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Small animal (fourth year) > Internal medicine (gastroenterology) > Flashcards

Internal medicine (gastroenterology) Flashcards

1
Q

what are the clinical signs of oropharyngeal/oesophageal disease?

A

dysphagia
saliva drooling
halitosis
odynophagia (painful swallowing)
regurgitation

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2
Q

what is odynophagia?

A

painful swallowing

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3
Q

what are the ways in which dysphagia can be described?

A

difficulty lapping or forming bolus
excessive jaw/head motion
dropping food from mouth
saliva drooling
persistent/ineffective swallowing
nasal discharge
gagging/coughing

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4
Q

what are the two reason dysphagia can occur?

A

functional - abnormal neuromuscular activity
morphological - structural abnormalities

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5
Q

what are some functional causes of neuromuscular dysphagia?

A

cricopharyngeal achalasia
myasthenia gravis
brainstem disease
peripheral neuropathy
polymyopathy

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6
Q

what could cause morphological dysphagia?

A

oropharyngeal inflammation/trauma
foreign bodies
neoplasia
congenital deformities

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7
Q

what is inflammation of the oral mucosa called?

A

stomatitis

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8
Q

what is inflammation of the lips called?

A

cheilitis

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9
Q

what is inflammation of the tongue called?

A

glossitis

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10
Q

what is inflammation of the gums called?

A

gingitvitis

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11
Q

what is inflammation of the pharynx called?

A

pharyngitis

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12
Q

what is inflammation of the tonsils called?

A

tonsilitis

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13
Q

what are some congenital morphological causes of dysphagia?

A

lip-fold deformities
cleft palate
malocclusion
craniomandibular osteopathy

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14
Q

how would regurgitation be described?

A

a passive event of undigested food covered in mucus/saliva being brought up the oesophagus (immediately after eating)

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15
Q

what is pseudoptyalism?

A

failure to swallow normal volume of saliva

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16
Q

what is ptyalism?

A

increased saliva production

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17
Q

what needs to be found out to define whether the animal is vomiting or regurgitation food?

A

what is brought up
when it is brought up (relation to feeding)
vomiting signs (active process)
concurrent disease
illness duration

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18
Q

what contrast can be used for GI tract?

A

barium mixed with food
iodine contrast (if perforation suspected)

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19
Q

what are some specialist test that can be used for oesophageal disease?

A

anti-ACh receptor antibody
2-M antibodies
ACTH stimulation test

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20
Q

what is the anti-ACh receptor antibody test used for?

A

primary oesophageal disease

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21
Q

what are 2-M antibody tests used for?

A

see if there are antibodies targeting the muscle of mastication (these are specific to there)

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22
Q

what is the definition of megaoesophagus?

A

oesophageal dilation with functional paralysis

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23
Q

what are the finding on radiograph of a patient with megaoesophagus?

A

uniformly dilated with gas/fluid filling
ventrally displaced trachea
possible secondary aspiration pneumonia

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24
Q

why is fluoroscopy occasional essential to diagnosing megaoesophagus?

A

can determine dysmotility of oesophagus

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25
Q

how can idiopathic megaoesophagus be treated?

A

feeding from a height (upright)
textured food/balls or slurry
metoclopramide (improve motility)

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26
Q

what is the prognosis for patients with idiopathic megaoesophagus?

A

guarded - often get aspiration pneumonia

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27
Q

what are possible causes of oesophagitis?

A

ingestion of caustics/irritants
foreign bodies
acute/persistent vomiting
gastric reflux

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28
Q

what are the clinical signs of oesophagitis?

A

anorexia
dysphagia
odynophagia
regurgitation
hypersalivation

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29
Q

how is oesophagitis treated?

A

(rest oesophagus)
frequent small soft feeds
liquid antacids
local anaesthesia

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30
Q

how can sucralfate aid oesophagitis treatment?

A

gastric protectant - coats mucosa of oesophagus

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31
Q

what is the aetiology of oesophageal strictures?

A

fibrosis after ulceration due to… foreign bodies, caustic agents, gastric reflux, drugs, severe oesophagitis

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32
Q

how can oesophageal strictures be treated?

A

dilation - bouginage or balloon

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33
Q

what is the disadvantage of using bougienage to dilate oesophageal strictures?

A

increased risk of perforations compared to balloon dilation

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34
Q

what is the most common place for oesophageal foreign bodies?

A

lower oesophageal sphincter (also heart base and thoracic inlet)

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35
Q

how are oesophageal foreign bodies treated?

A

removal via endoscopy (surgery is a last resort)

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36
Q

what should always be done after removal of an oesophageal foreign body?

A

radiograph (check for pneumomediastinum) - this can indicate a tear

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37
Q

what is primary vomiting due to?

A

underlying gastric disease

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38
Q

what is secondary vomiting due to?

A

non-GI disease

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39
Q

what is the events that happen after the vomiting centre is triggered to cause vomiting?

A

pylorus is contracted
stomach and lower oesophageal sphincter relaxes
abdominal muscles contract
glottis is closed
upper oesophageal sphincter opens
antiperastalsis propels food towards the mouth

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40
Q

what can switch on the vomiting centre of the brain?

A

duodenum
stomach
pharynx
vestibular system
chemoreceptor trigger zone

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41
Q

what are some possible secondary causes of vomiting?

A

infections, pyometra, renal failure, drugs, CNS disease, motion sickness, vestibular disease, neoplasia…

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42
Q

what can cause chronic vomiting?

A

intestinal/peritoneal disease
primary gastric disease
diffuse GI disease involving stomach

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43
Q

what are some causes of chronic vomiting secondary to intestinal/peritoneal disease?

A

inflammatory bowel disease
intestinal neoplasia
small intestinal obstruction
pancreatitis
peritonitis

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44
Q

what primary gastric diseases can cause chronic vomiting?

A

chronic gastritis
gastric retention disorders
gastric ulcers
gastric neoplasia

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45
Q

what diffuse GI diseases involving the stomach can cause chronic vomiting?

A

inflammatory bowel disease
alimentary lymphoma

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46
Q

what are the three basic models of the pathophysiology of gastric disease?

A

gastric outflow obstruction
gastroparesis
disruption of mucosal barrier

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47
Q

what diagnostic clinical pathological tests can be done for vomiting animals?

A

electrolytes
haematology
bile acid stimulation test
ACTH stimulation
urinalysis
pancreatic lipase

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48
Q

what are some possible causes of chronic gastritis?

A

dietary intolerance
chronic gastric parasites
hairballs
immune mediated

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49
Q

what are the clinical signs of chronic gastritis?

A

intermittent chronic vomiting
periodic early morning vomit with bile
poor appetite
gastric bleeding

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50
Q

what are the possible treatment options for chronic gastritis?

A

removal of aetiological agent
diet - trials, multiple small meals…
acid blockers
corticosteroids

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51
Q

what is the best diet for chronic gastritis cases?

A

hydrolysed protein diet

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52
Q

when does bilious vomiting usually occur?

A

vomiting occurs overnight/morning in dogs fed once a day (especially in the morning)

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53
Q

what is the presumed aetiology of bilious vomiting?

A

abnormal internal motility allowing bile reflux into the stomach

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54
Q

how can bilious vomiting be treated?

A

feed more often (later in the day)
prokinetics - ranitidine…

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55
Q

what is a gastric retention disorder?

A

food is retained in the stomach for >8 hours causing delayed vomiting of food (way longer than it should be retained)

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56
Q

what are the possible causes of gastric retention disorders?

A

anatomical obstruction
functional disorders - motility, inflammatory disease…

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57
Q

what are the possible outflow obstructions to the stomach causing gastric retention disorders?

A

pyloric stenosis
neoplasia/polyps
foreign bodies
chronic hypertrophic pyloric gastropathy

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58
Q

what prokinetics can be used to treat gastric retention due to a functional problem?

A

metoclopramide
ranitidine
erythromycin

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59
Q

how does metoclopramide work as a prokinetic for gastric retention?

A

stimulates normal gastric peristalsis

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60
Q

how does ranitidine work as a prokinetic for gastric retention?

A

stimulates peristalsis and hydrogen antagonist

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61
Q

how does haematemesis look if blood has been in then stomach for a while?

A

coffee grounds

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62
Q

what are some possible causes of haematemesis?

A

generalised bleeding
swallowed blood (oropharyngeal, nasal…)
severe gastritis
gastric ulcer
gastric neoplasia
duodenal disease

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63
Q

what are the clinical signs of gastric ulcers?

A

haematemesis
melaena
anaemia
weight loss
pain
peritonitis

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64
Q

what posture in associated with abdominal pain?

A

prayer posture

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65
Q

what are the possible causes of gastric ulcers?

A

drugs - NSAIDs, corticosteroids
head and spinal injuries
gastritis
liver/kidney disease
bile reflux
mastocytosis
helicobacter

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66
Q

what species of helicobacter causes gastric ulcers?

A

H. pylori

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67
Q

how are gastric ulcers treated?

A

sucralfate
acid blockers - antacids, H2 antagonists, proton pump inhibitors

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68
Q

what are some H2 antagonists used to treat gastric ulcers?

A

cimetidine
ranitidine
nizatidine

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69
Q

what proton pump inhibitor is used for gastric ulcer treatment?

A

omeprazole

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70
Q

what should not be given with omeprazole to treat gastric ulcers? and why?

A

NSAIDs as they can worsen intestinal ulceration

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71
Q

what is used to treat helicobacter?

A

triple therapy (two antibiotic plus an acid blocker)

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72
Q

what is an example of a triple therapy used to treat helicobacter?

A

amoxicillin, metronidazole, clarithromycin (triple antibiotics)
amoxicillin, metronidazole, omeprazole (2 antibiotics and acid blocker)

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73
Q

what are the majority of the neoplasms found in the stomach of dogs?

A

adenocarcinomas

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74
Q

where do gastric adenocarcinomas often metastasise to?

A

local lymph nodes and liver

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75
Q

when would you suspect a gastric adenocarcinoma?

A

older animals with chronic vomiting, anorexia, weight loss, haematemesis, anaemia and saliva drooling

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76
Q

what is the prognosis for gastric adenocarcinomas?

A

hopeless (surgical resection is rarely curative and often painful)

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77
Q

what is chronic diarrhoea?

A

diarrhoea that has been present for more than 2 weeks

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78
Q

what are the steps for approaching diarrhoea cases?

A

history/physical exam
symptomatic therapy
laboratory investigations
diagnostic imaging
GI biopsy
therapeutic trials

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79
Q

what are the main alimentary disease differentials diagnoses for diarrhoea?

A

adverse food reactions
inflammatory bowel disease
antibiotic responsive diarrhoea
lymphangiectasia
lymphoma/tumour
infectious diarrhoea
partial obstructions

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80
Q

what is lymphangiectasia?

A

effects the lymphatic system within the small intestine causing a blockage leading to dilation of the vessels

81
Q

what is a linear foreign body?

A

long thin foreign body such as string/wire (can wrap around tongue or other structure)

82
Q

what should be checked for in the oral cavity of diarrhoea cases?

A

CRT
gum colour
hydration (wet gums)
linear foreign bodies

83
Q

what is haematochezia?

A

fresh blood in faeces

84
Q

what are the features of small intestinal diarrhoea?

A

increased volume
colour change
normal/increased frequency
(weight loss, flatulence, borborygmi, halitosis - all evidence of malabsorption)

85
Q

why is an increased volume of faeces seen with small intestinal diarrhoea?

A

small intestine involved with digestion/absorption so damage to this means food isn’t being digested so maintains water in the large intestine (they have malabsorption)

86
Q

what are the features of large intestinal diarrhoea?

A

decreased volume
increased frequency
urgency/tenesmus
mucus/haematochezia
dyschezia
(can vary in consistency)
(less weight loss)

87
Q

what is melaena?

A

digested blood in faeces (before the small intestines)

88
Q

how does melaena appear?

A

dark tar colour

89
Q

where can diarrhoea most commonly be located to?

A

large intestine

90
Q

is fibre supplementation used for small or large intestinal diarrhoeas?

A

large intestine

91
Q

is sulfasalzine used for small or large intestinal diarrhoea?

A

large (only gets activated in the large intestine)

92
Q

if used for three consecutive days, what does fenbendazole treat?

A

Giardia (protozoal cause of diarrhoea)

93
Q

what are the three most common parasites causing diarrhoea in dogs/cats?

A

Giardia
Cryptosporidia
Tritrichomonas foetus (cats)

94
Q

what are the most common bacteria causing diarrhoea in dogs/cats?

A

salmonella
campylobacter

95
Q

what are the typical cats effected by Tritrichomonas fetus?

A

young cats
pedigree
cats in colonies

96
Q

does Tritrichomonas fetus produce large or small intestinal diarrhoea?

A

large intestinal (small intestinal much more common in cats so if you see signs of LI this is a top differential)

97
Q

what test can be ran to diagnose hyperthyroidism?

A

total thyroxine

98
Q

what test can be run to diagnose hypoadrenocorticism?

A

ACTH stimulation or basal cortisol

99
Q

what test is used for diagnosing exocrine pancreatic insufficiency?

A

trypsin like immunoreactivity

100
Q

what test can be run to diagnose malabsorption?

A

folate and cobalamin

101
Q

where is folate absorbed?

A

proximal small intestine

102
Q

where is cobalamin absorbed?

A

distal small intestine

103
Q

what can you tell about the outcome of a case if a hypocobalaminaemia is present?

A

this is a negative prognostic indicator (survival is worse)

104
Q

what are the two ways to get an intestinal biopsy?

A

endoscopy
surgical (coeliotomy)

105
Q

why is surgical (coeliotomy) biopsy better in cats with chronic diarrhoea?

A

often have other systems (liver and pancreas) effected with inflammation and disease

106
Q

what will be seen in cases of lymphangiectasia on intestinal biopsy?

A

lacteal dilation

107
Q

what should you ask an owner to keep a diary of in chronic diarrhoea cases?

A

frequency of diarrhoea
other signs (vomiting, pain…)
appetite and demeanour
compliance with treatment

108
Q

what is constipation?

A

difficult, incomplete or infrequent evacuation of dry hardened faeces from the bowels

109
Q

what are some possible aetiologies of constipation?

A

dietary
neuromuscular (idiopathic megacolon)
environmental (obesity, inactivity…)
colonic obstruction (stricture, pelvic trauma…)
electrolyte imbalance (dehydration, hypokalaemia…)
drug-induced

110
Q

what are some treatment options for constipation?

A

remove causative agent
oral laxative (lactulose)
enema
oral polyethylene glycol
gentle manual evacuation
surgery
dietary management

111
Q

what is a possible oral laxative for constipation treatment?

A

lactulose

112
Q

how much of the pancreas is exocrine tissue?

A

98%

113
Q

what are the exocrine cells of the pancreas called?

A

acinar cells

114
Q

what does the exocrine pancreas produce?

A

digestive enzymes
intrinsic factor
bicarbonate

115
Q

what is the function of intrinsic factor?

A

it binds to cobalamin to protect it through the small intestine and then allow it to be absorbed

116
Q

what are the two main diseases effecting the pancreas?

A

pancreatitis
exocrine pancreatic insufficiency

117
Q

what is the cause of acute pancreatitis?

A

inappropriate activation of digestive enzymes

118
Q

what is often the enzyme that drives pancreatitis?

A

trypsin (activates other enzymes)

119
Q

what are some possible predisposing factors for pancreatitis?

A

breed (spaniels/terrier)
gender (female>male)
obesity
drugs
concurrent disease
dietary factors

120
Q

what is the cause of most pancreatitis?

A

idiopathic

121
Q

what are some diseases associated with feline pancreatitis?

A

cholangitis
inflammatory bowel disease
hepatic lipidosis
diabetes mellitus

122
Q

what factors of a diet are associated with acute pancreatitis?

A

high dietary fat
hyperlipidaemia - obesity, diabete…
bin raiding, table scrap…

123
Q

what are the clinical signs of acute pancreatitis in dogs?

A

dehydration
anorexia
vomiting
weakness
abdominal pain (prayer position)
diarrhoea
jaundice

124
Q

what are the clinical signs of acute pancreatitis in cats?

A

lethargy
anorexia
vomiting
abdominal pain
diarrhoea

125
Q

what results on haematology/biochemistry suggests acute pancreatitis?

A

increased white blood cells
increased glucose/decreased calcium
increased liver enzymes
jaundice (increased bilirubin)

126
Q

what pancreatic enzyme tests are available for acute pancreatitis?

A

total amylase and lipase
pancreatic lipase

127
Q

will total amylase/lipase increase or decrease with acute pancreatitis?

A

increase

128
Q

what is the advantage of the pancreatic lipase test?

A

less affected by azotaemia
SNAP test available

129
Q

what is needed for a definitive diagnosis of pancreatitis?

A

pancreatic biopsy

130
Q

what is all of the treatment of pancreatitis based on?

A

supportive therapy (no cure for it)

131
Q

what treatment options are available for acute pancreatitis?

A

nutritional support
pancreatic enzymes
fluid therapy
analgesia
antiemetics

132
Q

what are the steps of dietary therapy for acute pancreatitis cases?

A

initial therapy - 3-7 days
interim diet - 3-28 days
long-term diet - 3 weeks onwards

133
Q

what is usually needed for the initial dietary therapy for acute pancreatitis (3-7 days)?

A

feeding tube (often anorexic and not wanting to feed on their own)

134
Q

what are the types of feeding tubes available?

A

enterostomy tube
nasooesophageal tube
oesophagostomy tube
gastrostomy tube

135
Q

what is fed in the interim diet therapy for acute pancreatitis patients? (3-28 days)

A

small amounts of water
low fat diet
small frequent meals
pancreatic enzymes

136
Q

what is the issue sometimes seen with pancreatic enzyme supplementation?

A

sometimes stops the patient wanting to eat

137
Q

what analgesic drugs should be avoided in patients with acute pancreatitis?

A

NSAIDs

138
Q

what are some good analgesic options for acute pancreatitis?

A

buprenorphine
paracetamol
tramadol
gabapentin

139
Q

what are the two main anti-emetics considered for acute pancreatitis cases?

A

maropitant (easier to administer)
metoclopramide

140
Q

what is the aetiology of exocrine pancreatic insufficiency?

A

pancreatic acinar atrophy (most common)
pancreatic hypoplasia
chronic pancreatitis

141
Q

what are the clinical signs of exocrine pancreatic insufficiency?

A

faecal changes
appetite changes
vomiting
poor coat quality

142
Q

what faecal changes are seen with exocrine pancreatic insufficiency?

A

large volume
foul smelling
greasy (steatorrhoea)
putty-like to overt diarrhoea

143
Q

what appetite changes can be seen with exocrine pancreatic insufficiency?

A

polyphagia - increased
coprophagia
pica - depraved appetite (eating weird things)

144
Q

what is the best ways to diagnose exocrine pancreatic insufficiency (EPI)?

A

trypsin like immunoreactivity

145
Q

are you looking for increased or decreased levels when carrying out a trypsin like immunoreactivity test for EPI?

A

decreased

146
Q

how can exocrine pancreatic insufficiency treated?

A

pancreatic enzymes - powder, enteric coated granules, fresh-frozen pancreas
dietary management - highly digestible diet (2x maintenance)
cobalamin supplementation

147
Q

why do dogs with EPI need cobalamin supplementation?

A

pancreas isn’t producing intrinsic factor

148
Q

what is a poor prognostic indicator of EPI outcome?

A

low cobalamin (if you need to supplement them)

149
Q

what is a possible complication of EPI?

A

bacterial overgrowth - food not absorbed so there is more substrate for bacteria to grow

150
Q

is EPI more common in dogs or cats?

A

cats

151
Q

what are the functions of the liver?

A

metabolism (protein, fat…)
storage
protein synthesis
bile production
detoxification…

152
Q

what is icterus also known as?

A

jaundice

153
Q

what is jaundice?

A

build up of bilirubin

154
Q

what is pre-hepatic jaundice due to?

A

haemolysis

155
Q

what is hepatic jaundice due to?

A

hepatic dysfunction
intrahepatic cholestasis

156
Q

what causes post-hepatic jaundice?

A

extra-hepatic cholestasis

157
Q

what clinical sign can be used to differentiate hepatic and post-hepatic jaundice from pre-hepatic jaundice?

A

mucous membranes will be pink/yellow in hepatic or post-hepatic jaundice
with pre-hepatic it will be yellow

158
Q

what metabolic dysfunctions can be seen with liver disease?

A

hypoglycaemia
hypoalbuminaemia
non-specific (condition/weight loss…)

159
Q

what clinical sign can hypoalbuminaemia lead to in liver disease cases?

A

ascites

160
Q

what effects does hepatic disease have that can cause circulatory disturbance (ascites)?

A

hypoalbuminaemia
portal hypertension
sodium/water retention

161
Q

what can cause an acquired portosystemic shunt?

A

cirrhosis
portal hypertension

162
Q

what is the main consequence of a portosystemic shunt?

A

hepatic encephalopathy - toxins that would normally be eliminated aren’t (build up of NH3 in blood)

163
Q

what are the clinical signs of hepatic encephalopathy?

A

anorexia, vomiting, diarrhoea
blindness, aggression, staggering, seizures

164
Q

what can make hepatic encephalopathy worse?

A

high protein meal
GI bleed
dehydration
acid-base imbalance

165
Q

what are clinical signs of hepatic encephalopathy in cats but not dogs?

A

copper-coloured irises
salivation

166
Q

why can excessive bleeding occur with liver disease?

A

liver produces/stores clotting factors
liver is responsible for vitamin K absorption
portal hypertension can cause GI bleeding

167
Q

why is the liver partly responsible for vitamin K absorption?

A

it is a fat soluble vitamin and the liver produces bile acids that help to absorb fat

168
Q

what are the clinical signs of liver disease?

A

icterus
faecal changes (grey, melaena)
hepatic encephalopathy
drug intolerance
ascites
stunted growth (due to metabolic effect)
vomiting/diarrhoea
PUPD
non-specific signs - anorexia, weakness…

169
Q

what are the two divisions of hepatopathies?

A

primary (problem arisen in liver)
secondary/reactive (liver reacting to issue elsewhere)

170
Q

what are the two types of primary hepatopathy?

A

inflammatory
non-inflammatory

171
Q

what are the two types of primary hepatopathy?

A

inflammatory
non-inflammatory

172
Q

what are some possible aetiologies of secondary hepatic disease?

A

anoxia
toxaemia
nutritional imbalance
metabolic changes
infection

173
Q

what are some bacterial causes of inflammatory hepatic disease?

A

leptospirosis
bacterial cholangiohepatitis

174
Q

what are some viral causes of inflammatory hepatic disease?

A

infectious canine hepatitis
canine herpes
feline infectious peritonitis

175
Q

what protozoa can cause inflammatory hepatic disease?

A

toxoplasma

176
Q

what are some non-infectious inflammatory causes of hepatic disease?

A

toxic hepatic disease
drug-induced hepatic disease
canine chronic hepatitis
feline lymphocytic cholangitis

177
Q

what are some causes of non-inflammatory hepatic disease?

A

congenital portosystemic shunt
juvenile heaptic fibrosis
feline hepatic lipidosis
neoplasia
telangiectasis
surgical - torsion/trauma

178
Q

what are some causes of non-inflammatory hepatic disease?

A

congenital portosystemic shunt
juvenile heaptic fibrosis
feline hepatic lipidosis
neoplasia
telangiectasis
surgical - torsion/trauma

179
Q

what is the reason for cats susceptibility to paracetamol and aspirin?

A

deficiency of gluruonyl transferase meaning they have difficulty conjugating toxins

180
Q

what is paracetamol toxic to cats?

A

deficiency of glucuronidation
deficiency of glutathione conjugation

181
Q

how is paracetamol toxicity treated?

A

N-acetylcysteine (precursor for glutathione)
vitamin C
supportive treatment

182
Q

why is coagulation often tested in cases of suspected hepatic disease?

A

check if a liver biopsy can safely be taken

183
Q

what do liver enzymes test for?

A

suggest liver disease (nothing to do with function!!!)

184
Q

what is the most common hepatocellular marker used in serum biochemistry?

A

ALT

185
Q

what is the most common cholestatic marker used in serum biochemistry?

A

ALP

186
Q

what can be tested to give an indication of liver function?

A

serum proteins (albumin)
glucose, urea, cholesterol
bilirubin
bile acids
ammonia

187
Q

what are the four reasons for low albumin?

A

protein losing enteropathy
protein losing nephropathy
decreased production
blood loss

188
Q

how can radiographs be used to determine overall liver size?

A

mass effect on other organs (stomach)

189
Q

what are the indications for a liver biopsy?

A

persistent increases in liver enzymes
altered liver size
monitoring progressive liver disease
evaluated response to treatment

190
Q

what must always be done before taking a liver biopsy?

A

clotting profile (APTT or PT)

191
Q

what are some contradictions for percutaneous liver biopsy?

A

lack of operator experience
small liver
focal disease
extrahepatic cholestasis
bleeding disorder
severe anaemia

192
Q

when does juvenile hepatic fibrosis occur?

A

first two years of life

193
Q

what breeds are predisposed to juvenile hepatic fibrosis?

A

German shepherd
Rottweiler

194
Q

what is the main pathology seen in juvenile hepatic fibrosis?

A

progressive fibrosis
minimal inflammatory reaction
central vein fibrosis/occlusion

195
Q

what caused acquired portosystemic shunts to develop?

A

secondary liver disease - juvenile fibrosis, cirrhosis…

196
Q

what are the four different patterns of canine chronic hepatitis?

A

idiopathic chronic hepatitis
lobular dissecting hepatitis
drug-induced chronic hepatitis
copper-associated hepatitis

197
Q

what are some features that are a poor prognostic indicator in chronic hepatitis?

A

hypoalbuminaemia
bridging fibrosis/severe necrosis and fibrosis

198
Q

what is hepatic portal hypoplasia?

A

microscopic intra-hepatic shunting often with no clinical signs (can have similar signs to portosystemic shunts)

199
Q

what are the two patterns of feline cholangitis complex?

A

suppurative cholangitis
lymphocytic cholangitis

Small animal (fourth year) (26 decks)

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