GIT Pathology 1 Flashcards

1
Q
  1. What overlies bone and muscle in the oral cavity?
  2. In oesophagus, forestomachs, stomach, intestine?
A
  1. Mucosa.
  2. Mucosa part of multi-layered wall of a tubular or saccular structure.
    Various specialisations for the mucosa
    - protective, increased SA.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. What type of epithelium lines the upper alimentary tract?
  2. What underlies the epithelium in the upper alimentary tract?
A
  1. Stratified squamous epithelium.
  2. Lamina propria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. In the oesophagus, what forms the boundary superficial to the mucosa?
  2. What underlies this boundary?
  3. What is the next layer?
  4. What is the most superficial layer?
A
  1. Muscularis mucosa.
  2. Submucosa.
  3. Muscularis externa (circular, longitudinal).
  4. Adventitia or serosa.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What defines the difference between an erosion and an ulcer at mucosal sites?

A

Erosion means damage only going into epithelium and no further, not getting through the basement membrane.
- will heal by epithelial proliferation.
Ulcer means damage goes into epithelium and through the basement membrane and into lamina propria - could go all the way.
- granular tissue will probably form.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Main disease mechanisms/processes affecting the alimentary tract.

A

Congenital anomalies.
Hypertrophy/hyperplasia.
Neoplasia.
Inflammation.
Circulatory disturbances.
FBs, obstruction, displacement, dilation.
Functional disorders - motility, digestion, absorption, secretory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Oral cavity abnormality types.

A

Congenital anomalies.
Inflammation.
Hypertrophy/hyperplasia.
Neoplasia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Oral cavity congenital anomalies.

A

Orofacial clefts.
- cleft lip (Harelip, Cheiloschisis) (primary).
- cleft palate (palatoschisis) (secondary).
- unilateral or bilateral.
- superficial or deep.
- one or the other, or concurrent.
Anomalies in jaw growth.
- brachygnathia = shortening of jaw.
- prognathia = elongation of jaw.
- mandibular or maxillary.
– can be difficult to establish which is abnormal relative to the other.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Potential consequences of cleft lip or cleft palate?

A

Impaired suckling.
Food enters nasal cavity.
Aspiration pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes an orofacial cleft?

A

Relatively common in some spp. and some breeds - relatively common in cattle and foals.
Often unknown cause.
Might include heritable factors or toxin/teratogens (some plants e.g. hemlock/drugs e.g. Griseofulvin).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Potential consequences of anomalies in jaw growth?

A

Malocclusion of the teeth.
- could result in orodental trauma.
- could result in abnormal tooth wear/overgrowth e.g. in rabbits.
- difficulty eating.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define…
1. Cheilitis.
2. Gingivitis.
3. Glossitis.
4. Pharyngitis.
5. Stomatitis.

A

Inflammation of…
1. lips.
2. gingiva.
3. tongue.
4. pharynx.
5. mouth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of oral inflammation.

A

Infectious agent.
- bacteria (oral microbiota), viruses, fungi/yeasts, parasites (Trichinella spiralis).
Physical injury.
- FBs, dental disorders, irritant/caustic chemicals, thermal injury.
Neoplasia (e.g. causing ulceration).
Uraemia - related to renal failure.
Some immune-mediated diseases.
Reduced secretions (e.g. saliva).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

General features of oral inflammation.

A

Acute or chronic:
- redness.
- swelling (less seen).
- heat.
- pain.
+/-
- vesicles.
- erosion/ulceration.
- necrotic debris.
- exudate.
- proliferative masses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can stomatitides (stomatitis) be classified?

A

Based on features of the primary/main lesion.
- vesicular.
- erosive/ulcerative.
- granulomatous.
- necrotising.
- lymphoplasmacytic.
- papular.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a vesicular stomatitides?
- Give examples.

A

Term generally used for oral vesicles caused by some epitheliotropic viral infections.
- E.g. FMDV in ruminants and pigs.
- E.g. vesicular stomatitis in ruminants, pigs, horses.
- E.g. Swine vesicular disease.
- E.g. vesicular exanthema of swine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. What is a vesicle?
  2. What can happen to vesicle in FMDV?
  3. Healing of vesicles in the mouth?
A
  1. Accumulation of fluid within the epithelium or between the epithelium and the lamina propria. They may coalesce to form bullae.
  2. Easily rupture and rapidly progress to erosions and ulcers due to fragility. Exudate and necrotic debris often then cover the surface of the ulcers/erosions, causing pain, hypersalivation, helping spread the virus.
  3. Granulation tissue formation and re-epithelialisation.
17
Q
  1. Erosive/ulcerative stomatitides.
  2. Causes of erosive/ulcerative stomatitides?
A
  1. Erosions/ulcerations common sequelae to many causes of injury or inflammation of mucosal surfaces.
  2. Infectious agents.
    - progression from vesicular stomatitis.
    - viral infections causing primary erosion or ulceration (e.g. BVDV, malignant catarrhal fever in cattle and deer (from ovine herpes), Bluetongue infection in sheep due to vasculitis, Feline calicivirus).
    Feline eosinophilic granuloma complex.
    Uraemia - often caused by renal failure.
    - ulceration of tongue, margins, bilateral.
    - foul smell, halitosis, dribbling.
    - bacteria in saliva can break down urea, w/ urease, into ammonia which is caustic.
    - vasculitis w/ thrombosis, losing blood supply.
    Trauma.
    - FBs e.g. grass awns, sticks, bones.
    - malocclusions.
    - iatrogenic e.g. dosing guns, dental instruments.
    Ingestion of caustic substances.
    Some rare autoimmune skin diseases.
18
Q

Granulomatous stomatitis.

A

Deeper secondary infections from ulcers and wounds by opportunistic bacteria – e.g. cellulitis, abscess due to Actinobacillus ligniereslii.
Leads to pyogranulomatous inflammation (wooden tongue),

19
Q

Necrotising stomatitis.

A

Wounds and damage to the oral cavity can lead to Fusobacterium necrophorum infection in cattle, pigs, sheep.
– bacterial toxins cause extensive necrosis, surface exudate, foul smell.
–> causes a diphtheritic membrane.
Animals can die of toxaemia, aspiration of the infectious material.

20
Q

Lymphoplasmacytic stomatitis.

A

Lots of lymphocytes and plasma cells dominating the inflammatory response.
E.g. feline chronic gingivostomatitis.
- severe inflammation, gingiva, buccal mucosa, and caudal oral mucosa.
- often ulcerative or proliferative lesions at the palatoglossal folds.
- may have evidence of concurrent oesophagitis on oesophagoscopy.
- suspected to be aberrant immune response to chronic antigenic stimulation – oral antigens.
- probably multifactorial – bacterial? viral? stress? –> bacteria in plaque thought to be main driving factor.
E.g. canine chronic ulcerative stomatitis.
- pain, ulcerative.
- “contact” or “kissing” ulcers often occur where mucosa lies against a tooth surface.
- obscure aetiology – abnormal immune response to dental plaque?

21
Q

Papular stomatitides - parapox viruses.

A

Sheep and goats = contagious ecthyma.
Cattle = bovine papular stomatitis.
Zoonotic.
Papules on lips, in oral cavity, may extend to oesophagus.

22
Q
A