Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVSOH 4 > Gastrointestinal Pathology > Flashcards

Gastrointestinal Pathology Flashcards

1
Q

Describe the mucosa of the gastrointestinal tract.

A

Oral cavity – mucosa overlying hard or soft tissues

Oesophagus, forestomaches, stomach, intestine – mucosa is part of a multi-layered wall of a tubular or saccular structure

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

What type of epithelium is in the upper alimentary tract?

A

Stratified squamous epithelium in the upper alimentary tract that may become keratinised. Beneath that there is another layer that supports that epithelium called the lamina propria, which is the supporting connective tissues that contains bloods vessels and glands.

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

Describe the histological layers of the oesophagus.

A
  • Mucosa made up of the epithelium and the lamina propria
  • Thin layer of muscularis mucosa and then submucosa beneath that
  • Deeper to that there is 2-3 layers of muscle and the outer layer in loose connective tissue
  • May/may not be covered by a mesothelial serosal surface (serosa or adevntitia if no serosal surface)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Erosion is going into the epithelium and not getting through the basement membrane. Ulcer can break through the basement membrane and can perforate through any number of deeper layers.

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

What are the main disease mechanisms affecting the alimentary tract?

A
  • Congenital anomalies
  • Hypertrophy/hyperplasia
  • Neoplasia
  • Inflammation
  • Circulatory disturbances
  • Foreign bodies, obstruction, displacement, dilation
  • Functional disorders – motility, digestion, absorption, secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is cheiloschisis and palatoschisis?

A

Orofacial clefts:

Cleft lip = harelip, cheiloschisis
Cleft palate = palatoschisis

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

What are the potential consequences of orofacial clefts?

A
  • Impaired suckling due to inability to generate the negative pressure due to cleft
  • Food enters nasal cavity
  • Aspiration pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is brachygnathia and proggnathia?

A

Anomalies in jaw growth:

Brachygnathia = short jaw
Prognathia = forward jaw

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

Define maxillary and mandibular jaw abnormalities.

A

Maxillary brachygnathism – shortness of the maxillae

Maxillary prognathism – prolongation of the maxillae

Mandibular brachygnathism – shortness of the mandibles

Mandibular prognathism – prolongation of the mandibles

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

What are the potential consequences of abnormalities in jaw growth?

A
  • Malocclusion of the teeth
  • Orodental trauma
  • Abnormal tooth wear/overgrowth
  • Difficulty feeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the potential causes of upper alimentary tract inflammation?

A
  • Infectious agents – bacteria (oral microbiota), viruses, fungi/yeasts, parasites
  • Physical injury – foreign bodies, dental disorders, irritant/caustic chemicals, thermal injury
  • Neoplasia, causing ulceration
  • Uraemia
  • Some immune-mediated diseases
  • Reduced secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the general features of upper alimentary tract inflammation?

A
  • Acute or chronic
  • Redness, swelling, pain, heat
  • With/without vesicles erosion or ulceration necrotic debris exudate proliferative masses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 6 classifications of stomatitides?

A

Vesicular
Erosive/ulcerative
Granulomatous
Necrotising
Lymphoplasmacytic
Papular

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

Describe the lesions of vesicular stomatitides.

A

Vesicles/bullae are fragile and easily ruptured and rapidly progress to erosions or ulcers

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

What are the causes of vesicular stomatitides?

A

Diseases with oral vesicles caused by epitheliotropic viral infections:

  • Foot and mouth disease (ruminants and pigs)
  • Vesicular stomatitis (ruminants, pigs, horses)
  • Swine vesicular disease
  • Vesicular exanthema of swine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some infectious causes of erosive/ulcerative stomatitides?

A
  • Progression from vesicular lesions in vesicular stomatitides
  • Viral infections causing primary erosion or ulceration
  • Feline calicivirus can cause oral vesicles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some non-infectious causes of erosive/ulcerative stomatitides?

A

Feline eosinophilic granuloma complex
Uraemia
Trauma
Ingestion of caustic substances
Some rare autoimmune skin diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does uraemia cause erosive/ulcerative stomatitides?

A

Uraemia caused by renal failure, ulceration of tongue, often bilaterally symmetrical, foul smelling, halitosis, dribbling

Urea converted to ammonia via oral bacteria and urease and/or peripheral vasculitis and thrombosis > mucosal ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the lesions of granulomatous stomatitides.

A

Mucosal ulcers and wounds are vulnerable to secondary infection, including by some bacteria in the normal oral flora.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the causes of granulomatous stomatitides?

A
  • Infection and inflammation may extend into deeper tissues
  • Actinobacillosis (stomatitis, glossitis, lymphadenitis)
  • Pyogranulomatous inflammation (Cattle, sheep, pigs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the lesions of necrotising stomatitides.

A

Surface exudate – fibrin, leucocytes and necrotic epithelium (diphtheritic membrane). Foul smelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the causes of necrotising stomatitides?

A

Necrotic stomatitis, oral necrobacillosis, calf diphtheria. Cattle, sheep, pigs, oropharyngeal mucosal damage with secondary infection with fusobacterium necrophorum. Bacterial toxins cause extensive necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How can feline chronic gingivostomatitis cause lymphoplasmacytic stomatitides?

A
  • Severe inflammation, gingiva, buccal mucosa and caudal oral mucosa
  • Ulcerative or proliferative lesions at the palatoglossal folds
  • Concurrent oesophagitis on esophagoscopy
  • Suspected aberrant immune response to chronic antigenic stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does canine chronic ulcerative stomatitis caused lymphoplasmacytic stomatitides?

A

Painful, ulcerative stomatitis. Contact or kissing ulcers often occur where the mucosa lies against a tooth surface. Abnormal response to dental plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What causes papular stomatitides?

A

Parapox viruses. Sheep and goats = contagious ecthyma, cattle = bovine popular stomatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe non-neoplastic and neoplastic oral masses.

A

Non-neoplastic – inflammatory and reactive hyperplastic or proliferative responses

Neoplastic – benign, benign but invasive, malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Define epulis.

A

A gingival growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the lesions of gingival/fibrous hyperplasia.

A
  • Result from chronic low-grade irritation, such as periodontal disease
  • Focal, multifocal or generalised
  • Pedunculated or sessile masses
  • Smooth or rough
  • May be ulcerated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What causes canine oral papillomatosis?

A
  • Canine papillomavirus-1 infection
  • Hyperplastic epithelial response to viral infection
  • Resolve spontaneously – 4-8 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the characteristics of peripheral odontogenic fibromas?

A
  • Arises from the periodontal ligament
  • Benign
  • Fibrous (collagenous) tissue
  • May contain hard tissues – bone, cementum, dentin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the characteristics of canine acanthomatous ameloblastomas?

A
  • Arises from odontogenic epithelium
  • Most frequently affects the rostral mandible but can occur anywhere in oral cavity
  • Benign (does not metastasise)
  • But often has aggressive behaviour with invasion of bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the most common oral neoplasm in cats?

A

Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the general features of squamous cell carcinomas?

A
  • Arises from stratified squamous mucosa lining the oral cavity, pharynx (and tonsils) and larynx
  • Malignant
  • Locally invasive
  • Tend to metastasize late in the clinical course
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the common sites of squamous cell carcinomas in cats?

A
  • Ventral surface of tongue/sublingual close to frenulum
  • Gingiva
  • Early tumour may appear as a small, raised, fleshy mass, or as an ulcerated area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Distinguish squamous cell carcinomas in cats and dogs.

A

Cats - highly invasive (soft tissues, bone) and may metastasize to local lymph nodes, rarely to lung

Dogs - common sites is gingiva (tonsils). Tonsillar SCC have much higher metastatic potential – metastatic spread is common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the most common malignant oral neoplasm in dogs?

A

Malignant melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the characteristics of malignant melanomas?

A
  • Common sites are the gums and lips
  • Can be very aggressive in infiltration
  • Local invasion of bone
  • Metastatic spread to local lymph nodes and often to distant sites
  • Often sessile, some pedunculated. May be ulcerated. Variable degree of pigmentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the common sites of fibrosarcomas?

A

Gingiva, palate

May invade underlying bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the metastatic ability of fibrosarcomas in dogs and cats?

A

Dogs - may metastasise, regional lymph metastases, pulmonary metastases

Cats - low metastatic potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How may cattle get neoplasms in the gastrointestinal or urinary tracts?

A

Cattle grazed on bracken fern can end up with neoplasms in the GIT or urinary tract due to the carcinogens they contain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the molar salivary gland?

A

In cats only – this is not a tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How do true salivary cysts form?

A
  1. Salivary gland duct blockage – congenital atresia, foreign body, salivary calculi, inflammation, strictures
  2. Duct remains intact
  3. Cystic dilation of the salivary gland or ducts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How do pseudocysts/sailoceles form?

A
  1. Salivary gland duct rupture – often small intraglandular duct
  2. Saliva pooling in soft tissues stimulate encapsulation and mild inflammation
  3. Fluid filled cavity in soft tissues of the mouth or neck
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are mucoceles and seroceles?

A

Mucocele – mucus content
Serocele – serous content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are ranula?

A

A smooth, rounded, fluctuant, cystic swelling on the floor of the mouth. May be a pseudocyst or true salivary cyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is sialoadenitis?

A

Salivary gland inflammation, may cause duct obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What causes sialoadenitis?

A

Infection via duct or haematogenous spread, or trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What may glandular atrophy be a result of?

A

From partial or complete duct obstruction or chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is necrotising sialometaplasia?

A

Salivary gland infarction

Areas of salivary gland infarction with coagulative necrosis, inflammation and swelling – variable degrees of pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is persistent aortic arch and the consequence of this?

A

When it forms on the right side instead of the left.

Entrapment and constriction of the oesophagus between the ligamentum arteriosum and the trachea at the level of the heart base = oesophageal obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the predisposed sites for obstruction to occur?

A

Larynx
Thoracic inlet
Heart base
Diaphragmatic hiatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the potential consequences of choke?

A

Scarring
Stricture
Perforation leading to periesophageal cellulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the causes of oesophagitis?

A
  • Traumatic injury or obstruction – foreign bodies, choke
  • Some viral diseases – mucosal disease/BVDV
  • Reflux of gastric acid (reflux oesophagitis) – chronic gastric regurgitation or vomiting
  • Ingestion of caustic/irritant chemicals, plants or drugs – doxycycline in cats if not flushed down the oesophagus and is left there
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are 2 oesophageal neoplasms?

A

Squamous cell carcinoma – cattle from bracken fern, may infiltrate local tissues, may metastasise to regional lymph nodes

Papillomas (viral) – cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is megaoesophagus?

A

Dilated hypomotile oesophagus, unable to effectively transport food from the pharynx to stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How does megaoesophagus develop?

A
  1. Muscular dysfunction
  2. Failure of peristalsis
  3. Accumulation of ingesta in the oesophagus
  4. Oesophageal dilation, regurgitation, may have secondary oesophagitis, ulceration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Which species can congenital megaoesophagus occur in?

A

Dogs, cats, horses and cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are some conditions that cause acquired megaoesophagus?

A
  • Idiopathic
  • Neurological diseases – such as, peripheral neuropathies, dysautonomia, toxins (lead poisoning), trauma (vagal nerve injury)
  • Neuromuscular diseases - myasthenia gravis, polymyositis
  • Hypoadrenocorticism
  • Prolonged oesophageal obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Which part of the stomach is prone to ulceration?

A

Glandular region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the primary causes of stomach dilation in horses?

A

Overconsumption of fermentable feeds, expansile or indigestible foods – changes osmolarity and draws in a lot of water

Ingestion of large quantities of water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the secondary causes of stomach dilation in horses?

A
  • Gastrointestinal obstruction
  • Ileus (gastrointestinal hypomotility)
  • Dysautonomia/grass sickness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What can be a consequence of stomach dilation in horses?

A

Can lead to bloat and then gastric rupture

Can happen ante or post mortem – differentiate by haemorrhage, inflammation, fibrin?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the primary causes of stomach dilation in dogs?

A
  • Overeating in young puppies
  • Component of gastric dilation and volvulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the secondary causes of stomach dilation in dogs?

A
  • Obstruction
  • Gastric ulceration
  • Gastric lymphomas
  • Uraemia (renal failure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What factors may be included gastric dilation?

A

Gastric distension by gas, fluid or feed

Gas source - aerophagia, bacteria?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Outline the pathogenesis of gastric dilation and volvulus.

A
  1. Normally positioned stomach
  2. As the stomach distends and rotates, the oesophagus twists and the pylorus begins to point upwards.
  3. The stomach twists and the pylorus moves to the opposite side. Air is trapped in the stomach and the stomach continues to dilate.
  4. In a nearly upside down and backwards position, the blood vessels to the stomach are compressed and/or torn. Early treatment can reduce this complication.
  5. Within minutes, the blood flow becomes compromised. Over time, this causes stomach tissue discolouration and irreversible damage. The bloated stomach presses on the caudal vena cava, causing decreased blood return to the heart and shock.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the potential consequences of gastric dilation and volvulus?

A
  • Gastric infarction > congestion, oedema, necrosis, may lead to gastric rupture
  • Venous obstruction from volvulus and pressure on surrounding tissues (vena cava) > reduced venous return from portal vein and caudal vena cava > circulatory shock
  • Respiratory compromise from increased intra-abdominal pressure on the diaphragm
  • Acid-base and electrolyte disturbances
  • Cardiac arrhythmias
  • Death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the causes of stomach obstruction?

A

Displacements and volvulus
Foreign bodies
Impaction
Pyloric stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the primary and secondary causes of stomach obstruction in horses and cattle?

A

Primary – high roughage feed, low water intake

Secondary – consequences of GI obstruction or impaired motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How does pyloric stenosis cause gastric obstruction?

A

Benign muscular pyloric hypertrophy/congenital pyloric stenosis = muscle of pyloric walls become thickened and causing an obstruction

Pyloric stenosis secondary to diseases causing pyloric obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What diseases can pyloric stenosis be secondary to?

A
  • Inflammatory disease
  • Neoplasia
  • Foreign bodies
  • Chronic hypertrophic pyloric gastropathy – hypertrophy of the pyloric mucosa and/or muscle layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the causes of gastritis/abomastitis?

A
  • Foreign bodies
  • Chemical/toxic - irritant/corrosive/toxic chemicals or plants, bile reflux from the duodenum
  • Hypersensitivity reaction
  • Secondary to systemic diseases – uraemia, septicaemia
  • Idiopathic
  • Infectious - BVD, clostridium septicum, helicobacter, fungi, ostertagia
  • Stress, diet, NSAIDs and glucocorticoids, hypoxia and ischaemia, paraneoplastic effects and gastric neoplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the features of gastritis?

A
  • Hyperaemia (reddening)
  • Thickening or swelling – oedema, inflammatory cell infiltrate, hypertrophy/hyperplasia, bocilated (cobblestone appearance)
  • Necrosis, erosion/ulceration
  • Haemorrhage
  • Fibrosis and atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Outline the pathogenesis of stomach ulceration.

A
  1. Increased acid and pepsin
  2. Decreased mucosal integrity and protection
  3. Ulceration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How does paraneoplastic release of histamine from mast cell tumours cause gastric ulceration?

A
  1. Mast cell tumour
  2. Release of histamine
  3. Bind to histamine receptor (H2) on gastric parietal cells on gastric glands
  4. Stimulates increased gastric acid secretion
  5. Gastric ulceration
75
Q

How does paraneoplastic release of gastrin from gastrinomas cause gastric ulceration?

A
  1. Gastrinoma – rare tumour of gastrin producing cells of the pancreas
  2. Release of gastrin
  3. Stimulates acid production by parietal cells of gastric glands
  4. Increased gastric acid secretion
  5. Gastric ulceration
76
Q

What are the factors that cause decreased mucosal integrity?

A
  • NSAIDs
  • Glucocorticoids
  • Mucosal trauma
  • Bile salts (damage to surface cell membranes)
  • Reduced mucosal perfusion or ischaemia
  • Stress (including strenuous activity)
  • Neurosurgery, spinal trauma
  • Dietary factors
77
Q

How do NSAIDs cause decreased mucosal protection?

A
  1. NSAIDs
  2. Inhibition of prostaglandin synthesis
  3. Reduced stimulation by prostaglandin
  4. Reduced bicarbonate secretion
  5. Increased acidity and reduced buffering
78
Q

How can acute superficial gastric ulcers progress?

A
  1. Acute superficial ulcer
  2. Progressive increase in depth in the mucosa (may be rapid)
  3. Submucosal involvement (larger blood vessels here)
  4. Increased risk of haemorrhage
  5. Reparative processes - granulation tissue. Some ulcers may come into equilibrium between ulcerative and reparative processes
  6. Progression into and through the muscularis externa and serosa layers will result in a perforating ulcer with potential for release of gastric content into the peritoneal cavity.
79
Q

What are the species specific most common gastric tumours?

A

Dogs – adenocarcinoma

Cats – lymphoma

Horses – squamous cell carcinoma

Bovine – lymphoma in countries with high levels of bovine leukaemia virus

80
Q

What are the characteristics of gastric adenocarcinomas in dogs?

A
  • Ulcerated, craterous masses
    may present as diffuse thickening of the gastric wall with no mass
  • Occasionally appear as an exophytic (outward growing) mass on the mucosal surface
  • Infiltrate the gastric wall
  • Often metastasize to local lymph nodes or distant sites
81
Q

What are the characteristics of gastric squamous cell carcinomas in horses?

A
  • Exophytic, vegetative, roughened and ulcerated mass
  • Can appear as diffuse thickening and ulceration without a detectable mass
  • Infiltrate the stomach wall and frequently metastasise
82
Q

What are some causes of functional intestinal obstructions?

A
  • Paralytic’ ileus – inhibition of peristalsis secondary to other conditions (peritonitis, abdominal surgery)
  • Dysautonomia – altered intestinal motility in horses (grass sickness)
  • Megacolon – from conditions causing colonic hypomotility
  • Colonic inertia
83
Q

What are the causes of colon inertia?

A
  • Idiopathic – middle-aged to older cats
  • Secondary to neurological disease
  • Secondary to prolonged colonic distension
84
Q

What are some examples of outlet obstructions?

A

Pelvic fracture malunion, stricture, intrapelvic mass

85
Q

How do outlet obstructions cause colonic inertia?

A
  1. Intractable constipation – obstipation
  2. Prolonged colonic distension
  3. Irreversible changes affecting colonic motility
  4. Secondary colonic inertia
86
Q

What do intestinal foreign body obstructions cause?

A
  • Pressure or traumatic injury may compromise intestinal wall circulation
  • Can lead to oedema, necrosis, ulceration, perforation
87
Q

What do linear intestinal foreign body obstructions cause?

A

May cause intestinal pleating or plication, and may cause ulceration and perforation

88
Q

What is atresia ani and atresia coli?

A

Atresia ani – failure to form anal orifice

Atresia coli – part of colon is blocked/missing

89
Q

How can lipomas cause strangulation?

A

Pedunculated lipoma can create a loop around intestine and not strangulate but cause constriction, and can also wrap around a loop of intestine which does cause strangulation.

90
Q

Outline the pathogenesis of intestinal ischaemia and infarction.

A
  1. Compression and obstruction of blood vessels – mesenteric veins affected first as they are thinner walled
  2. Vascular congestion and tissue ischaemia – mucosal epithelial necrosis starts within a few minutes and is extensive by 3-4 hours. External muscle layers can remain viable for 6-7 hours
  3. Necrosis, oedema and haemorrhage and effusion of tissue fluid and blood into the lumen
  4. Anaerobes proliferate – gas production and toxins
  5. Septic peritonitis with/without intestinal perforation
91
Q

What are the potential complications of hernias?

A
  • Intestinal obstruction
  • Intestinal strangulation
  • Incarceration – the herniated intestine cannot be returned back through the hernia (non-reducible)
92
Q

What is entrapment?

A

Entrapment of small intestine through a rent/tear in the gastro-splenic ligament. Can cause obstruction and infarction of the segment of entrapped intestine

93
Q

What is nephrosplenic entrapment?

A

Left dorsal displacement of the colon in horses

94
Q

What is volvulus?

A

Twisting of the intestine on its mesenteric axis

95
Q

What is torsion?

A

Torsion – twisting of a tubular organ along its long axis, both can cause mechanical obstruction and ischaemia

96
Q

What is an intussusception?

A

The intussusceptum telescopes in to the intussusscipiens

97
Q

What can cause an intussusception?

A

Intestinal irritability or hypermotility: foreign body, enteritis, parasites, tumours, handling of the intestine during surgery

98
Q

What can intussusceptions cause?

A
  • Partial or complete intestinal obstruction
  • Infarction and ischaemia of the affected intestine
99
Q

What can cause an intussusception to become irreducible?

A

Swelling, inflammation, adhesions

100
Q

Describe how diarrhoea develops from malabsorption.

A
  • Commonly results from villus atrophy
  • Reduced surface area for absorption – malabsorption of nutrients and solute
  • Osmotic retention of water in the intestine lumen
101
Q

Describe how diarrhoea develops from hypersecretion.

A
  • Excess of secretion over absorption results in a net influx of fluid and electrolytes
  • Some pathogens produce toxins that stimulate increased secretion of fluid into the intestine (with/without cellular injury depending on the pathogen) – E.coli
  • Some endogenous substances and mediators may cause increased secretion and contribute to the excess – prostinoids, histamine, some cytokines
102
Q

Describe how diarrhoea develops from increased permeability/effusion.

A

Condition causing effusion of fluid and solutes from the mucosa into the intestinal lumen. Increased effusion of fluid and proteins into the intestinal lumen = may cause a protein-losing enteropathy.

103
Q

What are the causes of increased intestinal permeability/effusion?

A
  • Damage to the mucosal integrity - injury to epithelial cells causing altered tight junction permeability or increased cell turnover, loss of epithelium, ulceration
  • Vascular damage – leakage of plasma components or haemorrhage
  • Inflammation
  • Increased hydrostatic pressure
  • Impaired lymphatic drainage
  • Hypoproteinaemia
104
Q

Describe how diarrhoea develops from altered motility.

A
  • Hypermotility = increased rate, intensity or frequency of peristalsis
  • Decreased gut transit time (mucosal contact time) may reduce the efficiency of digestion and absorption of nutrients and water
  • Hypermotility is probably a secondary mechanisms rather than a primary mechanism in diarrhoea in domestic animals
105
Q

Outline the pathogenesis of parvoviral enteritis in dogs and cats.

A
  1. Parvovirus infects proliferating enterocytes in crypts
  2. Necrosis of crypt enterocytes – loss of enterocyte proliferation to renew the surface epithelial layer as the cells are shed
  3. Early regenerative response with hyperplasia of surviving epithelium
  4. Collapse of the villus lamina propria and villus atrophy, resulting in short, blunted and denuded villi
  5. Diarrhoea results from the reduced absorptive surface area causing malabsorption and effusion of tissue fluids and blood from denuded mucosa contributes
106
Q
A
107
Q

What is lymphangiectasia?

A

Fat gets taken up and gets into lymphatics and causes obstruction of flow and lacteals become slow to empty and dilate

108
Q

What happen as a consequence of lymphangiectasia?

A
  • Obstruction of lymphatics with increased lymphatic pressure
  • Dilation of lacteals (villi) and intestinal and mesenteric lymphatics
  • Leakage of chyle from distended lymphatics can cause lipogranulomatous lymphangitis – cream/white nodular foci
109
Q

What are the causes of lymphangiectasia?

A

Include mucosal inflammatory cell infiltrates
Intestinal neoplasia
Mesenteric lymph node disease

110
Q

What are the clinical signs of idiopathic inflammatory bowel disease?

A

Consistent with malabsorption and/or plasma loss (effusion) from gut wall

111
Q

What is the histological appearance of idiopathic inflammatory bowel disease?

A
  • Microscopic mucosal features of inflammation, often lymphoplasmacytic, may be eosinophilic
  • Villi may variably appear normal, blunted, atrophic or sometimes fused
  • May also have inflammation affecting the large intestine and/or stomach
  • Lymphocytic infiltrate can sometimes be difficult to differentiate from lymphoma
112
Q

What are the most common intestinal tumours in cats and dogs?

A

Cats – lymphoma

Dogs – adenocarcinoma

113
Q

Describe the characteristics of intestinal adenocarcinoma.

A
  • May appear as an annular thickening of the wall or an intraluminal mass protruding from the wall
  • May be associated with fibrosis and stenosis
114
Q

Describe the characteristics of intestinal lymphoma.

A
  • Can be localised or diffuse, and may appear nodular, circumferential or plaque-like
  • Advanced diffuse tumours may give the mucosa a cobblestoned or granular appearance
115
Q

What are the causes of transudate/modified transudate in the peritoneal cavity?

A

Hypoproteinaemia
Congestive heart failure
Conditions causing portal hypertension
Lymphatic obstruction

116
Q

What is the cause of exudate inflammation in the peritoneal cavity?

A

Peritonitis

117
Q

What are the causes of gastrointestinal content, bile, urine and blood in the peritoneal cavity?

A

Gastrointestinal content – gastrointestinal tract rupture/perforation

Bile (biliary peritonitis) – bile duct or gall bladder perforation/rupture

Urine (uroperitoneum) – rupture of urinary bladder, urethra or ureter(s)

Blood (haemoperitoneum) – haemorrhage (trauma, neoplasia, coagulopathies)

118
Q

What are the causes of pneumoperitoneum?

A

Abdominal wall perforation, or gas from a perforated gastrointestinal tract. Rarely secondary to rupture of the urinary bladder or female reproductive tract.

119
Q

What are the causes of peritonitis?

A
  • Bacteria
  • Some viral infections - FIP, canine parvovirus
  • Migrating parasites - cysticercus tenuicollis, fasciola hepatica
  • Penetrating injuries - foreign bodies, traumatic reticulopericarditis, bite wounds
  • Gastrointestinal infarctions (volvulus)
  • Leakage of bile or pancreatic enzymes
  • Chemical peritonitis (leakage of barium)
  • Iatrogenic - after abdominal surgery – trauma, infection, foreign bodies/material
120
Q

How is peritonitis classified?

A
  • Local or diffuse
  • Acute or chronic
  • Septic or non-septic
  • Type of inflammation or exudate
121
Q

What are the common signs of stomatitis in horses?

A
  • Excessive drooling – sialorrhea
  • Rectance to eat/anorexia
  • Difficulty swallowing/dysphagia
  • Resistance to examination of the mouth
122
Q

Describe calculus in horses.

A

Deposition of mineralised supragingival and subgingival plaque formed by mineral and dead bacteria. In horses, the mineral component is mainly calcium carbonate

123
Q

What is infundibular necrosis?

A

Most common form of caries in horses. Dental caries is characterised by demineralisation of the inorganic part and enzymatic degradation of the organic matrix

124
Q

What is oral candidiasis in foals?

A

The superficial layers of the oral epithelium are involved. It appears as patchy pale grey pseudomembranous material of the oral cavity and tongue that can extend to the oesophagus and stomach. It may be indicative of immunosuppression

125
Q

What is vesicular stomatitis in horses?

A

Viral disease that affect mainly horses, donkeys, cattle and pigs. It is a notifiable animal disease. Vesicular lesions and secondary ulceration are the main lesions

126
Q

What is the aetiology of gastric ulceration in horses?

A

Stress, feeding type/frequency, enteric disease, colonic impaction, nonsteroidal anti-inflammatory drug therapy, exercise, and possibility of the involvement of an infectious agent such as Helicobacter spp

127
Q

Where do gastric ulcers in horses occur?

A

Within both the squamous and glandular regions of the equine stomach

128
Q

What are the main factors of gastric ulceration in horses?

A

Mucus secretion
Increased acid production
Blood flow
Epithelium regeneration

129
Q

What are ulcers of the glandular and non-glandular regions on the equine stomach associated with?

A

Reflux of the acidic content into the non-glandular regions associated with exercise and feeding patterns may happen

Ulcers of the glandular stomach have been associated with administration of NSAIDs

130
Q

What may deep ulcers of the equine stomach lead to?

A

To tearing of the stomach wall and rupture, but usually gastric ulcers are considered incidental post-mortem findings

131
Q

What is grade 0 gastric ulceration?

A

There is no appearance of hyperkeratosis or hyperaemia and the epithelial wall is intact

132
Q

What is grade 1 gastric ulceration?

A

Areas of hyperkeratosis and hyperaemia are visualised but the mucosa wall is still intact

133
Q

What is grade 2 gastric ulceration?

A

Minor, single lesions

134
Q

What is grade 3 gastric ulceration?

A

Large single lesions or extensive superficial lesions

135
Q

What is grade 4 gastric ulceration?

A

Extensive lesions are visualised deep to the mucosa

136
Q

What are 3 species that can cause parasitic gastritis in horses?

A

Gasterophilus spp
Draschia megastoma
Habronema species

137
Q

How do gasterophilus species cause parasitic gastritis in horses?

A
  • Larvae (botflies)
  • Intestinalis-the most common-cardias area
  • Nasalis-pyloric mucosa and duodenal ampulla
  • Lay eggs on the hairs of the face-migration oral mucosa-alimentary canal
  • Larvae infestations have been associated with gastric ulceration, reflux, peritonitis
138
Q

What is the pathogenesis of the disease caused by clostridium perfringes type C?

A
  1. Colonisation and proliferation in the intestine, and the production and secretion of the beta toxin, a trypsin-labile, cytotoxic protein.
  2. The toxin cause enterocyte necrosis and haemorrhage
  3. Toxin crosses the epithelial barrier and diffuses into the lamina propria, inducing damage to endothelial cells
  4. Increase in vascular permeability, leading to extravasation of fluid, proteins, and erythrocytes, contributing to the necrotic effect on enterocytes.
139
Q

What is the main pathological finding in clostridium perfringes type C?

A

A necrotising enterotyphlocolitis in neonates

140
Q

What is clostridium difficile?

A

A gram-positive bacillus in the soil and may be a normal inhabitant of the gastrointestinal tract of horses and other animals, including humans.

141
Q

What does clostridium difficile cause?

A

It causes diarrhoea in horses of all age groups due to the production of 2 major toxins, TcdA and TcdB responsible for the lesions.

Both toxins contribute synergistically to damage in the mucosal epithelial cells by different mechanisms

142
Q

Describe the lesions caused by clostridium difficile.

A

Lesions in foals are commonly located in the small intestine whereas the colon and cecum are most frequently affected in older animals.

143
Q

What is the main pathological finding of clostridium difficile?

A

Necrotising enterotyphlocolitis and submucosal gelatinous oedema colon and caecum

144
Q

What is rhodococcus equi?

A

Rhodococcus equi is a gram-positive coccobacillus that typically produces disease in foals up to 5-months. Survive and replicate within the macrophages

145
Q

What is the main pathological finding of rhodococcus equi?

A

Pyogranulomatous and ulcerative typhlocolitis

146
Q

What is caused by lawsonia intracellularis?

A

Malabsorption, and it is considered a protein-losing enteropathy. Intestinal mucosal hyperplasia that is the result of rapid and unchecked division of crypt epithelial cells

147
Q

What is the main pathological finding of lawsonia intracellularis?

A

A proliferative enteropathy affecting mainly the distal small intestine

148
Q

How does rotavirus affect foals?

A

Produce atrophy of the villi due to an increase in rate of loss of epithelium from the surface of villi and impairing sodium and/or glucose transport. Malabsorption is an important consequence

149
Q

How does coronavirus affect adult horses?

A

Gross and microscopic changes necrotising enteritis

150
Q

How is cryptosporidiosis characterised in horses?

A

Diarrhoea, which is mainly caused by villus atrophy and malabsorption

151
Q

How are strongylus vulgaris larvae characterised in horses?

A

Endoarteritis, in particular the cranial mesenteric artery and its main branches, that may lead to arterial infarction of the colon

152
Q

How is the acute syndrome of strongylus vulgaris characterised in foals?

A

Weight loss
Diarrhoea or constipation
Colic
Infarction of the intestine occurs when infected with large numbers of larvae for the first time

153
Q

How do NSAIDs and inflammatory drugs cause ulcerative colitis and typhlitis?

A

Ischemia caused by reduced perfusion, which is a consequence of inhibition of synthesis of prostaglandin by inhibition of the cyclooxygenase enzyme. Colic, diarrhoea and ulceration of the upper and lower alimentary system are the main aspects.

154
Q

Describe the lesions caused by foot and mouth disease.

A

Main lesion is the formation of epidermal vesicles in and around the mouth, on the feet, teats, and mammary glands. Foot lesions occur in the majority of cases

155
Q

Describe the lesions of vesicular stomatitis in farm animals.

A

The lesions occur mainly on the oral mucosa

The lesions are indistinguishable from those of foot and-mouth disease. Laboratory confirmation is essential

156
Q

Describe the lesions of bovine popular stomatitis.

A

Generally not clinically significant. The initial lesions are usually on the muzzle or lips and appears as erythematous, round macules, then papule, epithelial hyperplasia, and a central area of necrosis leaving a crateriform lesion with raised borders

157
Q

Describe the lesions of bovine virus diarrhoea/mucosal disease in farm animals.

A

Mucosae are hyperaemic and covered by a thin grey film of catarrhal exudate. Crusts, erosions, and shallow ulcers are present on the muzzle and nares of many affected cattle. Ulcers can be observed in the oral cavity

158
Q

What is the outcome of the ensuing viraemia due to bovine virus diarrhoea/mucosal disease due to?

A

A product of the genotype and virulence of the virus, the immune status of the host, whether or not the animal is pregnant, and if so, the stage of pregnancy

159
Q

Describe the lesions of infectious bovine rhinotracheitis.

A

Focal areas of necrosis, erosion, and ulceration sometimes linear (oesophagus) are the main lesion

160
Q

What are the clinical signs of malignant catarrhal fever/gammaherpesvirus/ovine herpesvirus-2?

A
  • Erosion/ulceration of nasal planum
  • Buccal cavity and tongue ulceration
  • Ocular/nasal discharge
  • Corneal opacity
161
Q

Describe the effect of bluetongue virus.

A

Endothelial damage caused by viral infection initiates local microvascular thrombosis and increased permeability leading respectively to ischemic necrosis and ulceration, oedema and haemorrhage

162
Q

What is the principle cause of calf diphtheria?

A

Fusobacterium necrophorum is the principal cause of oral necrobacillosis (calf diphtheria)

163
Q

What does calf diphtheria cause?

A

Causes an acute necrotizing ulcerative inflammation of the buccal and pharyngeal mucosa that can be fatal

164
Q

What is wooden tongue?

A

Actinobacillus lignieresii (gram negative). Stomatitis, glossitis, lymphadenitis. Pyogranulomatous lesions. Abnormal production of granulation tissue – this can become fibrous and harden

165
Q

What is lumpy jaw?

A

Actinomyces bovis (gram positive). Pyogranulomatous mandibular and maxillary osteomyelitis. Extension from dental alveoli of gums and tooth roots – penetrating wounds

166
Q

What do most disorders of the ruminant gastrointestinal tract relate to?

A

Aberrations of biota and motility

167
Q

What is primary ruminal tympany?

A

Frothy bloat - foam prevents gas from being eructated

168
Q

What is the formation of foam in primary ruminal tympany depend on?

A

Dependent on soluble proteins which are present in high levels in legumes, such as alfalfa and clover. Soluble proteins are degraded by the rumen microflora, they are denatured, become insoluble, and stabilise the foam

169
Q

What are the consequences of primary ruminal tympany?

A

Cardia blocked = decreased eructation

Respiratory function and haemodynamic of abdominal organs are severely affected

170
Q

What is secondary ruminal tympany?

A

Physical or functional defect in eructation

171
Q

What are the causes of secondary ruminal tympany?

A
  • Vagal damage
  • Failure of oesophageal groove closure
  • Ruminal and metabolic acidosis
  • Reticulorumenitis with necrosis and erosions
172
Q

What is the pathogenesis of ruminal acidosis?

A
  1. High carbohydrate/fermentable feedstuff diet
  2. Microbiota changes (responsive to the substrate available for fermentation) > increased lactic acid, pH- 4, 4.5 in fatal cases.
  3. Ruminal atony – volatile fatty acids act on receptors that mediate inhibition of reticuloruminal motility via vagovagal reflex
  4. Increase in ruminal acids, mainly lactate, causes increase osmotic pressure in RR
  5. Movement of fluids from the circulation to the rumen
  6. Dehydration (circulatory collapse)
  7. Death
173
Q

What are the consequences of ruminal acidosis?

A

Secondary bacterial infection - fusobacterium necrophorum necrotising ulcers embolise to liver > coagulative necrosis-abscesses

Mycotic rumenitis - opportunistic fungi penetrate the wall and cause peritonitis

174
Q

What are the predisposing factors of abomasal dilation, displacement and volvulus?

A
  • Abomasal atony/hypomotility
  • Alterations in the enteric nervous system
175
Q

What are the concurrent problems of abomasum dilation, displacement and volvulus?

A
  • Hypocalcaemia
  • Metritis and retained placenta
176
Q

What are consequences of abomasum dilation, displacement and volvulus?

A
  • Right displacement
  • Can progress to abomasal volvulus - the sequel to rotation of a loop formed by a distended abomasum and attached omasum and duodenum
  • Obstruction of duodenal outflow results in sequestration of chloride in the abomasal content and the development of metabolic alkalosis
177
Q

Distinguish the cause of abomasal ulceration in calves and dairy cows.

A

Calves – dietary change (recently weaned calves)

Dairy cows – postpartum period, concurrent disease

178
Q

Outline the pathogenesis of abomastitis.

A
  1. Contaminated fomite, high volume of feeds, failure of passive transfer, rapid diet change, or high osmolarity in abomasum
  2. Bacterial metabolic byproducts – toxins and gas
  3. Irritation of abomasal mucosa
  4. Tissue inflammation
  5. Reduced abomasal function
  6. Further toxins and gas production
  7. Tissue necrosis, ulceration and haemorrhage
  8. Abomastitis
  9. Death
  10. Bloat
  11. Further toxins and gas production or reduced abomasal function
179
Q

Describe the lesions caused by ostertagiosis in farm animals.

A
  • Nodules 2-3 mm diameter ‘Moroccan leather’ or ‘cobblestone’
  • Heavy infection – lesions confluent
180
Q

What does the emergence of ostertagia cause in farm animals?

A
  • Epithelial necrosis, sloughing, bacterial infection
  • Contents dark, fetid fluid
  • Causes ill-thrift, loss of protein, ascites, diarrhoea
181
Q

How does enterotoxigenic E.coli cause enteritis in neonatal farm animals?

A
  • Adhesion and attachment to villus enterocytes using fimbrial adhesins
  • Secretion of toxin(s)
  • Alteration of secretion and absorption of electrolyte and water by enterocytes
  • Profuse watery diarrhoea
  • Dehydration and acidosis
182
Q

How does cryptosporidium cause enteritis in young farm animals?

A

Young animals. Associated with villus atrophy of variable severity

183
Q

How does rotavirus cause enteritis in young farm ruminants?

A
  • Virus invades mature enterocytes of the villus
  • Decreased enterocytes
  • Lysis/exfoliation of surface enterocytes
  • Decreased absorption of Na+, glucose, H2O
  • Watery diarrhoea
  • Dehydration and acidosis
  • Increased mucus production and epithelial sloughing
  • Hyperaemic mucosa, covered in viscous, white/yellow/green fluid
184
Q

How does salmonella cause enteritis in ruminants?

A
  • Adhesion, colonisation and invasion of enterocytes
  • Proteins induce apoptosis of enterocytes and neutrophil recruitment
  • Neutrophils – increased tissue injury
  • Inflammation
  • Vascular damage/thrombosis
  • Loss of mucosal integrity
185
Q

What is diarrhoea the outcome of in salmonella in ruminants?

A

Outcome of active secretion of electrolytes, malabsorption resulting from reduced mucosal surface area and enterocyte competence, and inflammatory exudation

186
Q

How does Johne’s disease/mycobacterium avium paratuberculosis cause enteritis in the adult ruminant?

A
  • Attaches and crosses the epithelium at the ileal Peyer’s patches
  • Infected macrophages – focal granulomatous inflammation
  • Extension of granulomatous inflammation and villus atrophy
  • Lymphangiectasia and lymphatic rupture
  • Decreased absorption of nutrients and ions – loss of protein into lumen
  • Water loss into the lumen
  • Profuse watery diarrhoea
  • Dehydration and death

CVSOH 4 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions