Brainscape's Knowledge GenomeTM

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


See full index

Module 16 > Investigating Canine & Feline Liver Disease > Flashcards

Investigating Canine & Feline Liver Disease Flashcards

1
Q

how many lobes does the liver have

A

six lobes

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

what is the blood supply to the liver

A

dual blood supply

25% hepatic artery

75% portal vein (carries blood from GIT, GB, pancreas & spleen to the liver)

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

what are the functions of hepatocytes

A

metabolic and detoxifying functions

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

what are the functions of the liver (9)

A
  1. metabolism carbohydrates (glycogenesis, glycogenolysis, gluconeogenesis)
  2. bile acid synthesis and secretion
  3. storage of minerals (Fe, Cu) and vitamins
  4. metabolism lipids
  5. immune functions
  6. makes albumin
  7. production of coagulation factors
  8. drug metabolism and excretion
  9. production of urea from ammonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

when does liver failure occur

A

until >70% functional capacity is lost

hepatic injury must be considerable

chronic and recurrent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the biliary system

A

branched structure that transports bile from each individual hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

where does the biliary system connect to

A

duodenum by common bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the anatomic difference in pancreatic duct in cats vs dogs

A

dogs have a separate duct where cats have pancreatic duct that joins with common bile duct

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

what are the functions of the bile

A

emulsifies fat

neutralizes acid

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

what is a secondary (or ‘reactive’) hepatopathy

A

non specific reaction by hepatocytes to disorders other than primary hepatobiliary diseases

more common than primary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the signs of a secondary hepatopathy

A

increased liver enzymes

+/- ultrasound changes

+/- histopathology changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the categories of secondary hepatopathies (7)

A
  1. hypoxia/hypotension
  2. non hepatic inflammatory diseases
  3. drugs (dogs)
  4. endocrinopathies
  5. metastatic neoplasia
  6. right sided CHF
  7. pericardial effusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are hypoxic/hypotension changes that can cause secondary hepatopathies (4)

A
  1. shock
  2. surgery
  3. seizures
  4. anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are non hepatic inflammatory diseases changes that can cause secondary hepatopathies (4)

A
  1. GI disease
  2. pancreatitis
  3. sepsis
  4. toxemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what drugs can cause secondary hepatopathies (2)

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

what endocrinopathies can cause secondary hepatopathies (6)

A
  1. cushings
  2. addisons
  3. diabetes mellitus
  4. hyperthyroidism (cats)
  5. hypothyroidism (dogs)
  6. hyperlipidemia (min schnauzers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the clinical signs of secondary hepatopathies

A

extermely variable

none are pathognomonic for liver disease

anorexia, depression/lethargy, polyuria/polydipsia, vomiting/diarrhea, weight loss

jaundice, ascites, alerations in liver size, coagulopathies, hepatocutaneous syndromes (dogs),

hepatic encephalopathy, altered mentation, circling, headpressing, pytalasim (cats), coma (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are breeds associated with chronic hepatitis (4)

A
  1. springer spaniels
  2. dobermanns
  3. cocker spaniels
  4. labradors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what breeds are associated with copper storage disease (2)

A
  1. bedlington terriers
  2. labs (USA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what breeds are associated with gall bladder mucoceles (2)

A
  1. shetland sheepdogs
  2. border terriers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the signalment for feline hepatic lipidosis

A

middle aged overweight cats with recent history of anorexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what abnormalities are common in young ages (2)

A
  1. portosystemic shunts
  2. portal vein hypoplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are history questions to ask (4)

A
  1. acute or chronic problem
  2. try to differentiate between primary or secondary problem
  3. toxin exposure/current meds?
  4. vaccination status (Leptospirosis, CAV-1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what history questions would differentiate between a chronic and acute liver disease (6)

A
  1. healthy until recently? acute
  2. recent toxin exposure? acute
  3. drug administration? acute
  4. often weeks/months of non-specific signs - chronic
  5. often no clinical signs - chronic
  6. possible weight loss - chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what would be seen on a clinical exam with acute liver disease (3)

A
  1. fever
  2. dehydration
  3. cranial abdominal pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what would be seen with clinical pathology with acute liver disease

A

marked increase in ALT and AST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what could be seen on clinical exam with chronic liver disease

A

poor body condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what clinical pathology changes can be seen in chronic liver disease (2)

A
  1. persistent increase in liver enzymes
  2. +/- hypoalbuminemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are chronic liver diseases in dogs

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are chronic liver diseases in cats

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are hepatotoxic drugs (7)

A
  1. NSAIDs
  2. paracetamol (cats)
  3. azathioprine
  4. TMPS antibiotics (dogs)
  5. diazepam (cats)
  6. lomustine
  7. carbimazole/methimazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are infectious causes of acute hepatic disease (4)

A
  1. leptospirosis
  2. CAV-1
  3. clostridium spp
  4. acute neutrophilic cholangitis (cats)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are metabolic causes of acute hepatic disease

A
  1. hepatic lipidosis (cats)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are toxins that can cause acute hepatic disease (4)

A
  1. xylitol (chewing gum)
  2. mycotoxins, alfatoxicosis
  3. amanita mushrooms
  4. cyanobacteria – microcystin toxicosis (blue green algae)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are neoplasia’s that can cause acute hepatic disease

A
  1. diffuse infiltration (lymphoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are biochem indicators of liver damage (2)

A

1. ALT: alanine aminotransferase

2. AST: aspartate transaminase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are biochem indicators of cholestasis (3)

A

1. ALP: alkaline phosphatase

2. GGT: Gamma-glutamyl transferase

3. bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is cholestasis

A

the flow of bile from your liver is reduced or blocked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are biochem indicators of liver function (7)

A
  1. bile acids
  2. ammonia
  3. bilirubin
  4. glucose
  5. urea
  6. albumin
  7. cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what do hepatocellular leakage enzymes tell you

A

indicate hepatocellular membrane damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what are hepatocellular leakage enzymes

A

1. ALT: alanine aminotransferase

2. AST: aspartate aminotransferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

where is ALT found in the hepatocyte

A

in the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

where is AST found in the hepatocyte

A

mitochondria and the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

why is AST less specific than ALT to hepatocellular damage

A

because AST is also found in skeletal muscle, cardiac myocytes and kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what occurs if AST > ALT

A

check CK and troponins

need further investigations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the half life of ALT in dogs

A

60 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is the half life of ALT in cats

A

3-4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is the half life of AST in dogs

A

22 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is the half life of AST in cats

A

77 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

following an injury which enzmye ALT or AST is likely to increase first

A

ALT increases in the first 12 hours and peaks 1-2 days and takes about 2-3 weeks to return to reference intervals

AST release is later at about 24 hours and the magnitude is usually less and it returns to reference intervals around 48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are membrane bound markers

A

ALP

GGT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

where are membrane bound markers found

A

membrane bound location at bile canalicular surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what does an increase in membrane bound markers indicate

A

increased enzyme production stimulated by impaired bile flow (“cholestasis”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is the half life of ALP in dogs

A

77 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is the half life of ALP in cats

A

6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

at what time following an injury do ALP and GGT increase

A

ALP increases at around 4.5 days

GGT increases at around 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

why is ALP the least specific marker

A

because there are other isoforms of it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

where are ALP isoforms found (2)

A
  1. bone: osteoblasts, young growing animals, bone neoplasia
  2. steroid induced (dogs): exogenous (topical or systemic corticosteroid meds), endogenous (cushings disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

which is the more specific membrane bound marker ALP or GGT

A

GGT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is the problem with GGT as a membrane bound marker

A

it is more specific than ALP but it is less sensitive

it is not always increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

if you have a patient with no clinical signs but there is an elevation in liver enzymes what should you do

A

progressive monitoring important as function may not be abnormal until advanced disease

monitor every 2-4 weeks following an acute insult

may take months for a full recovery

be aware of high risks groups (dobermann, springer spaniels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

can the severity of increase in liver enzymes give you an indication of prognosis

A

no they cannot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

does liver damage equal liver dysfunction

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is the primary source of bilirubin

A

RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

how is bilirubin metabolized

A

transported to the liver and conjugated, secreted into bile and then stored in the gall bladder and excreted via the bile ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what are the categories of jaundice

A
  1. pre hepatic
  2. hepatic
  3. post hepatic
68
Q

what are causes of pre hepatic jaundice

A

hemolysis of red blood cells ex. hemolytic anemia

increased production exceeds capacity of hepatic excretion

69
Q

what are causes of hepatic jaundice (3)

A
  1. abnormal uptake
  2. defective conjugation
  3. abnomral excretion of bilirubin by hepatocytes
70
Q

what are causes of post hepatic jaundice (3)

A
  1. impaired excretion of bilirubin
  2. obstruction of common bile duct or gall bladder (ex. pancreatitis, neoplasia, choleliths, cholecystitis)
  3. bile duct rupture
71
Q

how would you determine if the cause of jaundice is pre hepatic

A

look at PCV

72
Q

how would you determine if the cause of jaundice is post hepatic (4)

A
  1. ALP, GGT > ALT, AST
  2. hypercholesterolemia?
  3. ultrasound biliary system assess for obstruction of bile duct, GB rupture
  4. pancreatic assessment (cPLI)
73
Q

how do you determine if the cause of jaundice is hepatic

A

rule out pre and post hepatic etiology

consider biopsy

74
Q

where is albumin synthesized

A

liver

75
Q

what is the half life of albumin

A

1-3 weeks

76
Q

how long does it take for significant decreases of albumin to occur

A

this develops very slowly

77
Q

at what % of liver function can hypoalbuminemia occur

A

30% liver function

78
Q

at what point would ascites occur

A

with significant hypoalbuminemia <15 g/l

79
Q

why does ascites occur with hypoalbuminemia

A

albumin is a major source of plasma colloid osmotic pressure

80
Q

what are other causes of hypoalbuminemia besides decreased liver production (2)

A
  1. gastrointestinal: protein losing enteropathy
  2. renal loss: protein losing nephropathy
81
Q

what are the sources of cholesterol

A

in the diet and made in the liver

82
Q

what is the major excretory pathway of cholesterol

A

bile

83
Q

what does hypocholestermia indicate

A

liver failure

84
Q

what does hypercholestermia indicate

A
  1. extrahepatic bile duct obstruction
  2. intrahepatic cholestatic disease
  3. marked hepatic regeneration
85
Q

where is urea produced

A

synthesized by hepatocytes from ammonia generated by catabolism of amino acids

86
Q

how is urea excreted

A

kidneys

87
Q

why does urea decrease with severe liver dysfunction

A

due to failure to convert ammonia to urea

88
Q

what other reasons beside failure to convert ammonia to urea can urea be decreased (3)

A
  1. decreased protein intake
  2. protein anabolism
  3. PUPD
89
Q

where is blood glucose derived from (2)

A
  1. glycogenolysis: breakdown of glycogen in the liver
  2. gluconeogenesis: production of glucose from amino acid precursors in the liver
90
Q

what other causes are there for hypoglycemia (6)

A
  1. hypoadrenocortism (addison’s)
  2. sepsis
  3. paraneoplastic
  4. insulinoma
  5. young/small toy breeds
  6. xylitol toxicity
91
Q

what % of hepatic function would hypoglycemia be seen

A

severe hepatic compromise

<30% function

not common

92
Q

what are the most specific test of liver dysfunction

A

bile acids

93
Q

describe how bile acids are synthesized (6)

A
  1. synthesized from cholesterol and stored in the liver
  2. ingestion of food stimulates a gall bladder contraction to help absorb fats
  3. secreted into the duodenum
  4. 95% reabsorbed by the ileum
  5. enter the portal circulation
  6. enter the liver
94
Q

what are 3 reasons why bile acids may be abnormally high

A
  1. reduction in hepatocellular mass
  2. impaired hepatocyte function
  3. distubred enterohepatic circulation (portal blood flow to liver or obstruction of biliary flow from liver)
95
Q

what are ddx of high bile acids (3)

A
  1. portosystemic shunt
  2. diffuse hepatic disease
  3. biliary stasis
96
Q

what is normal bile acid level pre prandial

A

0-10 umol/l

97
Q

what is normal bile acid level 2 hours post prandial

A

0-20 umol/l

98
Q

how is the bile acid stimulation test work

A

sensitivity improves measuring a pre prandial sample (starve patient 12 hours before measuring)

feeding causes gall bladder to contract and releases bile acids

99
Q

what do bile acids not tell you (4)

A
  1. no information about reversibility of conditions
  2. doesn’t determine specific etiology
  3. not helpful in differentiating a hepatic from a post hepatic jaundice
100
Q

why do bile acids not differentiate between a hepatic or post hepatic jaundice

A

bile acid increase occurs prior to jaundice in hepatobillary disease

don’t run if jaundice

101
Q

what occurs if bile acids are higher in the pre sample vs the post sample (3)

A
  1. gall bladder contracted just prior to the pre sample
  2. delayed gastric emptying
  3. lab error

interpret the higher of the two results

102
Q

what breed can have high bile acids

A

maltese

but also a breed that can get portosystemic shunts

103
Q

describe the ammonia cycle (3)

A
  1. endogenous NH3 enters the liver and enters the urea cycle
  2. converted to urea by liver
  3. excreted by the kidneys or enters the colon where it is converted to NH4+
104
Q

what are the causes of hyperammonia (3)

A
  1. abrnomal portal blood flow
  2. hepatic dysfunction
  3. urea cycle abnormality
105
Q

what coagulation factors does the liver produce

A

all of them except for VIII and vWF

106
Q

what % of coagulation factor depletion is needed for prolonged clotting times

A

>%70

107
Q

what can radiography evaluate

A
  1. liver shape and size
  2. choleliths

unhelpful with ascites

108
Q

what is ultrasound useful for (3)

A
  1. assessment of hepatic parenchyma, portal vein branches
  2. assessment of biliary tract – investigations post hepatic jaundice
  3. identify and sample nodules, massess, abdominal effusions
109
Q

what does ascites cause (4)

A
  1. imbalance in starlings laws (decreased oncotic pressure –> hypoalbuminemia, increased hydrostatic pressure –> portal hypertension)
  2. leakage from organs (bile)
  3. inflammation (peritonitis)
  4. leakage from vessels (blood)
110
Q

what is portal hypertension

A

high blood pressure in the hepatic portal system

111
Q

what are the consequences of portal hypertension (4)

A
  1. ascites
  2. hepatic encephalopathy
  3. multiple acquired shunting
  4. gastrointestinal ulceration
112
Q

what os post hepatic portal hypertension

A

the caudal vena cava

113
Q

what are the types of hepatic portal hypertension

A
  1. post sinusoidal: central vein
  2. sinusoidal: sinusoid
  3. pre sinusoid: portal vein
114
Q

what is pre hepatic portal hypertension

A

portal vein

115
Q

if the ascitic fluid is low protein transudate what could the site of origin of portal hypertension be (3)

A
  1. pre hepatic
  2. intra hepatic
  3. pre sinusoidal
116
Q

what are common causes of a low protein transudate (3)

A
  1. ligation of portosystemic shunts
  2. portal vein thrombosis
  3. portal vein hypoplasia
117
Q

if the ascitic fluid is high protein transudate what could the site of origin of portal hypertension be (4)

A
  1. post hepatic
  2. intra hepatic
  3. post sinusoidal
  4. sinusoidal intrahepatic
118
Q

what are causes of high protein transudates (2)

A
  1. chronic hepatitis
  2. right sided failure
119
Q

dif you have a low protein transudate what should you check

A

check serum albumin –> if that is low you need to rule out GI (PLE) or a kidney loss (PLN)

if it is normal –> then it is due to portal hypertension

120
Q

if the transudate is high in protein what type of portal hypertension is this and why

A

its post sinusoidal

somewhere between the hepatic sinusoids and the heart –> the fluid is higher in protein because the sinusoids in the liver are lined with fenestrated endothelial and are permeable to albumin

121
Q

what should you do before you decide to do a liver biopsy

A

check coagulation times and platelet numbers

if they are prolonged give plasma or vitamin K

monitor for signs of hemorrhage (RR, HR, mucus membranes)

122
Q

what are the pros of a FNA biopsy (5)

A
  1. minimally invasive
  2. little equipment
  3. sedation
  4. useful for lymphoma, mast cell tumours, and hepatic lipidosis
  5. bile samples
123
Q

what are the cons of a FNA biopsy (4)

A
  1. accuracy of cytology limited (30-50% agreement with histology)
  2. doesn’t evaluate hepatic architechture
  3. only cells that exfoilate
  4. iatrogenic damage gall bladder
124
Q

what size of needle is used for a FNA biopsy

A

23g

125
Q

what are the pros of using a cutting needle biopsy (3)

A
  1. larger sample size allows exam of hepatic architecture
  2. avoids laparotomy
  3. sample focal disease
126
Q

what are the cons of using a cutting needle biopsy (5)

A
  1. general anesthesia
  2. specialist equipment
  3. less accurate than surgical biopsies
  4. difficult with small livers or ascites
  5. hemorrhage
127
Q

what are the pros of a surgical biopsy (3)

A
  1. better diagnostic samples: larger sample allows better exam of hepatic architecture
  2. can get samples from multiple liver lobes and bile aspirate
  3. can visualize hemorrhage
128
Q

what are the cons of surgical biopsy (3)

A
  1. general anesthesia
  2. more invasive procedure
  3. risk of hemorrhage
129
Q

what are the clinical signs of biliary disease

A

non specific

+/- jaundice

+/- pale white feces

130
Q

what biochem changes can be seen with biliary disease (3)

A
  1. increase cholestatic liver enzymes: ALP, GGT > ALT, AST
  2. increase in cholesterol
  3. increase in bilirubin
131
Q

what are examples of biliary disease (5)

A
  1. pancreatitis obstructing common bile duct
  2. cholecystitis
  3. gall bladder mucocele (dogs)
  4. neoplasia: biliary carcinoma/adenoma (cats)
  5. cholelithiasis (dogs > cats)
132
Q

what is gall bladder mucocele

A

distention of gallbladder by an innappropriate accumulation of mucus

thick gelatinuous bile within gall bladder

133
Q

what will the gall bladder look like on US with gall bladder mucocele

A

kiwi appearance

134
Q

what secondary diseases should you check for if you suspect gall bladder mucocele

A

hypothyroidism

cushings

135
Q

what breed is gall bladder mucocele

A

shetland sheep dog (sheltie)

136
Q

how is gall bladder mucocele treated

A

surgical cholecystectomy required

137
Q

what is bile peritonitis

A

inflammatory response of the lining of the abdominal cavity to the presence of free bile

138
Q

what are the causes of bile peritonitis (5)

A
  1. trauma
  2. chronic inflammation
  3. obstructive lesions (cholelithiasis)
  4. neoplasia
  5. ruptured mucocele
139
Q

how would bile peritonitis present

A
  1. emergency
  2. signs of sepsis
  3. abdominal pain
  4. ascites
140
Q

what would the fluid look like in bile peritonitis

A

yellow/brown

measure bilirubin (>2x serum)

141
Q

how would you treat bile peritonitis

A

ex lap

consider referral

142
Q

what is chronic hepatitis

A

inflammation of hepatic parenchyma

143
Q

what are the breed related forms of chronic hepatitis

A
  1. lab
  2. english springer spaniel
  3. cocker spaniels
  4. dobermans
144
Q

what are indicators of poor prognosis with chronic hepatitis (3)

A
  1. ascites
  2. jaundice
  3. hepatic encephalopathy
145
Q

how is chronic hepatitis treated

A

immunosuppressives

146
Q

what is cholangitis

A

inflammation of the biliary duct

147
Q

what is commonly seen with cholangitis in cats

A

triaditis

duodenitis, pancreatitis, cholangitis

148
Q

what are the histological classifcations of cholangitis (4)

A
  1. neutrophilic cholangitis
  2. lymphocytic cholangitis
  3. chronic cholangitis due to liver fluke (tropical, subtropical climates)
  4. destructive cholangitis (uncommon, dogs)
149
Q

how is cholangitis diagnosed

A

biopsy

150
Q

what is neutrophilic cholangitis

A

suppurative inflammation on histology

151
Q

what is the signalment of neutrophilic cholangitis

A

tend to be younger cats

152
Q

what are the clinical signs of neutrophilic cholangitis

A

typically systemically unwell

pyrexia

lethargy

jaundice

153
Q

what is the etiology of neutrophilic cholangitis

A

ascending infection from intestines –> anatomical problem in cats

E. coli most common

154
Q

how is neutrophilic cholangitis treated

A

6-8 weeks of antibiotics

155
Q

what is lymphocytic cholangitis

A

suspected immune mediated disease

156
Q

what is the signalment of lymphocytic cholangitis

A

most cats are middle aged or older

157
Q

what are the clinical signs of lymphocytic cholangitis

A

long course (several weeks to months) of vague illness

systemically well – normothermic

increase in GGT

158
Q

how do you treat lymphocytic cholangitis

A

immunosuppressive (steroids)

159
Q

what is vacuolar hepatopathies

A

hepatocytes become markedly distended with cystolic glycogen

160
Q

what is vacuolar hepatopathies associated with (3)

A
  1. glucocorticoid administration
  2. hyperadrenocorticism (cushing’s disease)
  3. endogenous release of corticosteroids in response to chronic stress, illness, inflammation or neoplasia
161
Q

what biomarker is often elevated in vacuolar hepatopathies

A

ALP

162
Q

what are primary hepatobiliary neoplasias (3)

A
  1. biliary adenomas/carcinomas (cats), hepatocellular adenomas/carcinomas (dogs)
  2. hepatic lymphoma
  3. hepatic hemangiosarcoma
163
Q

what are secondary/metastatic hepatobiliary neoplasias (5)

A
  1. lymphoma
  2. leukemia
  3. mast cell tumour
  4. histiocytic
  5. HSA
164
Q

what is nodular hyperplasia

A

benign hyperplastic in older dogs

165
Q

what is increased in nodular hyperplasia

A

increase in ALP (+/- increase in ALT), diagnosed on biopsy

Module 16 (26 decks)

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