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Sem 6: SAM 2 > Liver Disorders > Flashcards

Liver Disorders Flashcards

1
Q

List indicators of decreased liver function that can be seen on bloodwork

A

- Hypoalbuminemia
- Hypocholesterolemia with end stage liver disease
- Hypoglycemia (when 75% loss of liver function)

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2
Q

List the cholestatic enzymes

A

ALP and GGT

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3
Q

What increased liver enzymes are always significant in cats?

A

ALT and ALP

Very short half life in cats, if elevated indicates acute liver injury

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4
Q

What drugs can cause an increase in ALT?

A
  • Phenobarbitol / Barbituates
  • Corticosteroids
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5
Q

What is different with ALP in cats vs dogs?

A
  • Cats lack steroid induced ALP isoenzyme, steroid hepatopathy only happens in dogs!!!
  • ALP is always significant in cats, very short half life
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6
Q

What can be seen on bloodwork with post hepatic jaundice?

A

- Hyperbilirubinemia
- Hypercholesterolemia
- Increased ALP (higher than ALT)
- Increased GGT
- Mild to mod increases in ALT, AST

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7
Q

When is hypoglycemia seen with liver disease?

A

when 75% of hepatic function is lots

chronic, end stage liver dz

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8
Q

At what times, pre and post prandial should bile acids be measured?

A

measure pre and 2 hours post prandial

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9
Q

Increases in serum bile acid concentration can be seen with?

A

- Hepatic dysfunction
- Portosystemic shunts
- Cholestasis

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10
Q

When would running a bile acids test be considered unnecessary?

A

Don’t run bile acids if BILIRUBIN is high on bloodwork …. you can assume bile acids is high if tbili is high

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11
Q

How is ammonia produced in the GI tract?

A
  • Urease producing bacT
  • Bacterial protein degradation
  • Enterocyte conversion of glutamine to glutamate
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12
Q

How is ammonia detoxified into urea?

A
  • Liverrr converts ammonia to urea
  • Also detoxified by conversion of glutamate to glutamine in muscle, brain, kidney, and liver
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13
Q

What are causes of increased ammonia?

A

- PSS
- Hepatic failure
- Urea cycle deficiency (arginine deficiency in anorexic cats

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14
Q

What is an important consideration when collecting a blood sample to measure ammonia levels?

A
  • Have to run sample ASAP
  • Result will be falsely elevated if left sitting
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15
Q

List CS of liver disease

A
  • Jaundice
  • Ascites
  • Anemia
  • PU/PD
  • Vomiting / Diarrhea (Extra GI cause of SI diarrhea)
  • Coagulopathy
  • Hepatic encephalopathy
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16
Q

Clinical icterus is visible when the bilirubin concentration exceeds ________

A

2-3 mg/dL

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17
Q

What are common causes of ascites secondary to liver disease?

A
  • Intrahepatic portal venous hypertension MOST COMMON
  • Reduced albumin & ↓ oncotic pressure
  • RAAs activation, Na+ and water retention worsens ascites
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18
Q

When is abdominocentesis indicated for treating ascites secondary to chronic liver disease?

A
  • Reserved for patients with discomfort due to the ascites or dyspnea / respiratory distress
  • Repeated ABDcentesis can further worsen protein loss
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19
Q

What is the treatment protocol for a patient presenting with ascites secondary to chronic liver disease?

A
  • Spironolactone (Aldosterone antagonist, K+ sparing, diuretic of choice)
  • Low Na+ diet
  • Abdominocentesis only if uncomfortable or in respiratory distress, avoid repeated taps
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20
Q

Which of the following clotting factors is not produced by the liver?

A. Factor IX
B. Factor III
C. Factor VIII
D. Factor X

A

C. Factor VIII

Liver makes all clotting factors EXCEPT Factor VIII

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21
Q

What anti-clotting proteins are produced by the liver?

A
  • AT III
  • Protein C
  • Protein S
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22
Q

Why is the assessment of bleeding risk in liver disease patients so challenging?

A
  • Hypo, hyper, or normocoagulable states
  • Liver produces clotting factors (hypocoagulable state), but also anti-clotting factors (hypercoagulable state)!
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23
Q

What is the treatment protocol for patients with coagulopathies secondary to liver disease?

A
  • Fresh frozen plasma, pRBCs, whole blood
  • Vitamin K
  • DDAVP
  • Indicated when spontaneous or procedure induced bleeding, no evidence to recommend prophylactically
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24
Q

How is the GI tract affected by hepatic disease?

A
  • Risk factor for GI ulceration and bleeding
  • Splanchnic congestion and poor blood flow may contribute
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25
Q

What is the treatment protocol for a patient with CS of GI bleeding secondary to hepatic disease?

A
  • Omeprazole
  • Sulcralfate

AVOID ulcerogenic meds like NSAIDS and Pred

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26
Q

How can liver disease lead to PU/PD?

A
  • Low Urea (medullary washout)
  • Thirst (manifestation of hepatic encephalopathy)
  • Excess cortisol secretion
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27
Q

How can severe liver disease result in secondary infections?

A
  • Results in immune dysfunction, increased risk of bacterial translocation, endotoxemia, septic peritonitis if biliary rupture
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28
Q

What are the 3 clinical scenerios which can cause hepatic encephalopathy?

A

- Acute severe total hepatic failure
- Chronic HE (most commonly from PSS)
- Deficiency in essential AAs in CATS & development of hepatic lipidosis (IMPT!)

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29
Q

True or False: Seizures are the most common clinical sign seen with hepatic encephalopathy

A

FALSE - rarely have seizures

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30
Q

What CS can be seen with hepatic encephalopathy?

A
  • Episodic with fluctuations between stages
  • Staring, decreased mentation
  • Ataxic
  • Head pressing
  • Blindness
  • Rarely seizures
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31
Q

What are precipitating factors for Hepatic Encephalopathy?

A
  • GI bleeding
  • Excessive protein intake
  • Infection
  • Drugs: Benzos, opioids
  • Hyponatremia, Hypokalemia
  • Metabolic alkalosis
  • Renal failure
  • Dehydration
  • Constipation
  • Overzealous use of Furosemide
32
Q

What is the treatment protocol for acute hepatic encephalopathy?

A
  • ID and remove underlying cause
  • Levetiracetam 1st line for seizures
  • Mannitol or Hypertonic saline for tx of increased ICP
  • Warm water enema followed by lactulose retention enema
33
Q

What is the treatment protocol for chronic hepatic encephalopathy?

A
  • Soy based (high protein) diet
  • Lactulose

Antibiotics NOT indicated for long term use

34
Q

What medication can be used to decrease blood ammonia levels in patients with hepatic encephalopathy?

A

- Lactulose
- Acidifies colon to convert ammonia into non-absorbable, ionized form
- Increases colonic motility which decreases ammoniagenic colonic microflora
- Decreases #’s of urease producing bacteria in lower GI tract

35
Q

Clinical signs of acute liver failure are visible when ___________

A

> 70% of liver function is lost

36
Q

What blood work changes can be seen with acute liver failure?

A
  • Hyperbili
  • Decreased BUN, Albumin, Cholesterol, etc
  • PT > 1.5x the upper reference range
  • +/- hepatic encephalopathy
37
Q

What is the treatment protocol for a patient presenting with evidence of acute hepatitis?

A
  • Neutraceuticals (Denamarin/SAMe)
  • Gastroprotectants like Omeprazole
  • IVFT
  • Vitamin K (for coagulopathies)
  • Abx ONLY if evidence of infection!
  • Treat HE
38
Q

What drugs are most associated with idiosyncratic hepatotoxicosis?

A
  • Carprofen
  • Methimazole
  • Diazepam
  • Sulfonamides
  • Mitotane
  • Zonisamide

(occurs even at standard doses)

39
Q

What drugs are most associated with dose dependent hepatotoxicosis?

A
  • Acetaminophen
  • Phenobarbital
  • Aflatoxin
  • Azathioprine
  • CCNU
  • Azole antifungals
  • Xylitol
40
Q

Why are cats more sensitive to acetaminophen toxicity than dogs?

A

Glucuronyl transferase deficiency, inability to convert to non-toxic metabolite

41
Q

What clinical signs can be seen in cats with acetaminophen toxicosis?

A
  • Cyanosis
  • Pale to muddy brown MM’s
  • Hematuria and hemoglobinuria (AKI)
  • Respiratory distress (hypoxia)
  • Facial or paw edema
  • Icterus
  • Hepatic encephalopathy
  • CV shock
  • Death

(CS of hemolytic anemia)

42
Q

What is the treatment protocol for a patient presenting with evidence of acetaminophen toxicity?

A
  • N-Acetylcysteine / NAC (1st line Antidote of choice) using a 0.22 um filter
  • Supportive care
  • Transition to oral Denamarin once stable
43
Q

What parasitic fluke is a differential for infectious liver disease in dogs?

A
  • Heterobilharzia americana

Results in granulomatous inflammation of the intestinal wall and/or chronic hepatic fibrosis

44
Q

How is infectious liver disease due to Heterobilharzia americana treated?

A
  • Praziquantel and Fenbendazole
45
Q

How is infectious liver disease due to suspect Heterobilharzia americana diagnosed?

A
  • Fecal PCR is best
  • eggs in Fecal smear or float
  • Biopsy from liver or GI tract
46
Q

What is reactive hepatopathy?

A

Liver damage secondary to disease elsewhere

(GI, pancreas, heart, anemia, endocrine disease)

47
Q

Define vaculolar hepatopathy

A

Liver syndrome where hepatocytes become swollen with fat, glycogen, or water

Most common secondary metabolic hepatopathy in dogs and cats

48
Q

List causes of vacuolar hepatopathy due to glycogen accumulation

A
  • Steroid hepatopathy DOGS only
  • Vacuolar hepatopathy in scottish terriers
  • Cobalamin deficiency in dogs
  • Secondary to hepatic insult from another disease process
49
Q

List causes of vacuolar hepatopathy due to fat accumulation

A
  • Feline hepatic lipidosis
  • Aflatoxin in dogs
  • Hypervitaminosis A in cats
  • Familial hyperlipidemia
  • Secondary to endocrine disease (HypoT, HyperT (occasionally), DM)
50
Q

What is a common cause of liver disease in scottish terriers?

A

Progressive vacuolar hepatopathy associated with hepatocellular carcinoma

51
Q

What is cirrhosis?

A
  • End stage chronic hepatitis
  • Occurs when substantial architectural distortion, fibrosis, and portal hypertension are present
52
Q

What is needed to definitively diagnose a patient with chronic hepatitis?

A
  • Biopsy required, laproscopic is best

Can’t diagnose chronic hepatitis with FNA!!

53
Q

What is the treatment protocol for a patient with chronic hepatitis?

A
  • Hepatoprotectants (Denamarin/SAMe)
  • Immunosuppressive trial with Cyclosporine only after biopsy and histological evidence to R/O neoplasia… used to differentiate immune-mediated CH from idiopathic CH
54
Q

How can you differentiate immune-mediated chronic hepatitis from idiopathic chronic hepatitis?

A
  • Requires an immunosuppressive trial with Cyclosporine to differentiate (only done after biopsy results)
55
Q

What are causes of Copper storage disease?

A
  • Altered copper excretion in bile
  • Excessive dietary intake
  • Or both
56
Q

What dog breed is overrepresented with Copper Storage disease?

A

- Bedlington terriers
- Doberman
- Dalmation
- Labs

57
Q

How is Copper storage disease diagnosed?

A
  • Biopsy required for definitive diagnosis
  • Rhodanine staining needed for copper
  • Copper quantification analysis from biopsy
  • Centrilobular copper indicates primary copper dz
  • Periportal copper indicates secondary copper dz
58
Q

What is the treatment protocol for patients with copper storage disease?

A
  • Penicillamine: Copper chelating drug of choice
  • Denamarin / SAMe + other neutraceuticals
  • Copper restricted diet lifelong

(add GI protectants due to GI side effects from Penicillamine)

59
Q

What is the most common cause of hepatobiliary disease in cats?

A

Hepatic lipidosis

60
Q

List secondary causes of hepatic lipidosis in cats

A
  • DM
  • Pancreatitis
  • GI disease
  • Renal failure
  • Neoplasia
  • Inflammatory hepatobiliary disease
61
Q

What is a primary cause of hepatic lipidosis in cats?

A

Obese, anorexic cats

(Primary is less common, secondary more common)

62
Q

What is hepatic lipidosis?

A
  • Accumulation of excessive triglycerides resulting in impairment of liver function and intrahepatic cholestasis
63
Q

Why are cats more prone to hepatic lipidosis than dogs?

A
  • Cats are carnivores, dependent on lipid and protein metabolism
64
Q

What clinical signs can be seen in cats with hepatic lipidosis?

A
  • CS typical of ACUTE liver failure
  • V/D
  • Hepatic encephalopathy
  • Palpable hepatomegaly
  • Jaundice
  • Recent weight loss
  • Cervical ventroflexion
65
Q

What bloodwork findings are seen with hepatic lipidosis?

A
  • High ALP with normal GGT if primary cause
  • High ALP with High GGT if secondary cause
  • Hypokalemia and Hypophosphatemia (poor prognostic indicator)
  • Mild hypoalbuminemia
  • +/- coagulopathies
66
Q

How is hepatic lipidosis diagnosed?

A
  • Definitive diagnosis made with biopsy but rarely necessary or recommended (cats usually really sick)
  • Usually diagnosed on FNA/cytology (only FNA liver AFTER giving Vitamin K)

Note: Liver biopsy only recommended if failure to improve w treatment or if suspect underlying hepatic disease

67
Q

What is the treatment protocol for cats with hepatic lipidosis?

A
  • Nutritional support is mainstay, tube feeding if needed
  • High protein, low carb diet
  • Increase feedings by 25-30% (at the max) per day to AVOID REFEEDING SYNDROME
  • Monitor potassium and phosphorus

(+ Antiemetics, prokinetics, hepatoprotectants, Vitamin K, Cobalamin)

68
Q

What is the prognosis for cats with hepatic lipidosis?

A
  • Good if survives initial 96 hours and rapidly treated
  • Can take months for cats to eat, requires long term feeding tube
  • Hypokalemia and Hypophosphatemia are poor prognostic indicators
69
Q

What electrolyte abnormalities can be seen with hepatic lipidosis?

A
  • Hypokalemia and Hypophosphatemia

(poor prognostic indicators)

70
Q

How is hepatocutaneous syndrome diagnosed?

A
  • Biopsy showing Parakeratotic hyperkeratosis and classic red, white and blue appearance
  • Swiss cheese or honeycomb appearance on liver ultrasound
  • Decreased plasma AA’s (hard to test)
71
Q

How is hepatocutaneous syndrome treated?

A
  • AA supplementation
  • Zinc + EFAs + egg yolks
  • High protein diet
  • Hepatoprotectants
  • Treat skin lesions

**(Avoid corticosteroids / Prednisone.. risk of precipitating DM)

72
Q

What is the prognosis for a patient diagnosed with hepatocutaneous syndrome?

A

Poor prognosis, 1-3 months

73
Q

What is the most common cause of acquired PSS?

A
  • Secondary to chronic portal hypertension from hepatic fibrosis/cirrhosis
74
Q

How is an acquired PSS diagnosed?

A

Doppler ultrasound of liver showing decreased velocity of portal vein blood flow or hepatofugal (backward) blood flow

75
Q

What test is most useful in differentiating between a PSS and microvascular dysplasia?

A
  • Protein C
  • Normal Protein C with Microvascular dysplasia

(SASx: protein C > 70% for MVD)

76
Q

FNA of the liver is a good method in diagnosing which conditions?

A
  • Hepatic lipidosis
  • Vacuolar hepatopathy
  • Round cell neoplasia
  • Rarely Toxoplasma or Leishmania

(NOT used to diagnose chronic hepatitis or copper hepatopathy.. biopsy required)

77
Q

What condition results in a swiss cheese or honeycomb appearance on ultrasound of the liver?

A

Hepatocutaneous syndrome

Sem 6: SAM 2 (34 decks)

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