Pancreatitis & EPI Flashcards

1
Q

Obj: Contrast how normal exocrine pancreatic physiology prevents pancreatitis and how disruptions cause acute pancreatitis

A
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2
Q

Obj: Based on different risk factors of pancreatitis in dog and cats, develop species’ specific treatment plans

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3
Q

Obj: Based on species’ differences in clinical signs and concurrent disease in both acute and chronic pancreatitis, formulate appropriate diagnostic plans to obtain an accurate diagnosis and exclude concurrent conditions

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4
Q

Obj: Given clinical signs, lab work, and imaging detect local (pancreatic/biliary) and systemic consequences of acute pancreatitis

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5
Q

Obj: Based on sensitivities and specificities of tests for pancreatitis and an individual patient, recommend the best test and/or interpret whether results rule-in/out pancreatitis

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6
Q

Obj: Explain the differences in pathophysiology and clinical signs of EPI between dogs and cats

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7
Q

Obj: Interpret diagnostic tests for EPI and recommend an individualized treatment and monitoring plan

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8
Q

Obj: Explain the prognosis of acute/chronic pancreatitis and EPI to owners, particularly duration of treatment, recurrence, and negative prognostic indicators

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9
Q

What are the exocrine pancreatic enzymes

A
  • Synthesized, stored, and secreted in inactive form
    • Trypsinogen
    • Chymotrypsinogen
    • Procarboxypolypeptidase
    • Proelastase
    • Prophospholipase A2
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10
Q

How is early activation of pancreatic enzymes prevented?

A
  • Activation by cleavage of pro-peptide within the duodenum
  • Packaged with pancreatic secretory trypsin inhibitor
  • Lysosomes and zymogens needed for activation stored as separate granules
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11
Q

What is the pathophysiology of Acute pancreatitis?

A
  1. Intra-pancreatic trypsin activation
  2. Concentration of activated trypsin overwhelms local trypsin inhibitor
  3. Trypsin activates self and other pancreatic enzymes within the pancreas
  4. Concentration of activated pancreatic proteases overwhelms local protease inhibitors
  5. Auto-digestion of pancreas
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12
Q

What are the net results of Acute Pancreatitis

A
  • Net Results:
    • Intra-pancreatic cell membrane injury by free-radicals
    • Systemic inflammatory response:
      • systemic free radical formation
      • activation of coagulation cascade
      • activation of complement cascade
    • bradykinin response → increased systemic inflammation by cytokines and chemokines (positive feedback)
      • → multi-organ failure and death
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13
Q

In dogs what are the clinical signs of Acute Pancreatitis?

A
  • Vomiting >90%
  • Anorexia 90%
  • Lethargy 90%
  • Abdominal pain 60%
  • Diarrhea 30%
  • Fever 30%
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14
Q

In cats what are the clinical signs for Acute Pancreatitis

A
  • Lethargy 100%
  • Anorexia 97%
  • Hypothermia 70%
  • Vomiting 40%
  • Abdominal pain 25%
  • Diarrhea 15%
  • Fever <10%
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15
Q

What are the risk factors for Acute Pancreatitis in Dogs?

A
  • Terrier/non-sporting breeds
    • Yorkshire terriers, Min Schnauzers, Shetland Sheepdogs
  • Middle-aged to older
  • Obesity
  • High-fat diet / dietary indiscretion
  • Hypertriglyceridemia
  • Ischemia
  • Pancreatic duct obstruction
  • Drugs/toxins
    • Azathioprine, potassium bromide, L-asparaginase, cisplatin…..etc.
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16
Q

What are the risk factors for Acute Pancreatitis in Cats?

A
  • Less common
  • High fat diet is NOT a risk factor
  • Possible factors:
    • Ischemia
    • abdominal trauma
    • infection (flukes, toxoplasma, virulent calicivirus)
    • hypertriglyceridemia
    • drugs (organophosphates
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17
Q

How is Acute Pancreatitis Diagnosed? (Broad Tests)

A
  • CBC
  • Chemistry - may be normal
  • UA - May be normal
  • Abdominal Imaging
  • Additional Bloodwork
    • Serum amylase and lipase conc
    • SNAP canine pancreatic lipase
    • Spec cPL or fPL
  • Cytology
  • Biopsy
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18
Q

What CBC findings are common with Acute Pancreatitis?

A
  • inflammatory leukogram
  • thrombocytopenia 60%
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19
Q

What Chemistry results are common with Acute Pancreatitis

A
  • Chemistry - may be normal
    • +/- Elevated ALP, GGT, t-bilirubin due to post-hepatic bile duct obstruction
    • elevated ALT secondary to hepatocellular damage from inflammation
    • +/- Hypoalbuminemia due to acute inflammation or systemic inflammation/vasculitis
    • +/- Hypocalcemia
    • Cats: hyperbilirubinemia 60%, hypocalcemia 50%
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20
Q

What UA results are common with Acute Pancreatitis?

A
  • UA - May be normal
    • mild proteinuria (systemic inflammation)
    • increased bilirubin if hyperbilirubinemia
    • Dilute USG is secondary acute kidney injury
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21
Q

What radiography findings are common for Acute Pancreatitis

A
  • Radiographs - non specific
    • decreased serosal detail, especially in right cranial abdomen
    • Right and ventral displacement of the duodenum
    • left displacement of the gastric axis
    • Gastric and proximal duodenal gas dilation
      • functional ileus due to inflammation
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22
Q

What Ultrasound findings are common with Acute Pancreatitis

A
  • US - can be normal Sensitivity 70%
  • Enlarged, hyperechoic pancreas with surrounding hyperechoic mesentery
  • Abdominal effusion due to inflammation
  • +/- mineralization in surrounding mesentery
  • +/- Common bile duct and gallbladder distention if extrahepatic biliary obstruction
  • Cats:
    • 85% pancreatic enlargement
    • 25% extrahepatic biliary dilation
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23
Q

How reliable are serum amylase and lipase concentrations for diagnosing Acute Pancreatitis?

A
  • Not specific
    • no useful in dogs/cats for diagnosis of pancreatitis
  • 50% of dogs with increased lipase do NOT have pancreatitis
  • 50% of dogs with pancreatitis do NOT have elevated lipase/amylase
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24
Q

How reliable is the SNAP canine pancreatic lipase test for diagnosing Acute Pancreatitis

A
  • High sensitivity 94%
    • A negative test can help rule out pancreatitis
  • Low specificity 70-75%
    • many false positives
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25
Q

How can results of a SNAP canine pancreatic lipase test be confirmed?

A
  • Confirmatory test
    • Spec cPL or fPL (pancreatic specific lipase) test
      • High sensitivity 80-94%
      • high specificity 90% if >400mcg/dL
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26
Q

What cytology findings are common with Acute Pancreatitis?

A
  • Acinar cell necrosis and neutrophilic inflammation
  • Not ruled out by normal cytology
    • samples difficult to obtain
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27
Q

What is the treatment for Acute Pancreatitis

A
  • Treat predisposing cause if known
  • Supportive Care
    • IV fluids
    • Antiemetic and anti-nausea drugs
    • Early enteral nutrition
    • Analgesia
    • Steroids
28
Q

Why are IV fluids part of Acute Pancreatitis treatment?

A
  • Correct:
    • hypervolemia
    • hypotension
    • electrolyte abnormalities
    • acid-base abnormalities
  • Pancreatic hypoperfusion can worsen pancreatitis
  • decreased perfusion of other organs increases risk for multi-organ dysfunction
29
Q

What fluids can be used for IV fluid therapy for Acute Pancreatitis

A
  • Crystalloids
    • Plasmalyte
    • Normosol
    • Lactated Ringers
  • Colloids
30
Q

What are the pros/cons of using Crystalloids for Acute Pancreatitis?

A
  • Pro:
    • widely available
    • Balanced electrolytes
    • Acid-buffering
  • Con:
    • Low oncotic pull
    • may easily leak through vascular
      • worsening of tissue edema and cavitary fluids
31
Q

What are the pros/cons of colloids for Acute Pancreatitis

A
  • Pro:
    • Improved microcirculation
    • low-volume resuscitation
  • Cons:
    • Dose-dependent coagulopathy
      • questionable clinical significance
32
Q

What parameters can be measured to adjust fluid rate based on need

A
  • Urine output
  • Body weight
  • blood pressure
  • improvement or worsening of effusion/edema
  • Biochemical changes
    • PCV/TS
    • lactate
33
Q

Why would potassium need to be supplemented while treating Acute Pancreatitis?

A
  • Hypokalemia common:
    • GI/urinary losses
    • decreased intake
    • iatrogenic diuresis form fluid therapy
  • K+max = 0.5 mEq/kg/h
34
Q

What Antiemetic and anti-nausea drugs are commonly used for Acute Pancreatitis? pros of each

A
  • Maropitant
    • additional visceral pain-relieving properties
  • Ondansetron
    • Low oral bioavailability
    • Good intravenous efficacy
  • Consider multi-modal approach
35
Q

What early enteral nutrition is recommended for Acute Pancreatitis?

A
  • Appetite stimulation once vomiting controlled
  • NG-tube support once vomiting controlled
  • Low-fat diet (dogs)
36
Q

What Analgesia options are there for Acute Pancreatitis?

A
  • Opioids
    • Buprenorphine
      • Mild - moderate pain
      • Expensive for large dogs
    • Butorphanol
      • Mild - moderate pain
      • Better for visceral pain than buprenorphine
      • Anti-emetic effects
      • Short-acting unless given as CRI
    • Hydromorphone
      • Good analgesia
      • Risk of Vomiting, ileus
    • Methadone
      • Excellent Analgesia
      • Best option as CRI for moderate - severe pain
      • Risk of ileus
    • Fentanyl
      • Excellent analgesia
      • Best option as CRI for moderate - severe pain
      • Risk of ileus
  • Adjunctive:
    • Lidocaine CRI
    • Ketamine CRI
    • Maropitant
37
Q

What is the benefit of early enteral nutrition in Acute Pancreatitis?

A
  • Improved GI mucosal barrier
  • Decreased vomiting
38
Q

What food can be provided to patients with Acute Pancreatitis?

A
  • Liquid diet
    • CRI
    • 25-30% RER on day 1
    • Increase caloric intake25-30% per day
    • Facilitate feeding with anti-emetics and prokinetics
  • Nutrient profile
    • Dogs: Low fat
      • 2.5-5 g/100kcal fat
    • Cats: High Protein
      • 9-12g/100kcal protein
39
Q

When could steroids benefit patients with Acute Pancreatitis?

A
  • Cases with extra-hepatic biliary obstruction
    • may benefit from decreased peripancreatic inflammation
40
Q

What treatments do not work for Acute Pancreatitis?

A
  • Plasma - in absence of SIRS/DIC
  • Antibiotics - in absence of sepsis
41
Q

When would antibiotics be indicated for use in Acute Pancreatitis cases?

A
  • Biochemical evidence of sepsis/GI mucosal translocation
  • Documented systemic infection
  • Documented infected pancreatic abscess
42
Q

What are the possible complications of Acute Pancreatitis?

A
  • Vasodilatory or hypovolemic shock
  • Hypovolemia
  • DIC
  • Thrombosis
  • Acute kidney injury
  • Diabetes mellitus
  • Pancreatic abscess/pseudocyt formatoin
  • Extrahepatic biliary obstruction
  • Systemic inflammatory response
    • → multiorgan failure → Death
43
Q

What in chronic pancreatitis

A
  • associated with pancreatic fibrosis and atrophy
  • Most common presentation of pancreatitis in cats
  • uncommon in dogs
44
Q

What are the clinical signs of chronic pancreatitis in dogs?

A
  • Lethargy 80%
  • Decreased appetite
  • Vomiting 60%
    • 35% chronic vomiting
  • Diarrhea 40%
45
Q

What concurrunt conditions affect dogs with Chronic Pancreatitis

A
  • Endocrine
    • Diabetes mellitus
    • hypothyroidism
  • Hepatobiliary diseae
  • IBD
46
Q

How is Chronic Pancreatitis diagnosed in dogs?

A
  • Blood work - usually normal
    • 70% spec cPL elevation
  • Abdominal US
    • Hyperechoic pancreas with increased/heterogenous echotexture
    • No peri-pancreatic changes
    • Normal in 50%
47
Q

How is Chronic Pancreatitis treated in Dogs?

A
  • Long term, low-fat diet
  • Avoid dietary indiscretion
  • Avoid predisposing drugs/risk factors
  • Treatment of concurrent GI or endocrine disease
48
Q

What are the clinical signs of Chronic Pancreatitis in Cat?

A
  • Chronic, intermittent vomiting/diarrhea
  • Chronic, intermittent dysrexia
  • Intermittent lethargy
  • Weight loss
49
Q

How is Chronic Pancreatitis diagnosed in cats?

A
  • Histopathology
    • rarely performed
  • Rule out other causes of Chronic Gi signs
  • Spec fPL
50
Q

What are common disease concurrent with Chronic Pancreatitis in cats?

A
  • Pancreatitis + Cholangitis + IBD
    • Triaditis
  • Pancreatitis + IBD
  • Pancreatitis + Cholangitis
51
Q

What is the treatment for Chronic Pancreatitis in Cats?

A
  • Supportive:
    • Anti-emetic/anti-nausea medications
    • fluid therapy
    • appetite stimulants
  • Avoid risk factors for exacerbation
  • Treatment of IBD and cholangitis if present
52
Q

What is a Pancreatic abscess? Etiologies?

A
  • Circumscribed collection of purulent material associated with the pancreas
  • Etiologies:
    • Complication of acute pancreatitis
    • Usually Sterile
53
Q

What are the clinical signs of a Pancreatic Abscess?

A
  • Abdominal pain
  • Anorexia
  • Fever
  • Vomiting/diarrhea
  • Lethargy/depression
  • Palpable abdominal mass
54
Q

How is a Pancreatic Abscess diagnosed?

A
  • Abdominal ultrasound:
    • circumscribed fluid-focus with hyperechoic rim
      • material may be hypoechoic to hyperechoic, depending on cellularity
  • Cytology of fluid:
    • high cellularity
    • non-degenerate neutrophils
55
Q

What is the treatment for Pancreatic abscess?

A
  • Pain management
  • Surgical resection
  • percutaneous drainage/conservative management if surgery is not possible
56
Q

What is a Pancreatic Pseudocyst? Etiology?

A
  • Sterile, focal collection of pancreatic fluid, surrounded by fibrous or granulation tissue
  • Etiology:
    • complication of pancreatitis
57
Q

What are the clinical signs of a pancreatic pseudocyst?

A
  • Non-specific - similar to pancreatitis
  • or asymptomatic
58
Q

How are Pancreatic pseudocysts diagnosed?

A
  • Abdominal US:
    • cyst-like structure associated with the pancreas
  • Cytology of fluid:
    • low cellularity
59
Q

What is the treatment for Pancreatic pseudocysts?

A
  • Medical: percutaneous drainage and monitoring
  • Surgery if medical management is unsuccessful
60
Q

What is Exocrine Pancreatic insufficiency? Etiologies?

A
  • Insufficient synthesis and secretion of pancreatic enzymes
  • Etiology:
    • Lack of pancreatic acinar cells secondary to acinar atrophy (most common in dogs)
    • Lack of pancreatic acinar cells secondary to chronic pancreatitis (most common in cats)
    • Obstruction of pancreatic duct secretion into the SI lumen, preventing effective secretion in the face of normal production
61
Q

What breeds are predisposed to acinar atrophy?

A
  • German Shepherd
  • Rough-coated collie
  • Eurasian
62
Q

What is the Pathogenesis of Exocrine Pancreatic insufficiency?

A
  • Pancreatic secretory products and pancreatic enzymes crucial for food digestion
  • Absence of secretory products = Maldigestion
    • undigested food components in GI tract → Diarrhea, microbiome dysbiosis, weight loss
63
Q

What are the clinical signs of Exocrine Pancreatic Insufficiency in Dogs?

A
  • Weight-loss with good to increased appetite
  • Diarrhea - often watery, malodorous and containing undigested food
  • Flatulence
  • Poor hair coat
  • Coprophagia, pica
64
Q

What are the clinical signs of Exocrine Pancreatic Insufficiency in Cats?

A
  • Clinical signs for appetite and diarrhea differ from dogs
  • Weight loss 90%
  • Anorexia 40%
  • Increased appetite 40%
  • Unformed stool 60%
  • Watery diarrhea 30%
  • Poor haircoat
  • Vomiting 20%
65
Q

How is Exocrine Pancreatic Insufficiency diagnosed?

A
  • Serum trypsin-like immunoreactivity (TLI) assay
    • severely decreased or undetectable
66
Q

What is the treatment for Exocrine Pancreatic Insufficiency?

A
  • Pancreatic enzyme supplementation
    • Dried pancreatic extract (porcine/bovine): Tablet, capsule, powder supplementation
      • 1 tsp/10kg body weight ON food
      • Enzyme activities of commercial products varies and are not strictly controlled.
      • Side-effects: Oral ulceration and bleeding
    • Raw, fresh pancreas
      • less ideal - risk of Echinococcus transmission
      • Option for pet that does not tolerate dried extract
  • Check serum cobalamin or methylmalonic acid and supplement cobalamin if decreased or increased, respectively
    • cobalamin deficiency in 80%
  • Diet:
    • no benefit to specific diet types in absence of concurrent intestinal disease
    • High-quality, maintenance diets
    • Avoid high fiber diets - may interfere with fat absorption
67
Q

What is the prognosis of Exocrine Pancreatic Insufficiency?

A
  • Life-long treatment needed
  • If lack of response, consider:
    • concurrent SI disease
    • Anti-acids: decrease destruction of supplemented enzymes within the stomach and decrease steatorrhea
  • Overall response in cats:
    • good 60%
    • partial 30%
    • poor 13%
  • Negative prognosis indicator: Untreated cobalamin deficiency