Gastrointestinal Pathology: General Principles Flashcards
General Philosoply of learning
- Observe all things, accurately and thoroughly
- Understand clearly what you have observed
- Evaluate wisely, in light of what you know
- Express in speech and writing waht you have observed, understood, and evaluated to others
Major Components of the tube
oral cavity
Esophagus
Forestomach
Stomach
Small intestine
Large intestine
Mucosa
- varies form stratified squamous in the oral cavity, esophagus and forestomach, to cuboidal to columnar in the stomach and intetines.
- has protective, asborptive, and secretory functions that vary based on location
Submucosa
loose connective tissue, vasculature and nerves that underlie the mucosa
Lymphoid affrefates taht contribute to enteric immunity are located here in some portions of the intestine
Enteric immunity is very active due to the constant exposure to antigens in ingesta
Muscularis
Varies between striated to smooth muscle, depending on the location within the digestive tract
Muscular contractions provide mixing and peristalsis to move ingesta through tje tract
Muscularis contians an extensive enteric nervous system that regulates gastrointestinal motility
Digestive Glands:
Salivary glands
produce seromucous secretions to moisten and lubricate food
Digestive Glands:
Pancreas
Produces enzymes that are important mediators of enzymatic digestion, including Trypsin, Chymotrypsin, lipase
Digestive Glands:
Liver
Produces bile and bile acids which are secreted to aid in digestion.
Enterohepatic circulation is an important aspect to digestion and hepatic function
GI Tract:
Function
The primary function is to uptake and break down ingested food into smaller units that can be absorbed and utilized for maintenance of the animal, and excretion of the non-absorbing materials
- Anterior end of the tube is modified to help prehension and initial grinding
- The distal end of the tube is modified for waste excretion
Proper digestive function is essential for an animal to maintain adequate nutrition
GI tract:
Dysfunction
- Clinical features of gastrointestinal disease are based mainly on the portion of the system affected
- signs of oral cavity disease include dysphagia, excess salivation
- Signs of gastric disease include vomiting
- Signs of intestinal disease include diarrhea
GI tract Dysfunction:
Developmental Anomalies
These are not common, but can affect any portion of the gastrointestinal system.
Examples include cleft palate and segmental hypoplasia within the tubular protion of the tract
GI tract Dysfunciton:
Metabolic Abnormalities
- Many dysfunctions of the gastrointestinal system will have metabolic consequences
- The purpose fo the system is to obtain and process nutrients needed to run metabolism
- Examples include gastritis due to uremia, fluid/e;ectrolyte imbalances due to diarrhea, mineralization, and nutrient dificiencies
GI tract Dysfunction:
Vascular Distrubances
Most common vascular problems of the gastrointestinal tract are related to physical occlusion of vessels
Various types fo gastrointestinal torsion are characterized by vascular occlusion and subsequent congestion, edema, and infarction
GI tract Dysfunctions
Cell/Tissue Injury
- Necrosis of enterocytes can occur due to a wide variety of insults
- common example is viral-induced enterocyte necrosis, which leads to malabsorptive or effusive diarrhea
- Stenosis of the tube can be the ultimate/end result of wound healing and fibrosis following cellular and tissue injury in the gastrointestinal tract
GI tract Dysfuction:
Inflammation
This is important as either a primary or secondary event in many infectious and non-infectious gastrointestinal conditions
GI tract Dysfunciton:
Immunological Reactions
The GI system is exposed to a wide variety of different antigens
Hypersensitivity to ingested antigens can result in malabsorption and diarrhea
GI tract Dysfunction:
Neoplasia
Specific types of neoplasia occur throughout the GI tract
Examples include oral melanoma and Fibrosarcoma, gastrointestinal adenocarcinoma and lymphosarcoma
Oral Cavity: Congenital
Goat Palatoshisis, secondary cleft palate
Pathogenesis: Genetic, Hypervitaminosis A, Griseofulvin, Toxic plants
Oral Cavity: Congenital
Cranio-facial Anomalies
Brachygnathia vs. Prognathia vs. agnathia
Superior maxilla, vs. inferior mandible
Pathogenesis: Most are presumed to be genetic
Oral Cavity: teeth
Dog teeth, enamal hypoplasia
Pathogenesis: CDV (BVD ruminants) infects ameloblasts → enamel hypoplasia
Oral Cavity: Teeth
Mdx: Sinus Empyema (purulent Sinusitis)
Pathogenesis: Demineralization or enzymatic digestion → Surface or pit cariers → loss of enamel, dentin → tooth infundibular impaction of feed material → continued loos of enamel/dentin → instability → tooth fracture → root inflammation and necrosis → extension into paranasal sinuses → empyema
MDx: sheep maxillary and mandibular premolar and molar teeth malocclusion
Pathogenesis: Inappropriate wearing , premature tooth attrition → ‘wave mouth”
Serous atrophy of fat bone marrow
MDX: Sheep bone marrow, serous atrophy of fat, also pericardial and perirenal adipose
Pathogenesis: Dental malocclusion → inability to prehend and chew food → starvation → mobalization of body fat stores/serous atrophy, this is a consequence of dental attrition
Stomatitis
Glossitis
inflammation of the tongue
Gingivitis
Inflammation of the gums
Tonsilitis
Inlfammation of tonsils
Pharyngitis
Inflamamtion of the pharynx
Oral Cavity: Inflammation
Superficial vs. deep
Superficial: surface, caustic, toxic, electric, sunburn, infection
Deep: involves the deeper connective tissues of oral cavity
Lip eosinophilic granuloam
MDx: Cat lip eosinophilic granuloma or ulcerative granulomatous cheilitis
Pathogenesis: Unknown, chronic, inflammation probably immune mediated
Stomatitis in cats
MDx: lymphocytic plasmacytic stomatitis; feline chonic gingivostomatitis
Pathogenesis: Linked to viruses (FeLV, FIV, FHV, FCV) ; Immune mediated
Stomatitis in dogs
Oral cavity: inflammation
MDx: Lymphocytic gingivitis/stomatisis ; Canine ulcerative paradental stomatitis/CUPS
Pathogenesis: Inappropriate oral care - periodontal disease ; Immune mediated, can be severe
ulcerative stomatitis
MDx: canine oral mucosa, ulcerative stomatitis
Pathogenesis: Migrating plant material/plant awns → lovalized trauma and inflammation
Bovine Oral Ulcer
Oral cavity: vesicles and ulcers
MDx: Bonie oral ulcer
Pathogensis: Direct epithelial damage by viruses, also potentially ischemic damage or trauma
In pigs consider seneca valley virus
Cat tongue vesicles and ulvers
MDx: Cat tongue vesicles and ulcers
Pathogensis: FCV, FHV-1, Uremia, immune mediated / pemphigus, trauma → Direct epithelail necrosis, possibly ischemic damage
Oral cavity: hyperplasia, papules
Mdx: Bovine oral cavity, proliferatie/papular stomatits and cheilitis
Pathogenesis: Bovine papular stomatitis virus → direct infection of oral epithelium → Proliferation of epithelium
Oral Cavity: Hyperplasia , papules
MDx: Goat/Sheep lip proliferatice cheilitis
Pathogenesis: Sheep parapox virus → infection of epithelium → proliferation, necrosis (Contagious ecthyma)
ZOONOTIC disease
Oral Cavity: Inflammation
MDx: Bovine pyogranulomatous / necrotizing glossitis
Pathogenesis: Actinobacillus lignieresi → infection via trauma damage or wound to oral epithelium → invades deeper structures, aka wooden tongue
Oral cavity: inflamamtion
MDx: Pyogranulomatous and necrotizing osteomyelitis
Pathogenesis: Actinomyces bovis → similar to A. lingieresi, but involves bone, aka lumpy jaw
Oral cavity: inflammation
MDx: Bovine fibrinous and necrotizing laryngitis
Pathogenesis: Fusobacterioum necrophorum → physical or viral-indiced damage or trauma to surface epithelium and cartilage → F. necrophorum invades form oral cavity
Ptyalism:
Ingestion of caustic substances; OP; foreign bodies ; rabies
Salivary ranula, mucocele/sialocele
accumulation of saliva in a dilated duct, or soft tissues of the mouth, respectively
Sialodenitis, sialoliths
Uncommon
Neoplasms
rare
Oral Cavity: Masses
Gingival or fibrous hyperplasia
Common in dogs more than cats, non-neoplastic
Oral cavity: masses
Peripheral odontogenic fibroma
Avoid the term epulis;
Stromal neoplasm of periodontal ligament origin;
can have bone dentin,
They are benign, can be difficult to completely excise
Oral cavity: Masses
Squamous cell carcinoma
1 in cats, #2 in dogs
Tongue > gingiva > tonsils;
Locally invasive into soft tissues, bone,
metastasize late to nodes and lungs
Oral Cavity: masses
Acanthomatous ameloblastoma
odontogenic epithelium
locally invasive into bone, but do not metastasize
Oral Cavity: Masses
Oral Melanoma
1 in dogs
can be pigmented or amelanotic
most are malignant with local invasion and distant metastasis
Oral cavity: masses
Fibrosarcoma
3 in dogs
Locally invasive with recurrence, can metastasize
Oral cavity: Masses
Oral papillomas
canine oral papillomavirus often spontaneously regress
Oral cavity: masses
Tumors of teeth
Uncommon
Oral cavity: masses
Others
Mast cell tumors, granular cell tumors, plasmacytomas, vascular tumors
Oral cavity: masses
inflammaotyr lesions
abcesses, granulomas
Esophagus: Inflammation/ulcerative
MDx: Canine mf Distal esophageal ulcers
Pathogenesis:
Chornic gastric reflux, direct damage to epithelium;
Could also be caused by viral infection, caustic substances, ischemic damage/vasculitis/thrombosis
esophagus: dilation
MDx: Canine Megaesophagus
Pathogenesis: Can be congenital → physical obstruction;
Also can be acquired → failure of nerves or muscle of the esophagus
Esophagus: obstruction
MDx: Bovine esophageal obstruction
Pathogenesis: Foreign body obstruction → inability to eructate gas/free gas bloat;
Also possible local ischemia, inflammation, perforation → wound healing → fibrosis/stricure
Esophagus: consequence of obstruction or ulceration
Esophagus: miscellaneous
MDx: Conine granulomatous esophagits
Pathogenesis: Spirocerca lupi infection → inflammation → esophageal sarcoma
Forestomachs: form, function
Nonglandular fermentation vat
Don’t overlook the forestomach/contents
Forestomachs: rumen Bloat
Mdx: Bovine rumen bloat
Pathogenesis: ante-mortem rumen bloat → diaphragm puched cranially → increased thoracic pressure → compressed venous returm → lack of venous flow into thorax
Rumen Bloat:
Frothy Bloat
Primary tympany due to foam production
Pathogenesis: Ingestion of legumes → foam formation at surface → prevention of gas cap formation → pervention of eructation → rumen bloat → increased intrathoracic pressure → inhibits respiration, cardiac function → reduced cardiac venous return
Rumen Bloat:
Free Gas Bloat
Secondary tympany due to physical or functional defect in eructation
Choke, peritonitis, abscesses
Forestomach: rumen acidosis
Mdx: Bovine rumen acidosis = neutrophilic ruminits and parakeratosis
Pathogenesis: excess CHO ingestion → altered microbial flora → excess lactic acid production → pH falls → rumen atony → reduced saliva production → Increase rumen osmotic pressure → direct epithelial damage → bacterial translocation across rumen mucosa
Forestomach: Consequences of rumen acidosis
MDx: Bovine rume erosion, ulceration, scarring; mf random hepatic abscesses
Pathogenesis: Rumen acidosis → rumen surface erosions and ulcers → loss of papilla → translocation of rumen organissms across compromised rumen wall into protal vein and liver with hepatic abscess formation OR chornic fibrosis/scarring
forestomach: rumen acidosis
MDx: Rumen infarction, can involve any forestomach compartment
Pathogenesis: Rumen acidosis → opportunistic oxygen-loving fungi travel across compromised rumen wall → invade blood vessels → vasculitis, thormbosis, ischemia, infarction
Forestomach: inflammation
MDx: Bovine diaphragm: foreign body penetration, fibrinous pleuritis and peritonitis
Pathogenesis: Acute or chornic consequence of foerign body penetration
Forestomach: other
parasites are uncommon
Neoplasia is uncommon
Papilloma; fibropapilloma in dogs; cattle
Squamous cell carcinoma in ruminants
Stomach, abomasum
Form and function; response to injury
Dilation, displacement
Obstruction
Circulatory distrubances
Inflammation: Gastritis, Gastric ulcerations
Disturbances of growth
Stomach Abomasum:
Form and function
The fundic mucosa is the source of HCl and pepsin
HCl is stimulated by histamine, acetylcholine, gastrin
They cardiac and pyloric mucosa also secrete mucus and HCO3
The squamous mucosa is highly sensitve to acid and bile
Protective protaglandin E stimulates mucus and HCO3, inhibits histamine production, causes vasodilation and increased bloodflow
Stomach, Abomasum:
Response to injury:
Restoration
can be complete following erosive physical or chemical trauma, rapid
Stomach, Abomasum:
Response to injury:
Atrophy
atrophy of parietal cell mass
Stomach, Abomasum:
Response to injury:
Metaplasia or hyperplasia
Mucous cell hyperplasia or metaphasisa
Gastric Rupture
MDx: Equine gastric rupture
Pathogenesis: Gastric distension or outflow obstruction → increased pressure → Rupture, typically along the greater curvature
Stomach: Dilation, displacemetn
MDx: Canine Gastric Distension with volvulus
Pathogenesis: Accumulation of gas/food/fluid and distention of stomach → dialtion +/- rotaion → venous infarction → reduced venous return → reduced cardiac output → Severe circulatory shock → Sudden/acute death
Stomach, abomasum: dilation, displacement
Bovine abomasal displacement:
Left: Most common, but rarely seen in necropsy
Right: less common but can progress to volvulus and death
Stomach, abomasum: Gastric ulcers
MDx: Pigs stomach: normal (left) progressing to partial then complete ulceration, with hemorrhage (right)
Pathogenesis varies: duodenal reflux, NSAIDs, increased acid, stress, finely ground grains, MCT/histamine, reduced protective mucus → hemorrhage, ulceration, perforation, peritonitis, healing/fibrosis, stricture
Stomach, Abomasum: Circulatory / Metabolic
MDx: Canine Gastric hyperemia, congestion, hemorrhage
Pathogenesis: Uremia (dogs >> cats, horses) → vasculitis of submucosal blood vessels and/or thrombosis → ischemia, can also affect other organs such as tongue, oral cavity, kidneys
stomach, abomasum: parasites
Stomach, Abomasum: Neoplasia
MDx: Bovine abomasal lymphoma
Pathogenesis: Linked to BLV in cattle, can involve other forestomachs, heart, uterus, spinal cord
Stomach, abomasum: neoplasia
MDx: Canine Gastric Adenocarcinoma
Pathogenesis: Spontaneous, these tend to be inflitrative and cause thickening, loss fo gastric rugae, but not pedunculated masses
Stomach, abomasum: neoplasia
MDx: Equine gastric squamous cell carcinoma with distnat metastasis
Pathogenesis: Spontaneous, may be linked to chornic gastric inflammation or ulceration; they tend to be inflitrative and widely metastaic
Intestine: anomalies
MDx: Equine (foal) severe diffuse colonic hypoplasia
Pathogenesis: Spontaneous in some species, but in foals intestinal aganglionosis is genetic, linked specifically to overo x overo paint horses, lethal white foal syndrome
Intestine: anomalies
MDx: Lamb small intestinal atresia
Pathogenesis: Spontaneous or genetic mostly, in callte that has benn linked to early rectal/pregnancy palpation
Intestine: Response to injury/villous Atrophy
Small intestine normal tall villi, short crypts.
Proliferative compartment is crypts, cells shed from tips in 2-8 days
Small intestine severe blunting and fusion of villi with crypt hyperplasia
more cells, crowding, proliferation, and they are less differential
Villous Atrophy
Common change in domestic animals that leads to malabsorption and/or plasma protein loss into the gut
- Atrophy with an intact or hyperplastic proliferative compartment
- Primary increased rate of loss or targeting of villar epithelium
- Primary crypt hyperplasia due to a chronic or persistent process which alters the microenvirnment
- Villous atrophy associated with damage to the proliferative compartment
Intestine: Protein Lossing Enteritis
Mechanisms
loss of enterocytes
protein into the lumen
Malabsorption
Intestine: Protein Lossing Enteritis
Causes
Lymphangiectasia
parasitism
Inflammation
Accumulation/amyloid
Intestine: Protein Lossing Enteritis
Lymphangiectasia
MDx: canine intestinal lymphangiectasia
Pathogenesis: Can be primary or secondary → failure of lymphatic flow, dilation of lymphatics and lacteals
Hyperproteinemia, lymphopenia, hypocholestrolemia
Intestine: Malassimilation
Maldigestion vs. Malabsorption
- Intraluminal phase:
- bile, pancreatic secretion
- Epithelial and delivery phase:
- nutrients are delivered from enterocytes to blood via interstitial fluid
- Reduced surface area
- Biochemical lesions of enterocytes
- nutrients are delivered from enterocytes to blood via interstitial fluid
MDx: Canine cancreatic atrophy or hypoplasia
Pathogenesis: Failure to form or damage and loss → exocrine pancreatic indufficiency
Intestine: Diarrhea
Secretions and intake = 9L/day
Jejunum and ileum are major sites of absorption
Colon absorbs also within limits
Intestine: Diarrhea
Small bowel diarrhea
infrequent passage of large volumes of fluid feces
Secretory: bacterial enterotoxins
Malabsorptive: osmotic retention of water in gut lumen, villus atrophy
Effusive: Increased permeability, elevated hydrostatic pressure of severe epithelial necrosis
Intestine: Diarrhea
Large Bowel Diarrhea
Frequent passage of small volumes of liquid feces, often with straining, blood, mucus
Malabsorptive: colitis, tumor
Secretory: Hydroxylated fatty acids, bile salts,
Large bowel not as leaky due to tight junctions
Intestine: Obstructions
Feline SI neoplasm
MDx: Feline SI neoplasm
Pathogenesis: Spontaneous; in cats linked to FeLV
NB: Other intrinsic obstructions include linear foreign bodies, intestinal parasitism, impactions, other intestinal neoplasia, foreign bodies intussesception
Intestine: Obstruction
SI localized congestion/hemorrhage
MDx: Canine SI localized congestion/hemorrhage, obstruction
Pathogenesis: Small Intestine foreign body luminal obstruction → Distenstion, pain → vomiting → rupture or perforation → peritonitis
Intestine: Intussusception
Luminal intrinsic obstruction and venous infarction
