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SAM II > Pancreatitis > Flashcards

Pancreatitis Flashcards

1
Q

Blue arrow: In the cat, the bile duct and pancreatic duct combine into the ______ ________ _______ before exit into the intestine.

A

Bile duct and pancreatic duct combine into the major duodenal papilla

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2
Q

Much of the parenchyma = exocrine acinar cells and ducts. Embedded amongst these cells are Islets of Landerhan cells.

T/F Endocrine cells are involved with insulin, glucagon etc.

A

True . . but pancreatitis aka what we’re doing now is NOT dealing with these cells. Pancreatitis deals with the EXOCRINE cells of the pancreas.

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3
Q

All of the following are digestive enzymes secreted from the pancreas except for:

Trypsin, chymotrypsin, carboxypeptidase (proteases to digest protein)
Amylase (digest carbs)
Lipases, cholesterol lipase, phospholipase (digest fats)

A

JK. They’re all correct.

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4
Q

What other things does the pancreas secrete?

A

Intrinsic factor: facilitates B12 absorption in ileum

Bicarb and water: epithelial cells of ducts; neutralize ingesta

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5
Q

**Digestive enzymes that are released in _______ (active/inactive) forms are called zymogens. These are necessary to prevent enzymes from digesting origin cells!!!

Enzyme activation mostly happens in the SI for pancreatic enzymes. Trypsin can become active IN the pancreas –> autohydrolizes to prevent damage.

A

INACTIVE form

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6
Q

There is a little release of enzymes btwn digestive periods. Neural control - stimulated by anticipation of a meal. What nerve does this?

A

Vagus n

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7
Q

Endocrine control of secretion regulation: stimulated by luminal contents of food to release what 3 things?

A
  1. cholecystokinin
  2. secretin
  3. gastrin
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8
Q

Pancreatitis is a disease of the _________ (endocrine/exocrine) pancreas. The _______ (acute/chronic) presentation is more associated with fatal consequences.

A

EXOCRINE; ACUTE

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9
Q

Besides pancreatitis, what are some other exocrine pancreatic diseases?

A

EPI: exocrine pancreatic insufficiency
Neoplasia: adenocarcinoma one of most common

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10
Q

What is the pathology of pancreatitis?

A

Zymogen activation in pancreatic tissue.

Inflammation and necrosis of pancreatic cells: clinical signs caused by cell death and inflammation. Leukocyte migration to inflammation = cytokine release. Severe systemic inflammatory affects.

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11
Q

What is the MOA of pancreatitis?

A

Occurs as response of pancreas to ‘noxious’ stimuli –> diet, medications, obstruction, trauma, secondary inflammation , infection etc

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12
Q

**List the 5 important af steps of MOA of pancreatitis

A
  1. decrease of secretion of enzymes
  2. development of giant vacuoles in cytoplasm of acinar cells
  3. zymogens of digestive enzymes & lysosomal enzymes (hydrolytic enzymes in cells) combine= BAD NEWS as digestive enzymes converted and released
  4. **Premature activation of zymogens and/or trypsin (bc remember: trypsin sometimes activates inside pancreas) and trypsin activates zymogens
  5. Overwhelming of natural defenses: trypsin and protease inhibitors and alpha macroglobulins

This all results in tissue necrosis and pancreatitis

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13
Q

What is the pathology result that we will get from this auto digestion of the pancreas?

A

Pancreatic edema, hemorrhage, necrosis, parapancreatic fat necrosis, profound local +/- systemic inflammation
This is all the disease process that we call pancreatitis

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14
Q

Acute pancreatits –> neutrophilic infiltrate
Chronic pancreatitis –> lymphocytic infiltrate
Acute on chronic –> neutrophil and lymphocytes

Blue box: Is all of this damage reversible or irreversible?

A

Damage is often REVERSIBLE!

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15
Q

What are some signs associated with acute pancreatitis?

A 
ADR = 'aint doin right'
Abdominal pain
Fever
V & D
Lethargy 
Inappetence --> anorexia
'prayer position'
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16
Q

What will we see on the PE of acute pancreatitis?

A 
Weakness
Dehydration
Abdominal pain 
HYPERsalivation
HYPERthermia
HYPOthermia (sick cats)
Hypovolemic shock
Icterus (bc pancreatic duct really close to hepatic ducts)
Petechia/ecchymosis
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17
Q

Blue box: When should you consider pancreatits?

A

VOMITING AND ABDOMINAL PAIN

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18
Q

What breeds, diets, drugs etc are canine inciting causes of acute pancreatitis?

A

Dietary indiscretion
High fat diet

Breed: Schnauzer

Organophosphate toxicity

Hyptertriglyceridemia: cause or effect?! We aren’t sure

Drugs: Calcium, KBr, Azathioprine, Estrogen etc

Trauma and/or hypo perfusion: post HBC or post sx

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19
Q

What are some feline inciting causes of acute pancreatitis?

A

Infections: FIV, FIP, Toxoplasmosis, Parasites (Amphimerus pseudofelineus)

Organophosphate toxicity

Concurrent GI or liver dz

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20
Q

What big difference is there btwn canine and feline inciting causes of acute pancreatitis?

A

In cats, acute pancreatitis is not at all related to food.

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21
Q

Amphimerus pseudofelineus infects bile ducts and can migrate to pancreas. It is treated with Praziquantel. Where in the world do we find it?

A

North and South America

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22
Q

What will our CBC show us for acute pancreatitis in dogs and cats?

A

Dogs: Leukocytosis +/- left shift
Leukopenia
Thrombocytosis or thrombocytopenia

Cats: Anemia **especially Heinz body*
Same as dog

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23
Q

Blue box: What predisposing cause or result of abnormal fat processing will we see on our chemistry for acute pancreatitis?

A

HYPERcholesterolemia

HYPERtriglyceridemia

24
Q

What will our coagulation patterns for acute pancreatitis show us?

A

Prolonged PT, PTT –> CONSUMPTION
Elevation of fibrinogen –> inflammation
D Dimer elevations –> making blood clots (& lysis) confirmed

25
Q

**T/F An increase in lipase and/or amylase is diagnostic for pancreatitis.

A

FALSE. Increases in these values is consistent w pancreatitis but NOT diagnostic. These enzymes are produced by the acinar cells andddddd other cells so

26
Q

T/F Trypsin Like Immunoreactivity is used to diagnose pancreatitis.

A

FALSE. TLI is used to dx EPI.

27
Q

**T/F Pancreatic Lipase Immunoreactivity (PLI) is our Gold Standard Test for pancreatitis.

A

True! You send our FASTED SERUM. It is QUANTITATIVE.

28
Q

Blue box: PLI increases with inflammation and necrosis. It is NOT predictive of histology severity. You must fast for 8-12 hours before drawing sample.

What are the abnormal values of PLI in dogs and cats?

A

Dogs: >5.4 ug/dL
Cats: > 400ug/dL

29
Q

What might we be able to see on abdominal rads of pancreatitis?

A

Loss of detail cranial abdomen- ‘Ground Glass

They could also be normal so

30
Q

**What is the classic picture of pancreatitis on an abdominal US?

A

HYPOechoic pancreas w HYPERechoic surrounding mesentery

May also see pseudocysts (pseudo= do not have epithelial lining) or abscesses

**Better than x ray but does not confirm all cases !

31
Q

What are some non pancreatic US findings that we could see associated with pancreatitis?

A

Peritoneal fluid
Peripancreatic fluid
Enlarged regional LNs
Liver-echogenicity changes; bile duct distension
Pain
Intestinal changes including gastric hypo motility or atony with distension of fluid, thickened intestinal wall, corrugation of duodenum and colon, hypo motility, ileum

32
Q

**What is our most definitive, magical, Gold Standard test for pancreatitis?

A

BIOPSY!

33
Q

Blue box: How do we tx pancreatitis?

A

SUPPORTIVE AND SYMPTOMATIC!!! NO direct tx for pancreatic inflammation!

34
Q

Blue box: Communicating with the owners about acute pancreatitis is gonna be super important. What should the clients know?

A

Early aggressive therapy is SUPER important: do NOT send home for a couple days and see what happens
\
Potential systemic and severe complications

Acute death is possible

Most tend to recover

Hospital stay could be anywhere form 2-10+ days

35
Q

Fluid therapy is necessary for pancreatitis. First give replacement + maintenance fluids (shock dose fluids often needed so start w 1/4-1/3 then reassess)

Attempt to replace losses in 8-12 hrs then start 1.5-2x maintenance

**PATIENT DEPENDENT–> monitor for fluid overload!!
What should we be looking at to monitor for fluid overload?

A

Monitor urine output, weight, skin turgor, respiratory effort

36
Q

Blue box: Colloid support is also an important aspect of pancreatitis tx. TAKE A LOT of care to make sure you don’t over hydrate.

Oncotic pressure support should be provided as needed. What colloid can we give?

A

Vet starch. 1/4 volume bolus over 30 mins then CRI

37
Q

Blue box: Fresh frozen plasma doesn’t have any literature to support it but people like to use it for it’s proposed anti inflammatory benefit. Even if this isn’t true, benefits of plasma include:

A
  1. replaces clotting factors
  2. provides colloid support
  3. alpha macs

1 and 2 are for sure true and 3 doesn’t have literature to actually support giving it to a pancreatitis patient but we figure that it couldn’t hurt

Alpha macs depleted in severe pancreatitis and this protein scavenges actuated proteases (i.e. trypsin)

38
Q

Blue box: T/F Another aspect to include in our multimodal therapy of pancreatitis are NSAIDS.

A

NoooOooO. NO NSAIDS and NO steroids in treating pancreatitis. But multimodal therapy is often needed.

Go to town w multimodal therapy(Methadone, Fentanyl, Lidocaine, Ketamine, Buprenorphine, Cerenia, Tramadol)

39
Q

T/F Antacids are yet another part of pancreatitis tx.

A

Yup.

H2 receptor antagonist: Famotidine; Ranitidine (also pro motility drug)
PPI: Pantoprazole; Omeprazole

40
Q

T/F Antiemetics are yet another part of pancreatitis tx.

A

Yup.
Cerenia (NK-1 antagonist)
Ondansetron & dolasetron (5-HT3 antag)
Metoclopramide (Dopamine Antagonist)

41
Q

What are some examples of pro kinetic drugs?

A

Metoclopramide
Ranitidine
Erythromycin
Cisapride

42
Q

T/F We also want to do some anti clot therapy in our tx of pancreatitis.

A

YUP
Low molecular weight heparin: Dalteparin= D & C
Clopidogrel= D & C
Rivaroxaban= just dogs

43
Q

Blue box: T/F Significant hospitalized cases of pancreatitis in dogs AND cats often receive antibiotics despite it being controversial.

A

True bc 1. necrotic pancreatic tissue can become an infected abscess

  1. GI mucosal barrier can be compromised leading to bacterial translocation –> especially in advanced diseases
  2. In the cline, common concurrent disease involves organs prone to infection in ill health (GI and liver)
44
Q

What antibiotics do we use?

A

Unasyn
Enrofloxacin
Metronidazole

45
Q

Gastric decompression is a great thing to do in pancreatitis bc gastric atony or hypo motility is often seen. What is the ideal way to do this?

A

NG tube ideal and it’s also a GREAT route for nutrition

46
Q

Blue box: Nutritional support is super super important with pancreatitis. Feed as soon as vomiting is under control +/- earlier. We no longer believe that fasting is a good approach.
‘Trickle feed’ and gradually increase
‘Feed Through’ so feed btwn bouts of vomiting
Early enteral feeding is VERY VERY important!!

What are the ways in which we get nutrition into body?

A

Enteral via intestinal tract

Parenteral IV

47
Q

T/F And finally, last but not least, surgery is a tx option for pancreatitis.

A

Noooope. Surgery almost never utilized.

48
Q

When can an animal with pancreatitis go home?

A

When it has its shit together.

Pain controlled.
No more vomiting.
Resolved fluid and electrolyte abnormalities.
Etc

49
Q

What kind of food should we give a dog with pancreatitis?

A

ALWAYS low fat

50
Q

What kind of food should we give a cat with pancreatitis?

A

WHATEVER they will eat!

51
Q

What is our protocol for monitoring a patient with pancreatitis?

A

Recheck in 2-3 weeks or sooner if having feeding tube or concerns

Repeat PLI only if clinical signs persist or recur

52
Q

What will the mild acute pancreatitis patient look like and what should we do for them?

A

They probably vomited a couple times but are well hydrated, no diarrhea, bouncing around, your PLI might come back positive but who cares bc they feel fine so you gotta treat the patient and not the tests!!

  • ** LOW FAT diet for DOG
  • **ANY diet for CAT
53
Q

What breed specific disposition does chronic pancreatitis have?

A

Miniature schnauzers

Gene abnormality: SPINK1 (protease inhibitor)
Test via ELISA kit

54
Q

T/F Chronic pancreatitis remains largely under diagnosed. You can see it with a biopsy. Patients are predisposed to diabetes mellitus and exocrine pancreatic insufficiency.

A

True

55
Q

If the cPL is elevated +/- US changes in a chronic pancreatitis patient then what should we do?

A

LOW FAT DIET and symptomatic tx

56
Q

What are some fun pussy pancreatitis facts?

A 
Lethargy 
Anorexia 
Only 35% vomit
Only 25% show pain 
Icterus possible
57
Q

Clicker question: You are treating a patient for pancreatitis who has not eaten in 24 hours. Your ideal next step should be:

A. continue fast until eats on own
B. force feed
C. feeding tube placement and feeding
D. send home

A

C. feeding tube placement and feeding

SAM II (20 decks)

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