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Systemic Pathology > Gastrointestinal Pathology: General Principles > Flashcards

Gastrointestinal Pathology: General Principles Flashcards

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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25
Q

Glossitis

A

inflammation of the tongue

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26
Q

Gingivitis

A

Inflammation of the gums

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27
Q

Tonsilitis

A

Inlfammation of tonsils

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28
Q

Pharyngitis

A

Inflamamtion of the pharynx

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29
Q

Oral Cavity: Inflammation

Superficial vs. deep

A

Superficial: surface, caustic, toxic, electric, sunburn, infection

Deep: involves the deeper connective tissues of oral cavity

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30
Q

Lip eosinophilic granuloam

A

MDx: Cat lip eosinophilic granuloma or ulcerative granulomatous cheilitis

Pathogenesis: Unknown, chronic, inflammation probably immune mediated

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31
Q

Stomatitis in cats

A

MDx: lymphocytic plasmacytic stomatitis; feline chonic gingivostomatitis

Pathogenesis: Linked to viruses (FeLV, FIV, FHV, FCV) ; Immune mediated

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32
Q

Stomatitis in dogs

A

Oral cavity: inflammation

MDx: Lymphocytic gingivitis/stomatisis ; Canine ulcerative paradental stomatitis/CUPS

Pathogenesis: Inappropriate oral care - periodontal disease ; Immune mediated, can be severe

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33
Q

ulcerative stomatitis

A

MDx: canine oral mucosa, ulcerative stomatitis

Pathogenesis: Migrating plant material/plant awns → lovalized trauma and inflammation

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34
Q

Bovine Oral Ulcer

A

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

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35
Q

Cat tongue vesicles and ulvers

A

MDx: Cat tongue vesicles and ulcers

Pathogensis: FCV, FHV-1, Uremia, immune mediated / pemphigus, trauma → Direct epithelail necrosis, possibly ischemic damage

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36
Q

Oral cavity: hyperplasia, papules

A

Mdx: Bovine oral cavity, proliferatie/papular stomatits and cheilitis

Pathogenesis: Bovine papular stomatitis virus → direct infection of oral epithelium → Proliferation of epithelium

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37
Q

Oral Cavity: Hyperplasia , papules

A

MDx: Goat/Sheep lip proliferatice cheilitis

Pathogenesis: Sheep parapox virus → infection of epithelium → proliferation, necrosis (Contagious ecthyma)

ZOONOTIC disease

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38
Q

Oral Cavity: Inflammation

A

MDx: Bovine pyogranulomatous / necrotizing glossitis

Pathogenesis: Actinobacillus lignieresi → infection via trauma damage or wound to oral epithelium → invades deeper structures, aka wooden tongue

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39
Q

Oral cavity: inflamamtion

A

MDx: Pyogranulomatous and necrotizing osteomyelitis

Pathogenesis: Actinomyces bovis → similar to A. lingieresi, but involves bone, aka lumpy jaw

40
Q

Oral cavity: inflammation

A

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
Q

Ptyalism:

A

Ingestion of caustic substances; OP; foreign bodies ; rabies

42
Q

Salivary ranula, mucocele/sialocele

A

accumulation of saliva in a dilated duct, or soft tissues of the mouth, respectively

43
Q

Sialodenitis, sialoliths

A

Uncommon

44
Q

Neoplasms

A

rare

45
Q

Oral Cavity: Masses

Gingival or fibrous hyperplasia

A

Common in dogs more than cats, non-neoplastic

46
Q

Oral cavity: masses

Peripheral odontogenic fibroma

A

Avoid the term epulis;

Stromal neoplasm of periodontal ligament origin;

can have bone dentin,

They are benign, can be difficult to completely excise

47
Q

Oral cavity: Masses

Squamous cell carcinoma

A

1 in cats, #2 in dogs

Tongue > gingiva > tonsils;

Locally invasive into soft tissues, bone,

metastasize late to nodes and lungs

48
Q

Oral Cavity: masses

Acanthomatous ameloblastoma

A

odontogenic epithelium

locally invasive into bone, but do not metastasize

49
Q

Oral Cavity: Masses

Oral Melanoma

A

1 in dogs

can be pigmented or amelanotic

most are malignant with local invasion and distant metastasis

50
Q

Oral cavity: masses

Fibrosarcoma

A

3 in dogs

Locally invasive with recurrence, can metastasize

51
Q

Oral cavity: Masses

Oral papillomas

A

canine oral papillomavirus often spontaneously regress

52
Q

Oral cavity: masses

Tumors of teeth

A

Uncommon

53
Q

Oral cavity: masses

Others

A

Mast cell tumors, granular cell tumors, plasmacytomas, vascular tumors

54
Q

Oral cavity: masses

inflammaotyr lesions

A

abcesses, granulomas

55
Q

Esophagus: Inflammation/ulcerative

A

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
Q

esophagus: dilation

A

MDx: Canine Megaesophagus

Pathogenesis: Can be congenital → physical obstruction;

Also can be acquired → failure of nerves or muscle of the esophagus

57
Q

Esophagus: obstruction

A

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

58
Q

Esophagus: consequence of obstruction or ulceration

A
59
Q

Esophagus: miscellaneous

A

MDx: Conine granulomatous esophagits

Pathogenesis: Spirocerca lupi infection → inflammation → esophageal sarcoma

60
Q

Forestomachs: form, function

A

Nonglandular fermentation vat

Don’t overlook the forestomach/contents

61
Q

Forestomachs: rumen Bloat

A

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
Q

Rumen Bloat:

Frothy Bloat

A

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

63
Q

Rumen Bloat:

Free Gas Bloat

A

Secondary tympany due to physical or functional defect in eructation

Choke, peritonitis, abscesses

64
Q

Forestomach: rumen acidosis

A

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
Q

Forestomach: Consequences of rumen acidosis

A

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
Q

forestomach: rumen acidosis

A

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
Q

Forestomach: inflammation

A

MDx: Bovine diaphragm: foreign body penetration, fibrinous pleuritis and peritonitis

Pathogenesis: Acute or chornic consequence of foerign body penetration

68
Q

Forestomach: other

A

parasites are uncommon

Neoplasia is uncommon

Papilloma; fibropapilloma in dogs; cattle

Squamous cell carcinoma in ruminants

69
Q

Stomach, abomasum

A

Form and function; response to injury

Dilation, displacement

Obstruction

Circulatory distrubances

Inflammation: Gastritis, Gastric ulcerations

Disturbances of growth

70
Q

Stomach Abomasum:

Form and function

A

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

71
Q

Stomach, Abomasum:

Response to injury:

Restoration

A

can be complete following erosive physical or chemical trauma, rapid

72
Q

Stomach, Abomasum:

Response to injury:

Atrophy

A

atrophy of parietal cell mass

73
Q

Stomach, Abomasum:

Response to injury:

Metaplasia or hyperplasia

A

Mucous cell hyperplasia or metaphasisa

74
Q

Gastric Rupture

A

MDx: Equine gastric rupture

Pathogenesis: Gastric distension or outflow obstruction → increased pressure → Rupture, typically along the greater curvature

75
Q

Stomach: Dilation, displacemetn

A

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
Q

Stomach, abomasum: dilation, displacement

A

Bovine abomasal displacement:

Left: Most common, but rarely seen in necropsy

Right: less common but can progress to volvulus and death

77
Q

Stomach, abomasum: Gastric ulcers

A

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
Q

Stomach, Abomasum: Circulatory / Metabolic

A

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
Q

stomach, abomasum: parasites

A
80
Q

Stomach, Abomasum: Neoplasia

A

MDx: Bovine abomasal lymphoma

Pathogenesis: Linked to BLV in cattle, can involve other forestomachs, heart, uterus, spinal cord

81
Q

Stomach, abomasum: neoplasia

A

MDx: Canine Gastric Adenocarcinoma

Pathogenesis: Spontaneous, these tend to be inflitrative and cause thickening, loss fo gastric rugae, but not pedunculated masses

82
Q

Stomach, abomasum: neoplasia

A

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
Q

Intestine: anomalies

A

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
Q

Intestine: anomalies

A

MDx: Lamb small intestinal atresia

Pathogenesis: Spontaneous or genetic mostly, in callte that has benn linked to early rectal/pregnancy palpation

85
Q

Intestine: Response to injury/villous Atrophy

A

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
Q

Villous Atrophy

A

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
Q

Intestine: Protein Lossing Enteritis

Mechanisms

A

loss of enterocytes

protein into the lumen

Malabsorption

88
Q

Intestine: Protein Lossing Enteritis

Causes

A

Lymphangiectasia

parasitism

Inflammation

Accumulation/amyloid

89
Q

Intestine: Protein Lossing Enteritis

Lymphangiectasia

A

MDx: canine intestinal lymphangiectasia

Pathogenesis: Can be primary or secondary → failure of lymphatic flow, dilation of lymphatics and lacteals

Hyperproteinemia, lymphopenia, hypocholestrolemia

90
Q

Intestine: Malassimilation

A

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
Q

Intestine: Diarrhea

A

Secretions and intake = 9L/day

Jejunum and ileum are major sites of absorption

Colon absorbs also within limits

92
Q

Intestine: Diarrhea

Small bowel diarrhea

A

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
Q

Intestine: Diarrhea

Large Bowel Diarrhea

A

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
Q

Intestine: Obstructions

Feline SI neoplasm

A

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
Q

Intestine: Obstruction

SI localized congestion/hemorrhage

A

MDx: Canine SI localized congestion/hemorrhage, obstruction

Pathogenesis: Small Intestine foreign body luminal obstruction → Distenstion, pain → vomiting → rupture or perforation → peritonitis

96
Q

Intestine: Intussusception

A

Luminal intrinsic obstruction and venous infarction

Systemic Pathology (4 decks)

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