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Year 1/2 > Digestion & Metabolism 2: Canine Hepatic Dz > Flashcards

Digestion & Metabolism 2: Canine Hepatic Dz Flashcards

1
Q

what 2 MAIN breeds are PREDISPOSED for HEPATIC DZ?

A
  1. WEST HIGHLAND TERRIER
  2. SKYE TERRIER
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2
Q

CHRONIC hepatitis…

LIKELY etiology?

signalment?

diagnosis tends to be made through… + 2 others

A

LIKELY etiology = IMMUNE-MEDIATED

signalment = MIDDLE-AGED FEMALES

diagnosis = tends to be from BLOODWORK with LIVER ENZYME ABNORMALITIES, +…
1. ULTRASOUND
2. BIOPSY

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3
Q

in EARLY CHRONIC HEPATITIS, on ABDOMINAL US, expect liver to be _____/_____ & in LATE CHRONIC HEPATITIS, expect liver to be _____/_____

A

HYPERECHOIC/LARGE, HYPOECHOIC/SMALL

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4
Q

what 2 biopsy findings should we expect in CHRONIC hepatitis?

A
  1. INFLAMMATION (lymphocytic, plasmacytic)
  2. HEPATOCELLULAR APOPTOSIS or NECROSIS
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5
Q

TREATMENT for CHRONIC HEPATITIS…

overall, aims to do what?

2 examples?

why is it important to determine if ANY treatment is necessary?

A

overall = AIMED AT MODULATING INFLAMMATION through IMMUNOSUPPRESSANTS

2 examples?
1. CORTICOSTEROIDS
2. CYCLOSPORINE

important to know if ANY tx necessary because STEROIDS CAN SOMETIMES CAUSE WORSE SIDE EFFECTS THAN DISEASE ITSELF

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6
Q

overall, prognosis for CHRONIC HEPATITIS IS ____

but once HEPATIC ____ present, then prognosis becomes ____, can see this on bloodwork….

once ____ develops, the prognosis becomes _____

A

VARIABLE, so many ranges of CHRONIC HEPATITIS

once HEPATIC FAILURE present, then prognosis becomes GUARDED –> can see DECREASED LIVER FUNCTIONAL PARAMETERS (ABC GLUCOSE)

once CIRRHOSIS (END-STAGE LIVER DZ) develops, prognosis becomes GRAVE

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7
Q

ALT/AST vs. ABC GLUCOSE?

A

ALT/AST = LIVER DAMAGE ENZYMES, TELL YOU NOTHING ABOUT LIVER FUNCTION

ABC GLUCOSE = LIVER FUNCTIONAL PARAMETERS

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8
Q

many breeds that develop CHRONIC HEPATITIS are also at risk of developing WHAT?

give 3 of these breeds

A

also at risk of developing INCREASED HEPATIC COPPER

3 breeds?
1. BEDLINGTON TERRIER
2. WESTIE
3. SKYE TERRIER

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9
Q

BEDLINGTON COPPER STORAGE DZ…

origin/pathophysiology? (3)

in CERTAIN BREED, presence of INCREASED HEPATIC COPPER leads to ____ ____

A

origin?
1. inherited as an AUTOSOMAL RECESSIVE trait in BEDLINGTON TERRIERS

  1. protein that NORMALLY excretes COPPER INTO BILE NO LONGER WORKS, so COPPER STAYS IN HEPATOCYTES
  2. causes INFLAMMATION, NECROSIS, FIBROSIS

in BEDLINGTON TERRIERS, INCREASED HEPATIC COPPER leads to development of CHRONIC HEPATITIS

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10
Q

2 diagnostics for INCREASED COPPER in CHRONIC HEPATITIS?

what do we expect to SEE in both?

A
  1. LIVER BIOPSY
    –> findings consistent with CHRONIC HEPATITIS
    –> COPPER STAINING primarily around CENTRILOBULAR REGION (around central vein)
  2. COPPER QUANTIFICATION
    –> copper >1,000 ug/g DRY WEIGHT
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11
Q

2 treatment options for INCREASED COPPER in CHRONIC HEPATITIS?

when is each treatment INDICATED?

A
  1. LOW COPPER DIET
    –> indicated when HEPATIC COPPER > 600 ug/g DRY WEIGHT
  2. COPPER CHELATION via D-PENICILLAMINE that BINDS COPPER so it can be EXCRETED
    –> indicated when HEPATIC COPPER > 1,000 ug/g DRY WEIGHT
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12
Q

CHOLANGITIS/CHOLANGIOHEPATITIS….

____ > ____

usually has a ____ component to the inflammation

what is the first and second MOST COMMON BACTERIAL causes?

2 treatments?

when is Sx indicated?

A

CATS > DOGS

usually has NEUTROPHILIC inflammation

bacterial causes?
1. E. COLI MOST COMMON
2. ENTEROCOCCUS second common

3 treatments?
1. ANTIBIOTICS
2. SUPPORTIVE THERAPY

Sx indicated if BILE DUCT OBSTRUCTED

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13
Q

CIRRHOSIS….

= definition

4 common causes?

on BLOODWORK, can see.. (2)

A

= END-STAGE condition resulting from ANY HEPATIC INSULT

3 common causes?
1. PORTAL HYPERTENSION
2. ASCITES
3. GASTRIC ULCERS
4. ACQUIRED PORTOSYSTEMIC SHUNTS

on BLOODWORK…
1. LIVER ENZYMES = NORMAL or HIGH
2. LIVER FUNCTION ABNORMALITIES = LOW ABC GLUCOSE

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14
Q

CIRRHOSIS…

2 BIOPSY findings?

treatment? (2)

prognosis?

A

BIOPSY findings…
1. DIFFUSE FIBROSIS
2. REGENERATIVE NODULES

treatment?
1. SUPPORTIVE THERAPY, not much you can do
2. ANTIFIBROTICS to help SLOW PROGRESSION of FIBROSIS
–> COLCHICINE
–> GCCs

prognosis = GENERALLY POOR

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15
Q

what should we keep in mind about HEPATIC SUPPORTIVE THERAPY?

A

typically safe w/ minimal side effects, but WE DO NOT HAVE EVIDENCE OF THEIR BENEFIT

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16
Q

URSODIOL

= what does it do?

A

INCREASES the FLOW OF BILE ACIDS to help PREVENT TOXIC BUILD-UP in LATE LIVER DZ

17
Q

S-ADENOSYLMETHIONINE (SAMe)

2 indications?

generates ___ which helps play a role in protecting ____ against ____ injury

also has ____-____ effects

A

2 indications?
1. HEPATIC LIPIDOSIS
2. HEPATOTOXICITY

generates GLUTATHIONE which helps play a role in protecting HEPATOCYTES against TOXIC injury

also has ANTI-INFLAMMATORY effects

18
Q

MILK THISTLE…

what is the active ingredient?

4 functions?

what POPULAR medication for liver dz is it in?

A

active ingredient = SILYMARIN or SILYBIN

4 functions?
1. ANTIOXIDANT
2. CHOLERETIC
3. ANTI-INFLAMMATORY
4. PROTECTION AGAINST MUSHROOM TOXICITY

often used in DENAMARIN

19
Q

75-80% of LIVER BLOOD SUPPLY is from the ___ ____, which contains _____ blood from….

20-25% of LIVER BLOOD SUPPLY is from the ____ ____ which contains _____ blood from…

A

75-80% = PORTAL VEIN, drains DEOXYGENATED blood from ALL INTRA-ABDOMINAL ORGANS

20-25% = HEPATIC ARTERY, contains OXYGENATED blood from SYSTEMIC ARTERIAL SYSTEM

20
Q

hepatic veins drain into the…

A

CAUDAL VENA CAVA

21
Q

describe the 3 types of PORTAL HYPERTENSION

A
  1. PRE-HEPATIC = something causing hypertension BEFORE portal vein
    –> PORTAL VEIN THROMBUS
    –> MASS causing COMPRESSION
  2. HEPATIC = LIVER DZ that causes INCREASED RESISTANCE TO BLOOD FLOW
    –> usually CHRONIC HEPATITIS causing FIBROSIS & increased VASCULAR RESISTANCE
  3. POST-HEPATIC = from a lesion that causes INCREASED PRESSURE in CAUDAL VENA CAVA
    –> CHF
    –> CAVAL SYNDROME
22
Q

when there’s both ASCITES & PROTAL HYPERTENSION, what type of fluid is present? (2)

A
  1. TRANSUDATE
  2. MODIFIED TRANSUDATE
23
Q

3 possible clinical manifestations of PORTAL HYPERTENSION?

A
  1. ASCITES
  2. GASTRODUODENAL ULCERATION/EROSION
  3. HEPATIC ENCEPHALOPATHY
24
Q

3 treatment options for dogs with ASCITES? + which MEDICATION is best for hepatitis?

what LIVER DZ is this usually associated with?

A

3 treatments?
1. DIETARY SALT RESTRICTION
2. DIURETICS –> SPIRONOLACTONE BEST
3. ABDOMINOCENTESIS for animals with SEVERE ABDOMINAL DISTENTION/DIFFICULTY BREATHING

usually associated with PORTAL HYPERTENSION

25
Q

HEPATIC ENCEPHALOPATHY…

usually patients with this have SIGNS of… because of….

has a ____ pathogenesis, with ____ being the MOST SIGNIFICANT REASON

A

usually have SIGNS of BILATERAL CEREBRAL CORTICAL DYSFUNCTION because of CIRCULATING SUBSTANCES THAT SHOULD BE METABOLIZED BY THE LIVER

usually because of AMMONIA, often need to treat HYPERAMMONEMIA

26
Q

what is the TREATMENT of HEPATIC ENCEPHALOPATHY centered around?

what are 2 examples of this treatment? which one is more common?

A

centered around treating HYPERAMMONEMIA

2 examples?
1. REDUCE DIETARY PROTEIN, can use DAIRY or VEGETABLE source
2. PREVENT GI HEMORRHAGE (ulcers, erosions, etc.) bc that could PRODUCE AMMONIA

27
Q

PREVENTION of FORMATION & ABSORPTION of AMMONIA via what 2 drugs?

give 2 examples for first

A
  1. ANTIBIOTICS to KILL BACTERIA THAT MAKE THE AMMONIA
    –> NEOMYCIN or METRONIDAZOLE
  2. LACTULOSE
    –> can be an ENEMA
    –> can be ORAL to PREVENT ABSORPTION OF AMMONIA
28
Q

LACTULOSE…

METABOLIZED BY ___ ___ into ____ ____

helps to INCREASE ____ in ____ and causes the formation of ____+, which….

also helps increase….

what DISEASE can it be used to treat? (1 secondary dz, 1 primary dz)

A

LACTULOSE

METABOLIZED BY COLONIC BACTERIA to ORGANIC ACIDS

helps to INCREASE ACID in COLON causing formation of AMMONIUM ION (NH4+), which CANNOT BE ABSORBED ACROSS GI EPITHELIUM

also helps increase INTESTINAL TRANSIT TIME, less time for BACTERIA TO MAKE AMMONIA

can be used to treat HYPERAMMONEMIA caused by HEPATIC ENCEPHALOPATHY

29
Q

SUPERFICIAL NECROLYTIC DERMATITIS…

aka? (2 names)

causes ___ disease

can be caused by WHAT medication?

what BREED can get this primarily?

3 skin lesions?

see WHAT on biopsy?

A

aka = HEPATOCUTANEOUS SYNDROME or ACHES

causes LIVER disease

can be caused by PHENOBARBITAL

SHIH TZUs can get this congenitally

3 skin lesions?
1. crusts
2. erosions
3. ulcers

see HYPERKERATOSIS on BIOPSY

30
Q

SUPERFICIAL NECROLYTIC DERMATITIS…

treatment options? (2)

prognosis?

MST?

A

treatment options?
1. AMINO ACID INFUSIONS
2. HIGH PROTEIN, HOME-COOKED DIET

prognosis is GUARDED

MST = 1 YEAR

31
Q

what is the MOST common PRIMARY liver neoplasia?

A

HEPATOCELLULAR CARCINOMA

32
Q

HEPATOCELLULAR CARCINOMA…

solitary vs. diffuse?

age of patients?

clinical signs are usually ___-___

diagnosis (3, which one is DEFINITIVE)

treatment?

prognosis for SOLITARY vs. DIFFUSE?

A

SOLITARY > DIFFUSE

patients tend to be OLD

clinical signs are usually NON-SPECIFIC

diagnosis?
1. US
2. RADS
3. BIOPSY for CONFIRMATION

prognosis for…
–> SOLITARY = GOOD if no metastasis
–> DIFFUSE = POOR

33
Q

HEPATIC LYMPHOMA…

usually a ____ cell ____ lymphoma

this is usually…

this can be a component of ____ lymphoma, putting the disease at stage ____, or it can be ____ in the liver

we can make a PRESUMPTIVE diagnosis based on… (2)

DEFINITIVE diagnosis? (2, which one tends to be SUFFICIENT)

prognosis for the TWO TYPES?

A

usually a LARGE cell LYMPHOBLASTIC lymphoma

this is usually INFILTRATIVE

this can be a component of MULTICENTRIC lymphoma, putting the disease at stage FOUR, or it can be PRIMARY in the liver

PRESUMPTIVE diagnosis?
1. ABNORMAL US FINDINGS
2. INCREASED LIVER ENZYMES on CBC

DEFINITIVE diagnosis?
1. CYTOLOGY usually sufficient
2. BIOPSY

prognosis for…
1. PRIMARY = POOR, MST 2 MONTHS
2. MULTICENTRIC = FAIR, MST 1 YEAR

34
Q

NON-SPECIFIC REACTIVE HEPATOPATHY…

see WHAT kind of inflammation? (2)

LACK of what 4 things?

associated with ____-____ disease, often ___ in origin

causes ____ in liver ____

A

inflammation?
1. MIXED inflammatory population
2. PORTAL INFLAMMATION

LACK of…
1. NECROSIS
2. APOPTOSIS
3. FIBROSIS
4. REMODELING

associated with EXTRA-HEPATIC dz, usually GI

causes INCREASE (mild) in LIVER ENZYMES

Year 1/2 (139 decks)

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