Small animal GI Learning objectives (10: pancreatitis dog/cat; 11/12/13: liver dz) Flashcards
1
Q
pancreatic protection
A
- intracellular compartmentalization
- enzymes are separate from lysosomes
- proteases made in inactive form
- zymogens
- PSTI secreted in parallel with trypsinogen
- acinar cells around acinus with duct that carries enzymes from acinar cells
- duct cells release bicard to neutralize acid -Na-Cl fluid from acinar cells
- pancreatic cells release trypsin inhibitor with pancreatic enzymes
- lysosomal hydrolases packaged separately, kept separate from zymogen granules
2
Q
zymogens + lysosomes
A
activated, digesting enzymes
3
Q
Critical element in activating zymogens
A
Calcium
4
Q
brush border enzyme
A
- enterokinase
- converts trypsinogen to trypsin
- trypsin activates zymogens by cleaving amino acids off polypeptide chain
- enterokinase is an enzyme located outside of pancreas (safety)
5
Q
process of pancreatitis
A
- pancreas digests itself
- lysosomal granules and trypsinogen and zymogens all released through apical side of pancreatic cell into the duct
- apical block of cell
- build up of zymogens and lysosomes => activation of pancreatic enzymes by hydrolases in lysosomes
6
Q
Risk factors for pancreatitis
A
- possibly high fat diet - makes pancreatitis worse
- indescretion of diet
- pancreatic ischemia
- reflux of duodenal contents - bile
- moreso cats
- duct obstruction: tumors, stones
- genetic factors: yorkies, poodles, schnauzers
- idiopathic
7
Q
DDX of pancreatitis
A
- acute gastroenteritis
- hemorrhagic gastroenteritis
- intestinal obstruction
- acute peritonitis
- IBD
- renal failure
8
Q
Clinical signs of pancreatitis
Dogs
A
- vomiting
- weakness
- abdominal pain
- large bowel diarrhea
- transverse colon runs underneath pancreas
9
Q
Clinical signs pancreatitis
Cats
A
- hypothermic
- lethargic
- anorexic
- dehydration
- abdominal pain
*could be triaditis
10
Q
Lab findings for pancreatitis
dogs
A
- neutrophilia and left shift
- thrombocytopenia
- anemia
11
Q
lab findings pancreatitis
cats
A
- bloodwork can be normal
- possible hemoconcentration if dehydrated
- anemia
12
Q
Diagnostic studies for pancreatitis
A
canine pancreatic lipase (cPLI) and feline pancreatic lipase (fPLI)
13
Q
DX pancreatitis
A
- high serum cPLI, fPLI
*avoid bx and irritating pancreas more (unless being performed for other reasons)
14
Q
TX: pancreatitis
A
- analgesic
- fentanyl patch
- buprenorphine
- epidural
- antiemetics
- metoclopramide
- maropitant
- ondansetron
- Plasma or plasma expander
*antibiotics if pancreatitis turns into enteritis
15
Q
Pancreatitis nutrition
A
- fast 3-5 days until vomiting stops for 1 day
- reintroduce food (low fat)
- if vomits, refast for another 24 hours
- reintroduce food (low fat)
- Parenteral nutrition possible
- enteral nutrition probably better
16
Q
Pancreatitis diet cats
A
- no idea
- make sure to treat any underlying dz
17
Q
Functions of liver
A
- Drains blood from digestive organs
- metabolic filter
- removes translocated intestinal bacteria
- carb metabolisim
- vitamin metabolism
- immunologic function
- detoxification and excretion
- Makes and releases bile acids
18
Q
Liver bile ducts
A
- flow parallel / opposite direction of artery and vein
19
Q
hepatic lobule
A
- has a hepatic vein in center
- surrounded by sinusoids
- portal trials on edges of lobules
20
Q
The triad
A
- made up of
- bile duct
- hepatic arteriole
- portal venule
21
Q
Sinusoids
A
- framed by hepatocytes
- make a weblike structure between central vein and portal triad
22
Q
Kupferr cells
A
- in the sinusoid lumen
- specialized macrophages
23
Q
Stellate cells
A
- in perisinusoidal space
- role is unclear
- involved in formation of liber fibrosis
24
Q
Signs of liver disease
A
- inappetance
- lethargy
- vomiting
- jaundice
- change in liver size, contour, margins
*signs can be extremely variable
25
ALT
| (cell damage)
* liver specific
* in cytoplasm
* increases with necrosis
* higher multiple fold inc over ALP when hepatocellular dz
* poor correlation between magnitude of inc and severity of dz
26
AST
| (cell damage)
* not liver specific (muscle trauma also)
* from cytoplasm to mitochondria
* inc with necrosis
* poor correlation between magnitude and severity of dz
27
ALP
| (cholestatic)
* from bone, liver, or steroid induced
* **except cats**
* **in cats ALP has 6 hr half life - if it's there, be worried**
28
GGT
cholestatic
29
signs of high bilirubin
icterus/jaundice
30
Bilirubinuria
* dogs: low renal threshold ok in dogs
* cats: high renal threshold, not ok in cats
31
albumin
* made in liver
* will decrease in liver disease
* will not decrease from anorexia/fasting
32
glucose
* liver is responsible for gluconeogenesis
* stores enough for about a month of fasting
* will dec in liver disease
33
cholesterol
* will dec in liver dz
* liver responsible for uptake, and synthesis
* will inc in choestatic dz
34
blood ammonia
* high blood ammonia is a sign of liver disease
* liver converts ammonia to urea
* fasting values
* inc in ammonia may be normal
* normal amonia in fasting animal may be liver disease
35
Serum bile acids
* not needed if patient is icteric
* does not conribute to encephalopathy
* can confirm liver function, but doesn't indicate type of liver dz
* in shunts
* bile acids get re-routed around liver so post-prandial bile acids are very high
36
what percent of liver can be removed before dysfunction
75%
37
Additional dx tests for liver dz
* CBC
* clotting function
* fecal exam to check for GI bleeding
* rads to eval liver size
* microhepatica: cranial shift of gastric axis
* ascites
* abdominocentesis: check for bile
* ultrasound
* many limitations
* only use if you are good at finding a focal lesion or obstruction
* liver aspiration
* cancer check, hepatic lipidosis check
* liver bx: for specific dx
38
Dog has ALT of 780 (10-100) and ALKP 220 (10-100)
more consistent with HEPATOCELLULAR DZ not choestatic b/c ALT is so increased
39
Causes of acute hepatitis
* hepatotoxins (carbon tetrachloride, mycotoxins, xylitol)
* drugs: acetaminophen (cats), azathioprine, trimethoprim-sulpha abx
* mushrooms: amanita
* viruses
* sage palm ingestions (FLORIDA)
\*varied causes, can be hard to find
40
DX of acute hepatitis
* inc in ALT and AST
* ALP usually normal or only mildly inc
* inc in serum bilirubin if many hepatocytes affected
* liver bx
* neither helpful nor essential
* done in chronic hepatitis
41
Causes chronic hepatitis
* leptospirosis
* drugs: phenobarb
* copper metabolism
* idiopathic
42
breed related chronic hepatitis
* dobie
* cocker spaniel
* labrador retreiver
43
Copper associated hepatopathy
* dalmation
* bedlington terrier
* west highland white terrier
* labradors
44
management of chronic hepatitis
* remove cause: drugs, copper
* anti-inflammatories
* glucocorticoids - may also reduce fibrosis
* anti-oxidants
* supportive therapy
* copper chelaters for 6+ months if copper related
* UCDA
45
UCDA
* ursodeoxycholic acid
* hydrophilic bile acid
* possibly prevents apoptosis and prevent mitochondrial damage
* inc flow of bile
* immunomodulating effects
46
Types of cholangitis in cats
* neutrophilic
* lymphocytic
\*based on type of infiltrate in bile duct lumen/biliary epithelium. Ultimately need bx and bile culture to dx
47
Neutrophilic cholangitis in the cat
* can be acute or chronic
* thought to be from ascending bacterial infection from intestine
* signs:
* fever
* lethargy
* vomiting
* jaundice
48
Lymphocytic cholangitis
* may be from some initiating factor that triggers immune-mediated mechanisms that perpetuate liver path
* signs
* ascites
* jaundice
49
Triaditis
* cholangitis +
* pancreatitis +
* IBD
50
Tx for neutrophilic cholangitis
* abx based on culture: usually E. Coli
* Glucocorticoids (pred) for inflammation
* cholecystectomy
* cases with inspissated bile and biliary duct obstruction
* fluid therapy and nutritional support
51
TX for lymphocytic cholangitis
* Glucocorticoids at immunosuppressive doses
* may breat with abx if suspect chronic neutrophilic cholangitis
* fluids, nutritional, antioxidant support
* if ascites: low Na+ diet and diuretics
52
Most common liver disease in cats
hepatic lipidosis
53
causes of hepatic lipidosis
* no confirmed etiology
* from formation of a metabolic disorder
* possibly related to malnutrition
* obesity inc risk
* inc risk from sudden rapid weight loss or dec caloric intake
* may be related to negative nitrogen balance
54
DX hepatic lipidosis
* lab
* dram inc ALP, inc ALT, mod inc AST, normal/slightly elevated GGT
* normocytic, normochromic, non-regenerative anemia
* Hx of fat cat with anorexia
* hepatomegaly on rads, rounded margins
* hyperechogenic ultrasound of liver
* tissue aspiration: don't misinterpret normal fat vacuoles
55
management Hepatic lipidosis
* nutritional support (60-90 kcal/kg/day at min)
* treat concurrent illness/underlying cause
* place e-tube
* metoclopramide/cisapride for delayed gastric emptying
* antiemetics if vomiting
56
extrahepatic biliary obstruction
impairment of bile flow in biliary system between liver and duodenum
57
clinical signs of extrahepatic biliary obstruction
* general
* vomiting
* lethargy
* innapetance
58
DX: extrahepatic biliary obstruction
* marked inc in ALP (always higher than ALT
* can only confirm by laparotomy
59
Causes of extrahepatic biliary obstruction
* dog: pancreatitis
* cat: pancreatic and biliary neoplasia
60
Management of extrahepatic biliary obstruction
* medically managed
* non-resolving, may surgerize
61
congenital portal systemic shunt
* abnormal development of hepatic portal circulation
* usually in young dogs, small for their age
62
portosystemic shunts breed disposition
* yorkies
* min schnauzers
* maltese
* irish wolf hound
63
Intrahepatic shunts more common in
large breed dogs
64
extrahepatic shunts more common in
cats and small breed dogs
65
Clinical presentation of portosystemic shunts
* small dogs: ADR
* cats: small stature, ptyalism, copper irises
* other signs
* PU/PD
* urate stones (not seen on rads)
66
lab Dx portosystemic shunts
* biochem profile may be normal
* ALT, AST, ALP, and GGT can be normal or mildly inc
* ammonium biurate crystals in urine
* may see low
* urea nitrogen
* albumin
* glucose
* microcytic anemia from low iron
* abnormal bile acids, ammonia
67
imaging dx portosystemic shunt
* ultrasound
* aortic to portal vein ratio
* renomegaly
* visualization of shunt
* CT angiogram
* Transplenic scintigraphy: no longer done
68
portosystemic shunt management
* sx ligation
* restricted protein
* high quality diet with lactulose
69
Cats have a common
bile and pancreatic duct that join before entering duodenal papilla
70
Cats are deficient in
* glucoronyltransferase
* cats have dec ability to excrete some compounds: NSAIDS
* cats are slower to secrete bilirubin
71
In cats, the gluconeogenensis pathway never
shuts down when fasting
72
Needed to conjugate bile acids in cats
taurine
73
AST increases in cats
often less dramatic and associated with muscle dystrophy
74
ALP in cats in produced in response to
epithelial stimulus
75
ALP increase in cats strongly suggests
on-going hepatic dz
76
Cats tend to develop jaundice earlier than dogs b/c
* reduced glutathione concentrations and
* dec secretory ability
77
In cats bilirubin is a very reliable sign of
* hepatopathy
* due to high renal threshold
78
In cats, bile acids are
* a sensitive test of liver function
* blood ammonia test is used same way as in dog
79
Cats with liver disease rarely have
hypoalbuminemia
80
Hyperglobulinemia in cats
* seen in a variety of diseases
* often concurrent with liver disease
