GI pt. 2 Flashcards
Hyperbilirubinemia
- elevated serum bilirubin
Jaundice/ Icterus
- yellowing of plasma/ tissues
Bilirubinuria
- bilirubin in urine (can be physiological in dogs, always abn in cats)
Cholestasis
- decreased bile flow
Icterus (Physical Exam)
- icterus most nosted in sclera, 3rd eyelid, pinnae, mucous membranes
- icterus detectable in tissues if serum bilirubin > 2mg/dl
3 Mechanisms of Icterus
- Pre-hepatic (hemolytic)
- Hepatic
- Post-Hepatic (obstructive)
Top Differentials for Pre-hepatic icterus
- IMHA (1 or 2)
- Heinz body anemia
- Infectious
- microangiopathic
Top Differentials for Hepatic Icterus (cats vs dogs)
Cats: - hepatic lipidosis - cholangitis - FIP - Lymphoma Dogs (cholestasis): - Cholangiohepatitis - chronic hepatitis - Cu-associated - cirrhosis
Top Differentials for Post-Hepatic Icterus
- obstruction (EHBDO)
- Rupture
Diagnostics for Icterus
- CBC
- Chem
- -> Pre - n cholesterol
- -> hepatic - low cholesterol
- -> Post - high cholesterol
- UA (bilirubinuria cats vs dogs)
- Ultrasound (hepatic vs post-hepatic)
- Other (coag, FNA, biopsy, CT scan)
Bile composition
- water, bile acids and salts, bilirubin, cholesterol, FA, electrolytes (bile released by CK)
- Bile acids - steroid acids made by liver
- Bile salts - salts of bile acids (Na/K)
Bile Functions
- fat emulsification and digestion
- absorption of fat-soluble vitamins
- bactericidal
- excretion of waste products (bilirubin and cholesterol)
2 surgical techniques for liver biopsy
- suture fracture technique
2. skin punch technique
Principle diagnostic feature of EHBDO
- hyperbilirubinemia
- high ALP, ALT< GGT
- hypoalbuminemia
- fecal exam - acholic feces, trematode eggs (Cats)
- bilirubin in the urine (maybe cysts)
Top 2 causes of EHBDO in feline
- Inflammatory (70%)
- Neoplastic (30%)
Indications for cholecystectomy in dogs
- biliary mucocele
- cholelithiasis
- GB neoplasia or trauma
- +/- functional EHBO but can catheterize
Dogs vs Cats Duodenal papilla differences
Dogs:
- major duodenal pappila –> exit for CBD + pancreatic duct separately
- minor duodenal pappila –> exit for accessory pancreatic duct
Cats:
- major duodenal pappila –> exit for conjoined CBD + PD
- minor duodenal pappila –> only 20% present
Understand bilirubin metabolism
- Spleen - breakdown heme to make biliverdin which is changed to unconjugated bilirubin
- unconjugated bilirubin is transported via blood + albumin to liver
- Liver - unconjungated –> conjugated bilirubin which is then secreted into bile in gallbladder
- Intestines - conj. –> urobilinogen which then gets excreted as stercobilin or reabsorbed and transported to liver or kidney
- liver pt2 - recycled
- kidney - excreted as urobilin in the urine
T/F: Icterus presents when bilirubin > 2mg/dL
T
Icterus:
Pre-hepatic = hemolysis (CBC)
Hepatic = intrahepatic cholestasis (Chem, n biliary u/s)
Post-hepatic = EHBDO or rupture (Chem, abn biliary u/s)
T
Blood Supply to Liver and Biliary Tract
Liver:
Hepatic Artery – (20% of blood and 50% of O2)
Portal Vein – (80% of blood and 50% of O2)
Biliary:
Cystic artery is a branch of the hepatic artery
T/F: the gallbladder lies between the quadrate and the right medial lobes of the liver.
T
Gall Bladder + Ducts Anatomy
Gall Bladder
Cystic Duct - gall bladder to first hepatic duct
Common bile duct - first hepatic duct to papilla
Feline megacolon
- middle aged, M > F
- a diagnosis of exclusion + radiographs
- Tx: Diet (canned diet), stool softeners, pro-kinetics, hydration, increase activity
- -> may require manual deopstipation under gen. anesthesia
- -> exhaust medical options prior to subtotal colectomy
T/F: the feline rectal exam should always be performed under sedation
T
Dyschezia
- difficult and painful defecation
Tenesmus
- ineffectual straining to defecate
Constipation
- infrequent, difficult evacuation of dry/ hard feces
Obstipation
- severe constipation to the point of inability to defecate
Megacolon
- irreversible colonic dilation ass/ w/ chronic constipation; usually based on radiograph
- idiopathic is the most common form
Underlying causes of constipation
- dehydration
- neurological
- obstruction (intra or extra luminal)
- Electrolyte disturbances
- idiopathic megacolon
Top 3 causes of obstipation
- Idiopathic megacolon (62%)
- ortho (23%)
- neuro (11%)
4 functions of the colon
- electrolyte and water absorption
- storage of feces
- fermentation of indigestible ingesta
- vitamin production
Diet modification for Feline Megacolon
- canned diet to inc water content
- increase digestibility to dec. stool volume
- increase fiber concentration
Indications for subtotal colectomy
- refractory idiopathic megacolon after exhausting all medical options ( ideally spare the ileocolic jxn)
Risk factors for Canine Pancreatitis
- hypertriglyceridemia (DM, hypoT4, Cushings, obesity)
- drugs (l-spar, diuretics, azathioprine)
- trauma/ ischemia
- diet?
- hypercalcemia?
Diagnostic pathway for Canine Pancreatitis
- CBC
- Chem (high ALT, ALP)(hyperbili, hypercholest, triglyc, hypocalcemia, hyperglycemia, azotemia)
- TLI is more for EPI
- spec cPL is ideal
- rads are insenstitve
- U/S is great, but operator dependent
T/F: there is no perfect test for canine pancreatitis
T, but spec cPL + U/S would is best
Treatment of Canine Acute Pancreatitis
- stabilize the patient first
- nutrition: many, small meals (low fat, high digest.)
- analgesia: partial and full u-agonists
- anti-emetics: 5HT3 (ondansetron) or NK1 (cerenia)
Pathobiology of Canine Acute Pancreatitis
- fusion of lysosomes and zymogen granules (vacuolization):
- -> premature activation of zymogens by proteases
- -> further activation by trypsin
- -> damage propagated by elastases and phospholipases
- systemic inflammatory response (TNF-a and IL-6 resulting in mutlisystemic inflammation)
Protective measures of the pancreas
- pancreatic secretory trypsin inhibitor
- pancreatic polypeptide
- plasma protease inhibitors
What types of pancreatitis to cats get?
- chronic suppurative pancreatitis (CP)
Etiology of Feline Pancreatitis
- IBD
- Cholangitis
- idiopathic
- -> all three would be a triaditis
Diagnosis of feline pancreatitis
- same as the dog
- use spec fPL and a good U/S
- histopath is gold standard (cats get the chronic mononuclear, firbosis and atrophy)
Therapeutics for feline pancreatitis
- hydration
- nutrition
- analgeisa
- treat underlying disease first if applicable
Canine vs feline pancreatitis (similarities)
- clinical signs
- clinpath evaluation
- diagnosis
Canine vs feline pancreatitis (differences)
- Nutrition (cats – hydrolyzed diet d/t IBD, dog – get them food)
- Chronicity (dogs are acute, cats are chronic)
- Clinical consequences (dogs can die, cats get hepatic lipidsosi and EPI)
Etiology (cats are triaditis and dogs are usually singular)
T/F; it is important to distinguish between a hepatopathy and liver dysfunction when it comes to anesthesia
T
How to distinguish between a hepatopathy and liver dysfunction
hepatopathy: AST, ALT, GGT,
Liver Dysfunction: BUN, Cholesterol, Albumin, bilirubin, glucose
T/F: the goal of anesthesia for liver disease is to maintain adequate blood supply to the liver
T
What are some drugs to avoid during anesthesia for liver disease/ dysfunction?
- acepromazine, alpha-2 agonists, benzodiazepines (if hepatic encephalopathies), ketamine
What are some drugs that are OK to use in anesthesia for liver disease/ dysfunction?
- opioids (no morphine or meperidine), propofol, etomidate, inhalents, and alfaxalone are fine
Functional parameters of the liver
- BUN (high w/ disease)
- cholesterol (low w/ disease)
- bilirubin (high w/ disease)
- glucose (low w/ disease)
- albumin (low w/ disease)
T/F: liver enzyme values (AST, ALT) tell us nothing about liver function
T
T/F: ALT and AST are leakage enzymes while ALP and GGT represent cholestasis
T
ALT
- more liver specific than AST
- also present in heart, kidneys, and muscle
- longer half life in dogs (60hrs) than cats (6hrs)
- any damage to the liver will cause leakage
AST
- less liver specific than ALT
- high concentrations in skeletal muscle
- necrosis and inflammation can increase AST
- most AST is bound to mitochondria so more damage is required vs ALT
ALP
- high sens., low spec in dogs
- membrane bound in liver, renal, bone, intestinal mucosa
- 3 causes of increase:
1. cholestasis
2. increased osteoblastic activity (growing)
3. admin. of corticosteroids - elevation in cats is of significant concern and we must find cause
T/F: GGT is more sensitive than ALP for inflammatory bile duct disease in cats than dogs. GGT»_space; ALP in most cholestatic disorders, except for hepatic lipisosis
T
T/F: Cats commonly develop marked hepatic fibrosis, cirrhosis, and acquired PSS compared to dogs
F; cats rarely develop these conditions
T/F: Bilirubinuria is rarely a concern in cats compared to dog
F; cats have roughly 7x higher renal threshold than dogs so bilirubinuria in cats is a huge concern
T/F: increased ALP is always important in cats
T
T/F: triaditis is more common in dogs than cats
F; triaditis (enteritis, pancreatitis, cholecystitis) is common in cats
How to run Bile Acids?
- fast dog for 12-18 hours
- take blood test (preprandial)
- feed small meal (CCK will trigger bile release)
- blood test post-prandially
How to read a bile acids
- hepatic disease will cause difficulty re-uptaking bile acids from blood causing increased [bile acids]
- PSS = normal pre and markedly elevated post
Feline hepatic diseases
- Hepatic Lipidosis (25-50%)
- Cholangitis (25%)
- Neoplasia (20%)
- 2nd* reactive hepatopathies (16%)
- Vascular - PSS (6%)
- Toxic (5%)
- FIP (<2%)
Feline Hepatic Lipidosis
- accumulation of excess triglycerides in hepatocytes
- obesity, stress, and anorexia
Feline Hepatic Lipidosis ( Pathogenesis)
- excessive fatty acid uptake
- inability to oxidize fa
- excessive lipogenesis
- inhibition of VLDL synthesis or secretion
Feline Hepatic Lipidosis ( Diagnosis)
- mod increased in ALT, ALP
- mod increase in serum bili
- n to mildly increase GGT
- enlarged hyperechoic liver on U/S
Feline Hepatic Lipidosis (Management)
- do not force feed the cat
- appetite stim. are not effective and may worsen a hepatopathy
- aggressive nutritional and fluid support
- do not restrict dietary fat or protein in cats w/ HL
- feed based on RER ( RER= 70*BW^0.75 / day)
Feline Hepatic Lipidosis (Prognosis)
- good w/ 80% survival w/ aggressive nutritional support
Cholangitis (3 forms)
- Neutrophilic (80%) (presents more sick than 2)
- Lymphocytic (20%)
- Chronic cholangitis d/t flukes
- can only differentiate via histopath
Cholangitis (Clinical signs)
- nothing specific (anorexia, weight loss, lethargy, vomiting, diarrhea)
- jaundice
- fever (lipidotic cats are not febrile)
T/F: a good way to differentiate between cholangitis and hepatic lipidosis in the cat is to take a rectal temp. Lipidotic cats will not have an elevated temperature
T
Neutrophilic Cholangitis
- think bacterial infection (E. coli, clostridia, bacteroides) (go to bile for culture)
- underlying cause unknown
Lymphocytic cholangitisi
- small lymphocytes mainly restricted to portal areas, variable portal fibrosis, biliary proliferation
Cholangitis (surgery)
- on indicated if discrete choleliths or complete biliary obstruction observed
Cholangitis (medical therapy)
- Ursodeoxycholic Acid (Actigall) (anti-inflammatory, immunomodulatory, and antifibrotic properties)
- Denamarin (antioxidant)
- Neutrophilic –> treat underlying dz
- lymphocytic –> pred or chlorambucil
Cholangitis (prognosis)
- extremely variable
What are the two components of Denamarin
- SAMe
- Silybin
Hepatic Disorders in the Dog
- Reactive Hepatopathy
- Chronic Hepatitis
- Copper Hepatotoxicity
- PSS
- Neoplasia
- Superficial Necrolytic Dermatitis
Copper Associated Hepatotoxicosis
- abnormal accumulation of copper in hepatic lysosomes
- up to 10k ppm (n <400ppm)
Cu-Ass Hepatotoxicosis (Bedlington terrier)
- autosomal recessive inherited gene
- deletion of commD1gene - inability to excrete Cu in bile ducts
Cu-Ass Hepatotoxicosis (Diagnosis)
- high ALT, ALP, bilirubin
- Quantification of hepatic copper from biopsy
- stain for copper (rhodanine)
- -> 1* metabolic disorders - centrilobular
- -> cholestasis - accumulation in the portal tracts (periportal region)
Cu-Ass Hepatotoxicosis (Treatment)
- dietary copper restriction
- Zinc Gluconate = decreased absorption via induction of metallothionein
- Cu chelating agent (d-penicillamine, trientine) (use when Cu >1000ppm)
- Anti-oxidants (denamarin)
- Ursodeoxycholic acid
Why is it inappropriate to give Zn-gluconate with d-penicillamine and denamarin?
D-penicillamine (a chelating agent) will chelate the Zn rather than the Cu
Chronic (Active) Hepatitis
- a canine disease
- active = neutrophils on biopsy
- idiopathic inflammatory condition ass. w/ Cu toxicity, infectious disease (lepto), drugs (tetracycline), idiopathic
Chronic (Active) Hepatitis (pathogenesis)
- immune mediated disease 2* to hepatocyte injury and release of hepatic antigens
Chronic (Active) Hepatitis (Signalment, Clinical Signs, types)
- female, middle-aged (dobermans)
- non-specific + icterus, jaundice, seizures, bleeding
3 types: - short fulminant = death
- progressive waxing and waning
- asymptomatic
Chronic (Active) Hepatitis (Lab findings)
- high ALT, ALP, bilirubin
- hypoalbuminemia
- abn bile acids
Chronic (Active) Hepatitis (Histo features)
- initial lympho-plasma infiltration
- bile duct hyperplasia
- bile stasis fibrosis, necrosis
Chronic (Active) Hepatitis (Treatment)
- manage excess copper if present
- arrest inflammation (cyclosporine)
- resolve fibrosis
- Zn gluconate
- antioxidants
PSS (3 classifications)
- congential vs acquired
- intra vs extra hepatic
- single vs multiple
T/F: toy breeds are predisposed to congenital, extrahepatic, single PSS while large breeds are predisposed to acquired, intrahepatic, single PSS
T
PSS (Diagnosis)
- signalment
- min. database (microcytosis, fx liver abn)
- serum bile acids
- abd rads, ultrasound
- hepatic scintigraphy (great y/n test)
- exploratory laparotomy
PSS (therapy)
Medical (for hepatic encephalopathy)
- decreased urease producing bacteria w/ an antibiotic (ampicillin, neomycin)
- avoid metro d/t neurotoxicity
- lactulose
- Diet (do not restrict protein unless encephalopathic)
Surgical
- Ameroid Ring Constrictor (ARC)
Why does administering lactulose help w/ hepatic encephalopathy?
- acidify the colon to converts NH3 –> NH4 which prevents re-absorption in the colon
Portal venous Hypoplasia
- type of microscopic PSS
- congenital in Cairn ter. Yorkies, toy breeds
- result of hypoplastic small intrahepatic portal veins
- high serum bile acids w/ no visible shunt
- biopsy –> similar to that of shunt dog
- do not need therapy and have great prognosis
Primary Survey of the Acute Abdomen
A- airways
B- breathing
C- circulation
D- disability/ dysfunction
Perfusion Parameters
- mentation
- mm color
- CRT
- heart rate
- pulse quality
- extremity temp
4 broad causes of abdominal pain
- distension
- traction
- ischemia
- inflammation
Hemoabdomen
- free blood in the abdomen that does not clot and pCV > circulating PCV
- causes: trauma, coagulopathy, ruptured viscera, torn blood vessel
Fluid Analysis (uroabdomen)
requires either:
- [creatinine] x 2 > serum
- [potassium] x 1.4 > serum
Fluid Analysis (bile peritonitis)
requires:
- [bilirubin] x 2 > serum
Fluid Analysis (septic peritonitis)
requires both:
- glc @ 20mg/dl < blood
- lactate @ 2mmol/L > blood
Because an elevation in AST can also come from a severe myositis, it is important to check this other chem panel value whenever we see that elevation?
CK
Why is an elevation of ALP in the cat more significant than in the dog?
- no steroid induced iso-enzyme
- a lot less ALP per gram of hepatocyte
- shorter half-life (6hrs)
T/F: ALP is made by bile caniliculi epithelium, GGT by bile duct epithelium
T
Classic PSS U/S findings
- microhepatica
- actual shunt
- possibly stones in the bladder
- slight renomegaly
Gold Standard for PSS diagnostics
- nuclear scintigraphy (tells us yes/ no for shunt)
Classical signs of SIBO
- low B12, high folate
- not necessarily required for diagnosis
2 breeds predisposed to BOTH canine chronic and acute pancreatitis
yorkies
schnauzers
pancreatitis ultrasound findings
- enlarged, hypoechoic pancreas
- hyperechoic mesentery surrounding it
What is the gold standard test for diagnosing a septic peritonitits
- intracellular bacteria present on cytology of the effusion
What is the gold standard test for diagnosing a uroabdomen
- positive contract cystourethrogram
Surgical treatment for hilar splenectomy (2 important arteries)
- ligation of the splenic and short gastric arteries
Adv./ Dis of Active Drain - Closed Suction for Septic Peritonitis
Adv. - closed system = dec nosocomials - relatively cheap - fluid samples for cytology Dis. - no opportunity to re-debride
Adv./ Dis of Open Abdominal Drainage for Septic Peritonitis
Adv. - improved drainage - inability to re-explore - discourages anaerobic growth Dis - cost - monitoring - hypoproteinemia - nosocomial infections common
5 factors that predispose to GDV
- large breed
- deep chest
- previous splenectomy
- fed once per day
- increasing age
Acute Hemorrhagic Diarrhea Syndrome
- acutely ill dog w/ bloody diarrhea
- often present in shock w/ normal to mild dehydration
- PCV = 10 x TP
AHDS (Signalment)
- younger to middle age small breeds
AHDS ( History)
- most commonly starts w/ vomiting
- progresses to hemorrhagic diarrhea w/in hrs - days
AHDS (Physical Exam)
- dehydration
- poor perfusion parameters
AHDS (pathogenesis)
- idiopathic
- disruption of intestinal permeability d/t inflammation –> acute transolcation of plsama like fluid –> hypovolemia and dehydration
AHDS (Treatment)
- resolve shock (often 1.5 - 3x blood volume in isotonic crystalloids)
- antimicrobials: concurrent sepsis or neutropenia
- GI protectants: consider ondansetron/ maropitant for first two day. Antacids not indicated
Parvovirus (signalment)
- a puppy w/ hemorrhagic diarrhea
Parvovirus (Diagnosis)
- ELISA snap test
- vaccines can induce weak positives
- PCR the feces if unsure
Parvovirus (2 major forms)
- myocarditis (almost nonexistent)
2. enteritis (v common)
Parvovirus (Clinical Signs)
- vomiting w/ or w/out diarrhea
Parvovirus (treatment)
- large volume IV fluids
- offer food daily (NG tube if truly anorexic)
- pain control?
Parvovirus (Prognosis)
- good w/ aggressive therapy
Parvovirus ( Outpatient treatment)
- give estimated deficit SQ
- daily calculate maintenance per TID SQ
- Antimicrobial once (cefovicin) SQ
- Antinausea/ antiemetic
Parvovirus ( post-infection immunity)
- immunity for rest of life
- some will never recover from bone marrow insult
