenitis
How does Mycobacterium avium spp. Paratuberculosis infection differ in sheep/goats versus cows
Diarrhea may not occur in sheep/goats. Hepatitis is much more likely and caseating granulmomas of the tuberculoate form and lymphangitis
What are the histological findings of Mycobacterium avium spp. Paratuberculosis infection
1) thickening of lamina propria by macrophages and multinucleated giant cells
2) acid-fast bacilli (Mycobacterium) within macrophages
3) Granulomatous inflammation can lead to mineralization of tissue, such as the aorta
Goat/Sheep Johne’s
typically isn’t diarrhea but have caseating granulomas and lymphangitis and granulomatous hepatitis
What is the mechanism of diarrhea in Johne’s disease
inflammatory, malabsorption
What causes proliferative ileitis in pigs?
Lawsonia intracellularis
proliferative ileitis in pigs
Caused by lawsonia intracellularis
affects pigs >4weeks
ileium is affected
Proliferative hemorrhagic enteropathy (large hemorrhagic cast in the lumen of thickened ileum with corrugated serosal surface
gross lesions of ileum: markedly thickened intestinal wall with cobblestone or cerebriform appearance
Is lawsonia intracellular more likely to affect pigs greater of less than 4 weeks
Greater than 4 weeks
What pathogen gives the gross lesion of cobblestone or cerebriform appearance in the intestinal wall of ileum due to mucosa being covered bt fibrinonecrotic (diphthertic) pseumembrane or cast
Lawsonia intracellularis
What part of the intestine does Lawsonia intracellularis typically affect in the pig?
Ileum
Lawsonia intracellularis histologic lesions
hyperplasia of crypt epithelium (tortuous) with crypt necrosis and hyperplasia
Silver stain highlights intracellular curved or slight spiral organisms in the apical cyotplasm of enterocyte
What is cause of intracellular curved or slight spiral organisms in the apical cytoplas of enterocytes causing hyperplasia and necrosis of crypt epithelium
Lawsonia intracellularis
What is the cause of swine dysentery
Brachyspira hyodysenteriae
Where part of the intestine does Brachyspira hyodysenteriae typically affect in pigs
Colon
Swine dysentery
Cause: Brachyspira hyodysenteriae
Pigs 8-14 weeks old
Colon affected
Gross lesions: bloody diarrhea, fibrinonecrotic pseudomembranes
Histolesions: Luminal spirochetes (silverstain)
E. Coli (Colibacillosis)
Neonatal pigs and calves most affected
Stress, overcrowding, infection with other pathogens
Types: ETEC, EHEC, Edema disease (enterotoxemic), Septicemic (EIEC), Enterpathogenic (EPEC,AAEC)
Edema disease (enterotoxemic colibacillosis)
Pigs 6 to 14 weeks old
E coli infection that produces an enterotoxin (verotoxin)
toxin produced in the small intestine then spreads hematogenously
Clinical signs neurologic signs, edema
What species is most affected by Salmonellosis
Horses
Cats and dogs on a raw diet
Salmonellosis
Acute, chronic, carrier
All species but esp horses or cats/dogs on raw diet
Small and large intestine
Gallblader
Mesenteric lymph nodes
What is the best tissue to culture Salmonellosis
Mesenteric lymph nodes
What animals are most affeced by peracute Salmonella septicemia
Young animal
acute necrosis of the blood vessels
What causes acute fibrinous cholecystitis in calves
Salmonella dublin
Acute Enteric Salmonellosis
Catarrhal enteritis with diffuse fibrinonecrotic ileotyphlocolitis
Mesenteric lymphadenopathy
fibrinous cholecystitis in calves with Salmonella dublin
What makes you highly suspicious of Salmonella Dublin
Fibrinous cholecystitis
Chronic enteric salmonellosis
lesion of pigs after chronic infection
button ulcers on the colon
Rectral strictures that can cause obstruction
What can cause rectal strictures that can lead to obstruction in pigs
chronic enteric salmonellosis
What is a likely result of cats on raw diets
Salmonella septicemia
Can nondiarrhea cats still shed salmonella
yes
Rhodococcus entercolitis in foals
Caused by Rhodococcus equi
Suppurative bronchopneumonia
Ulcerative colitis and pyogranulomatous lymphadenitis
What causes ulcerative colitis and pyogranulomatous lymphadenitis as well as suppurative bronchopneumonia is foals
Rhodococcus equi
What group pathogens are common in young animals and can compromise the GI mucosa resulting in secondary infection?
Viral enteritis
T/F some viruses can cause immunesuppression
True
What is the tropism for Parvovirus
Mitotically active cells suchs as
1) Crypts (immature secretory crypt epithelium)
2) Peyer’s patches (destruction of secondary lymphoid tissue)
What is the tropism for enteric Coronavirus
1) Tips and middle of villi resulting in fusion
2) Crypt epithelium leading to hyperplasia
3) Both small and large intestines
What is the tropism for Rotavirus
1) Upper two thirds of intestinal villi
2) Only small intestine
3) Vacuoliation of enterocytes
What portion of intestine does Rotavirus affect
Only the small intestine at the upper two thirds of the intestinal villi leading to vacuolation of enterocytes
Rotavirus enteritis pathogenesis
1)Fecal-oral route transmission
2) Viral replication in mature enterocytes
3) Necrosis and sloughing of absorptive cells
4)Villous atrophy
5) Maldigested/malabsorptive diarrhea
*Young animals
What diarrhea does Rotavirus lead to
Maldigested/malabsorptive diarrhea due to necrosis of absorptive cells
Rotavirus lesions
Possible only diarrhea grossly (hemorrhages, serosal glass appearance)
Histologically: villus blunting as rate of enterocyte loss exceeds replacement
What species does coronavirus enteritis typically affect
primarily a cat and pig disease
How is coronavirus enteritis spread
Fecal/oral spread through environmental contamination and fomites
Coronavirus enteritis pathogenesis
1)Ingestion
2) 1 to 4 day incubation
3) 2 days post-infection, virus enters and colonizes enterocytes of the upper duodenum
4) Spreads caudally through the small intestine and colon
5) Villus blunting and crypt hyperplasia
What part of the intestine does coronavirus affect?
Both the large and small intestine
villus blunting and crypt hyperplasia
Porcine coronavirus enteritis
Transmissible gastroenteritis (TGE)
highly contagious with high mortality in pigs less than 1 day
Gross: thin, gas or fluid filled intestine
Histology: severe villous atrophy
Feline coronavirus enteritis
generally mild and self-limiting disease of neonates ages 2 to 7 months
rarely fatal
repeat infection and long term shedders
Mutated virus and abnormal immune response can result in feline infectious peritonitis virus (FIP)
What is the gold standard diagnosis for Feline coronavirus enteritis
Immunohistochemistry
What is your #1 differential for a calf enteritis under 5 days old
Acute enterotoxigenic colibacillosis (ETEC)
Does Parvovirus 1 or 2 cause parvovirus enteritis
Canine parvovirus enteritis (CPV-2)
Canine parvovirus-2
a strain of feline panleukopenis virus (FPV) that infects dogs
virus receptor binding determines host susceptibility to parvovirus (transferrin receptor)
intersititial myocarditis in puppies is rare
Clinical signs of Canine parvovirus-2
Vomiting, diarrhea, sudden death from infection of intestinal crypts
Myocardial necrosis to puppies born to unvaccinated bitches and infected up to 8 weeks of age
Bone marrow and lymphoid depletion leading to immune suppression
How might you get myocardial necrosis of puppies with CPV-2
Puppies are born to unvaccinated bitches (no maternal antibodies)
Infected up to 8 weeks of age where the myocytes are still undergoing cell division
Lesions of CPV-2 infection
1) Serosal hemorrhage
2) Mucosal hemorrhage
3) Crypt necrosis
4) Immunohistochemical staining of parvovirus antigen in crypt epithelium
5) Myocardial necrosis
What affects on the host do nematodes have with intestinal infection
-Indirect undernourishment (Competition for nutrients)
-Local irritation (enterocolitis)
-Obstruction of gut lumen (if large burden)
-Loss of blood (anemia)
-Migration to other vital sites
Death due to Parascaris equorum infection is often due to:
A) Diarrhea and dehydration
B) Impaction and perforation
C) Salmonella spp
D) Poor doing and weight loss
Impaction and perforation
What ascarid commonly infects pigs
Ascaris suum
What is a sequela of Ascaris suum and Toxocara canis
Intestinal impaction +/- perforation
3 ways Ascarids are transmitted
1) Intrauterine
2) Through milk
3) ova - fecal - oral
*Larvae then penetrate the intestine and migrate to the liver
Ocular toxocariasis or neural larva migrans
a risk of zoonotic nematodes
What are the sequela of Ancylostoma caninum (hookworm) infection
hemorrhagic enteritis, anemia
Small strongyles in equine
cyathostomin parasites where larva emerge from the large intestinal walls (cecum and colon)
Large emegence of L4 can result in typhocolitis
What can result in typhocolitis of the horse?
Small strongyles/Cyathostomin parasites from the large emergence of L4 larva
Strongylus vulgarus in the horse can result in:
1) Verminous arteritis
2) Eosinophilic endarteritis with aneurysm
3) Non-strangulating intestinal infraction
What can cause verminous arteritis in the horse
Strongylus vulgarus
Larval Cyathostomosis
Synchronous development of arrested larvae and amergence of L4s leading to catarrhal or hemorrhagic enteritis and protein losing enteropathy
What are the sequela of Anoplocephala perfoliate infection in the horse
intussuception, impaction or rupture of the ileo-cecal valve
Coccidiosis
typically affect poultry, ruminants, and pigs
age: young
lesion: proliferative, hemorrhagic or necrotic lesions
Clinical signs: Poor doing associated with diarrhea
T/F coccidious can cause hemorrhagic enteritis
T
T/F enterocytes rupture in all stages on the coccidiosis life cycle
T
What is the pathogenic species of Eimeria in camelids
Eimeria macusaniensis
Eimeria macusaniensis
Pathogenic species of Eimeria in camelids
Usually young animals
Clinical signs: colic, protein losing enteropathy, does not usually cause diarrhea, Weight loss, death
difficult to do fecal flotation
Is Cryptosporidiosis from C. parvum zoonotic?
Yes
Cryptosporidiosis
Lines the surface of enterocytes
Histolesions: decreased villus height and fusion, hyperemia, increased mononuclear inflammation of the mucosa
Zoonoti
Giardiasis
Malabsorption due to damage to the microvillous border
Can be subclinical
Zoonotic
What kind of diarrhea does Giardia cause
Malabsorptive due to damage to the microvillous border
Pythium insidiosum
fungus like - water mold
usually affects the GI tract of dog but can also occur in skin
Leads to abdominal mass +/- obstruction
Oomycetes (Pythiosis)
Granulomatous inflammation with non-staining organims
Cause: Pythium insidiosum
Usually affects the GI tract of dogs (can also occut on skin)
Finding: abdominal mass +/- obstruction
What about history is important when considering diarrhea?
1) Number of animals affected
2) Duration, colic/diarrhea/vomiting, color of it
3) indoor vs outdoor, antibiotics treatment
4) Change in diet, indiscriminate eater
5) Access
Pulpy kidney and encephalomalacia in lambs in caused by what C. perfingens
Type C (A, e toxins)
Inflammatory bowel disease
Lymphoplasmacytic enteritis/gastroenteristis leading to malabsorption and protein losing enteropathy
Presence of eosinophils can suggest atopy or food hypersensitivity
What can cause Protein Losing Enteropathy
1) Physical or functional lymphatic obstruction
2) Cellular mediator release that increases vascular permeability
3) Mucosal inflammation
4) Increased pressure in lymphatics
PLE
Loss of albumin +/- loss of globulins, antithrombin, magnesium, calcium, cholesterol
can look like shag carpet grossly and will be float in water
caused by lymphatic obstruction, cellular mediator release that increases vascular permeability, mucosal inflammation, or increased pressure in lymphatics
Leading to diarrhea, vomiting, weight loss, edema, effusion, hypercoagulable state
What can result in protein losing enteropathy
-Diarrhea
-Vomiting
-Weight loss
-Edema
-Effusion
-Hyper coagulable state
What dog breeds does histiocytic ulcerative colitis or granulomatous colitis typically occur in?
Young boxers and french bulldogs
Boxer Colitis
Histiocytic ulcerative colitis or granulomatous colitis seen in young Boxers
Leads to blood mucoud diarrhea, anemia, hypoalbuminemia, and weight loss
Caused by infiliration of histiocytes that contain PAS positive material
Caused by invasive E Coli
Histiocytic ulcerative colitis /granulomatous colitis
seen in young Boxers
Leads to blood mucoud diarrhea, anemia, hypoalbuminemia, and weight loss
Caused by infiltration of histiocytes that contain PAS positive material
Caused by invasive E Coli
What is the cause of Histiocytic ulcerative colitis /granulomatous colitis
invasive E Coli leading to the infiltration of histiocytes that contain PAS positive material
How can you diagnose histiocytic ulcerative colitis
With the Periodic Acid Shift stain
What can cause right dorsal colitis in horses
NSAIDs
What might happen if a horse ingests blister beetle with cantharidin
necrohemorrhagic enteritis
Atresia
complete occlusion as seen in with
Atresia ilei
Atresia coli
Atresia ani
Leads to abdominal distension and obstruction
Persistent Meckel Diverticulum
Derived from the omphalomesenteric duct (stalk of the yolk sac)
Can be confused with the cecum
No importance clinically
What is the clinical importance of a Persistent Meckel Diverticulum
there is none, other than it gets confused with the cecum
White lethal foal syndrome
Inherited autosomal recessive disorder seen in paint horses leading to a mutation in the endothelin receptor B gene
Aganglionosis
Absence/Reduction of ganglion cells of the myenteric plexus (hypocellular) causing constipation and stasis and enterocolitis
What is another name for Aganglionosis
White lethal foal syndrome
Obstruction and Function Disorders
1) Obturation or occlusion (luminal) - plication
2) Compression (outside)
3) Stenosis (Stricture or scarring
4) Displacements
5) Functional (ileus or absence of peristalsis)
Intussusceptum
the entrapped segment during intussusception
Intussuscipiens
the enveloping segment during intussusception
Intussusception
telescoping to the intestine where the ileium telescopes inside ascending colon obstructing the intestinal contents and can cause blooding
blood vessels become trapped between layers leading to edema, strnagulation of bowel, gangrene, sepsis, shock, and death
causes: irritability, hypermotility
Causes of intussusception
irritability and hypermotility
Intestinal Torsion
Rotation along the long axis
can cause luminal and vascular compromise - infarction
results in a sharp line of demarcation due to obstruction of venous blood flow
Volvulus
twisting on the mesenteric axis
can cause luminal and vascular compromise - infarction
What is the sequela to vascular compromise to the intestine?
-Increased intestinal permeability
-Endotoxemia
-Sepsis
-Rupture
-Peritonitis
Different kinda of intestinal displacements
1) Equine colonic displacement
2) Displacement and entrapment (Equine epiploic foramen entrapment and hernias- umbilical, diaphragmatic, inguinal, scrotal)
3) rectal prolapse
Common intestinal neoplasms
-Lymphoma
-Adenoma/Adenocarcinoma
-Sarcomas
-Carcinoids
-Polyps
Intestinal/Alimentary lymphoma
Soft, white to tan, homogenous, soft mass or diffuse thickening of the GI wall leading to stenosis and ulceration
What is the most common GI neoplasm of cats and ruminants leading to stenosis and ulceration
Intestinal/alimentary lymphoma
What is the most common GI neoplasm in dogs and sheeps?
Intestinal adenocarcinoma
often have metastasized by diagnosis
Mesenchymal neoplasms of the GI tract
leiomyoma, leiomyosarcoma, gastrointestinal stromal tumors, hemangioma/hemangiosarcoma
What effect can mast cell tumors have on stomach and GI tract
predispose to gastric and GI ulceration and perforation
What do beavers have near their esophagus
cardiogastric gland, normal stricture, near the oesophagus entrance
Hepatic stricture
epithelium cells from the hepatic diverticulum and mesenchymal stroma surrounds vessels of the vitelline venous plexus
Caudal hepatic diverticulum develops into the gallbladder
Hepatocytes and biliary epithelial cells share_____
a common embryonic origin
Hepatic artery
supplies oxygen rich blood to the liver. approx 20% of blood to the liver
Blood leaves the liver through the hepatic vein which quickly enters the ________
caudal vena cava
Stellate (Ito) cells
Cells in the liver that store vitamin A and play a role in hepatic fibrosis
What do the stellate (ito) cells store
Vitamin A, play a role in hepatic fibrosis
Oval cell
Cells of the liver, of bone marrow origin, function in liver regeneration
differentiate into hepatocytes and biliary cells
Space of Disse
gap between endothelial cells and hepatocytes
What separates hepatic plates?
vascular sinusoids
Why are there microvilli of hepatocytes
take in, produce, and move products out
Kupffer cells
resident histiocytes
clear infectious agents and senescent cells
involved in cytokine driven interactions with hepatocytes, endothelial cells, lymphocytes and stellate cells
can function as antigen presenting cells
What are the resident histiocytes of the liver
Kupffer cells
What way does bile move in the liver
opposite of the flow of blood
from the centrilobular area through midzonal to the periportal area (inner to outer)
Zonal necrosis of the liver
pattern of hepatocellular degeneration and necrosis where it is pale, enlarged, friable, and enhanced lobular patter
1) Centrilobular (periacinar, zone 3) is the least oxygen in region and susceptible to hypoxia, seen with severe anemia or right sided heart failure. Also has the greatest enzymatic activity where activated compounds are turned into toxic forms
2) Midozonal necrosis: seen in pigs and horses with aflatoxicosis
3) Toxin exposure lacking requirement of metabolism by oxidases
What portion of the liver is most susceptible to hypoxia
Centrilobular, receives the least amount of oxygen
What portion of the liver is damaged in pigs and horses with aflatoxicosis
Midzonal
What portion of the liver has the greatest enzymatic activity and therefore targeted when metabolism is needed for activation of toxic metabolite
Centrilobular
What portion of the liver is most susceptible to immediate toxins that do not need to metabolized to be toxic?
Periportal because these cells lack oxidases and therefore are not readily broken down here
Bridging necrosis (Liver)
can link centrilobular areas or centrilobular to periportal areas
confluent areas of liver necrosis
Massive necrosis (liver)
Necrosis of the entire hepatic lobule
Regeneration does not occur because all hepatocytes in the lobule are affected
Can regeneration occur when all hepatocutes in a lobule are affected?
NO
What is a common cause of random necrosis?
infectious agents
Individual cell necrosis results in ______
proliferation and regeneration of hepatocytes
What area of pattern of necrosis is it if necrosis is occuring around the portal vein?
Zonal, periportal necrosis
Massive necrosis inhibits_______
hepatic replication. replacement occurs through the ductular reaction
What does prolonged liver regenerative effort with damaged reticulin result in?
nodular proliferation which distorts the architecture
Parenchymal regeneration of the liver can occur if_____
normal reticulin scaffolding remains intact without collapse
Hepatic fibrosis
occurs in hepatic injury
collagen scaffolding can extend into parenchyma
Stellate cells change towards a myofibroblastic function producing collagen synthesis
Perisinusoidal fibrosis affects hepatic function with capillarization of the sinusoids
What stains can be used for hepatic injury evaluation?
Trichrome (Blue stains collagen) and Reticulin (Tells if you have collapse of lobule)
Periacinal hepatic fibrosis can occur with _____
toxic injury and chronic passive congestion
Periportal fibrosis can result from______
chronic inflammation and some toxins
What can result in multifocal hepatic fibrosis
migrating nematodes
Hepatic cirrhosis
a diffuse process characterized by fibrosis and conversion of normal liver architecture into structurally abnormal lobes
-Parenchymal loss with increased reticulin network
-Fibrous tracts
-Hepatic regeneration between fibrous bands
-Vascular alterations such as acquired portosystemic shunts
What can 5 things can cause hepatic cirrhosis
1) Chronic toxic insult
2) Chronic hepatitis or cholangitis
3) Chronic biliary obstruction (typically portal)
4) Chronic passive congestion (central vein fibrosis)
5) Inherited disorders (copper, iron, dissecting hepatic fibrosis)
At end stage liver cirrhosis can you determine the inciting causes?
NO
Portal hypertension induced hepatic injury
diffuse liver fibrosis with chronic injury due to increased portal blood flow resistance and pressure elevation
collateral vascular channels open, shunting of portal vein into the central vein
Can lead to ascites. enhanced by hypoalbuminemia as (enhanced loss into intestinal lumen and reduced albumin synthesis)
If a patient presents with ascites, what likely happened
portal hypertension, shunting of blood from portal vein into the central vein through collateral vasculars
enhanced by hypoalbuminemia
Canaliculi
within the centrilobular (periacinar areas)
drain to canals of Herring lined by hepatocytes and biliary epithelium
then to cholangioles which drain to intralobular bile ducts
Flow of Bile
Canaliculi > Canals of Herring > intralobular bile ducts > gallbladder via common hepatic ducts
3 functions of Bile
1) Excretory- waste products eliminated in the bile
2) Digestion- intestinal secretions aid in the digestion of lipids within the intestine
3) Buffers- neutralizes the pH of ingesta released from stomach
What is the difference between cholestasis and hyperbilirubinemai
Cholestasis: blockage of bilirubin flow
Hyperbilirubinemia: increased bilirubin (conjugated or inconjugated) in blood
Where does bilirubin conjugation occur?
in the liver
Causes of prehepatic hyperbilirubinemia
Hemolysis- too much bilirubin for excretion
Causes of intrahepatic hyperbilirubinemia
1) liver injury affection the ability of hepatocytes to metabolize and excrete bile
2) Inherited abnormalities of bile synthesis inhibiting excretion
Causes of extrahepatic hyperbilirubinemia
-Obstruction of extrahepatic bile ducts
Intraluminal-calculi, parasites or
Extraluminal- neoplasia, adjacent inflammation (pancreatitis)
Icterus/jaundice
yellow discoloration of the tissues when bilrubin concentration must reach 2mg/dL
Maximus accumulation takes 2 days
What might you see if a horse has been deprived of feed for multiple days
icterus as hepatic bilirubin uptake is decreased
You are performing a necropsy on an animal with icterus. What systems will you check for the cause of icterus
Prehepatic: Spleen, blood, urinary tract
Hepatic: Liver
Post-Hepatic: Gallbladder, cystic duct, Duodenal papilla
Liver zone 1
Periportal area, low enzymatic activity
Liver zone 2
Midzonal area between the centrilolobular and portal areas
Liver zone 3
Centrilobular areas, least amount of oxygen, greatest enzymatic activity
Circulatory disorders of the liver
1) Disturbances of outflow (passive or venous congestion
2) Disturbances of inflow (Anemia, congenital porto-systemic shunts, portal hyper tension
3) Incidental (Telangiectasia)
4) Infarction- liver lobe torsion
How might acute passive liver congestion occur
acute right sided failure, can result in nutmeg liver
How might chronic passive liver congestion occur
valvular endocardiosis in dogs
What can chronic passive liver congestion lead to
Centrilobular hypoxia leading to atrophy (Degeneration, necrosis), sinusoidal ocngestion, periportal hepatocellular steatosis, and bridging hepatic fibrosis
Hepatic Steatosis
buildup of fat in the liver, can be from chronic passive congestion or other reasons tba
Would you expect passive congestion to cause icterus?
No, its an issue of blood flowing out of the liver
What clotting factors are made in the liver
5, 7, 9, 10
Bleeding tendencies with liver disease
-Impaired synthesis of clotting factors
-Reduced clotting products (fibrin degradation products, activated coagulation factors, plasminogen factors)
-Metabolic abnormalities affecting platelet function
*Clotting factors made in liver
Chronic disease factor II also deficient (Biliary obstruction, impaired fat absorption limiting vitamin K uptake from the intestine > inactivity of factor 2, 7, 9, 10
What clotting factors are impacted with biliary obstruction
impaired fat absorption (affects 2, 7, 9, 10)
Liver failure has reduced production of factors 5, 7, 9, 10. What other factor do you also see affected in biliary obstruction due to limited vitamin K uptake from the intestine
Factor II
What region of the hepatic lobule is most severely affected by anemia?
Centrilobular region
Congenital portosystemic shunts
Blood is shunted from the abdominal organs to the systemic circulation, bypassing the liver
Liver is unable to metabolize and detoxify the blood. Deprived of factors to enhance development (hepatic atrophy and insufficiency)
Can lead to stunted, hepatic-encephalopathy (ammonia) and ammonia biurate crystals
What dogs do you typically see single extrahepatic shunts in
Small and toy breeds
Portal vein to caudal vena cava, portal vein to azygous vein
What dogs do you typically see single intrahepatic shunts in?
Large breeds
Failure of ductus venosus to close at birth (often left side of liver)
What do you typically see with congenital portosystemic shunts in cats?
almost always extrahepatic and left gastric is the most common
What can lead to an acquired portosystemic shunt?
hepatic hypertension leading to multiple vessels being impacted
Intrahepatic shunts
failure of ductus venosus to close at birth
most commonly large breed dogs
left side of liver
Extrahepatic shunts
portal vein to the caudal vena cava
portal vein to azygous vein
small breeds of dogs and cats
What is a result of congenital portosystemic shunts
-Stunted
-Hepatic encephalopathy
-Hepatic atrophy and insufficiency
-Abnormal plasma ammonia leading to ammonia biurate crystals in the urine
What has the same histological lesions as a portosystemic shunt
Portal vein hypoplasia (microvascular dysplasia) leading to diminished hepatic perfusion leading to portal hypertension
Use clinical data, antemortem imaging, and portal vein pressure for dx.
Hepatic microvascular dysplasia (HMD)
histological diagnosis when ruled out portosystemic shunt
dogs are often 3-4 years of age
bloodwork less severe
Yorkshire and Cairn terrier most commonly affected but other small breeds are
Definitive diagnosis: proving dogs do not have any shunts but do have abnormal vessels on hepatic biopsy
some dogs can have both
Hepatic encephalopathy
Neurologic disease (depression, behavioral changes, convulsion) associated with hepatic failure
Unknown metabolites and increased plasma ammonia
Amines are absorbed from the intestine into the portal blood and not appropriately metabolized by the diseased liver
Toxic effects on the brain, seen in congenital or acquired shunts
Portal vein thrombosis
thrombosis of the extrahepatic portal system
seen in hyper coagulability or inflammatory disorders such as pancreatitis
What are some causes of hypercoagulability in the dog
*Liver disease
*Cushings
*Protein losing disease
*Neoplasia
*Immune mediated disease
*Infectious disease
* Pancreatitis
Causes of prehepatic portal hypertension
portal vein thrombosis
Causes of intrahepatic portal hypertension
chronic liver disease bridging disease
lobular abnormalities
regenerative nodules
lobular dissecting hepatitis
Veno-occlusive disease
amyloidosis
Schistomiasis
Granulomatous disease
Causes of post-hepatic portal hypertension
thrombosis of hepatic vein or caudal vena cava
congestive heart failure
Telangiectasis
dilation of sinusoids with hepatocellular loss
variable size dark, red to blue foci
common in cattle and older cats
can be incidental
Hepatic lipidosis or steatosis
occurs when the rate of triglyceride accumulation within the hepatocytes exceeds metabolic degradation or release of lipoproteins
causes: diet, toxins, hypoxia, ketosis, species syndromes, endocrine diseases
What could happen with sheep/goats on a high fat or deitary deficiencies of cobalt and vitamin B12
Liver steatosis
COMMD1 mutation
an autosomal recessive inherited mutation in dogs leading to impaired biliary excretion of copper
What does molybdenum do to copper
it antagonizes its uptake
What animals are most frequently affected by copper toxicity
Sheep (but also cattle, goats, and pugs)
How might copper toxicity occur
1) Excessive intake
2) Low molybdenum
3) Plants w hepatotoxic phytotoxins, pyrrolizidine alkoloids
4) COMMD1 mutation dogs (Dobermans, Labs, Skye and West Highland, Dalmations)
How does copper impact the liver
Hepatocellular necrosis from reactive oxygen species leading to hepatocellular apoptosis
Hemolysis and hemoglobinuria because decreased hepatic ability to deal with copper leading to elevated plasma copper leading to intravascular hemolysis
Acute: anorexia, abdominal pain, diarrhea, dehydration, and shock
Histologically: centrilobular hepatic necrosis and renal tubular necrosis
What is the most common recognizable size of canine chronic hepatitis
copper toxicity
Where does copper accumulate in the liver
centrilobular regions
What is the Rhodamine Stain used for
copper detection within the hepatocytes
What stains copper in the hepatocytes
Rhodamine
Lobular dissecting hepatitis
disease of young dogs, cirrhosis of the liver
similar to chronic active hepatitis but you see mild inflammation and increased fibrosis dissecting hepatic parenchyma isolating hepatocytes
Hepatosis dietetic
Acute hepatic necrosis in young, rapidly growing pigs
poorly understood but Vitamin E and/or selenium deficiency is like contributing to it because they are antioxidants and prevent oxidative injury leading to hemorrhagic centrilobular to massive hepatic necrosis
What might cause hepatosis dietetic in young rapidly growing pigs
vitamin e/selenium deficiency
Lipofuscin
pigment accumulation that increases with age due to incomplete oxidation of lipids
Ceroid
pigment accumulation due to peroxidation of fat deposits
Parasite hematin
pigment accumulation due to iron and porphyrin, fascioliasis
Hemosiderin
pigment accumulation due to the breakdown of erythrocytes
What is a consequence of portosystemic shunt
A) Chronic passive congestion
B) Massive hepatic necrosis
C) Nodular regeneration
D) Hepatic encephalopathy
D) Hepatic encephalopathy
What effect can steroids have on the liver
Hepatopathy, steatosis
What allows for cobalamin absorption
intrinsic factor
What secretes glucagon
alpha cells
What secretes insulin
beta cells
What secretes somatostatin
delta cells
Pacinian corpuscles
present on the pancreas of cats, mechanoreceptors for pressure and vibration
more suceptible for pain in abdomen
also in humans and primates
What is special about the cat pancreatic and common bile duct
they merge prior to going through the duodenal papilla while in dogs they enter separately
Canine juvenile pancreatic atrophy
cause of EPI in young dogs (loss of exocrine pancreas)
Primarily german shepherd, rough coated collies, chows, and english setters
Complex genetic disorders
Infiltration by small lymphocutes leading to atrophy and replacement fibrosis
autoimmune cell mediated process against acinar cells
What is a common cause of EPI in young german shephards
Canine juvenile pancreatic atrophy
EPI is a disease of
maldigestion and malabsorption
Clinical signs of EPI
Weight loss depsite normal to voracious appetite
Poor quality hair coat
muscle atrophy
Pale, soft, voluminous and malodourous feces “cow patty”
Mesenteric torsion, intussusception
Small intestinal bacterial overgrowth from increased volume of undigested nutrients
How do you diagnose EPI
Signalment and clinical signs
Serum trypsin-like immunoreactivity
<2.5 mcg/L dogs <8 mcg/L in cats
Cobalamin deficiency present
Agonal and postmortem finding of the pancreas
1) Interstitial hemorrhage from increased central blood pressure preceding the death
2) Autolysis- pancreas autodigests very rapidly- can look like pancreatitis/fat necrosis
Acute Pancreatitis
necrosis (primary lesion) and acute inflammation
Dogs>Cats
Cause: Not clear but
-High lipid/fat diet
-Abdominal trauma
-Hypotension and re-perfusion
-Hyperlipidemia: Cushings and hypothyroidism
Is acute pancreatitis more common in dogs or cats
Dogs
is chronic pancreatitis more common in dogs or cats
Cats
Gross findings of acute pancreatitis/ pancreatic necrosis
Red swollen parenchyma
Indistinct margins
hemorrhage
edema
fat necrosis / saponification
Fat necrosis/saponification
Release of pancreatic enzymes (lipase and amylase) leading to the breakdown of adipose into fatty acids and salts leading to necrosis and saponification
chalky, white to yellow deposits over the peri-pancreatic fat
histopath: purple to pink material, fibrin, mineral replacing adipose
surrounded by sheets of neutrophils and hemorrhage
How does fat necrosis/saponification occur
when pancreatic enzymes such as lipase and amylase are released to breakdown adipose into fatty acids and salts
What can zinc toxicity lead to
Pancreatic necrosis
Zinc toxicity
pancreas is a major route of zinc excretion
narrow margin between safe and unsafe exposure
exocrine acini are affected first
ingestion of pennies
Can also lead to heinz body hemolytic anemia
Sequelae of pancreatic necrosis
can lead to EPI
acutely- cytokine storms leading to SIRS (systemic inflammatory response syndrome) leading to acute respiratory distress syndrome and DIC
Necrotizing panniculitis- inflammation of subcutis due to circulating pancreatic enzymes: phospholipase A, lipase, amylase, and trypsin
Findings of Chronic Pancreatitis
Pancreas is firm, small, and nodular
Histopath: atrophy, fibrosis (pink bands of tissue) and lymphocytic or lymphoplasmacytic inflammation (blue aggregates)
What can cause chronic pancreatitis
1) Hepatic lipidosis due to inappetance
2) Repeated episodes of acute inflammation
3) Unresolved/ongoing necrosis or inflammation
4) Atrophy and fibrosis leading to loss of exocrine and/endocrine pancreas such as EPI or Diabetes mellitus
Feline Triaditis
due to the common bile duct and pancreatic duct merging together at the duodenal papilla
inflammation here can manifest 3
1) enteritis
2) pancreatitis
3) cholangitis or cholangiohepatitis
Pancreatic duct flukes
-Eurytrema procyonis (carnivores)
-Eurytrema pancreticum (ruminants)
Block the pancreatic duct, cause inflammation, atrophy and fibrosis
Pancreatolithiasis
Stones in the pancreatic duct
most commonly in cattle (incidental at slaughter)
mineralization following inflammation or necrosis
Rarely cause complete obstruction
Exocrine nodular hyperplasia
incidental finding that is constant adaptation to nutritional influences
seen in older dogs, cats, and cattle
nodules are pale due to less zymogen granules
can be confused with neoplasia but paler than surrounding pancreas
Adenocarcinoma of pancreas
tan to white
firm
multinodular
very infiltrative
Histo: acini, islands, cords
can have zymogen granules
can surround by dense stroma=desmoplasia/scirrhous response
carcinomatosis along serosal surface
Desmoplasia/Scirrhous response
the body response to wall off neoplasms with scar tissue to prevent spread. seem in pancreatic adenocarcinomas
Insulinoma
most common islet cell tumor
beta cells
secrete insulin and result in hypoglycemia
variable discrete, tan to red masses
common in ferrets (not malignant)
metastasis to liver and lymph nodes
histopath: lobules and packets of polygonal cells separated by fine connective tissue septa
Are insulimonas malignant
most are, except in ferrets
Where do insulinomas typically metastasize to in the dog?
lymph nodes and liver
mean survival time ranges between 12 to 18 months
T/F Herpes virus can cause hepatitis
T
Why is the first 2 weeks of life the most susceptible to herpesviral hepatitis
because of the lack of competent thermoregulation
Herpesviral hepatitis typically affects
the fetus or neonates
transplacental exposure, birth canal, infected littermates, oronasal secretion from dam
Herpesviral hepatitis leads to
multifocal, random hepatic necrosis with intranuclear inclusion bodies
What are your differentials for centrilobular necrosis of the liver
-Toxins (xylitol, aflatoxicosis, acetaminophen, carprogen
-Chronic passive congestion
-Canine Adenovirus 1
Canine adenovirus 1 and canine herpesvirus 1 both cause intranuclear inclusions but how do they differ in there hepatic necrosis
Canine Adenovirus 1 causes centrilobular necrosis while canine herpesvirus 1 causes random hepatic necrosis
T/F Canine Adenovirus causes random hepatic necrosis
F: it causes centrilobular necrosis
What is the causative agent of canine hepatitis
canine adenovirus 1
Infectious canine hepatitis
Caused by canine adenovirus 1
slight fever to severe depression, marked leukopenia and coagulation abnormalities
Hepatocullar necrosis and endothelial cell damage
immune complex deposition leading to uveitis, corneal clouding and glomerulonephritis
Intranuclear inclusions in liver, dx w PCR and FISH
also reported in wildlife
uncommon with routine vaccination
Clinical signs of Infectious canine hepatitis (ICH)
-Hepatocellular necrosis and endothelial cell damage ( centrilobular)
-Blue eye/corneal edema
-Glomerulonephritis
-Intranuclear inclusion boddies in the liver
Rabbit hemorrhagic disease causative agent
Calicivirus
Rabbit hemorrhagic disease
Calicivirus
Highly contagious, temperature resistance, direct contact, infected rabbit blood
Massive hepatocellular necrosis
NM, CA, CO, NV, TX
Pale enhanced lobular pattern, limp, friable texture
Necrosis is acute
Periportal to midzonal
Reportable to state veterinarian
Where does hepatic necrosis from rabbit hemorrhagic disease occur
Periportal to midzonal
Lymphocyctic cholangitis in cats
slowly progressive and chronic
usually >4 years of age
icterus (intrahepatic cholestasis)
Lymphocytes and plasma cells in the portal tracts and surrounding bile ducts
unknown cause
immune mediated?
must be differentiated from chronic suppurative cholangitis which is usually by ascending bacterial infections (cats > 11yo)
can occur with pancreatitis and IBD “Triaditis”
Why is the liver a common place for bacteria to manifest
bacteria can reach the liver through the portal vein, umbilican veins, hepatic artery, ascending from biliary, parasitic migration, direct extension from tissue adjacent to the liver
Ex: Fusobacterium in toxic ruminits, phlebitis, thrombosis, portal hypertension, septic thromboemoboli into lungs, sidden death, fungal disease with ruminal ulceration
enteric species of bacteria (Francisella, Nocardia, actinomyces)
Common bacterial causes of hepatitis
-Mycobacterim, tuberculosis
-Rhodococcus equi
-Corynbacterium pseudotuberculosis
-Francisella tularensis
-Salmonellosis: foci of necrosis with macrophages surround paratyphoid nodules
Paratyphoid nodules
aggregates of macrophages in the liver in response to salmonellosis
Clostridium piliforme hepatitis
young/immunocompromised animals
well recognized in lab animal
lead to pale foci of hepatocellular necrosis with surrounding neutrophilic and mononuclear infilitrate
Intracellular
What stain should you use for Clostridium piliforme (Tyzzer’s)
Warthin-Starry or Gomori’s silver stain
T/F Clostridium piliform is intracellular
T
Leptospirosis
gram -, thin spiral bacterial
enter body through mucous membranes or skin via contaminated water, bedding and soil, shed in urine, transplacental infection
intravascular hemolysis causing ischemic injury to centrilobular regions
icterus
can cause hepatic dissociation, bile casts, hemosiderin Kupffer cells, chronic active hepatitis
What disease causes hepatic dissociation and chronic active hepatitis
Leptospirosis
What disease causes intravascular hemolysis and ischemic injury to centrilobular regions
Leptospirosis
What bacteria can cause hepatic infarction
Clostridium Haemolyticum (novi type D)
What can cause bacillary hemoglobinuria
Clostridium Haemolyticum (novi type D)
Bacillary hemoglobinuria
Caused by Clostridium Haemolyticum (novi type D), found in poorly drained pastures with alkaline pH
After ingestion latent spores become embedded in liver
disease requires anerobic conditions (Fasciola hepatica)
High nitrate diet, liver puncture or biopsy, or other cause of localized hepatic necrosis
Produce beta toxin causing intravascular hemolysis and hemolytic anemia/hemoglobinuria and infarction
Signs: dehydration, anemia, bloody abdominal fluid, liver infarction, kidney petechiations, red to purple urine
dx: PCR, IFAT, IHC on liver
Prevent with vaccinations and control of liver flukes
What parasite is associated with clostridium haemolyticum
Fasciola hepatica, allows for anaerobic conditions
What bacteria is associated with Fasciola hepatica infection
Clostridium haemolyticum
How does Clostridium cause hemoglobinuria
It produces beta toxin that causes intravascular hemolysis and hemolytic anemia
How can you prevent bacillary hemoglobinuria
-Clostridium vaccination or fluke control
Black Disease causative agent
Clostridium novyi (type B)
Black’s Disease
Caused by Clostridium novyi (Type B)
most common in sheep and cattle but can occur in pigs and horses
germinate in regions of lowered oxygen tension and release exotoxin
Hepatic necrosis with migration of liver flukes
exotoxin causes discrete foci of coagulation necrosis and hemorrhage in the liver
Histo: necrosis surrounded by neutrophils and abundant gram + rods
What bacteria causes multifocla hepatic necrosis with black pigment with migration tracts of fluke pigment
Clostridium novyi (Type B)
Compare and contrast C. hemolyticum and C. novyi
spores are spread through fluke larval migration (areas of low oxygen) leading to bacterial proliferation. Both lead to death but hemolyticum toxins lead to intravascular hemolysis while novyi leads to infectious necrotic hepatitis
Name some causes of intravascular hemolysis
-Leptospirosis
-Bacillary hemoglobinuria
-Copper toxicity
What causes milk spotted liver in pigs
Ascaris suum migration
How might heartworm cause DIC and acute hepatic failure
it causes vena caval syndrome
Echinococcus
caused by ingested hydatid cysts
central necrosis
How does Fasciola hepatica differ from Fascioloides magna
-Fasciola hepatica inhabits the biliary system while Fascioloides magna inhabits the hepatic parenchyma
Where does Fasciola hepatica inhabit
the biliary system
Where does Fascioloides magna inhabit
the hepatic parenchyma
Trematode Hepatitis
Caused by F. hepatica or magna migration through the liver creates hemorrhagic tracts with fibrotic repair
leads to peritonitis, abscessation, widespread hepatic necrosis infiltration and Clostridium haemolyticum or novyi infection leading to bacillary hemoglobinuria or infectious necrotic hepatitis
Heterobilharzia americana
trematode of raccoons. ova shed in water from feces by infected racoons, release miracidia penetrate the host snails
Dogs infected wen skin is penetrated by cercariae released by snails
granulomatous diseasee in liver, pancreas, intestine, and mesentery in reaction to adult schistosomes
Theiler’s Disease
Equine Serum Hepatitis
Received inection of equine serum (such as tetanus antitoxin)
Late summer or early
Increasing evidence for a viral cause
Incubation period is prolonged
Rapid to often fatal
Hepatic failure with hepatic encephalopathy and icterus
intravascular hemolysis in terminal stages
What might occur with a horse receiving an injection of tetanus antitoxin
Theiler’s Disease (Equine Serum Hepatitis)
Hepatic failure with hepatic encephalopathy and icterus
Intravascular hemolysis with late stages
What hepatocytrs have the highest concentration of P450 enzymes
Centrilobular hepatocytes
Phases of liver metabolism
Phase I: chemicals bioactivated to high-energy reactive intermediate molecule (Bioactivation)
Phase II: formation of covalent bonds with polar molecules such as glucuronic acid (Conjugation)
Phase IIIL transport of molecules across the cell membranes into canaliculus
Old or young cats: Suppurative cholangitis/cholangiohepatitis
Young
Old or young cats: lymphocytic cholangitis
Old
What phase does conjugation happen
Phase II
What phase does bioactivation happen
Phase I
What phase does excretion happen
Phase III
Where does direct toxicity to hepatocytes occur
zone 1: periportal (no need to metabolism)
Where does indirect toxicity to hepatocytes occur
zone 3: Centrilolobular- injury occurs where there is most concentration of enzymes, toxic after metabolism by gi microbes
Acute toxic injury to liver
regeneration possible if submassive
Massive necrosis causes destruction of reticulin framework/limiting plate resulting in fibrosis
Chronic or recurrent toxic injury to liver
Necrosis and fibrosis and hepatocellular nodular regeneration- hepatic insufficiency
Name toxins of acute hepatic injury
1) Acetaminophen (cats)
2) Carprofen (dogs)
3) Microcystin LR (blue-green algae)
4) alpha-amanitin (Amanita mushrooms)
5) Acute aflatoxicosis
6) Xylitol (dogs)
What has red/white/blue lesions on histostaining
Hepatocutaneous syndrome
Acetaminophen toxicity
drug is metabolized by glucouronidation and sulfation
cats are deficient inpathways, dogs can still be affected
Causes methemoglobinemia and hepatotoxicity (Renal injury also possible)
liver damage more common in dogs
Centrilobular necrosis
Microcystin LR
Occur in cyanobacteria algal blooms in late summer/early fall
released by dying bacteria that accumulates on the water
ingested by livestoack
cause hemorrhagic gastroenteritis and hemorrhagic liver
Have centrilobular or massive hepatic necrosis and hemorrhage
Amanita mushrooms
high mortality rate lead to vomiting, bloody diarrhea to multiorgan failure
Massive hepatocellular necrosis, ductular reaction, hydropic degeneration
Xylitol
acutely toxic to dogs leads to hyperinsulinemia, hypoglycemia, icterus, and liver failure
vomitting, lethargy, weakness, seizures
found in sunscreens, medications, toothpastes, chewable vitamins, cosmetics, deodorants, and hair care
centrilobular to midzonal or massive necrosis and vacuolar degeneration
Aflatoxicosis
mycotoxin produced by fungus on feed in hot temperatures
Produced by Aspergillus flavus and parasiticus
metabolized in liver and can lead to carcinogenesis, teratogenesis, immunosuppression, and liver damage with reduced protein synthesis
inappetance, poor growth, hemorrhage, icterus, and death
What can be seen in subacute aflatoxicosis
Steatosis and Cholestasis
What can be seen with chronic aflatoxicosis
Bridging fibrosis (chronic) and biliary hyperplasia
Pyrrolizidine Alkaloid containing plants
Ragwort, Crotolaria, Senecio, Cynoglossum
Convered to pyrrolic esters by hepatic P450
Pigs most susceptible, chronic, lead to hepatic fibrosis
Megalocytosis, hepatic fibrosis, biliary proliferation +/- nodular regeneration
A horse present with icterus. Liver biopsy reveals hepatic dissociation, bile casts, and hemosiderin-laden macrophages. What would be a strong differential
A) Leptospirosis
B) Clostridium piliforme
C) Rhodococcus Equi
D) Salmonellosis
A) Leptospirosis
Hepatocellular nodular hyperplasia
common in dogs >6years
Not a result of hepatic dysfunction
multiple are present
Well demarcated and can compress adjacent parenchyma
Contain all elements of normal liver
Cytoplasmic lipid or glycogen common within hepatocytes
What should you not do when submitting liver biopsy
Say why you need to take the biopsy
Give as much information as you can
Provide what part of the liver
What are features of regenerative nodules (e.g hepatic cirrhosis) in contrast to nodular hyperplasia
They are not smooth or pale
Disease process (nodular hyperplasia is not)
Hepatocellular adenoma
single, compress adjacent tissue, variable size, unencapsulate. looks very similar to nodular hyperplasia
Is Hepatocellular carcinoma differentiated
well differentiated to atypical. but look for invasion at margin mitotic figures, and cellular atypia and help
Hepatocellular carcinoma
well differential to atypical
Common in ruminants (sheep) and dogs
solitary, involve entire lobe, well demarcated
Friable, more pale, divided into lobules
irregular trabeculae, three or more cells thick
multiple patterns can be found
distant metastasis uncommon
3 syndromes of hepatocellular carcinoma in dogs
1) Solitary or massive: low mitotic rate, low metastatic rate, usually amenable to surgery
2) Multifocal (nodular)-several masses
3) Diffuse- throughout the entire liver: nodular or diffuse can have metastasis, intrahepatic extension is most common, extraheptatic metastasis can occur to the local lymphnodes and lunges
What is the easiest hepatocellular carcinoma to treat in dogs
Solitary, can be surgically removed
Carcinoid
hepatic tumor of the neuroendocrine cells within the biliary epithelium
single or multiple nodules
use IHC to distinguish
What is the next common site for hemangiosarcoma after skin, spleen, and heart
Liver
What animal does not have a gallbladder
Rat
What is special about hepatosplic and hepatocytotropic T cell lymphoma
there is hepatic involvement with the absence of peripheral lymphadenopathy
Cholecystokinin
released in response of fatty food in intestine tract to stimulate bile emulsification of fats for better absorption
What is a result of biliary atresia
hyperbilirubinemia
Result of choleliths
can obstruct the gallbladder or bile ducts. bile cannot be released upon stimulation leading to hyperbilirubinemia and maldigestion of fats
pressure necrosis can rupture and cause acute peritonitis
What two viruses can cause cholecystitis
1) Rift valley fever
2) Infectious canine hepatitis
Gallbladder Edema causes
1) Non-sepecific inflammatory diseases
2) Anphylaxis-generalized venous congestion
3) Cardiac disease
T/F Biliary hamartoma is congential
T - biliary tree developmental abnormality
T/F Cholangiocellular carcinoma is benign
F- commonly to LN, lungs, or abdominal seeding
Cholangiocellular carcinoma
neoplasm of biliary epithelium from intrahepatic ducts
single or multiple masses
firm, raised, central depression, pale, unencapsulated
can have scirrhous response (firmness)
Metastasis is common to LN, lungs, or abdominal seeding
Cystic mucinous hyperplasia
benign
dogs and sheep
cystic spaces that thicken the gallbladder mucosa
asymptomatic but can become issue (gallbladder mucocele)
cause unknown
Gallbladder mucocele
progressive accumulation of mucin-laden bile
Can result in bile duct obstruction
Can lead to gall bladder ischemia and necrosis, bile peritonitis, and opportunistic infection
tx: with cholecystectomy
predisposing factors: endocrinopathies, hyperlipidemia, gallbladder dysmotilility, cystic hyperplasia
What could result from a gallbladder mucocele
1) Bile Duct obstruction
2) Gall bladder ischemia and necrosis
3) Bile Periotonitis
4) Opportunistic infection
What is the best treatment for gallbladder mucocele
Cholecystectomy
What can predispose animal to gallbladder mucocele
endocrinopathies, hyperlipidemia, gallbladder dysmotility, cystic hyperplasia
Are you more supspicious of steroid hepatotopy or hepatic lipidosis in a dog
steroid hepatotopy
What is your primary differential for multifocal hepatic abscesses in a horse
Rhodococcus equi
What is your top differential for disseminated foci of necrosis in the liver and spleen of a cat
Tularemia or Herpes
What is your differential for diarrhea, vomiting, coma, death. Liver with centrilobular to massive hepatocellular necrosis
Acute toxicity (Xylitol, Acetaminophen, Aflatoxin, Cyanobacteria, Amanita Mushroom)
