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Module 16 > Pancreatitis & Exocrine Pancreatic Insufficiency in Dog & Cat > Flashcards

Pancreatitis & Exocrine Pancreatic Insufficiency in Dog & Cat Flashcards

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1
Q

how many limbs are in the pancreas

A

2

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2
Q

what is the functional tissue of the pancreas

A

pancreatic acini

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3
Q

what are the functions of pancreatic acini

A

secrete pancreatic enzymes into the pancreatic ducts

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4
Q

how many pancreatic ducts do dogs have

A
  1. pancreatic duct
  2. accessory duct
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5
Q

where do the pancreatic ducts open to

A
  1. pancreatic duct opens at minor duodenal papilla
  2. the accessory duct opens at the common bile duct
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6
Q

how many pancreatic ducts do cats have

A

only the pancreatic duct

merges with the common bile duct before opening into the duodenum at the major duodenal papilla

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7
Q

what do the pancreatic acinar cells produce

A

produce and secrete enzyme precursors (zymogens), amylases and lipases

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8
Q

what do the pancreatic ducts secrete

A

bicarbonate under the influence of duodenal secretin

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9
Q

how is the pancreas essential for the absorption of cobalamin (vit B12)

A

it is a source of intrinsic factor (IF) which is needed for vit B12 absorption

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10
Q

what is the pathogenesis of acute pancreatitis

A

premature activation of zymogens within pancreatic acinar cells

“pancreatic autodigestion”

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11
Q

what is the defence mechanisms the pancreas has to prevent autodigestion (5)

A
  1. proteolytic enzymes are synthesized as inactive zymogens (ex. trypsinogen)
  2. packaging of these zymogens into granules to keep them separate from proteolytic processes –> released at apical membrane by exocytosis
  3. production of pancreatic secretory trypsin inhibitor (PSTI) –> incorperated into zymogen granules to prevent premature activation of trypsin
  4. trypsinogen activated to trypsin in SI by enterokinase
  5. hydrolases (amylases and lipases) are kept seperated from zymogens in lysosomes
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12
Q

what is the pathogenesis of acute pancreatitis (7)

A
  1. lysosomes & zymogen granules fuse to form vacuoles
  2. lysosomal enzymes activate trypsinogen to trypsin
  3. vacuoles rupture releasing active enzymes into cell
  4. other zymogens then activated
  5. causes cell necrosis and pancreatic autodigestion
  6. inflammatory mediators and cytokines etc cause cell necrosis and inflammaiton
  7. systemically plasma anti proteases are overwhelmed leading to systemic inflammatory response syndrome (SIRS) and associated signs
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13
Q

what are risk factors of acute pancreatitis (6)

A
  1. hypertriglyceridemia
  2. genetic predispositions in mini schnauzers and yorkshire terriers
  3. drugs KBr
  4. hypotension/ischemia/trauma
  5. hypercalcemia
  6. underlying neoplasia
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14
Q

what is the etiology of acute pancreatitis in cats (3)

A
  1. dietary factors unimportant
  2. hyperlipidemia unimportant
  3. not associated with body condition score
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15
Q

what are risk factors of acute pancreatitis in cats (6)

A
  1. biliary tract disease
  2. inflammtory bowel disease
  3. ischemia
  4. infection: toxoplasmosis, FIP
  5. organophosphate toxicity
  6. trauma
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16
Q

what are the clinical presentations of acute pancreatitis in dogs (8)

A
  1. dehydration
  2. anorexia
  3. vomiting
  4. weakness/lethargy
  5. abdominal pain
  6. diarrhea
  7. fever
  8. icterus
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17
Q

what are the clinical presentations of acute pancreatitis in cats (8)

A
  1. anorexia
  2. weakness/lethargy
  3. dehydration
  4. vomiting
  5. icterus
  6. fever
  7. abdominal pain
  8. diarrhea
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18
Q

how is acute pancreatitis diagnosed (7)

A
  1. clinical presentation
  2. hematology and serum biochem
  3. serum amylase and lipase
  4. trypsin like immunoreactivity (TLI)
  5. pancreatic specific lipase (PLI)
  6. diagnostic imaging
  7. cytology and pancreatic biopsy
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19
Q

what hematology changes can be seen with acute pancreatitis

A

inflammatory leukogram

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20
Q

what serum biochem changes can be seen with acute pancreatitis (4)

A
  1. elevations in ALT, ALP
  2. hyperbilirubinemia
  3. hypocalcemia
  4. azotemia and electrolyte disturbances
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21
Q

what occurs to serum amylase and lipase during acute pancreatitis

A

levels increased

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22
Q

why is serum amylase and lipase not very sensitive and specific to diagnose acute pancreatitis (3)

A
  1. levels are influenced by GFR and therefore increase in dehydrated patients
  2. originate from extra pancreatic tissue (gastric/intestinal mucosa)
  3. in dogs serum lipase may increased with neoplastic, hepatic and renal disease or following steroid administraion
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23
Q

what is serum TLI

A

trypsin like immunoreactivity

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24
Q

what is the sensitivity of TLI

A

pancreatic origin ~70%

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25
what is the issue with TLI in diagnosing acute pancreatitis (3)
1. increased early in acute pancreatitis but the half life is very short 2. levels fall rapidly resulting in poor sensitivity of the test (lots of false negative results) 3. delay in obtaining results (external test)
26
what is cPLI
canine pancreas specific lipase
27
what is the sensitivity and specificity of cPLI in diagnosing acute pancreatitis
sensitivity 91% specificity 77%
28
which is more accurate at diagnosing feline pancreatitis feline TLI or feline PLI
feline PLI is more sensitive and more specific
29
what other scenarios might cause cPL to be elevated
in dogs with upper GI foreign bodies
30
is abdominal radiography good at diagnosing acute pancreatitis
low sensitivity
31
what are radiographic changes associated with acute pancreatitis
loss of serosal detail or an increase in opacity in the R cranial quadrant displacement of duodenum and/or transverse colon
32
what is the appearance of the pancreas on US with acute pancreatitis
enlarged or ill defined hypoechoic to complex mass functional ileus of duodenum hyperechoic tissues around the pancreas --\> focal peritonitis
33
why is ultrasound useful in diagnosing acute pancreatitis
can detect concurrent disorders and complications of pancreatitis bile duct distention pancreatic abscesses or cysts local peritonitis
34
how is acute pancreatitis managed (5)
no definitive treatment supportive and symptomatic management 1. fluid and electrolyte balance 2. analgesia 3. anti emetic and anti ulcer therapy 4. nutritional support 5. management of complications
35
when would plasma be given in cases of acute pancreatitis
for coagulopathies and severely affected dogs
36
what does pancreatic extract do
decrease pancreatic stimulation analgesic?
37
when are antibiotics used in acute pancreatitis
if there is sepsis (uncommon) consider if pyrexia, GI ulceration, pancreatic abscess
38
why would corticosteroids be useful in acute pancreatitis
couteract almost all pathways of inflammation beneficial in people
39
what are potential sequelae of acute pancreatitis (5)
1. pancreatic abscess formation 2. necrotic masses 3. pancreatic pseudocysts 4. duodenal perforation/septic peritonitis 5. biliary tract obstruciton
40
why is it important to pay close attention to the volume status of the patient in acute pancreatitis
avoid hypoxic insult to an already compromised pancreas
41
what are pateints with acute pancreatitis more suspcetible to
GI ulceration so include anti ulcer therapy
42
what is the prognosis of acute pancreatitis based on in dogs
clinical presentation and development of complications requiring surgery
43
what is the prognosis of acute pancreatitis based on in cats
depends on severity of the disease negative prognostic indicators: dyspnea, hyperkalemia, high fPLI, low iCa
44
which is more common in cats: acute or chronic pancreatiits
chronic
45
what are the histological changes in chronic pancreatitis
non suppurative mononuclear infiltrate with fibrosis
46
how may chronic pancreatitis present (2)
1. acutely (acute on chronic inflammation) 2. may present due to progressive loss of exocrine and endocrine function
47
when should you suspect chronic pancreatitis (4)
1. intermittent, low-grade clinical signs 2. recurrent acute episodes of pancreatitis 3. exocrine pancreatic insufficiency 4. diabetes mellitus (PUPD, weight loss, polyphagia)
48
how do you differentiate acute vs chronic pancreatitis (3)
1. biopsy if having surgery for another reason 2. ultrasound 3. PLI: insensitive due to loss of pancreatic mass chronic pancreatitis is difficult to diagnose
49
how is chronic pancreatitis managed during the acute presentation
treat as for acute pancreatitis
50
how is chronic pancreatitis managed during low intermittent/low grade relapsing presentation (6)
1. analgesia (gabapentin) 2. low fat diet (esp if hyperlipidemia is a trigger) 3. vit B12 injections if low 4. consider appetite stimulants (cats ex. mirtazapine) 5. treat EPI if present or if chronic weight loss 6. treat DM if present consider corticosteroid therapy (cats and cocker spaniel)
51
what is exocrine pancreatic insufficiency (EPI)
decreased pancreatic secretory capacity clinical signs develop when 90% of secretory capacity is lost
52
what can exocrine pancreatic insufficiency (EPI) be caused by (3)
1. pancreatic acinar atrophy 2. aplasia (young dogs) 3. chronic pancreatitis
53
what causes pancreatic acinar atrophy
end stage autoimmune process
54
what breeds are predisposed for pancreatic acinar atrophy
GSDs and rough collies autosomal recessive
55
what is the main cause of chronic pancreatitis in cats
main cause of EPI
56
what are the clinical signs of EPI (6)
1. diarrhea 2. poor hair coat 3. increased appetite 4. flatulence 5. weight loss 6. steatorrhea
57
how is EPI diagnosed
measure trypsin like immunoreactivity (TLI) highly sensitive and very specific for EPI sample after 12h fast
58
what is the grey zone for diagnosing EPI
non fasted or early EPI
59
how is EPI managed (2)
1. enzyme supplementation 2. diet
60
what enzyme supplementation is used for EPI
powder or granules
61
what diet is used for EPI
highly digestible low fibre moderate fat diet may help little and often
62
why is cobalamin given in EPI
deficiency common in dogs and cats with EPI if deficiency plus small intestinal bacterial overgrowth (SIBO)
63
if treatment is not helping in EPI what would the reasons be (5)
1. enough enzyme in correct form? 2. dysregulation of GI flora: antibiotic responsive diarrhea, metronidazole, tylosin, tetracyclines 3. effect of gastric pH: consider H2 antagonists or proton pump inhibitors 4. diet change: fat restriction? 5. consider concurrent SI: chronic enteropathy, IBD, concurrent intestinal parasitism

Module 16 (26 decks)

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