Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3. Cat & Dog > hepatobiliary 1 > Flashcards

hepatobiliary 1 Flashcards

1
Q

Markers of Liver Disease: Hepatocellular injury

A
  • Alanine transferase (ALT)
  • Aspartate aminotransferase (AST)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Markers of Liver Disease: Induced / Cholestasis

A

A- lkaline phosphatase (ALP)
- Gamma-glutamyl transferase (GGT)
- Bilirubin (stasis - not induced)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Markers of Liver Disease: function

A
  • Synthetic biochemical products
  • Bile acids
  • Coagulation factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are ALT and AST markers for? which is more liver specific? cats vs dogs hald life?

A
  • Markers of hepatocellular injury
  • ALT is the most liver specific enzyme
    > Muscle and liver enzymes clinically significant in dogs and cats
  • Half-life shorter in cats vs dogs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

is AST always included on liver profiles? why, what can affect it?

A
  • AST another hepatocellular injury marker included on some profiles
  • Muscle isoenzyme can affect AST more than ALT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ALP & GGT: where do they come from, mostly? what is one of the strongest stimuli?

A
  • Synthesis & release from biliary tract
    > Cholestasis (bile retention) is one of the strongest stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Other sources of ALP, non-liver

A
  • Corticosteroid- and other drug (e.g., antiepileptics) induced (dogs only)
  • Bone
  • (Renal, GI isoenzymes less clinically relevant in serum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Elevated bilirubin usually due to:

A

increased production or decreased excretion of bile pigment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does bilirubin point to for the liver?

A

evere liver dysfunction
* Mononuclear phagocytic system cannot process bilirubin
* Increased due to lack of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

is bilirubin elevated due to pre-hepatic, hepatic, or post-hepatic causes?

A

all
- * Bilirubin can be elevated from pre-hepatic, hepatic, and post-hepatic (i.e., biliary) causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  • Markers of decreased synthetic function:
    what are they, when do they become abnormal?
A
  • Decreased albumin
  • Decreased cholesterol
  • Decreased urea
  • Decreased glucose
  • These values become abnormal (>55% hepatic mass) in course of liver disease (are not sensitive or specific)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

liver markers we can look at

A
  • ALP & GGT
  • Bilirubin
  • Liver Synthetic Products
    > Decreased albumin
    > Decreased cholesterol
    > Decreased urea
    > Decreased glucose
  • Coagulation profile (PT, PTT)
  • Bile acids (pre and post-prandial)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

range of slinical signs that can be due to the following liver issues:
Hepatocellular damage ….
Architecture change…
Intrahepatic biliary stasis …
loss of hepatocytes, fibrosis (cirrhosis)

A
  • None
    ()
    Non-specific signs:
  • Decreased appetite;
  • Lethargy;
  • Weight loss;
  • Vomiting, diarrhea
    ()
    More specific signs:
  • Icterus (if cholestasis)
    Also:
  • Abdominal pain
  • PU/PD
    ()
    Portal hypertension:
  • Ascites
    Failure:
  • Hepatic
    encephalopathy
  • Coagulopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

more specific signs of liver damage

A
  • Icterus (if cholestasis)
    Also:
  • Abdominal pain
  • PU/PD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Portal hypertension sign

A

Ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

liver failure signs

A
  • Hepatic encephalopathy
  • Coagulopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Gastrointestinal signs can be related to liver problems in these ways

A
  • Vomiting secondary to local inflammation, portal hypertension, encephalopathy
  • Liver disease can predispose to GI ulceration (hematemesis, melena)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

abdominal pain can be realted to liver problems in these ways

A
  • Liver capsule, biliary epithelium well innervated
  • Hepatomegaly (acute liver disease), biliary tract disease can cause pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Polyuria/polydipsia can be realted to liver problems in these ways:

A
  • Loss of renal medullary concentration gradient if low urea
  • Change in osmoreceptors in the liver
  • Manifestation of encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

jaundice point to pre-hepatic, hepatic, or post-hepatic issue?

A

can by any

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

pre-hepatic, hepatic, and post hepatic mechisms - which may be present in liver disease? how can we distinguish?

A
  • Hepatic and post-hepatic mechanisms may be present in liver disease
  • Ultrasound helpful in distinguishing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ascites realted to liver disease:
more common in dogs or cats? what is it? mechansim?

A
  • Dogs > cats
  • Transudate to modified transudate
  • Mechanisms:
  • Portal hypertension
  • Low albumin, decreased oncotic pressure
  • Activation of renin angiotensin aldosterone systemàsalt and water accumulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Physical Exam Findings that we may see in liver disease?

A
  • Jaundice
  • Hepatomegaly
  • Ascites
    > Palpable fluid wave
    > Ultrasound (point-of-care AFAST)
  • PE can be normal*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

possible reasons for acute elevation ALT:

A
  • Toxin, drugs
  • Infection (leptospirosis, other bacteria or viral)
  • Trauma
  • Hypoxia
  • Secondary to pancreatitis or enteritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

possible reasons for Chronic elevation ALT:

A
  • Ongoing toxin, drugs
  • Chronic infection
  • Chronic inflammatory disorder
  • Secondary to pancreatitis or enteritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Assessing Liver Enzyme Elevations
* When are these values concerning:

A
  • Any elevation in a cat (short half-lives
    of enzymes)
  • Both ALT and ALP elevation
  • > 2x upper limit in a dog
  • Persistence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Primary Hepatobiliary Disorders can be put into what 3 main categories

A
  • hepatocellular
  • biliary tract
  • vascular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

hepatocellular types of primary hepatobiliary disorders: (7) which is more common in dog vs cat?

A

Hepatocellular
* Nodular hyperplasia (aging)
* Chronic hepatitis (dog&raquo_space; cat)
* Toxicity
* Neoplasia
> Hepatoma
> Hepatocellular carcinoma
* Vacuolar hepatopathy
* Infectious
* Cirrhosis (end-stage change)

29
Q

toxicities that can cause hepatocellular related primary hepatobiliary disorders:

A
  • Mycotoxins (mushrooms, food aflatoxins)
  • Xylitol sweetened foods
  • Drugs
  • Unidentified
30
Q

infectious causes of hepatocellular related primary hepatobiliary disorders:

A
  • Viral: infectious canine hepatitis
  • Bacterial: leptospirosis
  • Fungal
  • Echinococcus multilocularis
  • Parasitic – cuterebra
31
Q

types of bililary tract primary hepatobiliary disorders (4)? which are more common in dog vs cat?

A
  • Gall bladder mucocele (dog&raquo_space; cat)
  • Cholangitis/cholangiohepatitits (cat&raquo_space; dog)
  • Neoplasia: bile duct carcinoma
  • Extrahepatic bile duct
    compression/obstruction
    > Pancreatitis
    > Neoplasia
    > Cholelithiasis
32
Q

vascular-related primary hepatobiliary disorders? which is more common in dog vs cat?

A
  • Portosystemic shunt (dog > > cat)
  • Portal vein hypoplasia without portal
  • hypertension (Microvascular dysplasia)
  • Neoplasia
  • Arteriovenous fistula
33
Q

Secondary hepatobiliary disorders

A
  • Pancreatitis
  • Endocrine
    > Diabetes mellitus
    > Hyperadrenocorticism: steroid hepatopathy
  • Hypoxemia
  • Trauma
  • Systemic infections
  • DIC
  • Neoplasia
    > Lymphoma
    > Metastatic neoplasia
    > Carcinoid: neuroendocrine tumour
  • Amyloidosis (Shar-Pei)
34
Q

possible reasons for Acute elevation ALT:

A
  • Toxin, drugs
  • Infection (leptospirosis, other bacteria or viral)
  • Trauma
  • Hypoxia
  • Secondary hepatobiliary disorder
35
Q

possible reasons for chronic elevation of ALT?

A
  • Ongoing toxin, drugs
  • Chronic liver infection
  • Chronic liver inflammatory disorder
  • Secondary hepatobiliary disorder
  • Neoplasia
36
Q

Chronic Hepatitis - what is it? potential causes?

A
  • Progressive inflammation of the liver
  • Potential causes:
    > Genetic predisposition
    > Previous or unrecognized infection
    > Previous toxin exposure
    > Immune mediated
37
Q

Copper Associated Chronic Hepatitis (CuCH) - is it primary or secondary? what can cause it?

A

Copper accumulation in the liver can be primary or secondary

  • Genetic predisposition causes copper deposition, leading to hepatitis
    > “Copper storage disease” of “Copper associated chronic hepatitis” (CuCH)
  • Hepatitis impairs copper excretion, leading to accumulation and further hepatitis
  • Normal dogs ingesting massive quantity of copper can have acute hepatitis
38
Q

Copper Storage Hepatopathy - types, what lesions are associated, and what copper levels?

A
  • Primary Copper Hepatopathy
    > Tends to be centrilobular
    > Copper quantification levels typically >1000ug/g
  • Secondary to cholestasis:
    > Often located in periportal zone (zone 1)
    > Associated with lower copper concentrations (typically <750ug/g)
    > Does not typically require chelation
39
Q

does copper storage hepatopathy secondary to cholestasis typically require chelation?

A

no

40
Q

copper storage hepatopathy accounts for what proportion of dogs with primary hepatopathy?

A

Accounted for 1/3 of all dogs with primary hepatitis in one study

41
Q

Chronic Hepatitis: Genetic Predispositions, what breeds

A
  • Varies geographically
  • North American predispositions:
  • Bedlington Terrier
  • Doberman (many have CuCH)
  • Labrador Retriever (many have CuCH)
  • Dalmatian (some have CuCH)
  • American & English Cocker Spaniels
  • West Highland White Terrier (possible CuCH)
42
Q

Chronic Hepatitis: Presentation - signalment, duration of disease prior to presentation?

A
  • Mean age 7 years
  • Dalmatians, Dobermans, Springers present younger & have female predisposition
  • Duration of disease prior to presentation unknown
43
Q

Chronic Hepatitis: Presentation - clinical signs? subclinical stage? enzymes? signs at presentation depend on what?

A
  • Clinical signs can be absent or non-specific
    > Decreased appetite, lethargy most common
    > More specific liver signs of icterus, ascites in ~1/3 of patients
    > Later stages can have signs of GI ulceration
  • Long subclinical stage
    > ~20% have increased enzymes noted without clinical signs
  • Variable signs at presentation, related to stage of disease
44
Q

Chronic Hepatitis: Diagnosis - what is earliest indicator?

A
  • Elevated ALT is earliest indicator
45
Q

Chronic Hepatitis: Diagnosis - enzyme tests and what they tell us

A
  • Elevated ALT is earliest indicator
  • Elevated ALP in later stages
    > Typically magnitude of ALT > ALP
    > End stage disease with lack of hepatocellular tissue could result in lower ALT
  • AST & GGT tend to mirror ALT & ALP, respectively
    > Less specific
46
Q

Chronic Hepatitis: Diagnosis - liver function test results and what they tell us

A

Liver function tests
* Elevated bilirubin in ~50%
* Decreased urea, cholesterol in 40%
* Hypoalbuminemia a late marker of synthetic failure
* Hypoglycemia rare (more common in acute liver failure)

47
Q

Chronic Hepatitis: Diagnosis - serum bile acids results and when useful

A

Serum bile acids
* Can be elevated in later stages (not sensitive for early disease)
* Not helpful if bilirubin elevated

48
Q

Chronic Hepatitis: Diagnosis - SOMETIMES HELPFUL CBC, URINALYSIS, AND PT/PTT RESULTS

A

Other clinicopathological abnormalities:
* CBCcanshowmildanemia
* Urinalysis can show isosthenuria if PU/PD
* PT/PTT can be prolonged in more advanced stages

49
Q

Chronic Hepatitis: Diagnosis - RADIOGRAPHS what we may see, and how useful

A

Abdominal radiographs can show microhepatica, ascites
* Not sensitive

50
Q

Chronic Hepatitis: Diagnosis - what might we see on ultrasound?

A

Abdominal ultrasound
* Hyperechoic liver parenchyma, or nodular changes later stages
* Liver often small in more advanced disease
* Allows investigation of alternative diagnoses and complications
> Ascites, thrombosis, portal hypertension, acquired portosystemic shunts

51
Q

Chronic Hepatitis: Diagnosis - what does true diagnosis require? how to interpret?

A
  • Diagnosis requires biopsy
    > Ultrasound guided or surgical
  • Biopsy interpretation:
    > Evaluate for extent & type of inflammation, presence of fibrosis
    > Copper quantification
52
Q

Chronic Hepatitis: Treatment - therapeutic targets and additional treatment targets

A

Therapeutic targets in CH (liver):
* Inflammation / immune mediated disease
* Fibrosis
* Oxidative injury
* Cholestasis
* Copper accumulation

Additional treatment targets:
* GI ulceration, ascites, coagulopathy
* Hepatic encephalopathy

53
Q

Anti-inflammatory/immunosuppressive drugs that can be helpful for chronic hepatitis? pros and cons? what are these reserved for?

A

Prednisone
* Beneficial in some case series
> Quantity of life
> Quality of life
* Potential side effects
* Steroid hepatopathy development (increased ALP)

  • Generally reserved for biopsy evidence of inflammation / immune mediated hepatitis
  • Can consider alternative immunosuppressives (e.g., cyclosporine)
54
Q

why is oxidative damage a particular concern for the liver? when might it occur?

A

Free radicals are normal by-product of aerobic metabolism of liver
* Increased in inflammation and toxicosis
* Hepatic antioxidant systems overwhelmed

55
Q

liver Oxidative injury - what can we give to help prevent?

A
  • S-adenosylmethionine (SAMe)
    > Improves liver glutathione (GSH) levels
    > Anti-inflammatory
  • Silymarin
    > Milk thistle extract
    > Silybin is major active constituent
    > Protective in experimental mushroom poisoning
  • Vitamin E
  • N-Acetylcysteine (IV)
56
Q

how can cholestasis be damaging to the liver?

A

Cholestasis: accumulation of bile acids > hydrophobic bile acids are toxic to hepatocytes

57
Q

Ursodiol - what is its use? how does it work and when should it be avoided?

A

Used to help in cases of cholestasis

  • Synthetic non-toxic hydrophilic bile acid
  • Enhances bile flow
  • Stimulates excretion of inflammatory produces (copper, leukotrienes, bilirubin)
  • Decreases by dilution concentrations of endogenous more toxic bile acids
  • Contraindicated in post-hepatic bile duct obstruction
58
Q

Copper Accumulation in CuCH - dietary reccomendations?

A
  • Lifelong dietary copper restriction
    > Diet: Hill’s l/d, Royal Canin Hepatic, homemade.diet
    > Protein level of these diets is relatively low and supplementing protein warranted if not encephalopathic
59
Q

Copper Accumulation in CuCH - if biopsy confirms high copper level, what is reccomended?

A

Copper chelation when biopsy confirmation that Cu level is high

60
Q

treatment for biopsy confirmed cases of chronic hepatitis? also with high copper?

A
  • If lymphocytic inflammatory infiltrate
    > Prednisone 1-2 mg/kg/day (max at 40 mg), slowly taper once disease status improves
  • If confirmed high copper levels
    > Dietary copper restriction
    > D-penicillamine for several months until ALT normalizes (or stabilizes)
  • Consider serology for leptospirosis
    > Or empirical treatment doxycycline for 2 weeks
  • Antioxidants (often SAMe & milk thistle; Vitamin E is less costly)
  • Ursodiol if evidence of cholestasis on biopsy and/or biochemical profile
  • Diet (if not CuCH):
    > Good quality maintenance diet
    > No protein restriction unless encephalopathic
61
Q

how do we treat a presumptive diagnosis of chronic hepatitis?

A
  • Initial treatment with antioxidants, +/- ursodiol (if cholestasis)
  • Consider immunosuppressive trial
    > Balanced with risk of complications
  • Consider serology for leptospirosis
    > Or empirical treatment doxycycline for
    2 weeks
  • Copper restricted diet if breed predisposed to CuCH
    > Generally not using D-penicillamine without confirmed quantification due to high side effect potential
62
Q

in a case of chronic hepatits where we see ascites - what should we condier for supportive care?

A
  • We see ascites because RAAS is upregulated
  • Consider spironolactone, mild sodium restriction
  • Occasional abdominocentesis (to relieve tension, maintain comfort)
63
Q

in a case of chronic hepatits where we see coagulopathy - what should we consider for supportive care? what kind of coagulopathy will we usually see?

A
  • Typically a “balanced coagulopathy” – spontaneous bleeding uncommon
  • Prior to biopsy, vitamin K +/- plasma
64
Q

in chronic hepatitis, why might we be at an increased risk of GI ulceration? what can GI bleeding exacerbate in this case?

A
  • Portal hypertension, other aspects of liver disease increase risk of ulceration
  • GI bleeding exacerbates hepatic encephalopathy
65
Q

in a case of chronic hepatitis with GI ulceration, what additional supportive care should we consider?

A
  • Weak evidence supportive prophylactic use of gastroprotectants
  • Consider sucralfate, omeprazole
66
Q

in a case of chronic hepatits with a bacterial infection, what type of infection do we expect and what is rarer?

A

Bacterial infection of parenchyma, primary bacterial cholangiohepatitis rare with CH

67
Q

supportive care for a case of chronic hepatitis with bacterial infection

A
  • Doxycycline if leptospirosis not ruled out
  • Consider antibiotics based on biopsy/ bile culture when available
68
Q

Chronic Hepatitis: Prognosis

A
  • Progressive disease, hepatic parenchyma lost over time
  • Cirrhosis (diffuse fibrosis of liver) at end stage
  • Median survival times 561 +/- 268 days in some studies
    > Ascites, presence of cirrhosis shorter survival (MST 21 days in some studies)

3. Cat & Dog (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions