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Gastrointestinal Pathology: General Principles Flashcards

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1
Q

General Philosoply of learning

A
  1. Observe all things, accurately and thoroughly
  2. Understand clearly what you have observed
  3. Evaluate wisely, in light of what you know
  4. Express in speech and writing waht you have observed, understood, and evaluated to others
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2
Q

Major Components of the tube

A

oral cavity

Esophagus

Forestomach

Stomach

Small intestine

Large intestine

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3
Q

Mucosa

A
  • 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
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4
Q

Submucosa

A

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

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5
Q

Muscularis

A

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

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6
Q

Digestive Glands:

Salivary glands

A

produce seromucous secretions to moisten and lubricate food

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7
Q

Digestive Glands:

Pancreas

A

Produces enzymes that are important mediators of enzymatic digestion, including Trypsin, Chymotrypsin, lipase

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8
Q

Digestive Glands:

Liver

A

Produces bile and bile acids which are secreted to aid in digestion.

Enterohepatic circulation is an important aspect to digestion and hepatic function

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9
Q

GI Tract:

Function

A

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

  1. Anterior end of the tube is modified to help prehension and initial grinding
  2. The distal end of the tube is modified for waste excretion

Proper digestive function is essential for an animal to maintain adequate nutrition

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10
Q

GI tract:

Dysfunction

A
  • 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
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11
Q

GI tract Dysfunction:

Developmental Anomalies

A

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

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12
Q

GI tract Dysfunciton:

Metabolic Abnormalities

A
  • 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
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13
Q

GI tract Dysfunction:

Vascular Distrubances

A

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

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14
Q

GI tract Dysfunctions

Cell/Tissue Injury

A
  • 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
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15
Q

GI tract Dysfuction:

Inflammation

A

This is important as either a primary or secondary event in many infectious and non-infectious gastrointestinal conditions

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16
Q

GI tract Dysfunciton:

Immunological Reactions

A

The GI system is exposed to a wide variety of different antigens

Hypersensitivity to ingested antigens can result in malabsorption and diarrhea

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17
Q

GI tract Dysfunction:

Neoplasia

A

Specific types of neoplasia occur throughout the GI tract

Examples include oral melanoma and Fibrosarcoma, gastrointestinal adenocarcinoma and lymphosarcoma

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18
Q
A

Oral Cavity: Congenital

Goat Palatoshisis, secondary cleft palate

Pathogenesis: Genetic, Hypervitaminosis A, Griseofulvin, Toxic plants

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19
Q
A

Oral Cavity: Congenital

Cranio-facial Anomalies

Brachygnathia vs. Prognathia vs. agnathia

Superior maxilla, vs. inferior mandible

Pathogenesis: Most are presumed to be genetic

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20
Q
A

Oral Cavity: teeth

Dog teeth, enamal hypoplasia

Pathogenesis: CDV (BVD ruminants) infects ameloblasts → enamel hypoplasia

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21
Q
A

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

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22
Q
A

MDx: sheep maxillary and mandibular premolar and molar teeth malocclusion

Pathogenesis: Inappropriate wearing , premature tooth attrition → ‘wave mouth”

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23
Q

Serous atrophy of fat bone marrow

A

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

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24
Q

Stomatitis

A
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Glossitis
inflammation of the tongue
26
Gingivitis
Inflammation of the gums
27
Tonsilitis
Inlfammation of tonsils
28
Pharyngitis
Inflamamtion of the pharynx
29
Oral Cavity: Inflammation Superficial vs. deep
Superficial: surface, caustic, toxic, electric, sunburn, infection Deep: involves the deeper connective tissues of oral cavity
30
Lip eosinophilic granuloam
MDx: Cat lip eosinophilic granuloma or ulcerative granulomatous cheilitis Pathogenesis: Unknown, chronic, inflammation probably immune mediated
31
Stomatitis in cats
MDx: lymphocytic plasmacytic stomatitis; feline chonic gingivostomatitis Pathogenesis: Linked to viruses (FeLV, FIV, FHV, FCV) ; Immune mediated
32
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
33
ulcerative stomatitis
MDx: canine oral mucosa, ulcerative stomatitis Pathogenesis: Migrating plant material/plant awns → lovalized trauma and inflammation
34
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
35
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
36
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
37
Oral Cavity: Hyperplasia , papules
MDx: Goat/Sheep lip proliferatice cheilitis Pathogenesis: Sheep parapox virus → infection of epithelium → proliferation, necrosis (Contagious ecthyma) ZOONOTIC disease
38
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
39
Oral cavity: inflamamtion
MDx: Pyogranulomatous and necrotizing osteomyelitis Pathogenesis: Actinomyces bovis → similar to A. lingieresi, but involves bone, aka lumpy jaw
40
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
41
Ptyalism:
Ingestion of caustic substances; OP; foreign bodies ; rabies
42
Salivary ranula, mucocele/sialocele
accumulation of saliva in a dilated duct, or soft tissues of the mouth, respectively
43
Sialodenitis, sialoliths
Uncommon
44
Neoplasms
rare
45
Oral Cavity: Masses Gingival or fibrous hyperplasia
Common in dogs more than cats, non-neoplastic
46
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
47
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
48
Oral Cavity: masses Acanthomatous ameloblastoma
odontogenic epithelium locally invasive into bone, but do not metastasize
49
Oral Cavity: Masses Oral Melanoma
#1 in dogs can be pigmented or amelanotic most are malignant with local invasion and distant metastasis
50
Oral cavity: masses Fibrosarcoma
#3 in dogs Locally invasive with recurrence, can metastasize
51
Oral cavity: Masses Oral papillomas
canine oral papillomavirus often spontaneously regress
52
Oral cavity: masses Tumors of teeth
Uncommon
53
Oral cavity: masses Others
Mast cell tumors, granular cell tumors, plasmacytomas, vascular tumors
54
Oral cavity: masses inflammaotyr lesions
abcesses, granulomas
55
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
56
esophagus: dilation
MDx: Canine Megaesophagus Pathogenesis: Can be congenital → physical obstruction; Also can be acquired → failure of nerves or muscle of the esophagus
57
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
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Esophagus: consequence of obstruction or ulceration
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Esophagus: miscellaneous
MDx: Conine granulomatous esophagits Pathogenesis: Spirocerca lupi infection → inflammation → esophageal sarcoma
60
Forestomachs: form, function
Nonglandular fermentation vat Don't overlook the forestomach/contents
61
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
62
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
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Rumen Bloat: Free Gas Bloat
Secondary tympany due to physical or functional defect in eructation Choke, peritonitis, abscesses
64
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
65
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
66
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
67
Forestomach: inflammation
MDx: Bovine diaphragm: foreign body penetration, fibrinous pleuritis and peritonitis Pathogenesis: Acute or chornic consequence of foerign body penetration
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Forestomach: other
parasites are uncommon Neoplasia is uncommon Papilloma; fibropapilloma in dogs; cattle Squamous cell carcinoma in ruminants
69
Stomach, abomasum
Form and function; response to injury Dilation, displacement Obstruction Circulatory distrubances Inflammation: Gastritis, Gastric ulcerations Disturbances of growth
70
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
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Stomach, Abomasum: Response to injury: Restoration
can be complete following erosive physical or chemical trauma, rapid
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Stomach, Abomasum: Response to injury: Atrophy
atrophy of parietal cell mass
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Stomach, Abomasum: Response to injury: Metaplasia or hyperplasia
Mucous cell hyperplasia or metaphasisa
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Gastric Rupture
MDx: Equine gastric rupture Pathogenesis: Gastric distension or outflow obstruction → increased pressure → Rupture, typically along the greater curvature
75
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
76
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
77
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
78
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
79
stomach, abomasum: parasites
80
Stomach, Abomasum: Neoplasia
MDx: Bovine abomasal lymphoma Pathogenesis: Linked to BLV in cattle, can involve other forestomachs, heart, uterus, spinal cord
81
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
82
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
83
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
84
Intestine: anomalies
MDx: Lamb small intestinal atresia Pathogenesis: Spontaneous or genetic mostly, in callte that has benn linked to early rectal/pregnancy palpation
85
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
86
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
87
Intestine: Protein Lossing Enteritis Mechanisms
loss of enterocytes protein into the lumen Malabsorption
88
Intestine: Protein Lossing Enteritis Causes
Lymphangiectasia parasitism Inflammation Accumulation/amyloid
89
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
90
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 MDx: Canine cancreatic atrophy or hypoplasia Pathogenesis: Failure to form or damage and loss → exocrine pancreatic indufficiency
91
Intestine: Diarrhea
Secretions and intake = 9L/day Jejunum and ileum are major sites of absorption Colon absorbs also within limits
92
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
93
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
94
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
95
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
96
Intestine: Intussusception
Luminal intrinsic obstruction and venous infarction

Systemic Pathology (4 decks)

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