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Certifying Examination > Pancreas > Flashcards

Pancreas Flashcards

1
Q

Which is the mechanism by hypertrigliceridemia produces pancreatitis?

A

High tryglicerides –> hydrolised by lipase –> high concentration of FFA that are toxic for acinar pancreatic cells.

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2
Q

Which drugs can potentially cause pancreatitis?

A
  • L asparginasa
  • Azathioprine
  • Phenobarbital and KBr
  • Glucocorticoids
  • Organophosphates
  • Furosemide
  • Sulfonamides
  • Clomipramine
  • Meglumine antimoniate
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3
Q

Which are the mechanism by with a pancreatits can predispose to DM?

A
  • Islet cell damage
  • Glucose toxicity
  • Initiation of autoimmune injury
  • Inflammation induced insulin resistance
  • Action of cytokines and adipokins
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4
Q

In what consist the mutation detected in Miniature Shnauzers prredisposing to pancreatitis?

A

SPINK1 mutation.

SPINK1 product is a secretory pancreatic trypsin inhibitor, which inhibits the premature zymogen activation –> if mutated, no inhibition –> premature zymogen activation –> pancreatitis

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5
Q

By which mechanisms trypsinogen and NFkB can be activated?

A
  • Calcium derrangement
  • Colocalization of lysosomes and zymogens
  • Impaired autophagia
  • Endoplasmic reticulum stress
  • Oxidative damage
  • Non esterified fatty acids production due to pancreatic fat lypolisis –> inflammation
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6
Q

Which is the action mechanism of fuzapladib?

A

LFA-1 inhibitor (integrin that permits neutrophil chemoatraction)

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7
Q

Which are the protective mechanisms for the development of pancreatitis?

A
  • Inactive zymogens
  • Distant lysosomes and zymogens
  • Secretory pancreatic trypsin inhibition
  • pH suboptimal for zymogens activation
  • Unidirectional flow
  • Antiproteases ciculating
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8
Q

Is vitamin D altered in pancreatitis?

A

Yes, it can be low, as well as vitamin D receptor is also low.

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9
Q

Which is normally the ultrasound change that appear earlier in an acute pancreatitis in dogs?

A

Mesenteric hyperecogenicity

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10
Q

Which is the histopathologic prevalence of pancreatitis in cats?

A

66% (C>A)
But clinical prevalence much lower.

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11
Q

Which is the pathophisiology of chronic pancreatitis?

A

Insult –> oxidative damage –> activation of pancreatic stellate cells –> fibrosis.

This last step is potentiated by:
- Mild inflammation
- LPS on TLR4 (endothoxemia??
- Duct obstruction –> activation trypsin
–> vicious cycle

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12
Q

Which are the most differences in clinical signs between feline and canine pancreatitis?

A

While dogs show specially gastrointestinal signs, most common detected signs in cats is apathy and anorexia, followed by gastrointestinal signs

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13
Q

Which is the interpretation of fPLI?are the

A

It has a high specificity but lower sensitivity –> a positive result can confirm a pancreatitis, but a negative result cannot discard it.

SNAP fPLI has the same interpretation than dogs: a negative result discard pancreatitis, but a positive result has to be confirmed with PLIf.

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14
Q

Which are the histopathologic parameters evaluated in feline pancreatitis (both acute or chronic)?

A

Acute:
- Neutrophilic inflammation
- Edema/necrosis

Chronic:
- Lymphoplasmocytic/mononuclear inflammation
- Fibrosis
- Cyst degeneration

(each parameter punctuated from 0-3)

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15
Q

Which subtypes of acute pancreatitis can be distinguished?

A
  • Acute necrotizing pancreatitis: with substantial necrosis
  • Acute suppurative pancreatitis: necsrosis is not a feature
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16
Q

How is the dietary treatment in a pancreatitis?

A

CATS:
- Acute: don’t need a low fat diet –> highly digestible diet (GI diet)
- Chronic: no modification

DOGS: Low fat (both acute and chronic=

17
Q

What is alfa2 macroglobulin

A

Is a scavenger protein for activated proteases
–> if reduced –> increase activated proteases –> activation trypsin –> worse pancreatitis.

–> FFP has alfa2 macroglobulin, suggesting that the administration would improve the clinical status, but there is no studies confirming it utility.

18
Q

Which is the evidence regarding the use of corticosteroids in pancreatitis?

A

There is a concern about GC as a cause of pancreatitis, but there is not any studying confirming that (most studies confirm only a mild increase in PLI but no clinically).

There is evidence in humans and dogs that the use of GC in acute pancreatitis improve the outcome (study in dogs: reduce faster CRP and hospitalization days), due to the inflammatory rol as well as treating the GC deficit due to the critical illness.
No evidence in cats regarding the use of GC

19
Q

Which are the poor prognosis indicators of acute panceratitis in cats?

A
  • Low calcium
  • Low glucose
  • Azotemia
20
Q

Which is the prevalence of AKI development in dogs with acute pancreatitis?

A

25%
Worse prognosis
Can be detected by higher electrolyte fraction excretion and higher NGAL1 concentrations.

21
Q

Which is the etiology of a EPI?

A
  • Lack of acinar pancreatic cells:
    —- 2ary to chronic pancreatitis
    —- Exocrine pancreatic atrophy (immunemediated)
    —- Congenital aplasia/hypoplasia
  • Obstruction of pancreatic duct
22
Q

When appear signs of EPI?

A

When > 90% of exocrine pancreatic function have been lost:
- GI is redundant and there are a lot of different enzymes with the same function
- The expocrine pancreas has a high reserve capacity

23
Q

What does TLI measures?

A
  • Cationic trypsin
  • Cationic trypsinogen
  • Cationic trypsin bound to proteinase inhibitor molecule
24
Q

In which situations a normal TLI can be a false negative?

A
  • Pancreatic insufficiency limited to lipase
  • Pancreatic duct obstruction
25
Q

Which is the association of cobalamin and folate and prognosis in EPI?

A

Low cobalamin associated to worse prognosis, specially when it is not associated with a high folate (high folate, better prognosis)

26
Q

Which are markers of bad prognosis for pancreatitis in dogs?

A
  • SIRS signs
  • Coagulopathy
  • Low calcium
  • Azotemia
27
Q
A

Certifying Examination (10 decks)

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