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General Principles of GI System Flashcards

1
Q

What is the causes of palatoschisis (hard and soft palate)?

(cleft palate)

A
  • Genetic
  • hypervitaminosis A
  • Griseofulvin
  • toxic plants
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2
Q

What is “brachygnathia”

A

to short

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3
Q

what is “prognathia”?

A

too long

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4
Q

what is “agnathia”?

A

not there

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5
Q

What is wrong with this calf?

A

superior (maxilla) brachygnathia

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6
Q

What is Dental caries and its pathogenesis to causing sinus empyema (purulent sinusitis)

A
  • Loss of dental matrix
  1. Demineralization or enzymatic digestion
  2. Surface or pit caries
  3. Loss of enamel, dentin
  4. Tooth infundibular impaction of food material
  5. continued loss of enamel/dentin
  6. Instability
  7. Toot fracture
  8. Root inflammation and necrosis
  9. Extension into paranasal sinuses
  10. empyema
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7
Q

What is going on in the picture? What most likely caused it?

A
  • Enamel hypoplasia
  1. Canine Distemper Virus (or BVD in ruminants) infects ameloblasts
  2. enamel hypoplais
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8
Q

What is going on in the picture? how did this happen?

A
  • Maxillary and mandibular premolar and molar teeth malocclusion
  • Inappropriate wearing / premature toot attrition
    • “Wave mouth”
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9
Q

What is going on in the picture? How would this develop from dental malocclusion?

A
  • Serous atrophy of fat, pericardial and perirenal adipose (not pictured)
  1. Dental malocclusion
  2. Inability to prehend and chew food
  3. Starvation
  4. mobilization of body fat stores/serous atrophy
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10
Q

What are the different inflammations that can occur in the oral caviy?

A
  • Stomatitis
  • glossitis
  • gingivitis
  • cheilitis
  • tonsilitis
  • pharyngitis
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11
Q

What is the difference between deep and superficial inflammation?

A
  • Superficial = surface
    • caustic, toxic, electric, sunburn, infection
  • Deep = deeper connective tissues of the oral cavity
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12
Q

give a morphologic diagnosis and a possible cause

A
  • Cat lip eosinophilic granuloma or ulcerative granulomatous cheilitis
  • Unknown path, chronic inflammation probably immune mediated
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13
Q

Diagnosis and possible pathogenesis?

A
  • Lymphocytic gingivitis/stomatitis
    • Inappropriate oral care ⇢ periodontal disease
  • Canine ulcerative paradental stomatitis (CUPS)
    • immune mediated can be severe
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14
Q

Morphologic diagnosis and possible pathogenesis?

A
  • Bovine oral ulcer
  • Direct epithelial damage by virus, potentially ischemic damage or trauma
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15
Q

If this lesion was in a pig what virus should be considered?

A

Seneca Valley Virus (Picornavirus)

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16
Q

Morphologic diagnosis and possible pathogenesis?

A
  • Cat tongue vesicles and ulcers (vesicular/ulcerative glossitis)
  • FCV, FHV-1, uremia, immune-mediated/pemphigus, trauma ⇢ direct epithelial necrosis, possibly ischemic damage
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16
Q

Morphologic diagnosis and possible pathogenesis?

A
  • Cat tongue vesicles and ulcers (vesicular/ulcerative glossitis)
  • FCV, FHV-1, uremia, immune-mediated/pemphigus, trauma ⇢ direct epithelial necrosis, possibly ischemic damage
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17
Q

Morphologic diagnosis and possible pathogenesis?

A
  • bovine oral ulcer (ulcerative stomatitis)
  • BVDV, IBR, MCF, vesicular dzs, caustic substances ⇢ direct epithelial necrosis, possibly ischemic damage
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18
Q

Morphologic diagnosis and possible pathogenesis?

A
  • Bovine oral cavity, proliferative/papular stomatitis (oral mucosa) and cheilitis (lips)
  1. Bovine papular stomatitis virus (parapox)
  2. Direct infection of oral epithelium
  3. Proliferation of epithelium a
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19
Q

Morphologic diagnosis and possible pathogenesis?

A
  • Lip proliferative cheilitis
  1. Sheep parapox virus
  2. Infection of epithelium
  3. Proliferation, necrosis (contagious ecthyma)

*******ZOONOTIC*******

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20
Q

Morphologic diagnosis and possible pathogenesis?

A
  • Bovine pyogranulomatous / necrotizing glossitis
  1. Actinobacillus lignieresi infection via trauma damage or wound oral epithelium
  2. Invades dep structures (connective tissue and muscle) “Wooden Tongue”
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21
Q

Morphologic diagnosis and possible pathogenesis?

A
  • Pyogranulomatous ad necrotizing osteomyelitis
    1. Actinomyces bovis - similar to A. ligniersi but also involves bone “Lumpy Jaw”
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22
Q

Morphologic diagnosis and possible pathogenesis?

A
  • Bovine fibrinous and necrotizing laryngitis (calf diphtheria)
  1. physical or viral -induced damage or trauma to surface epithelium and cartilages
  2. Fusobacterium necrophorum invades from the oral cavity
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23
Q

what is ptyalism

A
  • over production of saliva
  • Causes:
    • ingestion of caustic substances,
    • OP
    • foreign bodies
    • rabies
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24
Q

what is a salivary ranula, mucocele/sialocele?

A

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

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25
Q

What is this mass?

A
  • Gingival or fibrous hyperplasia
  • Common Dogs>cats
  • Non-neoplastic
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26
Q

What is this mass?

A
  • Peripheral odontogenic fibroma
  • Stromal neoplasm of periodontal ligament of origin
  • Can have bone, dentin
  • Benign
  • can be difficult to completely excise
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27
Q

What is this mass?

A
  • acanthomatous ameloblasta
  • Odontogenic epithelium (ameloblasts)
  • Locally invasive into bone, do not metastasize
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28
Q

What is this mass?

A
  • Squamous cell carcinoma
  • # 1 in cats
  • # 2 in dogs
  • Tongue>gingiva>tonsils,
  • locally invasive into soft tissue and bone
  • metastasize late to node or lungs
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29
Q

What is this mass?

A
  • oral (malignant) melanoma
  • # 1 in dogs
  • can be pigmented or amelanotic
  • most are malignant with local invasion and distant metastasis
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30
Q

What is this mass?

A
  • Oral papillomas
  • Canine oral papillomavirus
  • Often spontaneously regress
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31
Q

Morphilogical Dx? Pathogenesis?

A
  • Canine mf distal esophageal ulcer
  • chronic gastric reflux ⇢ direct damage to epithelium
  • Viral infection
  • Caustic substance
  • Ischemic damage/vasculitis/thrombosis
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32
Q

Morphilogical Dx? Pathogenesis?

A
  • Canine megaesophagus
  • Can be congenital ⇢ physical obstruction
  • Can be acquired ⇢ failure of nerve or muscle of the esophagus
    • Due to myasthenia gavis, SLE, polyneuritis/myositis
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33
Q

Morphilogical Dx? Pathogenesis?

A
  • Bovine esophageal obstruction (choke)
  1. foreign body obstruction ⇢inability to eructate gas/free gas bloat
  2. Or local ischemia, inflammation, perforation
    1. wound healing
    2. fibrosis/stricture
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34
Q

Morphilogical Dx? Pathogenesis?

A
  • Canine granulomatous esophagitis
  1. Spirocerca lupi infection
  2. Inflammation
  3. esophageal sarcoma
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35
Q

What are Forestomachs?

A
  • nonglandular fermentation vat
  • pH 5.5-7
  • Some definitive diagnoses can be made here
36
Q

Morphilogical Dx? Pathogenesis?

A
  • Bovine rumen bloat
  1. Ante-mortem rumen bloat
  2. diaphragm pushed cranially
  3. increased thoracic pressure
  4. compressed venous return
  5. lack of venous flow into thorax
37
Q

What chases Rumen bloat?

A
  • Frothy bloat:
    • primary tympany due to foam production (soluble proteins of legumes, pectins, pH, reduced saliva production)
    • Path:
      1. Ingestion of legumes
      2. foam formation at surface
      3. prevention of gas cap formation
      4. prevention of eructation
      5. rumen bloat
      6. increased intrathoracic pressure
      7. inhibits respiration, cardiac function
      8. reduced cardiac venous return (at least up to the thoracic inlet
  • Free gas bloat
    • secondary tympany due to physical or functional defect in eructation (chock peritonitis, abscesses)
38
Q

Morphological Dx? Pathogenesis?

A
  • Bovine rumen acidosis = neutrophilic ruminitis and parakeratosis (Sticky papilla)
  1. excess CHO ingestion
  2. altered microbial flora
  3. excess lactic acid produciton
  4. pH falls
  5. rumen atony
  6. reduced saliva production (reduced buffering capacity)
  7. increase rumen osmotic pressure
  8. direct epithelial damage
  9. bacterial translocation across rumen mucosa
39
Q

Morphological Dx?

A

parakeratosis, neutrophilic rumenitis

40
Q

Morphological Dx? Pathogenesis?

A
  • Bovine rumen erosion, ulceration, scarring (fibrosis) random hepatic abscesses (not pictured)
  1. Rumen acidosis
  2. rumen surface erosion and ulcers
  3. loss of papilla
  4. translocation of rumen organisms across compromised rumen wall into portal vein and liver with hepatic abscess formation Or chronic fibrosis/scarring
41
Q

Morphological Dx? Pathogenesis?

A
  • Rumen infarction (vascular thrombosis, necrosis and hemorrhage)
  • Can involve any forestomach compartment
  1. Rumen acidosis
  2. opportunistic oxygen-loving fungi travel across compromised rumen wall
  3. invade blood vessels
  4. vasculitis, thrombosis, ischemia, infarction
42
Q

Morphological Dx? Pathogenesis?

A
  • Bovine diaphragm, foreign body penetration , fibrinous pleuritis and peritonitis
    1. Acute or chronic consequence of foreign body penetration
43
Q

Morphological Dx? Pathogenesis?

A
  • Bovine reticulum focal fibrosis
    1. chronic consequence of foreign body penetration
44
Q

Morphological Dx? Pathogenesis?

A
  • Bovine fibrinous peritonitis
  1. foreign body penetration through forestomachs into abdomen
  2. inflammation
45
Q

What are some injuries of the stomach?

A
  • Dilation, displacement
  • obstructions
  • circulatory distrubances
  • Inflammation
    • gastritis
    • gastric ulceration
  • Distrubances of growth
46
Q

What is the normal form and function of the stomach/abomasum?

A
  • Fundic mucosa is the source of HCl (parietal cells) and pepsin (chief cells)
  • HCl is stimulated by histamine, acetylcholine, gastrin
  • The cardiac and pyloric mucosa also secrete mucus and HCO3
  • The squamous mucosa is highly sensitive to acid and bile
  • protective prostaglandin E, stimulates mucus and HCO3 inhibits histamine production, causes vasodilation and increased blood flow
47
Q

What are the stomach’s responses to injury?

A
  • Restoration
    • can be completed following erosive physical or chemical trauma
    • rapid
  • Atrophy of parietal cell mass
    • with chronic inflammation
  • Mucous metaplasia and hyperplasia
    • with chronic inflammation
48
Q

Morphologic Dx? Pathogenesis?

A
  • Equine gastric rupture
  1. Gastric distension (excess CHO) or outflow obstruction
  2. increased pressure
  3. rupture, typically along the greater curvature
49
Q

Morphologic Dx? Pathogenesis?

A
  • Canine gastric dilation with volvulus, venous infarction of spleen and stomach
  1. Accumulation of gas/food/fluid and distention of stomach
  2. dilation +/- rotation
  3. venous infarction
  4. reduced cardiac outpute
  5. severe circulatory shock
  6. sudden/acute death
50
Q

Can the bovine abomasum become displaced?

A
  • Left displacement
    • most common - rarely seen in necropsy
  • Right displacement
    • less common, can progress to volvulus and death
51
Q

Morphologic Dx? Pathogenesis?

A
  • Pig stomachs (squamous portion) the cardia:
    • normal (left) progressing to partial then complete ulceration, with hemorrhage (right)
  • Path varies:
  1. Duodenal reflux (bile salts), NSAIDs, increased acid, ‘stress’ glucocorticoids, finely ground grains, MCT/histamine, reduced protective mucus/HCO3
  2. hemorrhage, ulceration ,perforation, peritonitis, healing/fibrosis, and stricture
52
Q

Morphologic Dx? Pathogenesis?

A
  • Canine gastric hyperemia, congestion, hemorrhage (and mineralization)
  1. Uremia (dogs>>cats, horses)
  2. vasculitis of submucosal blood vessels (circulating toxins) and/or thrombosis
  3. Ischemia (can also affect other organs such as tongue, oral cavity, kidneys
53
Q

Morphologic Dx? Pathogenesis?

A
  • Horse gastric bots
  • Gasterophilus sp
54
Q

Morphologic Dx? Pathogenesis?

A
  • Bovine abomasum proliferative abomasitis
  • Chronic Ostertagia ostertagii
55
Q

Morphologic Dx? Pathogenesis?

A
  • Dog stomach Physaloptera canis
56
Q

Morphologic Dx? Pathogenesis?

A
  • Sheep abomasum
  • Haemonchus contortus
57
Q

Morphologic Dx? Pathogenesis?

A
  • Bovine abomasal lymphoma (with mf ulcers)
    • Note thickened white firm tissue in wall of abomasum
  1. Linked to BLV in cattle (can involve other forestomachs, heart, uterus, spinal cord
58
Q

Morphologic Dx? Pathogenesis?

A
  • Canine gastric adenocarcinoma (with ulceration)
    1. Spontaneous, tend to be infiltrative and cause thickening, loss of gastric rugae, but not pedunculated masses
59
Q

Morphologic Dx? Pathogenesis?

A
  • Equine gastric squamous cell carcinoma
    1. spontaneous, may be linked to chronic gastric inflammation or ulceration, tend to be infiltrative and widely metastatic
60
Q

Morphologic Dx? Pathogenesis?

A
  • Equine sever diffuse colonic hypoplasia
  1. Spontaneous is some species, in horses intestinal aganglionosis is genetic
    1. Overox overo paint horses, lethal white foal syndrome
61
Q

Morphologic Dx? Pathogenesis?

A
  • Lamb small intestinal atresia (blind end)
  1. Spontaneous or genetic mostly
    1. in cattle this has been linked to early rectal/pregnancy palpation
62
Q

What is the normal intestine?

A
  • SI normal tall villi, short crypts
    • crypt/villus ratio varies by species and age
  • Proliferative compartment is crypts
  • Cells shed from tips in 2-8 days
63
Q

What is the SI response to injury?

A
  • SI severe blunting and fusion of villi with crypt hyperplasia
  • More cells, crowding, proliferation (more mitotic figures) and they are less differentiated (loss of polarity)
64
Q

What is Villous atrophy?

A
  • Common change in domestic animals that leads to malabsorption and/or plasma protein loss into the gut
  • Villous atrophy with an intact or hyperplastic proliferative compartment:
    • Primary increased rate of loss or targeting of villar epithelium
      • Ex: coronavirus, rotavirus, coccidia, enteroinvasive bacteria, transient ischemia, some necrotizing toxins
    • Primary crypt hyperplasia due to a chronic or persistent process which alters the microenvironment
      • Ex: nematode parasitism, chronic coccidial infection, giardiasis, granulomatous enteritis, chronic IBD, Lawsonia
  • Villous atrophy associated with damage to the proliferative compartment
    • Ionizing radiation, cancer therapeutics, parvovirus, BVDV and rinderpest viruses
65
Q

What are the mechanisms and causes of Protein Loss enteritis (PLE)

A
  • Mechanisms
    • Loss of enterocytes
    • Protein into the lumen
    • malabsorption
  • Causes:
    • lymphangiectasia
    • parasitism
    • inflammation
    • accumulation/amyloid
66
Q

Morphologic Dx? Pathogenesis?

A
  • Canine intestinal lymphangiectasia (intestinal mucosa is thickened and ‘shaggy’
  • Also Hypoproteineia, lymphopenia, hypocholesterolemai
  1. Primary (idiopathic) or secondary (to lymphatic obstruction)
  2. Failure of lymphatic flow
  3. Dilation of lymphatics and lacteals
67
Q

What is the difference between maldigestion and malabsorption

A
  • Maldigestion
    • Intraluminal Phase - bile, pancreatic secretion (exocrine pancreatic insufficiently)
  • Malabsorption
    • Epithelial and delivery phase - nutrients are delivered from enterocytes to blood via interstitial fluid
      • reduced surface area - villus atrophy, short-bowel syndrome
      • Biochemical lesion of enterocyte - lipids, polysaccharides, protein
68
Q

Morphologic Dx? Pathogenesis?

A
  • Canine pancreatic atrophy or hypoplasia (not there)
  1. Failure to form or damage/loss
  2. exocrine pancreatic insufficiency
69
Q

What are the mechanisms of diarrhea?

A
  • Malabsorption - osmotic diarrhea, usually SI
  • Hypersecretion - intact mucosa, occurs as a result of net efflux of fluid and electrolytes independent of permeability changes or absorptive capacity
  • Effusive - increased capillary pressure or epithelial permeability (PLE)
  • Hypermotility - uncommon in domestic animals
70
Q

What is Small bowel diarrhea and causes?

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 or severe epithelial necrosis
71
Q

What is Large bowel diarrhea and causes?

A
  • Frequent passage of small volumes of liquid feces, often with straining, blood, mucus
  • malabsorptive - colitis, tumor
  • secretory - hydroxylated fatty acids, bile salts, lare bowel not as ‘leaky’
72
Q

What are the types of intestinal obstructions?

A
  • Intrinsic - from inside
  • extrinsic - from outside
  • functional - no physical blockage
73
Q

Morphologic Dx? Pathogenesis?

A
  • feline Si neoplasm (lymphoma - hx)
  1. Spontaneous
    1. linked to FeLV
74
Q

Morphologic Dx? Pathogenesis?

A
  • Canine SI localized congestion/hemorrhage, obstruction
  1. SI foreign body - luminal obstruction
  2. distension, pain
  3. vomiting
  4. rupture / perforation
  5. peritonitis
75
Q

What is the difference between intussuscipiens and intussusceptum

A
  • During intussusception
  • Red = intussuscipiens - outer intestine
  • Blue = Intussusceptum - inner intestine
  • Also in picture - luminal intrinsic obstruction and venous infarction
76
Q

Morphologic Dx? Pathogenesis?

A
  • localized intestinal venous infarction
  1. mesenteric lipoma
  2. stalk wraps around small intestine
  3. strangulation (implies involvement of vascular supply
77
Q

Morphologic Dx? Pathogenesis?

A
  • megacolon
  1. distal spinal cord deformity (see inset picture)
  2. clononic neuropathy
  3. Adynamic ileus of colon
  4. functionobstruction
  5. megacolon
78
Q

Morphologic Dx? Pathogenesis?

A
  • Horse diaphragmatic (interna) hernia; intestinal displacement (into thoracic cavity), venous infarction
  1. usually acquired and traumatic
  2. diaphragmatic perforation
  3. moves into wrong space; others include epiploic foramen entrapment, mesenteric rent entrapment
79
Q

Morphologic Dx? Pathogenesis?

A
  • Calf umbilical hernia
  • # 1 congenital defect of cattle
  1. congenital defect
  2. failure to close
  3. passage of intestinal or other abdominal contents into sac
80
Q

Morphologic Dx? Pathogenesis?

A
  • Calf, mesenteric root volvulus, with SI venous infarction
    1. Spontaneous, possibly linked to peristalsis
81
Q

Left or right dorsal displacement?

A
  • Right dorsal displacement: colon moved to the right of cecum
  • Left dorsal displacement:* left colons are moved laterally and dorsally and trapped between spleen and abdominal wall and kidney (nephrosplenic entrapment)
82
Q

What causes ischemia in the intestines?

A
  • Inadequate blood supply to a local area
  • Causes:
    • obstruction of efferent vessels
    • blockage of afferent arterioles
    • reduced flow through an open circulation
83
Q

What is the timeline of ischemia in the SI?

A
  • 5-10m - changes at villar tips (swelling, separation of epithelium
  • 30m - advanced changes, progress towards crypts
  • 1-2hr - villus epithelium gone, mesenchymal core and villi collapse
  • 2-4hr - epithelium completely necrotic and sloughed
  • 4-6hr - basement membrane is damaged, ischemia beyond this will not recover
  • 6-7hr - muscularis externa becomes necrotic
84
Q

What is reperfusion?

A
  • Tissue changes occurring after blood flow has been restored
  • Complex interplay between:
    • Free radicals xanthine oxidase is key enzyme; NADPH oxidase in leukocytes
    • Microvascular damage by free radicals
    • neutrophils (resident and recruited)
    • Complement
    • Proinflammatory cytokines such as TNFa, IL1, etc…
85
Q

What is the sequela of ischemia?

A
  • Short term (3-4hr) ischemia: crypts are preserved and re-epithelialization occurs in 1-3 days
  • Small ulcers ⇢ acute inflammatory response ⇢ granulation tissue
  • Larger ulcers are unble to be fully resolved ⇢healing by fibrosis ⇢strictures
86
Q

What are the types of infarction?

A
  • Atrial
  • venous
87
Q

Morphological Dx? Pathogenesis?

A
  • Cranial mesenteric arteritis with parasite larva and thrombosis
  1. Ingestion of L4 S. vulgaris
  2. Migration to cranial mesenteric artery
  3. arteritis/thrombosis
  4. downstream effects of thromboembolization

Systemic Pathology (19 decks)

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