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Doctor of Veterinary Medicine (Work in progress) > Veterinary Medicine - Pancreas & Liver Diseases > Flashcards

Veterinary Medicine - Pancreas & Liver Diseases Flashcards

1
Q

Pancreatitis - Etiologies

A

Primary hypertriglyceridemia (e.g. Familial hypertriglyceridemia of Miniature Schnauzers)

Secondary hypertriglyceridemia:
-High fat diet / Garbage eating
-Endocrinopathies: DM, Hypothyroidism, Cushing’s disease
-Hypercalcemia
-Ischemia (e.g. Dehydration, Shock, Anesthesia)
-Trauma (e.g. Iatrogenic)
-Drugs: TMS, Phenobarbital + KBR, Azathioprine, L-Asparaginase
-Toxins (e.g. Organic phosphates, Lilly flower in cats)
-Translocation of bacteria from the GI (Cats) -Idiopathic

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2
Q

Pancreatitis - Possible complications (Local, Systemic)

A

Local:
Peritonitis (Aseptic)
Necrosis
Cholestasis (Cats more than Dogs)
Gastritis
Enteritis
Colitis (Anatomical proximity)
Ileus

Systemic:
SIRS\MODS
ARDS\ALI
Pleural effusion
PTE
AKI
DIC
Arrhythmias

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3
Q

Chronic Pancreatitis - 3 Possible causes

A

Sequela to episodes of acute Pancreatitis

Immune-mediated

Repeat translocations of bacteria from the GI (Cats)

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4
Q

Chronic Pancreatitis - 2 Possible complications

A

Exocrine pancreatic insufficiency (EPI)

Diabetes mellitus (DM)

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5
Q

Acute Pancreatitis - US Sensitivity

A

70% (but dependent on the skill of the radiologist)

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6
Q

Pancreatitis - Possible CBC findings

A

Leukocytosis\Leukocytopenia

Anemia (e.g. GI Bleeding, Anemia of inflammation\neoplasia )

Thrombocytosis (Inflammation) \ Thrombocytopenia (e.g. Vasculitis ,DIC)

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7
Q

Pancreatitis - Possible panel findings and their respective explanations

A

-Hypoalbuminemia (Negative APP, GI bleeding) \ Hyperalbuminemia (e.g. Dehydration)
-Hypoproteinemia (GI bleeding)
-Hyperbilirubinemia (Cholestasis)
-Elevation of liver\bile enzymes (Cholestasis, Hepatic damage)
-Hyperamylasemia (Pancreatitis, GI damage, AKI)
-Hypercholesterolemia (Cholestasis)
-Hypertriglyceridemia (Lipolysis of peripancreatic\abdominal fat)
-Hypocalcemia (Saponification)
-Hypoglycemia (Destruction of beta-cells and release of Iinsulin) \ Hyperglycemia (depletion of beta cells)
-Azotemia: Dehydration, AKI, GI bleeding)
-Hyponatremia, Hypokalemia, Hypochloridemia (Diarrhea, vomiting)

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8
Q

Pancreatitis - Amylase - Why is it considered non-specific to pancreatitis? When can it be considered specific?

A

Elevation can also be secondary to: Damage to the duodenum, Decreased Renal GFR (e.g. AKI)

3x-4x the normal range - specific to pancreatitis

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9
Q

Pancreatitis - Specific enzymes - More useful for acute or chronic pancreatitis?

A

Acute Pancreatitis

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10
Q

General Lipase - Specific to pancreatitis? Why?

A

No

Many lipases in the body besides pancreatic lipase: Lipoprotein-lipase, Hormone-sensitive lipase, Stomach and liver.

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11
Q

Pancreatitis - Most sensitive test to diagnose pancreatitis

A

Snap PLI

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12
Q

Pancreatitis - Most specific test to diagnose pancreatitis

A

Spec PLI

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13
Q

Pancreatitis - Specific testing is more sensitive for cats or dogs?

A

Dogs > Cats

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14
Q

Pancreatitis - Snap PLI - More useful for confirming or rule out pancreatitis?

A

Rule-out (High sensitivity, low specificity)

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15
Q

Pancreatitis - DGGR Lipase - When ia it considered specific to pancreatitis?

A

3x Upper reference interval

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16
Q

Pancreatitis - What are the effects on coagulation? Explain the pathophysiology

A

First hypercoagulability and then Hypocoagulability and DIC

Release of proteases => Endothelial damage, Inflammation and consumption of anti-coagulants (e.g. AT-3, Alpha-2-macroglobulin, Alpha-1-proteinase) => Hypercoagulability => Consumption of pro-coagulation factors and platelets => Hypocoagulability and DIC

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17
Q

Pancreatitis - Diagnosis - Gold standard? When is it performed?

A

Histology\Cytology

Almost never, unless neoplasia is suspected

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18
Q

Acute Pancreatitis - Treatment (Dog)

A

Fluids, Electrolytes

Low fat diet: Enteral as soon as possible is preferred. Tube feeding if anorexic after a few days

GI support: Anti-emetics, GI protectants (if GI bleeding is suspected,) Appetite stimulants, Pro-motiles

Analgesia (e.g. Butorphanol/Buprenorphine/Fentanyl )

Antibiotics - not indicated in MOST cases of canine pancreatitis. Only if sepsis is suspected

*Plasma - Low AT-3/ suspected DIC - No proven efficacy

*Steroids - Last resort

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19
Q

Chronic pancreatitis - Treatment (Dog)

A

Low fat diet

Analgesia

Anti-emetics

*Immunosuppression - recurrent episodes of acute on chronic \ No response to therapy

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20
Q

Pancreatitis - Treatment - What’s different in cats (2 main differences)

A

Antibiotics - bacterial translocation more common than in dogs

Low fat diet - unless there is underlying hypertriglyceridemia - Not necessary

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21
Q

Pancreatitis - Prognosis

A

Depends:

1) Mild disease that passes with supportive treatment and dietary restriction (Low fat) for an indeterminate period (few weeks to life-long depending on the case) - good prognosis

2) Serious systemic disease that might require prolonged admission and with life threatening complications (SIRS, AKI, ALI/ARDS etc.) - fair to guarded

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22
Q

Pancreatitis - What are the top 3 associated disease with Pancreatitis In cats? (Concurrent together with Pancreatitis)

A

IBD

Cholangiohepatitis

Hepatic Lipidosis

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23
Q

What are the 2 most common sequelas of Pancreatitis?

A

DM

EPI

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24
Q

Exocrine pancreatic insufficiency (EPI) - Most common etiologies in both cats and dogs

A

Dogs: Sequela to chronic pancreatitis (50% of cases), Pancreatic acinar atrophy (Other 50% of cases)

Cats: Sequela to chronic pancreatitis (almost 100% of cases)

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25
Q

Exocrine pancreatic insufficiency (EPI) - Clinical signs

A

Common:
Weight loss
Polyphagia
Small intestine diarrhea (often with undigested food particles, Steatorrhea)

Possible additional signs (with prolonged disease):
Behavioral changes, Tremors
Seizures
Coma

Rare: Spontaneous bleeding

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26
Q

Exocrine pancreatic insufficiency (EPI) - Common bloodwork findings

A

Panel:
Hypocholesterolemia
Hypocalcemia (Total and ionized)
Hypophosphatemia (Rare)
Decreased B12, Increased Folate (less common)
Prolonged clotting times (Rare)

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27
Q

Exocrine pancreatic insufficiency (EPI) - Diagnosis (what is the gold standard)

A

Trypsin-like immunoreactivity (TLI)

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28
Q

Exocrine pancreatic insufficiency (EPI) - Treatment & Prognosis

A

Pancreatic enzyme extract - add with every meal\snack for life!

B12 Supplements (In case of deficiency)

Vitamin D analogs + Calcium supplements (in cases of clinical hypocalcemia) and taper off according to repeat blood tests

Excellent with normal life expectancy

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29
Q

Exocrine pancreatic insufficiency (EPI) - Reasons for treatment failure

A

Pancreatic extract ineffective\Poor quality\Owners fail to comply with giving extract according to instructions

B12 deficiency

Concurrent diseases: ARD, IBD, DM

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30
Q

How does dysbiosis affect bile acid metabolism? Specific treatments?

A

Dysbiosis can create secondary bile acids (which are harmless) into primary bile acids which are irritant to the GI - causing diarrhea

Colestid, Ursolit (Synthetic)

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31
Q

How would feces look like in cholestasis?

A

White (no stercobilirubin to give it color)

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32
Q

Clinical signs associated with liver disease - Causes for Hyperammonemia

A

Liver shunts (e.g. PSS, MVD)

Liver failure

B12 Deficiency

Arginine deficiency (Cat)

Congenital urea-cycle enzyme deficiency

Sepsis with urease positive urease-positive

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33
Q

Clinical signs associated with liver disease - For liver function to be affected - how much of the liver needs to be compromised?

A

70-80%

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34
Q

Clinical signs associated with liver disease - What causes vomiting in liver disease?

A

GI Ulcers caused by decreased metabolism of gastrin

Decreased detoxification activities

Hepatomegaly creating mechanical pressure on the GI

Portal hypertension

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35
Q

Clinical signs associated with liver disease - What causes Pu/Pd in liver disease

A

Decreased urea production

Hypercortisolemia

Due to behavioral changes (e.g. 2nd to hyperammonemia)

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36
Q

Clinical signs associated with liver disease - Hyperammonemia - Important clinical sign in cats

A

Hypersalivation

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37
Q

Clinical signs associated with liver disease - How can liver disease cause lower urinary tract signs (e.g. Pollakiuria, Stranguria, Hematuria)

A

Ammonium biurate crystals\uroliths

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38
Q

Clinical signs associated with liver disease - What causes Melena in liver disease

A

Hypergastrinemia

Coagulopathy

Portal hypertension

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39
Q

Clinical signs associated with liver disease - What causes white feces in liver disease

A

Cholestasis

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40
Q

Infectious diseases of the liver - DDs

A

Bacterial:
-Ascending infection from the GI (Cholangiohepatitis)
-Leptospirosis
-Mycobacteria
-Bartonellosis

Viral:
-Canine adenovirus
-FIP

Fungal:
-Aspergillosis
-Cryptococcosis

Parasitic:
-Leishmaniasis
-Neosporosis
-Toxoplasmosis.

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41
Q

Clinical pathology of the liver - CBC - Common findings

A

Non-regenerative anemia:
Anemia of inflammation\neoplasia

Regenerative anemia:
Bleeding (Coagulopathies, GI ulcers)
Hemolysis (e.g. Heinz-bodies)

Platelets:
Thrombocytopenia (Portal vein thrombosis, DIC)
Thrombocytopathy

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42
Q

Clinical pathology of the liver - Extra-hepatic causes for increase in liver enzymes

A

Reactive hepatopathy: Pancreatic\Biliary\GI Diseases

Muscle diseases (ALT from muscles)

Bone diseases

Growing animals (ALP) (B-ALP)

Drugs\Toxins (e.g. GC, Phenobarbital, Cycad)

Endocrinopathies (e.g. Cushing’s disease, Hypothyroidism, DM)

Vascular congestion (e.g. R-CHF)

Ischemia (e.g. Shock)

Cholestasis of sepsis (Cat).

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43
Q

Clinical pathology of the liver - What are the common patterns for muscle and liver damage using ALT,AST and CK?

A

Hepatic damage: ALT > AST

Muscle damage: AST,CK > ALT

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44
Q

Clinical pathology of the liver - ALP - Is a singular rise in ALP in a dog with no clinical signs or increase in additional liver enzymes requires further investigation? Why? and what about cats?

A

ALP Is non-specific and can increase from benign reasons: Hepatic nodular hyperplasia in older dogs, Overweight animals, Growing animals

In cats on the other hand - any increase in ALP is significant and is a marker for hepatic lipidosis

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45
Q

Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Drugs

A

Corticosteroids - ALP (+++), GGT (++), ALT (+), AST (+)

Barbiturates: ALP (++), GGT (+), ALT (+), AST (+)

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46
Q

Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - DM, Cushings disease

A

DM: ALP > ALT

Cushing’s disease: ALP (+++), GGT (+), ALT (+), AST (+)

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47
Q

Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Hypoxia

A

ALT (++), ALP (+), GGT (+), AST (+)

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48
Q

Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Muscle damage

A

AST (++), CK (+), ALT (+)

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49
Q

Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Hepatic lipidosis

A

ALP (+++), ALT (+), GGT (Normal)

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50
Q

Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Chronic hepatitis

A

ALT (+++), ALP (+ or Normal)

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51
Q

Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Cholangiohepatitis

A

GGT (+), ALT (+), ALP (+ or Normal)

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52
Q

Clinical pathology of the liver - What are the markers for liver function and how are they affected in liver failure?

A

Cholesterol - either hypercholesterolemia due to cholestasis, or hypocholesterolemia due to decreased production

Albumin - Hypoalbuminemia

Bilirubin - Hyperbilirubinemia

Glucose - Hypoglycemia

Urea - Decrease

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53
Q

Clinical pathology of the liver - What is the liver function that is usually affected last in liver failure?

A

Glucose

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54
Q

Clinical pathology of the liver - How is glucose affected in liver failure/PSS and what is the pathophysiology

A

Decrease (Hypoglycemia)

Liver failure - Decrease in gluconeogenesis, Increased insulin production

PSS - Glycogen storage decreases, response to glucagon decreases.

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55
Q

Clinical Pathology of the Liver - DDs For Hypoglycemia

A

Sepsis

Storage Diseases

Neoplastic

Addison’s disease

Polycythemia

Pancreatitis

Insulin overdose (e.g. for diabetics, Insulinoma)

Liver failure

Young - Fasting in puppies

Toy breeds

Xylitol

Tremors

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56
Q

Clinical pathology of the liver - Liver leakage enzymes (ALT/AST) are specific to liver damage in cats (as opposed to Extra-hepatic damage like Biliary tract/Pancreas/GI) - True/False

A

False

Because bile tract leakage enzymes in cats are not sensitive

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57
Q

Clinical pathology of the liver - Liver and biliary tract leakage enzymes are sensitive but not specific (True/False)

A

True

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58
Q

Clinical pathology of the liver - In clinically healthy dogs, a sole increase in ALT warrants further follow up but a sole increase In ALP doesn’t necessarily (True\False) - Why

A

True

ALT - Very specific to liver damage and could be an early sign for disease such as chronic hepatitis, neoplasia

Should invite for a follow up in a month for repeat bloodworks and possibly imaging

ALP - Not specific and can increase for many benign reasons, such as nodular hyperplasia, Growing animals, Steroids, Obesity etc.

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59
Q

Clinical pathology of the liver - Common Urinalysis findings in dogs and cats in liver failure

A

Isosthenuria (USG between 1.008 - 1.012)

Ammonium biurate crystal\uroliths

Bilirubinuria

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60
Q

Clinical pathology of the liver - Coagulation-related findings in liver disease

A

Thrombocytopenia

Thrombocytopathy

Prolonged PT/PTT

Decreased AT-3

Decreased fibrinogen

TEG/\EM: Hepatic disease can cause either hypo or hypercoagulability.

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61
Q

Liver failure\DIC - How to differentiate

A

D-dimer - raises in DIC (and less affected in liver failure)

Thrombocytopenia, Prolonged PT/PTT and decreased AT-3 can be found in both instances

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62
Q

Clinical pathology of the liver - Ammonia challenge test - What to give? What’s the sensitivity for detecting PSS? For detecting parenchymatic disease?

A

High protein meal \ Ammonium chloride

Acquired PSS - 80%

Congenital PSS - 90%-100%

Parenchymatic liver disease - 50%

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63
Q

Clinical pathology of the liver - Ammonia challenge test - Possible complication

A

Causing\worsening hepatic encephalopathy

64
Q

clinical pathology of the liver - Ammonia challenge test - What is the test most sensitive for?

A

PSS (congenital PSS the highest sensitivity)

65
Q

Clinical pathology of the liver - Bile acids challenge test - Sensitivity to PSS? To parenchymatic disease?

A

PSS - 90%-100%

Parenchymatic disease - 50%-70%

66
Q

Liver US - Highly sensitive and specific tool for detecting liver disease (True/False)

A

False

67
Q

Liver US - High velocity portal vein blood flows can signify what?

A

Liver shunt

68
Q

Liver US - low velocity portal vein blood flows can signify what??

A

Portal hypertension (e.g. due to decreased liver parenchyma in cirrhosis, Portal vein thrombosis)

69
Q

Liver radiography - Useful for what disease? 2 Useful methods to perform it

A

PSS

Contrast injection US Guided to Splenic vein

Contrast injection to Cranial Mesenteric vein during a surgical operation

70
Q

Liver US - What is it good for especially?

A

Detecting shunts

Detecting obstruction patterns

71
Q

What is the best imaging modality for detecting liver shunts

A

Angio-CT

72
Q

Liver FNA - What types of diseases is it most useful for?

A

Diffuse diseases: Such as vacuolar diseases (e.g. Hepatic Lipidosis), Diffuse neoplasia (Lymphoma)

73
Q

Liver Biopsy - “Tru-Cut” - 2 Main Contraindications

A

Hypocoagulation (bleeding state)

Ascites

74
Q

Liver biopsy through laparotomy - Main advantages as opposed to US-guided, and how to prepare for it, in terms of trying to prevent bleeding as much as possible

A

Better visualization

Larger samples

Larger quantity of samples

Samples from hard to reach location

Better control of bleeding

Vitamin K Supplementation, Plasma, Monitor PT/PTT

75
Q

Treating hepatic diseases - Hepatic encephalopathy (and explain the reasoning behind each element)

A

Fluids (Correcting hypoglycemia, hypokalemia and alkalemia => in order to prevent a catabolic state and further translocation of ammonia from the intestine to the blood stream)

Low-medium protein Diet (e.g. K\d, L\d) (No aromatic AAs and short-chain FAs which can act as neurotransmitters)

Lactulose: Osmotic laxative which decreases overall bacterial load, Promotes growth of bacteria which prefer to metabolize carbohydrates, lowers colonic pH and promotes production of ammonium over ammonia

Antibiotics: Ampicillin and\or Metronidazole (To lower Intestinal bacterial load)

Flumazenil (In depressed animals) or Gabapentin (In hyper animals)

Additional supportive hepatic treatment if necessary (e.g. anti-oxidants, Ursolit, Vitamin K supplement, L-carnitine in cats with hepatic lipidosis)

76
Q

Treating hepatic diseases - Portal hypertension

A

Low-sodium diet (to prevent systemic hypertension)

Diuretic: Spironolactone (First choice because of it being a K-sparing diuretic - not causing hypokalemia and potentially worsening hepatic encephalopathy

Furosemide (second choice)

Abdominocentesis (In case of ascites which leads to dyspnea).

77
Q

Treating hepatic diseases - Cholestasis (Non-obstructive) - Treatment

A

Treat underlying cause

Ursolit

78
Q

Treating hepatic diseases - Anti-oxident drugs

A

PO:
Alpha-tocopherol (vitamin E)
Thistle
SAMe

IV:
N-Acetylcysteine

79
Q

Treating Hepatic Diseases - Important instructions to to tell the owners when administering SAMe

A

Give on an empty stomach

80
Q

Treating hepatic diseases - Coagulopathy

A

Vitamin K supplements

Plasma\Full blood transfusion

81
Q

Treating hepatic diseases - Coagulopathy - Why is it important to give vitamin K as soon as possible when suspecting bleeding tendencies?

A

It takes 24-36h before it takes effect so give it first so you can do FNA\Biopsy the next day without needing to wait longer than necessary

82
Q

Treating Hepatic Diseases - Coagulopathy - Vitamin K toxicity is a danger in what animal and why?

A

Cats (Can cause Heinz-bodies anemia)

83
Q

Treating hepatic diseases - Cirrhosis/ Hepatic fibrosis - What is the most effective treatment? Why?

A

Find and treat the underlying issue causing the fibrosis (If possible)

Liver might still be able to regenerate

84
Q

Treating hepatic diseases - Copper storage disease - treatment options

A

Low copper diet (L\d)

D-Penicillamine (chelation

Zinc in diet (Competes with copper absorption)

85
Q

What is the most common liver disease in cats?

A

Neutrophilic cholangiohepatitis

86
Q

Neutrophilic cholangitis/cholangiohepatitis - Signalment, Possible cause, Clinical signs

A

Middle aged-old cats

Translocation of bacteria from the GI

Lethargy, Anorexia
Fever
Vomiting
Diarrhea
Jaundice

87
Q

Neutrophilic cholangitis/cholangiohepatitis - Classic CBC, Panel, US findings

A

Neutrophilia

Increased GGT

Increased ALT+-AST

Increased ALP

Hypercholesterolemia

Hyperbilirubinemia

Thickening of extra-hepatic biliary tract walls, Widening of biliary tract, thickening of gall bladder wall, Pus +- calculi in biliary tract

88
Q

Neutrophilic cholangitis/cholangiohepatitis - Cytology and biopsy findings, Treatment, Prognosis

A

Neutrophils + Bacteria (Send to C&S)

Antibiotics (4-6 Weeks. Treat for 1 week after enzymes normalize)
Anti-oxidants (e.g. NAC, SAMe)
Ursodiol
Anti-emetics
Appetite stimulant
Analgesia

Good. Recurrence is possible. Worse in case of gall bladder stones

89
Q

Lymphocytic cholangitis/cholangiohepatitis - Signalment, Possible Cause, Clinical Signs, Jaundice?

A

Middle age - old cats

Immune-mediated

Anorexia, Lethargy
Weight loss
Vomiting
Diarrhea
Jaundice

Less common: Ascites, lymphadenopathy, Hepatomegaly

90
Q

Lymphocytic cholangitis/cholangiohepatitis - CBC, Panel findings

A

Lymphopenia

Possible neutrophilia

Increased GGT

Increased ALT+-AST

Increased ALP

Hypercholesterolemia

Hyperbilirubinemia.

91
Q

Lymphocytic cholangitis/cholangiohepatitis - Biopsy, Treatment, Prognosis

A

Lymphocytic infiltrate (Mainly around portal zone)

Immunosuppression (GC +- additional Immunosuppression)
Anti-oxidants
Ursolit
GI support
Analgesia

Guarded

92
Q

Dogs/Cats - Which tend to have cholangitis (+/- hepatitis) and which tends to have hepatitis?

A

Dogs - Hepatitis

Cats - Cholangitis

93
Q

Chronic hepatitis in dogs - What is the best marker?

A

ALT

94
Q

Chronic hepatitis (Dog) - What is the gold standard for diagnosis

A

Histology

95
Q

How do you differentiate between a primary copper-associated chronic hepatitis and secondary copper-related hepatitis (Due to cholestasis, inflammation etc.)

A

Primary: Copper staining on histology revels aggregates of copper in the centrilobular area

Secondary: Aggregates are in the peri-portal area

96
Q

Copper-related chronic hepatitis - What are some common poster breeds of the disease?

A

Bedlington terrier, Labrador retriever, Dalmatian, WHWT

97
Q

Chronic hepatitis - Clinical signs

A

Lethargy, Anorexia

Weight loss

Vomiting , Diarrhea, Melena\Hematochezia\ Hematemesis

Pu/Pd

Jaundice

Ascites\Pleural effusion\Peripheral edema

Spontaneous bleeding

Hepatic encephalopathy

Hemolysis (Copper-associated chronic hepatitis)

98
Q

Copper-related chronic hepatitis - How soon to screen for the disease in a Bedlington Terrier

A

1 Year of age

99
Q

Copper-Related Chronic Hepatitis - 2 important diagnostic tests - for achieving diagnosis of copper storage disease and prognosis

A

Copper staining (Qualitative assessment)

Copper quantification (Achieved with biopsy taken through laparotomy)

100
Q

Breed-associated/Idiopathic chronic hepatitis - What are the 2 main processes going on in the liver?

A

Inflammation

Fibrosis

101
Q

Breed-associated/Idiopathic chronic hepatitis - 3 possible histological findings?

A

1) Moderate to severe lymphocytic infiltrate +- fibrosis. Eventually can progress to cirrhosis

2) Lobular dissecting hepatitis - Severe fibrosis cutting through the lobules with little to no inflammation

3) Reactive hepatopathy - Mild portal inflammation. Secondary process Indicative of an extra-hepatic pathology (e.g. Pancreatitis, Cholangitis, Enteritis)

102
Q

Breed-associated/Idiopathic chronic hepatitis - Signalment

A

Young-young adult dogs

103
Q

Breed-associated\Idiopathic chronic hepatitis - Diagnosis, Treatment

A

Biopsy (Also rule out infection, toxins, copper-storage disease)

If inflammation is present on histology - worth trying GC +- 2nd Immunosuppression (e.g. Cyclosporine, Azathioprine, Cellcept)

Diet for liver disease (e.g. L\d)

Hepatic support:
Anti-oxidants
Ursodiol
Vitamin K supplements

GI support (e.g. anti-emetics, PPI, appetite stimulant)

Treat complications: Hepatic encephalopathy, Portal hypertension.

104
Q

Breed-associated/Idiopathic chronic hepatitis - Prognosis

A

If there is still inflammation on biopsy - Regeneration might be possible and worth a try

In general: MST of 1.5-2 years from diagnosis.

-Cirrhosis on histology: MST of 1 month

-Ascites: MST of 1 month

-Lobular dissecting hepatitis: MST of 1 month

105
Q

Idiopathic canine acute hepatitis - What is the main cell infiltrate and what is the treatment

A

Neutrophils

Hepatic and GI support + Antibiotics

106
Q

Vascular anomalies of the liver - Congenital Porto-systemic shunts - What is common in what breed sizes: Extra/Intra-hepatic shunts, Large/Small breeds dogs

A

Small breeds - Extra hepatic

Large breed - Intra hepatic

107
Q

Vascular anomalies of the liver - Congenital Porto-systemic shunts - Classic history & clinical signs. Also what is the typical onset of clinical signs

A

Growth retardation (smaller than expected/littermates)

Pu\Pd - due to decreased urea production, Hypercortisolemia, Psychogenic polydipsia due to hepatic encephalopathy

Intolerance to anesthesia (e.g. Long recovery period post neutering) - decreased hepatic metabolism of anesthetic drugs

Neurological signs (e.g. Behavioral changes, Star-gazing, Head pressing) - due to hepatic encephalopathy

Pollakiuria\Stranguria\Hematuria - due to ammonium biuate stones

Onset - usually up to 6 months of age

108
Q

Vascular anomalies of the liver - Congenital Porto-systemic shunts - Common complications include ascites and portal hypertension (True/False)

A

False

PSS leads to increased blood velocity through the portal vein, as opposed to other hepatic diseases (e.g. cirrhosis, NCPH)

109
Q

Vascular anomalies of the liver - Congenital Porto-systemic shunts - Common lab findings

A

Mild non-regenerative anemia

Normal to mild increase in liver enzymes

Hypocholesterolemia

Hypoalbuminemia

Hypoglycemia

Low urea

Increased bile acids

Hyperammonemia

110
Q

Vascular anomalies of the liver - Congenital Porto-systemic shunts - Definitive diagnosis

A

US (80-100% Sensitivity)

Contrast X-ray

Angio-CT (Gold standard)

111
Q

Vascular anomalies of the liver - Congenital Porto-systemic shunts - Treatment

A

Medical:
Low protein diet (e.g. L\d or k\d)

Lactulose

Antibiotics

Anti-oxidants (SAMe)

Surgical:
Closer of the shunt with:
Surgical knot \ Cellophane \ Stent (Mainly for intra-hepatic shunts) \ Ameroid constrictor)

**It is recommended to first stabilize the animal with medical treatment for 2-3 weeks and then perform surgery.

112
Q

Vascular anomalies of the liver - Congenital Porto-systemic shunts - Surgical procedure success rate and possible complications

A

65-85% (Better in extra-hepatic shunts)

Complications:
-Acute portal hypertension post-surgery
-Seizures
-Incomplete closure of the shunt
-Hepatic encephalopathy

113
Q

Vascular anomalies of the liver - Multiple acquired shunts - Signalment, Clinical signs, Diagnosis

A

Older dogs.

GI signs

CNS signs (Hepatic encephalopathy)

Ascites (Portal hypertension)

Jaundice

Pu\Pd

Abdominal US

114
Q

Vascular anomalies of the liver - Multiple acquired shunts - Treatment

A

Treat primary hepatic disease if possible

Medical supportive treatment only:
GI support
Livet diet
Anti-oxidant
Ursodiol
Treat hepatic encephalopathy (i.e. lactulose, Antibiotics)
Treat portal hypertension (i.e. Spironolactone

Cannot be fixed surgically

115
Q

Vascular anomalies of the liver - Multiple acquired shunts - Cause

A

Severe chronic liver disease which leads to portal hypertension (e.g. NCPH, Arteriovenous malformation, Idiopathic chronic hepatitis)

116
Q

Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Pre-sinusoidal/Sinusoidal/Post-sinusoidal anomaly

A

Pre-sinusoidal\Sinusoidal

117
Q

Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Signalment

A

Small breed dogs & Cats

118
Q

Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Diagnosis

A

History and clinical signs indicative of shunting (GI signs, CNS signs, Dysuria, Pu\Pd)

Can be milder to-non clinical as opposed to cPSS. Also with no signs of portal hypertension!

Blood results that might suggest shunting (previously discussed, such as hypocholesterolemia, Hypoalbuminemia, decreased urea, Hyperammonemia) - usually to a milder degree than those found in cPSS

Gold standard - a combination of the following:
1) No evidence of shunts on US \ angio-CT
2) Histology - Underdeveloped portal veins + abundance of portal arterioles

119
Q

Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Pathogenesis

A

Microscopic intra-hepatic connections between portal veins and systemic circulation

120
Q

Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Treatment

A

Main treatment - Low protein diet

GI\Hepatic encephalopathy medical treatment if further indicated

121
Q

Portal vein hypoplasia with portal hypertension (Non-cirrhotic portal hypertension) - Pathogenesis

A

Hypoplasia of the portal system, but as opposed to HMD - Does cause portal hypertension - leading to both HE and ascites

No evident fibrosis/cirrhosis

122
Q

Portal vein hypoplasia with portal hypertension (Non-cirrhotic portal hypertension) - 2 main clinical signs

A

CNS signs (hepatic encephalopathy)

Ascites

123
Q

Portal vein hypoplasia with portal hypertension (Non-cirrhotic portal hypertension) - Treatment, Prognosis

A

Supportive:
Treat HE (i.e. Lactulose, Antibiotics, Low-protein diet +- Gabapentin/Flumazenil)

Treat ascites (Low sodium diet, Spironolactone, Abdominocentesis if indicated)

Prognosis: Poor - MST 2 years

124
Q

Post-sinusoidal diseases - Arteriovenous malformation - Pathology

A

Fistula between hepatic artery and portal vein

125
Q

How can you differentiate between pre and post-sinusoidal portal hypertension based on the abdominal effusion

A

Based on the TS of the effusion:

Pre-sinusoidal: Transudate (<3 g\dL)

Post-sinusoidal - Modified transudate (~3 gr/dL)

126
Q

Post-sinusoidal diseases - Arteriovenous malformation - Diagnosis

A

Angio-CT

127
Q

Post-sinusoidal portal hypertension - Etiologies

A

Arteriovenous malformation

R-CHF

Tamponade

Budd-Chiari syndrome

Thrombus in the Vena Cava

128
Q

Post-sinusoidal diseases - Best diagnostic tools

A

CT

R-CHF \ Cardiac Tamponade - US

129
Q

Vacuolar hepatopathy - Common etiologies

A

Hypothyroidism

Cushing’s disease

DM

Tetracycline

Obesity

130
Q

Hepatic lipidosis (Cat) - Signalment, Classic history

A

Middle-aged-old cats

Overweight cat that hasn’t eaten for a few days (2-7 days) or lost weight lately

131
Q

Hepatic lipidosis (Cat) - Pathogenesis

A

Cats are obligatory carnivores and when they become anorexic, they stop getting essential amino acids and fatty which are necessary for fat metabolism:

-L-Carnitine deficiency: responsible for transporting fatty acids to the mitochondria for beta-oxidation and transport from the hepatocytes to the blood stream

-Apoprotein deficiency: VLDL production decreases - reducing transport of fat from the liver to the blood stream

Overweight cats: abundant amount of fat that can be transported to the liver (Main reason for the classic signalment of the disease

Diabetogenic hormones increase and insulin secretion decreases

HSL levels Increase and LPL levels Decreases

132
Q

Hepatic lipidosis (Cat) - Clinical signs

A

Anorexia, Lethargy, GI signs (e.g. Vomiting, Diarrhea), CNS signs (e.g. Aimless walking, Star gazing, Seizures), Jaundice

133
Q

Hepatic lipidosis (Cat) - Classic bloodwork findings

A

Mild non-regenerative anemia

ALP (+++), ALT (++). GGT Normal

Hypocholesterolemia (Liver failure) or hypercholesterolemia (Cholestasis)

Hypoalbuminemia

Hyperbilirubinemia

Decreased urea

Hyperglycemia (Hypoglycemia less common)

High ammonia levels

Low B12

134
Q

Hepatic lipidosis (Cat) - Diagnosis (Gold standard)

A

FNA of the liver showing hepatocytes with vacuolar changes

135
Q

Hepatic lipidosis (Cat) - Treatment, Prognosis

A

Treat underlying cause (i.e. Pancreatitis, Cholangiohepatitis)

Feeding (The most crucial principal). Mostly done through an esophageal tube. High protein diet (Some protein might be necessary in cases of hepatic encephalopathy)

Liver support:
L-Carnitine supplement
Anti-oxidant
Vitamin B1 supplement (Thiamine)
Vitamin K supplement
Vitamin B12 supplement
*Ursodiol is contraindicated

GI support (e.g. anti-emetics, Pro-motile, Appetite stimulant)

Treat hepatic encephalopathy if present (e.g. Lactulose, Antibiotics, Gabapentin/Flumazenil)

65-90% - depending on the primary cause. First 24-48h after feeding has started is the most crucial due to refeeding syndrome

136
Q

Hepatic lipidosis (Cat) - Possible life threatening complication when starting to treat hepatic lipidosis

A

Refeeding syndrome:
Hypokalemia
Hypomagnesemia
Hypophosphatemia
Hypoglycemia
Low Thiamine levels

Can cause GI signs, CNS signs, Arrhythmias and can lead to death

137
Q

Give examples for drugs that can cause hepatotoxicity (6)

A

Acetaminophen

Carprofen (Idiosyncratic)

Phenobarbital

Tetracyclines

Ketoconazole

TMS

138
Q

Mucocoele - Predisposing diseases\etiologies

A

Hypothyroidism

Cushing’s disease

Hypertriglyceridemia

139
Q

Mucocoele - Treatment

A

2 Approaches:

Surgical - Cholecystectomy (Removal of the gallbladder) - Considered the preferred approach in order to avoid risk of bile peritonitis

Medical - Ursodiol, Anti-oxidant, GI support and analgesia if indicated
Antibiotics if indicated.

140
Q

Mucocoele - Possible complications

A

Cholangitis

Gallbladder rupture and bile peritonitis

141
Q

Copper-related chronic hepatitis - Age of onset

A

Bedlington Terrier - as soon as 1 year of age

Other breeds - middle-age adults

142
Q

Vascular anomalies of the liver - Congenital Porto-systemic shunts - commonly causes hyperbilirubinemia (True\False)

A

False

PSS does not cause cholestasis and therefore does not cause hyperbilirubinemia

143
Q

When is it indicated to perform a Bile Acid test? When is it indicated to perform a Post-Prandial Bild Acid test? What result is considered abnormal\elevated?

A

Animal with GI signs and decreased liver functions +- elevated liver enzymes that is not Icteric!

If fasting bile acids levels are normal

> 25 micromol\L for both tests

144
Q

Mucocele - Treatment

A

Conservative:
Low fat diet
Ursodiol
Antioxidants (e.g. SAMe / Thistle)
Antibiotics

Surgical: Cholecystectomy

145
Q

GGT Elevation - Which organs should Be suspected to be involved?

A

Biliary tract

Pancreas

Small Intestine

146
Q

What is the mean age for copper-associated chronic hepatitis in Labradors?

A

7 Years

147
Q

Copper-associated chronic hepatitis - common breeds (5)

A

Bedlington terrier, Labrador retriever, WHWT, Doberman Pinscher, Dalmatian

148
Q

Chronic hepatitis - diagnosis

A

Signalment & Clinical signs

Blood works (Most common - elevation in ALT, other liver & bile enzyme elevations possible, Changes in Liver functions (Chol, Alb, Bili, Glu, Urea, Bile Acids, Ammonia, Coagulation factors)

Urinalysis (Isosthenuric USG, evidence of ammonium biurate crystals)

Abdominal US (Liver size, shape, echogenicity, Evidence of Portal hypertension)

Screening for infectious diseases (e.g. Leptospira, Leishmaniasis, Toxoplasmosis, Bartonella, Mycobacterium, Aspergillosis)

Liver biopsy, copper staining & Quantification

Culture and sensitivity for bacteria and mycology.

149
Q

Copper-associated chronic hepatitis - Treatment

A

D-Penicillamine

Zinc supplementation

Low copper diet

Anti-oxidants

150
Q

Chronic Hepatitis - Common Breeds (5)

A

Labradors, Doberman, Dalmatian, Cocker Spaniel, WHWT

151
Q

Chronic hepatitis - Treatment

A

Treat underlying causes

Supportive treatment (e.g. GI Protectants, anti-emetics, Apatite stimulant)

Liver diet

Anti-oxidant

Ursodiol

Ascites => Abdominocentesis, Spironolactone, Low sodium diet

Hepatic encephalopathy => AB + Lactulose

Prednisone +- Immunosuppressant (If indication of active inflammation on histology)

Treat for copper-accumulation (if indicated)

152
Q

In which species (Dog/Cat) Is GGT elevation more specific to biliary tract disease

A

Cats

153
Q

Neutrophilic Cholangitis - Treatment

A

Treat underlying cause

Supportive treatment

ABs (C&S Preferred) for a period of 4-6 weeks

Ursodiol

Anti-oxidants

If recurrent episodes and Lympho-plasmacytic cholangitis suspected - consider glucocorticoids\Immunosuppressant.

154
Q

Destructive cholangitis - Common histological findings (3)

A

Ductopenia

T-Cell Predominate - Infiltrate to duct walls

Lipograuloma

155
Q

What is the algorithm of analyzing cytologic samples?

A

1) Is the cellularity low\moderate\high

2) Is the slide Inflammatory?

3) What is the dominant cell type - Epithelial \ Mesenchymal \ Round Cell

4) What is the morphology of the cells - Hypercellularity\Anisocytosis\Anisokaryosis || Prominent Nucleoli\Multiple Nucleoli\Vacuolation\Basophilic Staining\Mitosis\Cytophagia (Not Macrophages)\Cells in wrong location\Nuclear molding

156
Q

EPI - Most dogs have TLI levels of…?

A

> 2.5microgram\L

Doctor of Veterinary Medicine (Work in progress) (17 decks)

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