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VET377 > Lecture 24 - Alimentary 5 > Flashcards

Lecture 24 - Alimentary 5 Flashcards

1
Q

Name the structures that are shown in the diagram below:

A
  1. Muscularis mucosae
  2. Lamina propria
  3. Lumen
  4. Epithelium
  5. Adventitia or serosa
  6. Submucosal plexus
  7. MALT
  8. Submucosa
  9. Myenteric plexus
  10. Inner circular muscle
  11. Outer longitudinal muscle
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2
Q

Name the structures that are shown below:

A
  1. lamina propria
  2. villus
  3. mucosa
  4. peyers patch
  5. submucosa
  6. muscularis mucosae
  7. muscularis
  8. crypt
  9. serosa
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3
Q

Can the following clinical signs be localised to the upper of lower alimentary tract? - malaise, lethargy, weakness, inappetance, anorexia, weight loss, dehydration, haemorrhage and melaena

A

No - these are sign that are common to both the upper and the lower alimentary tracts (as well as multiple other organ systems)

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4
Q

Can the following clinical signs be localised to the upper of lower alimnetary tract?

Abdominal pain and colic, polyphagia/hyperphagia (excessive eating)

A

Yes - These clinicial signs are consistent with diseae of the lower alimentary tract and of other abdominal organs

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5
Q

Where can the following clinical signs be localised to?

Dysphagia, gagging, retching, regurgitation, ptyalism, halitosis, bloat in ruminants

A

These are specific to the upper alimnetary tract - oropharynx, oesphagus, ruminan forestomachs

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6
Q

Where the following clinical signs be related to?

Vomiting, diarrhoea, haematochezia, dyschezia (excessive straining with stools), gas accumulation, borborygmi, eruction, bloat, flatulence, faecal incontinence

A

lower digestive tract

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7
Q

Compare erosion veruses ulceration (including their sequelae):

A

Erosion: loss of epithelium, basement membrane is intact - heals quickly (re-epithelialistion ) and returns to normal

Ulcer: loss of epithelium and basement membrane - heals by second intention without scarring, may lead to perforations/strictures/stenosis in tubular GIT organs

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8
Q

Define halitosis:

A

Bad breath

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9
Q

Define ptyalism:

A

Increased salivation

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10
Q

Term for oral cavity inflammation

A

Stomatitis

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11
Q

Term for inflammation of the lips:

A

Cheilitis

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12
Q

Term for inflammation of the gingiva:

A

Gingivitis

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13
Q

Term for inflammation of the teeth and gums (periodontia - teeth and gums):

A

Periodontitis

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14
Q

Term for inflammation of the pharynx:

A

Pharyngitis

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15
Q

Term for inflammation of the tonsils (MALT) :

A

Tonsillitis

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16
Q

Term for inflammation of the salivary glands:

A

Sialodentitis

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17
Q

What is the term for inflammation of the oesphagus?

A

Oesphagitis

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18
Q

Breifly describe the pathogenesis of viral vesicular stomatitides:

A
  1. Epitheliotropic virsus - clefts filled with serum form within/beneath epithelium
  2. Coalesce to form bullae/vesicles
  3. Abraded (scraped of)
  4. Erosion /ulcer
  5. Granulate and heal rapidly if they are not infected by secondary bacterial/mycotic infection
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19
Q

What are the 4 main diseases seen in viral vesicular stomatitis and what is the cause of each?

A
  1. Foot and mouth - caused by picornavirus
  2. Vesciular stomatitis - caused by rhabdovirus
  3. Swin vesicular disease - enterovirus
  4. Vesicular exanthema of swine - calicivirus
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20
Q

Fill in the table below for the causes and species distribution of viral vesicular stomatitides:

A
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21
Q

What is the pathogenesis of viral erosive/ulcerative stomatitides?

A
  1. Endothelial damage (+/- epithelial necrosis)
  2. Microvascular thrombosis
  3. Increased vascular permeability
  4. Vasculitis –> ischaemic necrosis, odema and haemorrhage
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22
Q

Name the disease that are shown below that are causing viral erosive/ulcerative stomatitides and state which ones are seen in Australia:

A
  1. Bovine viral diarrhoea
  2. Bluetongue
  3. Malignant cattarhal fever

Note BVD and MCF is in Australia - Bluetongue is but sheep are not allowed above a certain latitude

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23
Q

Why are viral vesicular stomatitides and erosive/ulcerative stomatitides often difficult to differentiate?

A

Viral/vesciular stomatitides can often differentiate to the point where they cannot be differentiated from erosive/ulcerative stomatitides grossly.

24
Q

What causes papillomas in the oral cavity?

A

They can be spantanous or viral

25
Q

What are some examples of benign neoplasia in the oral cavity of animals?

A

Fibromatous epulis of the peridontal ligament

Acanthomatous ameloblastoma (invasive but don’t metastasise)

26
Q
A
27
Q

What are some examples of malignant neoplasia in the oral cavity of animals?

A
  1. Squamous cell carcinoma (very locally invasive)
  2. Malignant melanoma (rapid metastasis)
  3. Fibrosarcoma
28
Q

Name the proliferative lesions seen in the oral cavity below:

A
  1. Fibrogingival hyperplasia
  2. Fibromatous epulis
  3. Squamous cell carcinoma
  4. malignant melanoma
29
Q

What are some abnormalities that are seen in tooth developement?

A
  1. Adontia, oligodontia, polydontia
  2. Enamel/dentin defects (CDV, BVDV)
30
Q

What are the general causes of peridontal disease?

A
  • Plaque = bacterial mass + organic matrix
  • Calculus = mineralised mass
  • Caires/infundibular impaction - gingivitis, periodontics, pulpitis, alveolar osteomyelitis
31
Q

Name the condition that is shown below:

A

Feline odontoclastic resorptive lesions (ideopathic)

32
Q

Name the condition that is shown below and provide a possible aetiological agent:

A

Enamel hypoplasia due to canine distemper virus

33
Q

Name the condition that is shown in the image below:

A

Dental calculus and purulent gingivitis

34
Q

What is an important condition to rule out in cases of ptyalism?

A

Rabies

35
Q

What are three potential causes of degeneration and necrosis of the ruminal epithelium?

A
  1. Degeneration and necrosis of the ruminal epithelium with inflammation –> stellate scars
  2. Secondary to mechanical or other chemical injury (urea, kikuyu poisoning, sulfur)
  3. Due to primary viral diseases causing erosion and ulceration (BVD, MCF, FMD, bluetongue)
36
Q

What are some potential sequelae to ruminal acidosis?

A

Trueparella pyogenes, fusobacterium necrophorum –> can spread haemotogenously to the liver –> causing abscesses

Aspergillis, Mucor, Rhizopus spp. –> spread haematogenously –> hepatitis and mycotic placentitis (aborption)

37
Q

What are some of the potential sequalae to acute ruminal acidosis?

A
  1. liver abscesses
  2. laminitis
  3. mycotic placentitis (abortion)
  4. polioencephalomalacia (thiamine deficiency)
38
Q

What is the term for inflammation of the stomach?

A

gastritits

39
Q

What is the term for inflammation of the small intestine?

A

enteritis

40
Q

What is the term for inflammation of the caecum?

A

Typhlitis

41
Q

What is the term for inflammation of the colon?

A

Colitis

42
Q

What is the term for inflammation of the rectum?

A

Proctitis

43
Q

What is the term for inflammation of the anus?

A

anusitis

44
Q

State three factors that are critical to normal gastric function:

A
  1. Motility
  2. Patency of pyloric outlet
  3. Mucosal integrity
45
Q

What are the clinical signs of gastric dysfunction?

A
  1. Anaemia, haematemesis, melaena
  2. Vomting (in some species)
  3. Decreased appetite and weight loss
  4. Variably severe abdominal pain (cloic, bruxism, ptyalism)
46
Q

Briefly describe the pathogenesis of gastric/abomasal ulceration:

A

Pathogenesis poorly understood - imbalance between acid secretion and mucosal protection

  1. Regional disruptions to blood flow –> ischaemia
  2. Prostaglandins stimulate HCO3 secretions having a general protective effect - drugs inhibiting prostaglandins (e.g. steroids and NSAID’s) –> promotion of ulcers
  3. Local disturbances/trauma to mucosal epithelial barrier
  4. Gastric hyperacidity (Zollinger-Ellison syndrome)
  5. Other factors e.g. neoplasia
47
Q

Name the process that is occuring the images below:

A

Gastric ulceration

48
Q

What are the clinical signs that may be seen as a result of GIT haemorrhage?

A
  1. Haematemesis
  2. Malaena
  3. Haematochaezia
49
Q

Briefly explain the pathogenesis of ostertagia ostertagia (cattle) and teladorsagia circumcinta (small ruminants):

A
  1. L3, L4 and L5 stage larvae reside in abomasal glands
  2. Induces glandular hyperplasia and metaplasia (glands become predominantly mucous secreting)
  3. Lumen pH increases –> reduced conversion of pepsinogen to pepsin (increased pesinogen in blood) and bacterila fermentation causing osmotic diarrhoea
  4. Emergence of immature adults causes physical damage to mucosa –> inflammation
  5. Weight loss, diarrhoea and hypoproteinaemia
50
Q

What are the pathological mechanisms of diarrhoea?

A
  1. Maldigestion/malabsorption (malassimilation) - ingestion of poorly absorbed solutes (increased osmotic pressure in lumen), disease causing loss of mucosal surface area (villous atrophy)
  2. Increased secretion of ions (‘hypersecretion’) - bacterial toxins, inflammatory mediators, endogenous laxatives
  3. Increased intestinal permeability (PLE) - acute inflammation, chronic inflammation, neoplasia
  4. Changes in intestinal motility - viral enteritis, radiation enteritis
51
Q

What are the sequalae of severe diarrhoea?

A
  1. XS faecal fluid –> dehydration –> hypovolaemia –> haemoconcentration –> inadequate tissue perfusion
  2. Resutlant hypoglycaemia –> switch to anaerobic glycolysis and ketoacidosis (decreasedblood and tissue pH) –> pH-dependant enzyme system functions
  3. Acidosis compounded by faecal bicarb loss in the diarrhoea and inadequate absorption of bicarb (late effect of inadequate renal perfusion)
  4. Resultant electrolyte imbalance –> increases intracellular [H+] and decreases intracellular [K+]
  5. Imbalances lead to decreased neuromusuclar control of myocardial contraction and further decreases in tissue perfusion
  6. Viscous cycle that –> hypovolaemic shock
52
Q

Name the condition that is shown below:

A

Perianal fistula

53
Q

What are the mechanisms by which NSAID’s cause intestinal ulceration?

A
  1. Inhibition of prostaglandin synthesis
  2. Altered microcirculation
  3. Delayed GIT healing (decreased cell turnover and mucous production, stimulate gastrin secretion that causes increased acid production)
54
Q

What is peritonitis and what are the two potential routes from which it can arise?

A

Inflammation of peritonium and structures contained therein

  • gastrointestinal tract rupture
  • systemic infections
55
Q

What is ascites and what can be done to further classify this fluid?

A

Ascities = excessive intraperitoneal fluid - it can be further characterised by performing an aseptic abdominocentisis to characterise the fluid

VET377 (60 decks)

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