Exam 2 Flashcards
Lecture 12
Hepatobiliary Diseases
Acinus Model
Zone 1 Cells
-Protein synthesis
-Urea, cholesterol production
-Gluconeogenesis
-Bile formation
-Beta oxidation of fatty acids
-Most oxygen area
Zone 2
-Produce albumin
-Glycolysis
-Pigment formation
Zone 3
-Liponeogenesis
-Ketogenesis
-Drug metabolism (P450)
-Most susceptible to toxins and lowest in oxygen supply (Centrilobular) - Hypoxic damage
Signs & Symptoms
- Abdominal enlargement
-Ascites and or hepatomegaly, organomegaly - Microhepatica
-Chronic disease
-Cirrhosis - Diarrhea
-Cholestasis: decreased bile acids secretion, decreased fat ingestion/absorption - hyper osmosis
-Portal vein hypertension: decreased water absorption from GI - Vomiting
-Shunting: increased toxins activate CRTZ, hepatomegaly or biliary obstruction: increased vagal tone - Icterus
-Decreased clearance of bilirubin - Hepatic encephalopathy
-2nd to congenital or acquired PSVA, Cats: HE 2nd to hepatic lipidosis without shunting (lack of AA) - PU/PD
-HE: abnormal neurotransmission stimulate ACTH production increased cortisol
-Decreased urea production medullary washout
-Vomiting and diarrhea - Dysuria
-From urolithiasis (ammonium biturate) - Anesthesia intolerance
-Decreased hepatic metabolism, avoid GABA-ernig drugs (ie. benzodiazepines) - Alcoholic feces
-Signs of endocrine pancreatic insufficiency (pale grey), but patients different
-Extra hepatic bile duct obstruction - Hypoglycemia
-Young animals, no glycogen stores
-Portosystemic shunt older animals, synthetic hepatic failure or hepatic neoplasia-insulin like growth factor - GI bleeding
-Portal hypertension, coagulopathies, DIC
Abdominal enlargement - Ascites
- Abdominal muscle weakness
- Organomegaly: hepatomegaly, hepato-splenomegaly
- Abdominal effusion/ascites
-Transudare or modified transudate
-Exudate
-Hemorrhagic
-Chylous
Ascites/edema mechanisms
1. Decreased oncotic pressure (low albumin)
2. Vasculitis: leaking vessels
3. Increased hydrostatic pressure (venous obstruction, volume overload)
4. Lymphatic obstruction
Ascites & Liver
-Low to moderate protein
-Low to moderate cell count
-Transudate (pure or modified)
Primary Ddx for Transudate
- Heart disease
- Hepatic disease
- Marked hypoproteinemia associated with decreased production and or excessive loss
- Vasculitis: unusual
Pre hepatic Ascites
-Portosystemic shunt (acquired)
-Portal vein obstruction or hypoplasia
Intrahepatic
-Fibrosis/cirrhosis
-Microvascular shunting/intrahepatic shunt
Post-hepatic “passive hepatic congestion”
-Obstruction of intrathoracic caudal vena cava
-Congestive heart failure
-Pulmonary hypertension
-Pericardial disease
RAAS activation
-Pooling of blood in the splanchnic circulation secondary to portal hypertension
-Decrease in cardiac output activates the RAAS
-This leads to volume expansion, an increase in hydrostatic pressure, and this worsens ascites
Ascites - Hypoalbuminemia
-Associated with advanced liver disease
-Lowers vascular osmotic pressure further aggravating ascites formation
-Ascites associated with chronic hepatitis is a poor prognostic indicator
Microhepatica
Jaundice = Icterus
-Bile pigment (bilirubin) staining of tissues
Mechanisms
1. Large, persistent increase of bilirubin (hyperbilirubinemia), exceeds capacity o liver to take up and excrete it
2. Major impairment of bile excretion. Cholestasis with hyperbilirubinemia
Cholestasis
-Inability to take up, process within the hepatocytes or excrete bilirubin into the bile canaliculi are primary causes of cholestasis in liver disease.
-Obstruction of bile duct near duodenum, such as thrombus, cholelith, extraluminal compression (tumor or swelling due to inflammation), pancreatitis
-Jaundice may or may not be present depending on degree of stasis or blockage
Bilirubinuria
2+ to 3+ on dipstick
May be normal in concentrated urine for dogs (especially intact males)
-Bilirubinuria in cats is always pathologic due to their high tubular resorptive capacity 9x >dogs
-Rising bilirubinuria often precedes onset of icterus
Hepatic Encephalopathy
-Abnormal mentation, gait, neurologic function
-Accumulation of toxins in the blood
1. Marked reduction of functioning hepatic mass to process toxins
2. Portal blood flow is diverted around the liver via portosystemic shunting (congenital shunt)
Clinical syndrome
Type A
-Acute hepatic failure in the absence of pre-existing liver disease (Hepatic lipidosis in cats)
Type B
-Associated with congenital PSS
Type C
-Marked hepatic parenchyma disease and portal hypertension or acquired PSS, and divided into episodic, persistent, and minimal subcategories
HE, Ammonia theory
C/S
-Hypersalivation: especially cats with hepatic lipidosis. Dogs with advanced disease
-Polyuria in dogs: neurotransmitter changes imparing dopaminergic ACTH impaired release due to reduced inhibition of pituitary
-High cortisol throughout to induce partial inhibition of renal tubular response to vasopressin
Grading
1. Asymptomatic
2. Mild increase inapthy, decrease motility, or both
3. Mild ataxia, severe apathy
4. Combination of ptyalism, severe ataxia, head pressing, circling
4. Coma, seizures, stupor
C/S
-Reflective of diffuse (bilateral) cerebral cortical dysfunction
-Often episodic
-May be precipitated by a meal
-Reversible with treatment of underlying hepatopathy
Pathogenesis
-Not fully understood
Theories - Ammonia
-Biggest toxin implicated
-Ammonia detoxification mainly performed in liver via portal circulation unless shunt present
-Urea cycle: ammonia into urea in periportal hepatocytes and urea excreted by the kidneys
Brains lacks effective urea cycle
-Hyperammonia, glutamine formation increases
-Ammonia metabolized to glutamine in astrocytes by ATP
-Cellular swelling, neuronal edema, formation of reactive oxygen and nitrogen species.
-In cats with lipidosis, arginine deficiency leads to hyperammonemia
-Ammonia plays a role in regulation of GABA and Glutamate
Endogenous Benzodiazepines, Manganese, Pro-inflammatory cytokines
Benzodiazepines
-Biggest category of anesthesia meds
-Problem when liver function is compromised
-HE liver makes compound that act like diazepam and valium
-GABA inhibitory neurotransmitter regulated by GABA/benzodiazepine receptor/chloride ionophore complex
-Chloride ionophore complex-receptors for barbiturates and ivermectins. Receptor binding allows chloride to enter the cell
-Benzodiazepine-like ligands increased in plasma of human patients with fluminant liver failure
-Concentration of ligands correlated with severity of HE
-40% of cirrhotic human patients in hepatic coma responded to FLUMAZENIL
-Source of benzodiazepine unknown (food?)
Manganese
-Essential trace element
-Decreased hepatobiliary excretions with PSS
-Toxic to basal ganglia: astrocytes area sire of early destruction dysfunction/damage
Pro-inflammatory Cytokines
-Strong positive correlation
-TNF-alpha and severity of HE in patients with cirrhosis
-Dogs with cPSS and HE have significantly higher serum [CRP] than asymptomatic dogs with cPSS
HE - Predisposing factors, Prognosis
-High protein meal
-GI bleeding bc RBCs are treated as protein in the gut, ammonia and amine acids in RBCs
-Azotemia
-Hypokalemia
-Alkalemia
-Blood transfusion
-Bacterial infection: increases nitrogen load
-Sedatives, anesthetics, organophosphates
-Diuretics: secondary hypokalemia and azotemia
-Methionine: converted to mercaptans by GI bacteria
Arginine deficiency in CATS
Prognosis
-Fair to good for mild cases
-Guarded to poor with more severe C/S
-Varies depending on whether the underlying cause can be successfully treated
-Extrahepatic PSS good with surgical therapy
Poor if
-PT>100 seconds
-Hyperbilirubinemia
-Aflotoxin toxicosis
-Very young or very old
-Viral infections
Causes of death HE
-Edema
-Sepsis
-Hemorrhage
Coagulopathies
Liver synthesizes
-Protein C, S
-Antithrombin
-Fibrinogen, plasminogen
-Vit-k dependent factors: VII, IX, X, II (prothrombin)
-Factors V, XI, XII, XIII
Vitamin K deficiency when bile flow is decreased
75-85% factors not functioning or present before coagulator function is prolonged
-Thrombocytopenia can be observed due to consumption or sequestration
Bleeding risk assessment is important in clinical work-up of the hepatic patient
-Conversely, dogs and cats with hepatic disease may occasionally be predisposed to hypercoagulability. This may lead to microvascular thrombosis or portal vein thrombosis
-Bleeding can occur with portal hypertension-induced vascular fragility
-Hematemesis and melena may be seen with hepatic disease
-Upper GI most commonly affected
Metabolic Disturbances
Hypoalbuminemia
-Associated with hepatic production >/= 80% loss
-Hypoglycemia: decreased gluconeogenesis, severe PSS or hepatocellular dysfunction, possible neoplasia
Lecture Diagnostic tests Hepatobiliary diseases
History, Signalment, PE
Laboratory testing - CBC
-Few changes are consistent with hepatobiliary disease
-Normochromic to mildy hypochromic microcytosis (decreased MCV) = iron deficiency, unable to use iron available, such as in cirrhosis or PSS
>60% dogs PSS
<30 % cats PSS
Ddx: GI bleeding or breed specific
Anemia
-Mild microcytic anemia - consider PSS
-Marked microcytic anemia - consider GI bleeding
-Regenerative, microcytic anemia in jaundiced patient: consider hemolytic anemia (immune, infectious)
-RBC morphology: related to altered lipoprotein metabolism in cell membrane abnormalities
-Poikilocytes (abnormally shaped RBCs): particularly in cats with PSS or other hepatobiliary disease
Serum Enzyme Activity
ALT (SGPT) & AST
-Present in the hepatocyte cytosol and are released as a result of hepatocellular membrane damage LEAKAGE
-Specific to hepatocellular injury
-Alanine transaminase, Serum glutamic pyretic transaminase.
Related to extent of hepatic injury but not necessarily prognosis/reversibility
-Generalized hypoxia, regeneration, and metabolic activity also increase ALT levels
-Glucocorticoid activity in dogs mild to moderate increase in ALT
AST (SGOT)
-Aspartate transaminase
-Glutamic oxaloacetic transaminase (SGOT)
-Not liver specific
-Found in muscle also
-Consider in reference to Hx, c/s, and muscle specific enzyme activity Creatine kinase (CK or CPK)
-AST more reliable in cats for hepatocellular damage prediction
SAP (ALP) and GGT
SAP, ALKP, ALP: Alkaline Phosphatase
-Low concentration in the hepatocellular cytosol, so not leakage associated
-Not specific but association in cholestasis
-Found in bone, GI tract, kidney, and placenta
Glucocorticoids, phenobarbital, induction ALP in dogs
Increased level always significant in cats
-Growing bones, young dogs, common elevation
-Are serum enzymes that reflect new synthesis and release of enzymes from the biliary tract in response to certain stimuli such as cholestasis
GTT
-Gamma-glutamyltransferase
Specific for cholestasis in dogs and cats
-Post hepatic cholestasis and diseases affecting the biliary tree association
-Longer half life than ALKP in cats, so it is useful for monitoring treatment and progression of biliary disease
What tests estimate hepatic function?
- Glucose
- Cholesterol
- Albumin
- BUN
Functional testing - Bile Acids
Serum Bile Acids
Bile Acid Stimulation Test
-Collect a 3ml sample of blood in a serum tube after animal was fasted for 12 hours
-Feed a small amount of food that is normal in fat content (~20% fat dry matter basis in dogs)
-Collect another sample 2 hours after the meal
-Generally, postprandial abnormal SBA concentration using the enzymatic method in animals without icterus exceeds 20umol/L in cats and 25 umol/L in dogs
Urine Bile Acid (UBA)
-Reflects the average SBA concentrations during that time interval of urine formation
-Random UBA sampling has the advantage of nor requiring timing to meals or enterohepatic challenge
-UBA elevations correlate with hepatobiliary disease and PSS in dogs and cats
-Do not correlate as well for hepatic neoplasia in the dog compared to SBA
Functional test - Ammonia
- A high ammonia concentration helps in confirming suspicion of HE
-Reduced hepatic mass available to process ammonia
-Presence of portosystemic shunting, which disrupts the presentation of ammonia to the liver for detoxification
-Overproduction of ammonia in the GI tract (ie, SI bacterial overgrowth)
Ammonia Testing
-Pretest: draw after fast of minimum 6 hours - 12 hours
-Then feed a meal of 25% daily caloric requirement
-Post test draw 6 hours after a meal, must be collected in iced, heparinized (green top tube) and spun immediately in a refrigerated centrifuge and separated
-Canine samples - assay within 30 minutes
-Feline samples can be frozen (-20 degrees Celsius, and assay within 48 hours)
Coagulation Tests
APTT & PT
-Both prolonged if impaired liver function
-Thrombocytopenia is not uncommon in hepatobiliary disease, may be secondary to bleeding (GI), consumption (DIC), and or decreased production
-Ideally platelet function should be assessed prior to biopsies of the liver
-Buccal mucosal bleeding test (BMBT) is the only cage side test available to practitioners, but should be interpreted with caution
Ultrasound
-Does not tell you anything about function but it tell us about architecture, explain to client
-Widely used and valuable
-Limited sensitivity and specificity for hepatic disease
-Abdominal effusion enhances ultrasound images, but bone and gas densities block with acoustic shadowing
CT
-Used to image a variety of hepatic disease and masses
-Most commonly indicated in imaging PSS or better defined masses and vascular as pre surgical planning
-Provides excellent anatomic detail particularly with 3D renditions
MRI
Scintigraphy
-Utilization of radioactive isotopes that are taken up by tissues
-Technetium-99m
-Gamma camera
-Animal isolated for 24-48 hours until radioactivity has decreased to background levels
Laboratory, Coagulation, Imaging
Liver Sampling (Cytology or Biopsy)
Cytology: cells on a slide
Biopsy: tissue architecture
-In most cases of primary liver disease, liver biopsy is needed to establish a definitive diagnosis, prognosis and a basis for treatment
-Therapy without biopsy is non specific and may actually do more harm than good
-Strongly recommended before committing to the use of steroid, copper-chelating and antifibronic therapies
Reasons for cytology/biopsy
1. Explain abnormal tests, especially those persisting for more than a moth
2. Explain hepatomegaly
3. Determine hepatic involvement in systemic disease
4. Stage neoplastic disease
5. Objectively assess response to treatment
6. Evaluate progression of disease
Liver sampling - FNA
Advantages
-Minimizes trauma and risk for patient
-Least invasive
-Useful for diagnosing hepatic lipidosis in cats and suspected lymphoma
Disadvantages
-Low diagnostic yield
-Potentially misleading results
-Low correlation diagnosis of liver disease
Lecture Hepatobiliary Disease in the Cat 1&2
Cats vs. Dogs
Cats
-Higher prevalence of heapatobilirary disease
-Concurrent biliary tract disease, pancreatitis, IBD “Triad disease”
-Clinically serious hepatic lipidosis more common
Relatively deficient in gluconoryl transferase
-Reduced ability to metabolize drugs or toxins
-Cats are more discerning in consuming food, less likely to scavenge toxins
-Do not produce steroid-induced isoenzyme of SAP
-SAP half-life is short in cats (6 hours)
-HAC (Cushing’s disease) is rare in cats
-Obligate carnivores: post prandial gluconeogenesis
-High dietary requirement for Arginine and Taurine (essential)
Dogs
-Chornic parenchymal disease is more common (fibrosis, cirrhosis, portal hypertension)
-Biliary tract disease occurs but is uncommon
-Secondary hepatic lipidosis is generally not clinically important
-No deficiency of hepatic enzymes, but some breeds variation
-Dogs are more likely to scavenge, exposing them to more potential hepatotoxins
-Produce steroid-induced isoenzyme of SAP
-SAP half-life is long, 66 hours - 74 hours induced
-HAC is common
-Adapted to use starch dietary post prandial release of insulin results in glucose storage
-Lower requirement for Arginine
-No obligate carnivores, no dietary requirement for Taurine, though some breeds predisposed to Taurine deficiency cardiomyopathy
Icterus = Hyperbilirubinemia
- Pre hepatic = hemolysis (anemia)
- Intra-hepatic
- Post hepatic = bile duct/gall bladder/duodenum
The Icteric Cat
- Hepatic lipidosis
- Cholangitis/cholangiohepatitis
- FIP
- Lymphoma
Hepatic Lipidosis
CATS
Case
CBC
-Mild mature neutrophilia
-Rare Heinz bodies (oxidative stress)
Chemistry profile
-ALP elevated
-ALT, GGT, Cholesterol may be normal
-BUN, Creatinine and serum Bilirubin may be normal
Urinalysis
-Bilirubinuria
-SG concentrated, pH6.5, Inactive sediment
Ultrasound
-Large hyper echoic liver
-Falciform ligament fatty - noticeable
Tx
Always vitamin K
-Impaired bile flow, impaired vitK from helpful bacteria production
-IV fluids: Normosol R + KCl + VitB
-Dolasetron PRN for nausea
-Next day: liver FNA ultrasound guided after coagulation panel performed and WNL
Dx
-80% hepatocytes filled with vacuoles = lipid accumulation
-Hepatic lipidosis
Primary Hepatic Lipidosis
-Middle aged and older cats
-Massive accumulation of fat in hepatocytes
-Can be reversible if treated early
Secondary
-May occur secondary to any disease leading to anorexia
-Seen most often with pancreatitis, diabetes mellitus, IBD, and other hepatic disorders
-Pathogenesis is the same as primary HL
Pathogenesis
-Mobilization of peripheral lipids to the liver
-Deficiency of dietary proteins and nutrients important to fat metabolism and mobilization
Methionine, Arginine, Taurine
-Concurrent inappetence or anorexia: caused by stress in cat with obesity = metabolic abnormalities
Hepatic Lipidosis Tx, Dx, Px
Principles of HL Tx
-Restore fluid deficits and correct electrolytes
-Initiate nutritional support promptly
-Treat underlying disease concurrently
-Treat HE to control C/S
IV fluid
-0.9% saline (avoid lactate)
-K supplement
-NO dextrose (reduces beta oxidation of intrahepatic fats)
-Add water-soluble vitamins B
Nutrition
-Feeding tube
-High protein diet
-Start gradually 20-50% RER on day 1, then increase over several days
Control Nausea/vomiting
-Maropitant, ondansetron or metoclopramide
-Adding SAM-e and Vitamin E helps
HE control
-Lactulose, amoxicillin, or low dose metronidazole
-Prebiotics and probiotic may help acidify the colon promoting the proliferation of non-ammoniagenic bacteria
-Vitamin K SC or IM q12 hrs x3d
Ursodiol
-Synthetic hydrophilic bile acid (promotes choloresis = bile flow healthy bile formation)
-Choleretic, anti-inflammatory, anti-fibrotic, cytoprotective, antioxidant
-No available date in humans to demonstrate efficacy though
Carnitine Supplement
-Higher survival rate
Prognosis
-55-80% survival rate in intensively fed cats
-Mortality high without supportive feeding
-Success with secondary HL depends on primary disease
Cholangitis (biliary tree)
Cholangiohepatitis (biliary tree and hepatic parenchyma
Biliary disease is the second most common liver disorder in cats in the US
-Often concurrent pancreatitis, and or intestinal disease
-Cholangitis: inflammation of the biliary tract
-Cholangiohepatitis: inflammation of the binary tract that extends to the hepatic parenchyma
Feline CCHS - Cholangiohepatatis Syndrome
-Any age
-Insidious history
-Vague signs
-Neutrophilic cholangitis: primary bacterial infection
-Lymphocytic cholantitis: Primary cholangitis
Neutrophilic (suppurative) cholangitis
Pathogenetis
-Ascending bacterial cause originating in the SI
-E. coli; Streptococcus spp, Clostridium spp, occasionally Salmonella spp.
-Results in neutrophilic infiltration of the bile duct lumen and walls, along with edema and neutrophils within the portal areas
C/S
-Acute
-Most often seen in dogs young, and middle aged cats
-Biliary stasis, septic, fever, jaundice, lethargy, vomiting, weight loss
Dx
-Findings are neither sensitive nor specific for the disease
-Most have variable elevations (mild to severe) of bilirubin, ALT/AST, SAP, GGT and neutrophilia
Acurate diagnosis requires cytology, biopsy Laparoscopic, laparotomy
-Ultrasound: risk of leakage; general anesthesia strongly recommended to prevent patient movement and gallbladder laceration
Tx
-Based on cytology and culture/sensitivity ideally
-4-6 weeks
-Amoxicillin or amoxicillin/clavulanic acid
-Ursodeoxycholic acid (URSODIOL) may be given as a choleric and anti inflammatory agent
-Septic or very ill cat: hospitalization, IV fluids, antibiotics, and feeding support
-Critical to ensure feeding to prevent secondary hepatic lipidosis
Neutrophilic CCHS Tx
Lymphocytic cholangitis
Pathogenesis
-May overlap with chronic neutrophilic cholangitis
-Slowly progressive
-Infiltration of hepatic portal areas with small lymphocytes, occasionally plasma cells and eosinophils
-Lymphocyte inflitrate is primarily T-cells with portal B cell aggregates
-No acute signs like fever
May be difficult to distinguish from lymphoma
-Bile inflammatory infiltration is common
-Inciting cause is unknown, mediates? infectious?
C/S
-Young to middle aged cats, Persians
-Older cats
-Long history (months to years) of low grade illness that comes and goes
Weight loss, intermittent anorexia, lethargy
-Jaundice if often observed
-Less likely to be febrile
Clinicopahtologic abnormalities
-Values may be normal
-Mild to moderate increases: ALT/AST, SAP, GGT
-Less likely to have peripheral neutrophilia than cats with acute neutrophilic cholangitis
Dx
-Radiographs non-specific, may include hepatomegaly and effusion
-Ultrasound can aid in identifying dilation of the biliary tree
-Primary ultrasound differential is extra hepatic bile duct obstruction (EBDO)
Dx
-Biopsy needed for definitive diagnosis
-PT/PTT testing and VitK therapy should be done prior to biopsy
-PCR for antigen receptor rearrangement (PARR) assay may help distinguish lymphoma from inflammatory disease
-May consider testing for Bartonella via serology or PCR
General Tx
-Look for underlying disease and manage it
-EHBDO, choleliths, trematodes, IBD, pancreatitis
-Antimicrobials: empiric coverage gram (-) and anaerobes
-Tx neutrophilic: several months
-Tx non-neutrophilic until biopsies return & based on C/S
Ursodeoxyxholic acid: cytoprotectivem antifibrotic, choleric, antioxidant
-Maintain adequate nutrition
-Supplement water soluble vitamins B12 deficiency
-Vitamin K if jaundice
-Fluid therapy
-Maintain normal serum potassium
-Antioxidant therapy
-Vitamin E
-SAMe
Lymphocytic cholangitis Tx
-Differing opinions
-Often immunosuppressive corticosteroids but may not lead to resolution/cure
-URSODIOL recommended
-SAMe and VitE recommended
-Very ill cats require hospitalization, IV fluids, medical feeding support
-Critical to ensure feeding, prevention of hepatic lipidosis
-Concurrently treat associated disease such as IBD or pancreatitis
Portosystemic Shunt (PSS)
-More common in dogs than cats
-Congenital more common than acquired
-Congenital: extra hepatic or intrahepatic, single (most commonly) or double vessels
-Purebred cats are overrepresented
C/S
-GI: intermittent diarrhea, vomiting
-Urinary: Cystitis associated with rate stones
-PU/PD
-Neurologic: signs of HE
-Poor or stunted growth
-Copper colored irises
Dx
-History and C/S
-Elevated pre and post prandial bile acids
-Radiographs 50% show small livers
-Clinpath: Low BUN, mild increased liver enzymes and microcytosis
-Visualization of the shunt or imaging, ultrasound, CT angiography, or portal venography
Tx
-Complete or partial ligation of the shunt
-Cats need more than medical management due to higher obligate protein metabolism = production of > ammonia than dogs
Prognosis
-Good if it can be ligated
-Post operative mortality higher in cats than dogs
Pancreatitis in cats
-Inflammation of the pancreas, duodenum, and or biliary tree is common in cats and is known as “Triad disease”
-Pancreatitis can lead to bile duct obstruction EBDO leading to severe cholestatic hepatopathy
Treatment of Complications of Hepatic Disease and Failure
Hepatic Encephalopathy
Ammonia NH3 is the most important cause of HE
-Lipophilic and highly lipid soluble passes freely across cell membranes
-Ammonium NH4, is not lipid soluble and must be transported across cell membranes
Case
Case
Lecture 8
Exocrine pancreatic disease
General
Acinar: secrete digestive enzymes, aqueous NaCHO3 90%
Endocrine: Hormones, insulin, glucagon. 10%
Intrinsic factor: health of the intestinal cells. Vitamin B12 needed by ileum, when enteropathy present = deficiency in Vitamin B12 possible. Cats get it more than dogs, triaditis
Modified Organ Scoring System
-Based on clfinicopathologic criteria
-Hepatic: elevated liver enzymes >3x upper normal range
-Renal: elevated BUN, Creatinine
-Leukocytes: >10% bands or WBC >24 x 10^3/uL
-Blood glucose elevated (endocrine pancreas)
-Abnormal bicarbonate or anion gap = acid-base imbalance
Diagnosis
-High index of suspicion based on breed, C/S and history
PLI gold standard test for pancreatitis
-Amylase, lipase: not sensitive or specific for diagnosis
-RAdiographs
-Ultrasound
