GIT Path Flashcards
Define: Cholestasis
Bile without motion
Define: Icterus
Yellowing of the skin and other tissues due to deposition of bilirubin (aka jaundice)
What could elevated AST mean?
Indicates cell damage, not necessarily hepatic
What could elevated ALT in a dog or cat mean?
Could be indicative of hepatic disease, or corticosteroids and some anticonvulsants.
What would elevated GGT be indicative of?
Cholestasis
What would elevated creatinine kinase be indicative of?
Cardiac/skeletal muscle cell damage
What tests look for reduced functional hepatic mass?
Bile acids, BSP test, blood ammonia/ urea
What is significant about ALP elevation in cats, and why?
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.
What is the difference between ALP and GGT?
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.
What drugs are ALP and GGT affected by in dogs?
ALP: anticonvulsants, anaesthetics, barbiturates GGT: corticosteroids
What could the presence of GGT in urine indicate?
Tubular damage
Elevated ALT?
Does not necessarily mean cell death as changes in permeability also increase ALT
What are anorexia, vomiting depression, weakness, abdominal pain, dehydration, diarrhoea, fever and jaundice common clinical signs of ?
Acute necrotizing pancreatitis
Amylase increases in the dog differentials?
1) pancreatic injury 2) renal dysfunction 3) GIT disease 4) hepatic disease 5) neoplasia
Amylase elevation is…
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
Amylase in cats and horses with pancreatic injury?
Cats: usually NOT increased, occasionally decreased; can increase with pre-renal and post- renal azotaemia Horse: slight if increased at all
Amylase in horses
increases seen in - 50% of horses with proximal enteritis - 25% of horses with other causes of intestinal colic
Lipase elevation
Magnitude of the increase is important. If 2x higher than upper limit highly suggestive of pancreatic injury Dogs recieving CST up to 5x increases
Lipase in cats
Not a reliable indicator of pancreatic injury
What % of cats show evidence of pancreatitis on necropsy?
67%
Pancreas specific lipase immunoassay
Pancreatitis = increase Reduced Pancreatic Mass = decrease
Two types of hyperproteinemia
- Dehydration 2. True Increase
Reasons for a true hyperproteinemia
- neonatal 2. acute inflammation and tissue injury 3. chronic inflammation 4. chronic liver disease 5. neoplasia
Hypoproteinemia causes
- Decreased protein intake/production - malabsorption - starvation - exocrine pancreatic insufficiency - liver disorders - cachexia (neoplastic) 2. Increased protein loss - in urine (glomerulopathy) - gut (PLGE) - haemorrhage - parasitism
Hypoproteinaemia if significant will result in
Oedema
Serum Trypsin immunoreactivity (TLI)
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)
Supportive findings for pancreatic necrosis (7)
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
dysphagia
difficulty/ discomfort in swallowing as a symptom of disease
ptyalism
excess salivation
halitosis
bad breath
stomatitis
inflammation of the oral cavity mucosa
pharyngitis
inflammation of the pharynx
glossitis
inflammation of the tongue
tonsilitis
inflammation of the tonsils
gingivitis
inflammation of the gingiva
enamel hypoplasia
virus infects ameloblasts during enamel formation. Enamel is fully formed when the teeth erupt
catarrhal
thick mucus exudate
Causes of stomatitis
direct injury (foreign body) or chemicals, systemic or local disease
Types of stomatitis
vesicular stomatitis catarrhal stomatitis erosive or ulcerative stomatitis necrotising stomatitis granulomatous stomatitis papular stomatitis eosinophilic granuloma complex
What is this?
Vesicular stomatitis
What disease is going on here? Hint: This is a section of oral mucosa
Food and mouth disease
What agent causes foot and mouth disease?
Picornavirus
What are the main routes of administration for food and mouth disease?
Inhalation and ingestion
Bonus points! Viraemia, localises in lymphoid and epithelial tissue, vesicles then provide a source of infection for other hosts
What autoimmune disease process is this?
Pemphigus
Ulcerative or Erosive Stomatitis is a feature of?
Uraemia
Viruses: Calicivirus, BVD, Blue Tongue, Equine Viral Rhinotacheitis
What is this?
Feline calicivirus
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?
Feline Calicivirus (FCV)
Scabby mouth
Parapox virus
Enters through abrasions in the epidermis
Zoonotic: orf (ecthyma contagiousum)
Scabby mouth lesions (sheep)
mouth, udder, coronary band, anus
What is this?
Scabby mouth
Pathology of scabby mouth
- begins as raised red lesions
- forms pustules which turn into scabs
- eosinophilic cytoplasmic inclusion bodies may be seen early in the disease
What is actinobacillosis more commonly known as?
“wooden tongue”
What are the main clinical symptoms of actinobacillosis?
Enlarged firm tongue
Diffuse fibrous proliferations on tongue (inc granulomas)
Multifocal well demarcated yellow lesions on the retropharyngeal lymph node
What is eosinophilic granuloma complex?
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.
What are the 3 identifiable lesions of an eosinophilic granuloma complex?
- indolent (rodent) ulcer
- eosinophilic (or linear) granuloma
- eosinophilic plaque
What is thought to be the cause of eosinophilic granuloma complex?
Thought to be a hypersensitivity or autoimmune reaction (think eosinophils and mast cells)
A genetic component is also suspected.
What type of eosinophilic granuloma complex is this?
Indolent
What type of eosinophilic granuloma complex is this?
Where else could it occur in the body?
Linear
on the skin
What type of eosinophilic granuloma complex is this?
Its this the most common distribution for this type of complex?
Eosinophilic plaque
Define cheiloschisis?
Cleft lip
What is the medical term for a cleft palate?
palatoschisis
Define brachygnathia
‘parrot mouth’
short mandible
Define prognathia
elongated mandible
What would be the primary cause for concern with an abnormal oral cavity?
(brachygnathia, prognathia)
Dysphagia
What is this disorder known as?
what type of breed does it effect?
Gingival hyperplasia
most common in brachycephalic breeds
(30% of boxers > 5 years affected)
What is epulis?
excessive growth of gingiva
Are all epulis considered benign?
No
What are acenthomatous epulides?
Why are they significant?
malignant acanthomatous ameloblastomas
only epulides not considered benign as they invade bone and are prone to reoccurrence
What can (potentially bad outcome) happen to a papilloma wart?
it can undergo a malignant transformation to a SCC
e.g cervial cancer
What is this?
What is its pathology?
What does it look like histologically?
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
What is the prognosis of most (90%) oral melanomas in the dog?
Poor as 90% are malignant
What should you be careful of when diagnosing oral melanomas?
some melanomas are amelanotic
What is the most common oral tumour in cats?
What cell type does this tumour arise from?
Oral fibrosarcoma
Fibroblasts
Where are the common sites of oral SCCs in cats and dogs?
Cats: Tongue
Dogs: Tonsils
What are the four symptoms that would cause you to include intestinal disease in your differential diagnosis?
- D+
- V+
- Abdominal paint
- Weight loss
What are the 3 mechanisms of diarrhoea
- osmotic
- secretory
- increased permeability
What are the 4 causes of intestinal obstruction?
- stenosis and atresia
- extrinsic obstruction
- functional obstruction
- intestinal displacement
What are the six causes of stenosis and atresia?
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)
What are the four causes of extrinsic obstruction?
- neoplasms
- abscesses
- peritonitis
- fibrous adhesions
What % of hepatocytes have to be destroyed or removed for chronic liver failure to occur?
80-90%
Hepatic lipidosis
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
Feline idiopathic hepatic lipidosis
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
Pyrrolizidine Alkaloidosis
Pattersons curse poisoning.
Antimitotic but hypertrophic hepatocytes
Nuclei and cytoplasm up to 10-20x greater in volume
Biliary duct proliferation
Copper storage diseases
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
focal necrosis (liver)
scattered foci due to bacterial infection or parasite migration
centrilobular (periacinar) necrosis
often due to hypoxia and anoxia (cardiac failure)
periportal necrosis
(zone 1) hepatocytes can occur due to inflammation around portal triads
massive necrosis (hepatic)
iconnecting whole acini are affected
bridging necrosis
confluent areas of necrosis linking centrilobular areas or periportal areas.
followed by bridging fibrosis as a prelude to cirrhosis
In herbivores what are the predisposing factors to copper deposition?
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
Hepatitis
inflmmation involving the plates of hepatocytes
what is significant about viral hepatitis (and some bacterial hepatitis)
cause death so quickly that inflammatory cells have little time to accumulate
cholangiohepatitis
inflammation of the bile ducts and hepatocytes
cholangitis
inflammation of the biliary system
cholecystitis
inflammation of the gall bladder
Blacks disease (pathology)
Clostridial (clostridium novyi)
Spores lodge in the hepatic sinusoids
Usually follows mass necrosis by the liver (faciola hepatica)
What is the correct order of the life cycle of fasciola hepatica
egg -> miracidium -> germinal balls -> cercariae -> metacercariae -> fluke
9 days to 1 month 24-30 hr 30-50 days
Gram negative rod, features pili and flagella, oxidase negative
causes: diarrhea (may be bloody), cramps
Pathology: eating expired food, orofaecal route of administration
Salmonella enterica
Differentials for acute vomiting/ abdominal pain in a dog
hepatopathy, pancreatic necrosis, GIT inflammation or obstruction, peritonitis/splenitis, (less likely) acute nephropathy
deh
Gingivitis pathology
Reversible! inflammation of the gingiva
Bacteria in gingival sulcus stimulate inflammatory reaction
Usually G+
If untreated -> periodontitis
Periondontal disease
Irreversible destruction of tooths supporting structures
Switches to G-
Inflammatory reaction -> periodontal soft tissue = alveolar bone loss
Likely suspects for periodontitis
NSFA porphyromonas, prevotella, fusobacterium, bacteroides
G+ NSFA
Proprionibacterium, lactobacillus, eubacterium, bifidobacterium, actinomyces, peptostreptococcus, peptococcus
Three sites where NSFA causes disease
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
Why does periodontal disease occur?
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)
Scientific name for the bacteria causing wooden tongue
Actinobacillus lignieresii
What is are the features of actinobacillus lignieresii
G- rods
O2 +/-
Oxidase +
Normal Flora
What is the pathology of actinobacillus lignieresii
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
What is the genus of bacteria responsible for lumpy jaw?
Actinomyces
What are the features of Actinomyces?
Filamentous G+ rods
+/- O2
Endogenous
