Hepatobiliary + pancreas Flashcards
1
Q
What stimulates release of pacnreatic enzymes?
A
Secretion stimulated by Ach, CCK and secretin binding to receptors…
- Vagal response to sight/smell of food = cephalic phase and causes release of ACh.
- The gastric phase is when the stomach distends, causing a vagovagal reflex.
- The intestinal phase is from the distension of the duodenum, causing release of ACh.
- Peptides and fat in duodenum cause CCK release, low pH in the duodenum causes secretin release
2
Q
What are the 3 types of pancreatitis in cats?
A
Cat pancreatitis:
Three types:
-
Acute Necrotizing Pancreatitis = acinar cell and peripancreatic fat necrosis as the primary characteristic with varying inflammation, hemorrhage, mineralization, and fibrosis.
- Premature activation of zymogens within acinar cells leads to acinar cell necrosis from trypsin, chymotrypsin, carboxypeptidase, hemorrhage due to elastase digestion of blood vessels and saponification due to lipase digestion of pancreatic and peripancreatic fat. Lots of inflammatory mediators, free radicals, etc come into the mix as well.
- Acute Suppurative Pancreatitis = neutrophilic inflammation predominates. Is less common than acute necrotizing pancreatitis, affects younger animals.
- Chronic Non-suppurative Pancreatitis = characterized by lymphocytic inflammation, fibrosis, acinar atrophy as the predominant feature. Is a histo diagnosis, can’t differentiate from the
3
Q
What is a pancreatic pseudocyst?
A
Pancreatic Pseudocyst:
- A sterile collection of pancreatic fluid surrounded by a fibrous or granulation tissue capsule.
- Considered a complication of pancreatitis, clinical signs are same as for pancreatitis.
- Aspiration is safe and should be attempted for dx (low cellularity) and tx (drainage is accepted therapy, either surgically or via US) - if persists, clinical signs do, too.
- On US can’t distinguish pseudocyst from abscess or necrosis unless gas points to an abscess. Neoplasia can also mimic or be associated with abscess or necrosis.
4
Q
What is a pancreatic abscess?
A
Pancreatic Abscess:
- A pocket of pus associated with the pancreas, almost all are NOT infected.
- A complication of pancreatitis, with similar clinical signs
- Drainage is the therapy of choice- surgery may be risky, so manage medically
5
Q
What is exocrine pancreatic insufficiency?
A
Exocrine Pancreatic Insufficiency:
- Insufficient production and secretion of pancreatic enzymes.
- Most common cause is lack of acinar cells due to atrophy (dogs) or chronic pancreatitis (cats).
- Pancreatic Acinar Atrophy most common cause- exclusively in GSD, Rough Coated Collies, Eurasians (genetic marker not found). Maybe autoimmune destruction of the pancreas.
- Chronic pancreatitis destroys acinar cells and fibroses them
- Theoretically also could be from obstruction of the pancreatic duct (which in itself can lead to pancreatitis, pancreatic atrophy or both)
- Pancreatic aplasia and hypoplasia suspected in young animals but not proven
- There is lots of redundancy in digestion and a huge excess of digestive enzymes so EPI only occurs if >90% of exocrine pancreatic function is lost.
Clinical signs:
- Diarrhea
- Weight loss in part due to maldigestion and buildup of ingesta in gut w/ changes in microbes as well but also loss of bicarb which normally buffers stomach acid and trophic factors for GI maintenance.
6
Q
What are some causes of pancreatic edema?
A
Causes:
- Pancreatitis
- Portal hypertension
- Hypoalbuminemia
Fluid goes between all the little lobes so have a ‘tiger-striped’ appearance.
7
Q
What are the 2 different types of DM?
A
In dogs:
- Almost exclusively type I, insulin dependent, from destruction of beta cells- usually just have fewer beta cells, rarely they are all gone.
- Type II almost always from an insulin antagonistic drug or disease.
In cats:
- Almost always type II…a small number of cats have antibodies to islet cells, but 80% are non-insulin dependent. So they have impaired response to insulin in muscle, liver, fat, and have beta cell failure
- Risk factors in cat:
- Age
- Male
- Neutered
- Inactivity
- Glucocorticoid administration
- Progestin administration
- Obesity
Cause is likely multifactorial:
- Autoimmune mechanisms - ab against beta cells and intracellular glutamic acid decarboxylase
- Genetic- more common in female dogs, male cats, some families predisposed
- Insulin-antagonistic diseases, drugs
- Obesity - beta cell degeneration secondary to chronic insulin resistance
- Pancreatitis
- Environmental factors
Clinical signs:
- PU/PD- blood glucose of 180-220 overwhelms the renal tubular cells ability to resorb so get osmotic polyuria and compensatory polydipsia
- PP - glucose entering the satiety center of the brain is mediated by insulin, so no insulin, no feeling of satiety.
- Weight loss - there is decreased tissue utilization of glucose, fatty acids and amino acids without insulin as well as accelerated hepatic glycogenolysis so the body is basically starving
Complications:
- Cataracts - very common in dogs. Rare or at least less severe in cats. Due to altered osmotic relationships in the lens from accumulation of fructose and sorbitol which cause water influx, swelling and rupture of lens fibers
- Anterior uveitis is secondary to rupture of the lens fibers and exposure of lens proteins to local immune response, KCS
- Hepatic lipidosis
- Peripheral neuropathy - rare in dog, common in cat. From peripheral demyelination and remyelination, axonal degeneration and regeneration. Cause is likely multifactorial and associated with vascular and metabolic factors.
- Diabetic nephropathy- can be the result of diabetes but commonly can have renal failure concurrently but from a separate cause. Is associated with glomerulonephropathy/glomerulosclerosis
- Bacterial infections, esp UTI
- Pancreatitis
- Rarely, glomerulonephropathy, retinopathy, EPI, diarrhea, dermatopathy
8
Q
What are some clinical signs of hepatic disease and why?
A
- Early signs are PU/PD (unknown why), anorexia, vomiting, lethargy
- GI ulceration
- Hepatic encephalopathy- ammonia, created in the GI tract by bacterial degradation of amines, amino acids and purines, isn’t detoxified to urea by the liver.
-
Jaundice - bilirubin is formed in the reticuloendothelial system from heme. The reticuloendothelial system (RES) is phagocytic cells (monocytes and macrophages) in connective tissue-accumulate in lymph nodes and the spleen. The Kupffer cells of the liver and tissue histiocytes are also part of the RES. Released from RES, bound to albumin, taken up by the liver and secreted into bile.
- Prehepatic - severe hemolytic anemia
- Hepatic
- Post-hepatic - biliary obstruction
- Coagulopathies - hepatocytes produce all clotting factors but VIII. Also clears activated coag factors, plasminogen activators, and fibrin degradation products. Also the site of activation of the vitamin K dependent factors (II, VII, IX, X). Also less bile means less absorption of fat-soluble vitamin K.
- Ascites - from neoplasia, portal hypertension, bile peritonitis
- Urolithiasis - ammonium biurate from chronic hyperammonemia and hepatic processing of uric acid
9
Q
What are some hepatic toxins?
A
- Phalloidin mushrooms
- Acetaminophen
10
Q
What are some causes of granulomatous hepatitis?
A
Granulomatous hepatitis characterized by macrophage infiltration.
Lots of causes:
- Idiopathic common
- Bacterial (Nocardia, mycobacterium, etc)
- Fungal (histo, cocci)
- Parasitic (hepatozoon, heterobilharzia)
11
Q
How do hepatic abscess occur?
A
HEPATIC ABSCESS - from ascending infection, portal umbilical veins in newborns, direct penetration or central necrosis of tumor.
- Very commonly in older dogs abscesses are secondary to tumor so *make sure* you biopsy appropriately.
- Most commonly found are Staph and Clostridia.
- In adults, abscesses associated with Yersinia, Nocardia asteroides, Actinomyces
Predisposing conditions to any hepatobiliary infections include:
- Obstructed bile flow
- Impaired hepatic perfusion +/- oxidant injury (chronic hepatitis, cirrhosis, PSS, neoplasia, torsion, trauma)
- Immunocompromise (cushings, diabetes, etc),
- Increased translocation of enteric organisms (IBD, neoplasia, liver disease, ileus, pancreatitis)
- Omphalitis in a neonate
- Visceral larval migrans.
- Granulomas associated with mycobacteria, fungi, migrating nematodes, schistosomiasis, leishmania (dogs), Bartonella (dog), Cytauxzoon felis (cat), non-infectious causes (drug rxns, lymphangectasia, immune-mediated, idiopathic)
12
Q
What are some hepatic storage diseases and what breeds are predisposed to it?
A
Copper Overload
- Copper Overload of Bedlington Terriers- chelation therapy is used to decrease inflammation and prevent recurrence
- Doberman hepatitis- seen in female 5-7 years old, poor prognosis. Recently found to be from copper storage
- Other copper hepatopathies seen in Westies, Dalmatians, Labs, Skye Terriers, Cockers, Springers, Siamese cats
- Copper overload causes inflammation as a result of hydroxyl radical formation
Hepatic Amyloidosis
- Amyloid proteins with a beta pleated structure can be associated with systemic disease and lots of different disease processes- is from acute phase reactions associated with chronic inflammatory, neoplastic or infectious processes or as a familial trait.
- Predisposition in Shar-Peis, Abyssinian, Oriental, Siamese cats
- Predisposes to spontaneous liver lobe fracture bc organ fragility or coagulopathy- often present bc sudden death or hemorrhagic shock
- On US the liver is hypoechoic with masses suggestive of hematomas
Lysosomal storage disorders
- Normal lysosomes degrade cellular and extracellular fats, proteins, CHOs and nucleic acids for reuse. May combine and create secretory lysosomes.
- Usually are systemic disorders (eg mucopolysaccharidosis) but many are hepatocellular or Kupffer cell related.
13
Q
Dsscribe cholangitis
A
CHOLANGITIS
- Cholangitis is second most common liver disease of cats, after lipidosis
Neutrophilic:
- Usually from ascending bacterial infection
- Neutrophilic cholangitis in cats- suppurative or acute cholangitis
- Suppurative
- Acute cholangitis
- Inflammatory cells start in bile duct lumen or epithelium and extend out form there
- Usually E. coli, rarely staph or other- usually ascending from bowel
Ultrasound findings:
- On US often see dilated gall bladder with thickened wall (>1mm) and inspissated bile and distended bile ducts (>5mm).
- The hepatic parenchyma may be patchy and echogenic
- **Diagnosis often can be made via percutaneous bile aspiration but 25% result in bile peritonitis and it is contraindicated if the gall bladder wall looks bad or in cases of emphysematous cystitis
- Can be found in conjunction with biliary obstruction- choleliths are common
- Coexisting features include pancreatitis (usually mild) and IBD
- TRIADITIS= cholangitis, pancreatitis + IBD
Lymphocytic cholangitis in cats- aka cholangiohepatitis, non-suppurative cholangitis, sclerosing cholangitis
- Often in young cats
- Inflammatory cells center on periportal areas but don’t infiltrate bile ducts
Utrasound findings:
- Chronic inflammation causes distended, fibrotic bile ducts seen on US as irregular, wide ducts, which are prone to infection.
- In general the liver appears heterogeneous on ulrasound
- On US need to ddx from extrahepatic bile duct obstruction
Destructive cholangitis- almost always an idiosynchratic reaction to sulfonamides
- Necrosis of smaller intrahepatic ductules- take off drugs to save remaining ones is only hope
- End result is porto-portal bridging fibrosis which can lead to portal hypertension, acquired shunts, etc.
Chronic cholangitis associated with liver fluke infection
- Similar to lymphocytic cholangitis
- Infection is via raw fish that ate a water snail, the fluke goes up bile duct from the intestine
- See large bile ducts with papillary projections and periductal and portal fibrosis. Rarely see the flukes or eggs.
14
Q
How long does it take for biliary obsrtuction to show sonographic signs?
(extra- vs. intrahepatic)
A
- Extrahepatic bile duct distention in 48 hours
- Intrahepatic in 5-7 days
15
Q
Are biliary carcinoma benign or malignant?
A
Biliary cystadenoma
- Arise primarily from intrahepatic bile ducts. Rarely extrahepatic.
- In cats is considered benign but can be a problem if it’s in the porta hepatis. There can be rare malignant transformation characterized by calcification and solid tumor mass.
- Male predisposition.
