Brainscape's Knowledge GenomeTM

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


See full index

Gastrointestinal Pathology > GIT Path > Flashcards

GIT Path Flashcards

1
Q

Define: Cholestasis

A

Bile without motion

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

Define: Icterus

A

Yellowing of the skin and other tissues due to deposition of bilirubin (aka jaundice)

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

What could elevated AST mean?

A

Indicates cell damage, not necessarily hepatic

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

What could elevated ALT in a dog or cat mean?

A

Could be indicative of hepatic disease, or corticosteroids and some anticonvulsants.

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

What would elevated GGT be indicative of?

A

Cholestasis

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

What would elevated creatinine kinase be indicative of?

A

Cardiac/skeletal muscle cell damage

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

What tests look for reduced functional hepatic mass?

A

Bile acids, BSP test, blood ammonia/ urea

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

What is significant about ALP elevation in cats, and why?

A

There are lower levels in feline hepatocytes and biliary epithelium and it has a shorter half life when compared to dogs (6 hours vs 72). Any elevation in ALP in cats is therefore investigated.

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

What is the difference between ALP and GGT?

A

Both are used to show cholestasis. ALP is useful for dogs and cats and rarely horses. GGT is more commonly used in horses. ALP is NEVER used in sheep and cattle.

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

What drugs are ALP and GGT affected by in dogs?

A

ALP: anticonvulsants, anaesthetics, barbiturates GGT: corticosteroids

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

What could the presence of GGT in urine indicate?

A

Tubular damage

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

Elevated ALT?

A

Does not necessarily mean cell death as changes in permeability also increase ALT

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

What are anorexia, vomiting depression, weakness, abdominal pain, dehydration, diarrhoea, fever and jaundice common clinical signs of ?

A

Acute necrotizing pancreatitis

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

Amylase increases in the dog differentials?

A

1) pancreatic injury 2) renal dysfunction 3) GIT disease 4) hepatic disease 5) neoplasia

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

Amylase elevation is…

A

Not a specific indicator of pancreatic injury, magnitude of the increase is important. 3x increase of upper limit is highly suggestive of pancreatic disease/injury HOWEVER Amylase activity 3x occurs in azotaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Amylase in cats and horses with pancreatic injury?

A

Cats: usually NOT increased, occasionally decreased; can increase with pre-renal and post- renal azotaemia Horse: slight if increased at all

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

Amylase in horses

A

increases seen in - 50% of horses with proximal enteritis - 25% of horses with other causes of intestinal colic

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

Lipase elevation

A

Magnitude of the increase is important. If 2x higher than upper limit highly suggestive of pancreatic injury Dogs recieving CST up to 5x increases

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

Lipase in cats

A

Not a reliable indicator of pancreatic injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What % of cats show evidence of pancreatitis on necropsy?

A

67%

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

Pancreas specific lipase immunoassay

A

Pancreatitis = increase Reduced Pancreatic Mass = decrease

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

Two types of hyperproteinemia

A
  1. Dehydration 2. True Increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Reasons for a true hyperproteinemia

A
  1. neonatal 2. acute inflammation and tissue injury 3. chronic inflammation 4. chronic liver disease 5. neoplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hypoproteinemia causes

A
  1. Decreased protein intake/production - malabsorption - starvation - exocrine pancreatic insufficiency - liver disorders - cachexia (neoplastic) 2. Increased protein loss - in urine (glomerulopathy) - gut (PLGE) - haemorrhage - parasitism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Hypoproteinaemia if significant will result in

A

Oedema

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

Serum Trypsin immunoreactivity (TLI)

A

Sensitive indicator of early pancreatitis Increases inconsistently with necrotising pancreatitis and some clinically healthy animlas may have TLI values in the same range as animals with pancreatitis Assess in combination with renal function (amylase lipase and TLI all increase with decreased renal function)

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

Supportive findings for pancreatic necrosis (7)

A

1) haematology -inflammatory demand (left shift), stress neutrophilia + toxic changes -haemoconcentration (dehydration) - anaemia 2) hyperlipidemia (fasting) 3) fluid imbalance (vomiting and loss of HCl) 4) pre-renal azotemia (urea) 5) non-septic exudate in peritoneal cavity (+lipase and amylase) 6) mild transient hyperglycaemia 7) transient hypocalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

dysphagia

A

difficulty/ discomfort in swallowing as a symptom of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ptyalism

A

excess salivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

halitosis

A

bad breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

stomatitis

A

inflammation of the oral cavity mucosa

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

pharyngitis

A

inflammation of the pharynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

glossitis

A

inflammation of the tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

tonsilitis

A

inflammation of the tonsils

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

gingivitis

A

inflammation of the gingiva

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

enamel hypoplasia

A

virus infects ameloblasts during enamel formation. Enamel is fully formed when the teeth erupt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

catarrhal

A

thick mucus exudate

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

Causes of stomatitis

A

direct injury (foreign body) or chemicals, systemic or local disease

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

Types of stomatitis

A

vesicular stomatitis catarrhal stomatitis erosive or ulcerative stomatitis necrotising stomatitis granulomatous stomatitis papular stomatitis eosinophilic granuloma complex

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

What is this?

A

Vesicular stomatitis

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

What disease is going on here? Hint: This is a section of oral mucosa

A

Food and mouth disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What agent causes foot and mouth disease?

A

Picornavirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the main routes of administration for food and mouth disease?

A

Inhalation and ingestion

Bonus points! Viraemia, localises in lymphoid and epithelial tissue, vesicles then provide a source of infection for other hosts

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

What autoimmune disease process is this?

A

Pemphigus

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

Ulcerative or Erosive Stomatitis is a feature of?

A

Uraemia

Viruses: Calicivirus, BVD, Blue Tongue, Equine Viral Rhinotacheitis

46
Q

What is this?

A

Feline calicivirus

47
Q

I am a non enveloped RNA virus. I cause serous nasal discharge, chemosis and conjunctivitis. My trademark pattern of inflammation however involves the oral cavity of cats. What am I?

A

Feline Calicivirus (FCV)

48
Q

Scabby mouth

A

Parapox virus

Enters through abrasions in the epidermis

Zoonotic: orf (ecthyma contagiousum)

49
Q

Scabby mouth lesions (sheep)

A

mouth, udder, coronary band, anus

50
Q

What is this?

A

Scabby mouth

51
Q

Pathology of scabby mouth

A
  1. begins as raised red lesions
  2. forms pustules which turn into scabs
  3. eosinophilic cytoplasmic inclusion bodies may be seen early in the disease
52
Q

What is actinobacillosis more commonly known as?

A

“wooden tongue”

53
Q

What are the main clinical symptoms of actinobacillosis?

A

Enlarged firm tongue

Diffuse fibrous proliferations on tongue (inc granulomas)

Multifocal well demarcated yellow lesions on the retropharyngeal lymph node

54
Q

What is eosinophilic granuloma complex?

A

firstly it is a reaction pattern and not a disease.

It is a group of lesions that affects the skin, mucocutaneous junctions and the oral cavity of cats and (rarely) dogs.

55
Q

What are the 3 identifiable lesions of an eosinophilic granuloma complex?

A
  1. indolent (rodent) ulcer
  2. eosinophilic (or linear) granuloma
  3. eosinophilic plaque
56
Q

What is thought to be the cause of eosinophilic granuloma complex?

A

Thought to be a hypersensitivity or autoimmune reaction (think eosinophils and mast cells)

A genetic component is also suspected.

57
Q

What type of eosinophilic granuloma complex is this?

A

Indolent

58
Q

What type of eosinophilic granuloma complex is this?

Where else could it occur in the body?

A

Linear

on the skin

59
Q

What type of eosinophilic granuloma complex is this?

Its this the most common distribution for this type of complex?

A

Eosinophilic plaque

60
Q

Define cheiloschisis?

A

Cleft lip

61
Q

What is the medical term for a cleft palate?

A

palatoschisis

62
Q

Define brachygnathia

A

‘parrot mouth’

short mandible

63
Q

Define prognathia

A

elongated mandible

64
Q

What would be the primary cause for concern with an abnormal oral cavity?

(brachygnathia, prognathia)

A

Dysphagia

65
Q

What is this disorder known as?

what type of breed does it effect?

A

Gingival hyperplasia

most common in brachycephalic breeds

(30% of boxers > 5 years affected)

66
Q

What is epulis?

A

excessive growth of gingiva

67
Q

Are all epulis considered benign?

A

No

68
Q

What are acenthomatous epulides?

Why are they significant?

A

malignant acanthomatous ameloblastomas

only epulides not considered benign as they invade bone and are prone to reoccurrence

69
Q

What can (potentially bad outcome) happen to a papilloma wart?

A

it can undergo a malignant transformation to a SCC

e.g cervial cancer

70
Q

What is this?

What is its pathology?

What does it look like histologically?

A

Papilloma wart (viral)

Regress spontaneously, usually occurs in dogs < 1 year old, leads to long lasting immunity to the virus

Histological: composed to stratified squamous epithelium and folds of proliferating stroma

71
Q

What is the prognosis of most (90%) oral melanomas in the dog?

A

Poor as 90% are malignant

72
Q

What should you be careful of when diagnosing oral melanomas?

A

some melanomas are amelanotic

73
Q

What is the most common oral tumour in cats?

What cell type does this tumour arise from?

A

Oral fibrosarcoma

Fibroblasts

74
Q

Where are the common sites of oral SCCs in cats and dogs?

A

Cats: Tongue

Dogs: Tonsils

75
Q

What are the four symptoms that would cause you to include intestinal disease in your differential diagnosis?

A
  • D+
  • V+
  • Abdominal paint
  • Weight loss
76
Q

What are the 3 mechanisms of diarrhoea

A
  1. osmotic
  2. secretory
  3. increased permeability
77
Q

What are the 4 causes of intestinal obstruction?

A
  1. stenosis and atresia
  2. extrinsic obstruction
  3. functional obstruction
  4. intestinal displacement
78
Q

What are the six causes of stenosis and atresia?

A

1. congenital e.g atresia ani

2. acquired stenosis due to process in intestinal wall (e.g neoplasm)

3. foreign body (enterolith, phytobezoar, trichobezoar)

4. parasites (either a huge number of parasites or sudden death of large numbers)

5. impaction of the colon (pain causes suppression of defecation causing a backup)

6. impaction of the caecum (change in diet, water intake, poor dentition)

79
Q

What are the four causes of extrinsic obstruction?

A
  1. neoplasms
  2. abscesses
  3. peritonitis
  4. fibrous adhesions
80
Q

What % of hepatocytes have to be destroyed or removed for chronic liver failure to occur?

A

80-90%

81
Q

Hepatic lipidosis

A

Degenerative change to liver

Caused by hypoxia, nutritional factors, bacteria, toxins

involves hepatomegaly and fat inclusion droplets in hepatocytes

If its severe it may be necrotic, if mild can recover

Common in preweaned animals

82
Q

Feline idiopathic hepatic lipidosis

A

Obese cats now anorexic with no other observable disease

Enlarged jaundiced friable livers with accentuated lobular pattern

liver floats in 10% formalin

only 50% survival

Therapy aimed at reversing catabolic state by force feeding high protein

83
Q

Pyrrolizidine Alkaloidosis

A

Pattersons curse poisoning.

Antimitotic but hypertrophic hepatocytes

Nuclei and cytoplasm up to 10-20x greater in volume

Biliary duct proliferation

84
Q

Copper storage diseases

A

copper excess distributed throughout the cytoplasm but eventually aggregates into lysosomes causing a golden brown pigmented histological appearance

causes hepatocellular damage leading to fibrosis and alteration of lobular structure

85
Q

focal necrosis (liver)

A

scattered foci due to bacterial infection or parasite migration

86
Q

centrilobular (periacinar) necrosis

A

often due to hypoxia and anoxia (cardiac failure)

87
Q

periportal necrosis

A

(zone 1) hepatocytes can occur due to inflammation around portal triads

88
Q

massive necrosis (hepatic)

A

iconnecting whole acini are affected

89
Q

bridging necrosis

A

confluent areas of necrosis linking centrilobular areas or periportal areas.

followed by bridging fibrosis as a prelude to cirrhosis

90
Q

In herbivores what are the predisposing factors to copper deposition?

A

herbivores grazing on pastures with a soil deficiency of molybdenum but normal copper levels. = excessive intake of copper

herbivores grazing pastures containing hepatotoxins (usually pyrr aka) copper is normally excreted in bile any disease causing chronic cholestasis may produce excessive storage of copper within hepatocytes

91
Q
A
92
Q

Hepatitis

A

inflmmation involving the plates of hepatocytes

93
Q

what is significant about viral hepatitis (and some bacterial hepatitis)

A

cause death so quickly that inflammatory cells have little time to accumulate

94
Q

cholangiohepatitis

A

inflammation of the bile ducts and hepatocytes

95
Q

cholangitis

A

inflammation of the biliary system

96
Q

cholecystitis

A

inflammation of the gall bladder

97
Q

Blacks disease (pathology)

A

Clostridial (clostridium novyi)

Spores lodge in the hepatic sinusoids

Usually follows mass necrosis by the liver (faciola hepatica)

98
Q

What is the correct order of the life cycle of fasciola hepatica

A

egg -> miracidium -> germinal balls -> cercariae -> metacercariae -> fluke

9 days to 1 month 24-30 hr 30-50 days

99
Q

Gram negative rod, features pili and flagella, oxidase negative

causes: diarrhea (may be bloody), cramps

Pathology: eating expired food, orofaecal route of administration

A

Salmonella enterica

100
Q

Differentials for acute vomiting/ abdominal pain in a dog

A

hepatopathy, pancreatic necrosis, GIT inflammation or obstruction, peritonitis/splenitis, (less likely) acute nephropathy

101
Q
A

deh

102
Q

Gingivitis pathology

A

Reversible! inflammation of the gingiva

Bacteria in gingival sulcus stimulate inflammatory reaction

Usually G+

If untreated -> periodontitis

103
Q

Periondontal disease

A

Irreversible destruction of tooths supporting structures

Switches to G-

Inflammatory reaction -> periodontal soft tissue = alveolar bone loss

104
Q

Likely suspects for periodontitis

A

NSFA porphyromonas, prevotella, fusobacterium, bacteroides

105
Q

G+ NSFA

A

Proprionibacterium, lactobacillus, eubacterium, bifidobacterium, actinomyces, peptostreptococcus, peptococcus

106
Q

Three sites where NSFA causes disease

A

1) normal overgrowth e.g periodontal disease
2) extension of the normal flora into sterile part of the same system
3) traumatic instillation into distant sites e.g CFA

107
Q

Why does periodontal disease occur?

A

THINK HPE

Host factors: immunity, genetics, systemic illness, stress, diet

Local Factors: Calculus, tooth crowding, morphology, saliva

Plaque Factors: Volume and type (beneficial vs. non beneficial)

108
Q

Scientific name for the bacteria causing wooden tongue

A

Actinobacillus lignieresii

109
Q

What is are the features of actinobacillus lignieresii

A

G- rods

O2 +/-

Oxidase +

Normal Flora

110
Q

What is the pathology of actinobacillus lignieresii

A

Results from the trauma to oral cavity caused by hard or sharp plant fibres, rough milking bale or trough

Organisms penetrate into underlying soft tissue through penetration of mucosal barriers

Can be “outbreak” pattern

111
Q

What is the genus of bacteria responsible for lumpy jaw?

A

Actinomyces

112
Q

What are the features of Actinomyces?

A

Filamentous G+ rods

+/- O2

Endogenous

Gastrointestinal Pathology (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions