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Anatomic Pathology 2 > Unit 3 - GI Lecture 1 > Flashcards

Unit 3 - GI Lecture 1 Flashcards

1
Q

What is the most vital structural defense in the digestive tract?

A

the mucosal epithelium

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2
Q

What is the role of the mucosal epithelium in the digestive tract?

A

it forms a physical barrier between the luminal contents and the more susceptible deeper structures

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3
Q

What can losing mucosal integrity lead to (generally)?

A

focal fungal/bacterial infection of surface mucosa or access of organisms to depper tissues leading to bacteremia/septicemia

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4
Q

How does ruminal acidosis lead to mycotic rumenitits?

A

ruminal acidosis causes a disruption of mucosal intergity allowing normal rumen fungi to colonize mucosal defects and cause mycotic rumenitis

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5
Q

How does gastrointestinal venous drainage pass through the liver?

A

the GIT mucosal integrity is lost, the bacteria enter venous circulation and thus there is a bacterial infection of the liver

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6
Q

What is the result of gastrointestinal venous drainage passing through the liver?

A

multifocal hepatic abscesses

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7
Q

What are the biochemical protective mechanisms of the digestive tract?

A

gastic acid secretion, buffers in secretions, mucus, and secretion of digestive enzymes in an inactive proenzyme form

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8
Q

What are consequences of biochemical protective mechanism failure?

A

microbial overgrowth and gastric ulceration

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9
Q

What is achlorhydria?

A

when there is no gastric acid in the stomach

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10
Q

What does achlorhydria lead to?

A

microbial overgrowth, an increased risk of infections, and diarrhea

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11
Q

What can cause gastric ulceration?

A

NSAIDs cause decreased production of gastric mucus and bicarbonate which can facilitate gastric ulcer formation

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12
Q

What is the pathogenesis of NSAIDs causing ulcer formation?

A
  1. NSAIDs
  2. Decreased prostaglandin E2 production
  3. Decreased bicarbonate and decreased mucus secretion and decreased blood flow
  4. gastic ulcer formation
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13
Q

How is motility in the digestive tract a protective mechanism?

A

it keeps ingesta, secretions and gas moving through the intestinal tract with eventual removal of waste products and does not allow organisms to build up in segments of the GIT

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14
Q

What is the consequence of failure of motility in the GI tract?

A

localized bacterial overgrowth

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15
Q

What can predispose to pigs to get E.coli enteritis?

A

low temperatures due to decreased peristalsis

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16
Q

How are microflora protective mechanisms of the GIT?

A

colonization with commensal bacteria and protozoa aids digestion, stimulates proper mucosal development and helps to prevent pathogenic organisms from attaching and invading the mucosa

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17
Q

What can result in aberrant microflora?

A

neonates not having competitive microflora, disruption by dietary changes, and disruption by antibiotics

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18
Q

How does Clostridium difficile colonize?

A

the colonic flora are disrupted by antibiotics

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19
Q

How is inflammation and nonspecific immunity protective in the GIT?

A

inflammation and nonspecific immunity helps control invasion of organisms, specific humoral and cell mediated immunity act locally and systemically to eliminate specific pathogenic organismsf

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20
Q

What is TGE?

A

transmissible gastroenteritis

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21
Q

What is TGE caused by?

A

coronavirus

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22
Q

What is largely protective against TGE?

A

lactogenic immunity

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23
Q

When are pigs most susceptible to TGE?

A

when they are less than 2 weeks of age

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24
Q

What are the structures in the upper digestive tract?

A

oral cavity (teeth, tongue, mucosa, pharynx), esophagus, forestomachs

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25
Q

What population of dogs is retained deciduous teeth common in?

A

toy breeds

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26
Q

How can retained deciduous teeth cause disease?

A
  1. Permanent teeth to erupt in abnormal positions
  2. Overcrowding of teeth
  3. Accidental bites to the palate/gums
  4. Abnormal jaw position
  5. Development of plaque with associated gingivitis/periodontal disease
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27
Q

What is enamel formed by?

A

ameloblasts

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28
Q

When is enamel formed?

A

only during tooth development

29
Q

What is required for proper enamel development?

A

healthy ameloblasts and proper tooth nutrition

30
Q

What can cause focal insult to ameloblasts?

A

infection and trauma

31
Q

What can cause generalized ameloblast damage?

A

severe pyrexia, epitheliotrophic viruses, toxins, and nutrition

32
Q

What do teeth look like with enamel hypoplasia?

A

teeth will have a roughened, discolored surface with discreet pitting or circumferential band-like irregularities

33
Q

Localized insult such as trauma causes enamel hypoplasia to how many teeth?

A

usually just a single tooth

34
Q

A systemic condition can cause damage to how many teeth?

A

usually widespread involvement affecting portions of several teeth producing enamel at the time of the insult

35
Q

True or False: Enamel defects are present at tooth reuption

A

TRUE

36
Q

What is the pathogenesis of enamel hypoplasia from CDV?

A
  1. Canine Distemper virus infects epithelial cells
  2. CDV causes epithelial necrosis, including necrosis of infected ameloblasts during tooth development
  3. Enamel hypoplasia of the tooth being formed at the time of infection
37
Q

What is the pathogenesis of enamel hypoplasia caused by fluorine in cattle?

A
  1. Flourine is toxic to ameloblasts and dentinoblasts

2. Exposure to escessive fluoride during tooth formation results in enamel hypoplasia

38
Q

How do teeth typically appear with enamel hypoplasia due to flourine?

A

teeth are mottled, stained, and have a pitted, chalky surface

39
Q

What is dental attrition?

A

wearing down of the teeth by friction

40
Q

Irregularities of wear are common in what animals?

A

in animals that chew a lot especially in horses

41
Q

If a horse isn’t eating and there is weight loss what should you suspect as the cause?

A

sharp enamel points which can lacerate the tongue and cause horses to stop eating

42
Q

What is malocclusion?

A

misalignment of teeth of the upper and lower arcade

43
Q

What are clinical signs associated with malocclusion in rabbits?

A

anorexia, weight loss, facial abscesses, exophthalmos, ocular discharge, drooling, small fecal pellets

44
Q

What are the three general categories of diseases of the oral cavity?

A

congenital/developmental
vesicular, ulcerative, exudative lesions
mass lesions

45
Q

What things can cause vesicular, ulcerative, exudative lesions?

A

viral, bacterial, fungal, parasitic, metabolic, traumatic/toxic, immune mediated/autoimmune, invasive neoplasia

46
Q

What are the processes that cause mass lesions?

A

hyperplasia, neoplasia, inflammation

47
Q

What is cleft palate?

A

inadequate growth and failure of fusion of the palatine shelves

48
Q

What is cleft palate bad?

A

because it allows communication between the oral and nasal cavitites

49
Q

What are important sequelae to cleft palate?

A

aspiration pneumonia and chroniic rhinitis

50
Q

What are some common differentials for oral vesicular lesions?

A

viral infections or immune mediated

51
Q

What is the pathogenesis for viral vesicular/ulcerative lesions?

A
  1. Viral-induced vacuolar degeneration of mucosal epithelial cells
  2. Degenerate cells die and form small vesicles
  3. Small vesicles coalesce
  4. Large vesicles form that are fragile and rupture
  5. Ruptured vesicle develops into an ulcer
52
Q

What feline viruses typically cause oral cavity lesions?

A

feline calicivirus and feline viral rhinotracheitis

53
Q

What systemic signs are associated with vesicular viral oral cavity lesions?

A

fever, upper respiratory tract disease, and conjunctivitits

54
Q

What lesions are associated with calicivirus?

A

oral vesicles and ulcers

55
Q

What oral lesions are associated with viral stomatitis of ruminants?

A

multifocal vesicular to ulcerative glossitis and stomatitis

56
Q

What systemic signs are associated with vesicular/Ulcerative viral stomatitis of ruminants?

A

fever, oculonasal discharge, diarrhea

57
Q

What species are affected by pemphigus vulgaris?

A

dogs, cats, and horses

58
Q

What lesions are associated with pemphigus vulgaris?

A

vesiculobullus and ulcerative lesions identified in the oral cavity and mucocutaneous junctions

59
Q

What causes pemphigus vulgaris?

A

antibodies directed against desmosomal antigens of keratinocytes and the mucosal epithelium

60
Q

What are some common differentials for ulcerative oral lesions?

A

neoplasia, trauma, bacterial, fungal, metabolic, and toxic

61
Q

What is the pathogenesis of bacterial stomatitis?

A
  1. Disruption of integrity of the oral mycosa (primary viral infection, trauma, uremia)
  2. Colonization of defect by bacteria, often normal flora
  3. Ulcerative bacterial stomatitis
62
Q

What are some bacteria associated with bacterial stomatitis?

A

Fusobacterium necrophorum, Actinobacillus lignieresii, Trueperella pyogenes

63
Q

What oral lesions are associated with uremia?

A

fetid, ulcerative stomatitis, ulcerative glossitis, gastric congestion, edema +/- focal ulcerations

64
Q

What is thrush?

A

a fungal infection of the mouth -

65
Q

What species are typically affected by thrush?

A

foals, pigs, dogs, and avians

66
Q

What lesions are associated with thrush?

A

whitish, velvety plaques in the mouth and on the tongue

67
Q

What can cause mycotic stomatitis?

A

disruption of normal microflora and immunosuppresion

68
Q

What can cause immunosuppresion that leads to mycotic stomatitis?

A

steroid administration, chemotherapy, very old or very young, immunodeficiency

Anatomic Pathology 2 (48 decks)

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