Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

Pancreatitis & Exocrine Pancreatic Insufficiency in Dog & Cat Flashcards

1
Q

how many limbs are in the pancreas

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the functional tissue of the pancreas

A

pancreatic acini

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the functions of pancreatic acini

A

secrete pancreatic enzymes into the pancreatic ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how many pancreatic ducts do dogs have

A
  1. pancreatic duct
  2. accessory duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what do the pancreatic acinar cells produce

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what do the pancreatic ducts secrete

A

bicarbonate under the influence of duodenal secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the pathogenesis of acute pancreatitis

A

premature activation of zymogens within pancreatic acinar cells

“pancreatic autodigestion”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what hematology changes can be seen with acute pancreatitis

A

inflammatory leukogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what occurs to serum amylase and lipase during acute pancreatitis

A

levels increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is serum TLI

A

trypsin like immunoreactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the sensitivity of TLI

A

pancreatic origin ~70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the issue with TLI in diagnosing acute pancreatitis (3)

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is cPLI

A

canine pancreas specific lipase

27
Q

what is the sensitivity and specificity of cPLI in diagnosing acute pancreatitis

A

sensitivity 91%

specificity 77%

28
Q

which is more accurate at diagnosing feline pancreatitis feline TLI or feline PLI

A

feline PLI is more sensitive and more specific

29
Q

what other scenarios might cause cPL to be elevated

A

in dogs with upper GI foreign bodies

30
Q

is abdominal radiography good at diagnosing acute pancreatitis

A

low sensitivity

31
Q

what are radiographic changes associated with acute pancreatitis

A

loss of serosal detail or an increase in opacity in the R cranial quadrant

displacement of duodenum and/or transverse colon

32
Q

what is the appearance of the pancreas on US with acute pancreatitis

A

enlarged or ill defined hypoechoic to complex mass

functional ileus of duodenum

hyperechoic tissues around the pancreas –> focal peritonitis

33
Q

why is ultrasound useful in diagnosing acute pancreatitis

A

can detect concurrent disorders and complications of pancreatitis

bile duct distention

pancreatic abscesses or cysts

local peritonitis

34
Q

how is acute pancreatitis managed (5)

A

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
Q

when would plasma be given in cases of acute pancreatitis

A

for coagulopathies and severely affected dogs

36
Q

what does pancreatic extract do

A

decrease pancreatic stimulation

analgesic?

37
Q

when are antibiotics used in acute pancreatitis

A

if there is sepsis (uncommon)

consider if pyrexia, GI ulceration, pancreatic abscess

38
Q

why would corticosteroids be useful in acute pancreatitis

A

couteract almost all pathways of inflammation

beneficial in people

39
Q

what are potential sequelae of acute pancreatitis (5)

A
  1. pancreatic abscess formation
  2. necrotic masses
  3. pancreatic pseudocysts
  4. duodenal perforation/septic peritonitis
  5. biliary tract obstruciton
40
Q

why is it important to pay close attention to the volume status of the patient in acute pancreatitis

A

avoid hypoxic insult to an already compromised pancreas

41
Q

what are pateints with acute pancreatitis more suspcetible to

A

GI ulceration so include anti ulcer therapy

42
Q

what is the prognosis of acute pancreatitis based on in dogs

A

clinical presentation and development of complications requiring surgery

43
Q

what is the prognosis of acute pancreatitis based on in cats

A

depends on severity of the disease

negative prognostic indicators: dyspnea, hyperkalemia, high fPLI, low iCa

44
Q

which is more common in cats: acute or chronic pancreatiits

A

chronic

45
Q

what are the histological changes in chronic pancreatitis

A

non suppurative

mononuclear infiltrate with fibrosis

46
Q

how may chronic pancreatitis present (2)

A
  1. acutely (acute on chronic inflammation)
  2. may present due to progressive loss of exocrine and endocrine function
47
Q

when should you suspect chronic pancreatitis (4)

A
  1. intermittent, low-grade clinical signs
  2. recurrent acute episodes of pancreatitis
  3. exocrine pancreatic insufficiency
  4. diabetes mellitus (PUPD, weight loss, polyphagia)
48
Q

how do you differentiate acute vs chronic pancreatitis (3)

A
  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
Q

how is chronic pancreatitis managed during the acute presentation

A

treat as for acute pancreatitis

50
Q

how is chronic pancreatitis managed during low intermittent/low grade relapsing presentation (6)

A
  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
Q

what is exocrine pancreatic insufficiency (EPI)

A

decreased pancreatic secretory capacity

clinical signs develop when 90% of secretory capacity is lost

52
Q

what can exocrine pancreatic insufficiency (EPI) be caused by (3)

A
  1. pancreatic acinar atrophy
  2. aplasia (young dogs)
  3. chronic pancreatitis
53
Q

what causes pancreatic acinar atrophy

A

end stage autoimmune process

54
Q

what breeds are predisposed for pancreatic acinar atrophy

A

GSDs and rough collies

autosomal recessive

55
Q

what is the main cause of chronic pancreatitis in cats

A

main cause of EPI

56
Q

what are the clinical signs of EPI (6)

A
  1. diarrhea
  2. poor hair coat
  3. increased appetite
  4. flatulence
  5. weight loss
  6. steatorrhea
57
Q

how is EPI diagnosed

A

measure trypsin like immunoreactivity (TLI)

highly sensitive and very specific for EPI

sample after 12h fast

58
Q

what is the grey zone for diagnosing EPI

A

non fasted or early EPI

59
Q

how is EPI managed (2)

A
  1. enzyme supplementation
  2. diet
60
Q

what enzyme supplementation is used for EPI

A

powder or granules

61
Q

what diet is used for EPI

A

highly digestible

low fibre

moderate fat diet may help

little and often

62
Q

why is cobalamin given in EPI

A

deficiency common in dogs and cats with EPI

if deficiency plus small intestinal bacterial overgrowth (SIBO)

63
Q

if treatment is not helping in EPI what would the reasons be (5)

A
  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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions