Pancreas Flashcards
Which is the mechanism by hypertrigliceridemia produces pancreatitis?
High tryglicerides –> hydrolised by lipase –> high concentration of FFA that are toxic for acinar pancreatic cells.
Which drugs can potentially cause pancreatitis?
- L asparginasa
- Azathioprine
- Phenobarbital and KBr
- Glucocorticoids
- Organophosphates
- Furosemide
- Sulfonamides
- Clomipramine
- Meglumine antimoniate
Which are the mechanism by with a pancreatits can predispose to DM?
- Islet cell damage
- Glucose toxicity
- Initiation of autoimmune injury
- Inflammation induced insulin resistance
- Action of cytokines and adipokins
In what consist the mutation detected in Miniature Shnauzers prredisposing to pancreatitis?
SPINK1 mutation.
SPINK1 product is a secretory pancreatic trypsin inhibitor, which inhibits the premature zymogen activation –> if mutated, no inhibition –> premature zymogen activation –> pancreatitis
By which mechanisms trypsinogen and NFkB can be activated?
- 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
Which is the action mechanism of fuzapladib?
LFA-1 inhibitor (integrin that permits neutrophil chemoatraction)
Which are the protective mechanisms for the development of pancreatitis?
- Inactive zymogens
- Distant lysosomes and zymogens
- Secretory pancreatic trypsin inhibition
- pH suboptimal for zymogens activation
- Unidirectional flow
- Antiproteases ciculating
Is vitamin D altered in pancreatitis?
Yes, it can be low, as well as vitamin D receptor is also low.
Which is normally the ultrasound change that appear earlier in an acute pancreatitis in dogs?
Mesenteric hyperecogenicity
Which is the histopathologic prevalence of pancreatitis in cats?
66% (C>A)
But clinical prevalence much lower.
Which is the pathophisiology of chronic pancreatitis?
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
Which are the most differences in clinical signs between feline and canine pancreatitis?
While dogs show specially gastrointestinal signs, most common detected signs in cats is apathy and anorexia, followed by gastrointestinal signs
Which is the interpretation of fPLI?are the
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.
Which are the histopathologic parameters evaluated in feline pancreatitis (both acute or chronic)?
Acute:
- Neutrophilic inflammation
- Edema/necrosis
Chronic:
- Lymphoplasmocytic/mononuclear inflammation
- Fibrosis
- Cyst degeneration
(each parameter punctuated from 0-3)
Which subtypes of acute pancreatitis can be distinguished?
- Acute necrotizing pancreatitis: with substantial necrosis
- Acute suppurative pancreatitis: necsrosis is not a feature
How is the dietary treatment in a pancreatitis?
CATS:
- Acute: don’t need a low fat diet –> highly digestible diet (GI diet)
- Chronic: no modification
DOGS: Low fat (both acute and chronic=
What is alfa2 macroglobulin
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.
Which is the evidence regarding the use of corticosteroids in pancreatitis?
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
Which are the poor prognosis indicators of acute panceratitis in cats?
- Low calcium
- Low glucose
- Azotemia
Which is the prevalence of AKI development in dogs with acute pancreatitis?
25%
Worse prognosis
Can be detected by higher electrolyte fraction excretion and higher NGAL1 concentrations.
Which is the etiology of a EPI?
- Lack of acinar pancreatic cells:
—- 2ary to chronic pancreatitis
—- Exocrine pancreatic atrophy (immunemediated)
—- Congenital aplasia/hypoplasia - Obstruction of pancreatic duct
When appear signs of EPI?
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
What does TLI measures?
- Cationic trypsin
- Cationic trypsinogen
- Cationic trypsin bound to proteinase inhibitor molecule
In which situations a normal TLI can be a false negative?
- Pancreatic insufficiency limited to lipase
- Pancreatic duct obstruction
Which is the association of cobalamin and folate and prognosis in EPI?
Low cobalamin associated to worse prognosis, specially when it is not associated with a high folate (high folate, better prognosis)
Which are markers of bad prognosis for pancreatitis in dogs?
- SIRS signs
- Coagulopathy
- Low calcium
- Azotemia
