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
What population of dogs is retained deciduous teeth common in?
toy breeds
26
How can retained deciduous teeth cause disease?
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
27
What is enamel formed by?
ameloblasts
28
When is enamel formed?
only during tooth development
29
What is required for proper enamel development?
healthy ameloblasts and proper tooth nutrition
30
What can cause focal insult to ameloblasts?
infection and trauma
31
What can cause generalized ameloblast damage?
severe pyrexia, epitheliotrophic viruses, toxins, and nutrition
32
What do teeth look like with enamel hypoplasia?
teeth will have a roughened, discolored surface with discreet pitting or circumferential band-like irregularities
33
Localized insult such as trauma causes enamel hypoplasia to how many teeth?
usually just a single tooth
34
A systemic condition can cause damage to how many teeth?
usually widespread involvement affecting portions of several teeth producing enamel at the time of the insult
35
True or False: Enamel defects are present at tooth reuption
TRUE
36
What is the pathogenesis of enamel hypoplasia from CDV?
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
What is the pathogenesis of enamel hypoplasia caused by fluorine in cattle?
1. Flourine is toxic to ameloblasts and dentinoblasts | 2. Exposure to escessive fluoride during tooth formation results in enamel hypoplasia
38
How do teeth typically appear with enamel hypoplasia due to flourine?
teeth are mottled, stained, and have a pitted, chalky surface
39
What is dental attrition?
wearing down of the teeth by friction
40
Irregularities of wear are common in what animals?
in animals that chew a lot especially in horses
41
If a horse isn't eating and there is weight loss what should you suspect as the cause?
sharp enamel points which can lacerate the tongue and cause horses to stop eating
42
What is malocclusion?
misalignment of teeth of the upper and lower arcade
43
What are clinical signs associated with malocclusion in rabbits?
anorexia, weight loss, facial abscesses, exophthalmos, ocular discharge, drooling, small fecal pellets
44
What are the three general categories of diseases of the oral cavity?
congenital/developmental vesicular, ulcerative, exudative lesions mass lesions
45
What things can cause vesicular, ulcerative, exudative lesions?
viral, bacterial, fungal, parasitic, metabolic, traumatic/toxic, immune mediated/autoimmune, invasive neoplasia
46
What are the processes that cause mass lesions?
hyperplasia, neoplasia, inflammation
47
What is cleft palate?
inadequate growth and failure of fusion of the palatine shelves
48
What is cleft palate bad?
because it allows communication between the oral and nasal cavitites
49
What are important sequelae to cleft palate?
aspiration pneumonia and chroniic rhinitis
50
What are some common differentials for oral vesicular lesions?
viral infections or immune mediated
51
What is the pathogenesis for viral vesicular/ulcerative lesions?
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
What feline viruses typically cause oral cavity lesions?
feline calicivirus and feline viral rhinotracheitis
53
What systemic signs are associated with vesicular viral oral cavity lesions?
fever, upper respiratory tract disease, and conjunctivitits
54
What lesions are associated with calicivirus?
oral vesicles and ulcers
55
What oral lesions are associated with viral stomatitis of ruminants?
multifocal vesicular to ulcerative glossitis and stomatitis
56
What systemic signs are associated with vesicular/Ulcerative viral stomatitis of ruminants?
fever, oculonasal discharge, diarrhea
57
What species are affected by pemphigus vulgaris?
dogs, cats, and horses
58
What lesions are associated with pemphigus vulgaris?
vesiculobullus and ulcerative lesions identified in the oral cavity and mucocutaneous junctions
59
What causes pemphigus vulgaris?
antibodies directed against desmosomal antigens of keratinocytes and the mucosal epithelium
60
What are some common differentials for ulcerative oral lesions?
neoplasia, trauma, bacterial, fungal, metabolic, and toxic
61
What is the pathogenesis of bacterial stomatitis?
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
What are some bacteria associated with bacterial stomatitis?
Fusobacterium necrophorum, Actinobacillus lignieresii, Trueperella pyogenes
63
What oral lesions are associated with uremia?
fetid, ulcerative stomatitis, ulcerative glossitis, gastric congestion, edema +/- focal ulcerations
64
What is thrush?
a fungal infection of the mouth -
65
What species are typically affected by thrush?
foals, pigs, dogs, and avians
66
What lesions are associated with thrush?
whitish, velvety plaques in the mouth and on the tongue
67
What can cause mycotic stomatitis?
disruption of normal microflora and immunosuppresion
68
What can cause immunosuppresion that leads to mycotic stomatitis?
steroid administration, chemotherapy, very old or very young, immunodeficiency