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G.I. > Ch.33Dzesofthehepatobiliarysystem > Flashcards

Ch.33Dzesofthehepatobiliarysystem Flashcards

1
Q

Pathologic changes in the liver

A

biliary hyperplasia
death of hepatocytes
fibrosis

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2
Q

What percentage of reserve capacity does the liver have?

A

close to 80% can be removed before regeneration and recovery are no longer possible

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3
Q

In which part of the biliary tree does most cell division take place?

A

Rappaport’s zone 1 (the portal area)
–>Then cells pushed to central lobular area

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4
Q

What are reasons the liver will not regenerate?

A

-antimitotic agents such as pyrrolizidine alkaloid metabolites or antineoplastic drugs that prevent cell division
-restricted by connective tissue
-fibrosis

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5
Q

Icterus is due to

A

failure of uptake, conjugation or excretion of bilirubin

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6
Q

Why is diarrhea in cattle seen with chronic liver disease?

A

-related to portal hypertension & increased hydrostatic pressure

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7
Q

Why does ascites occur with liver failure?

A

-portal hypertension caused by venous blockage producing INC hydrostatic pressure
-protein leakage into peritoneal cavity
-lymph leakage caused by cirrhosis or veno-occlusion

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8
Q

C/S of pruritus with liver disease occurs because

A

retention of bile salts
**not usually seen in cases of liver dz in horses

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9
Q

What does hepatic photosensitization, dermatitis lesions look like:

A

-white areas–> skin becomes erythematous, then thickend with keratin crusts and then becomes necrotic

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10
Q

Hepatic photosensitization is caused by what agent?

A

photodynamic agent phylloerythrin
–formed in the GI tract of lg animals by bact degradation of chlorophyll
- after absorption into portal circulation, phylloerythrin should be conjugated by liver and excreted into bile
-phylloerythrin accumulates in skin & reacts to sunlight & emits energy that causes lesions

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11
Q

A change in fecal color is not usually seen in adults with liver dz, however can see changes in young animals with simple digestive tracts. What fecal color changes can you see in young animals?

A

Stercobilin metabolism of bilirubin seen with cholestasis–> feces are lighter in color

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12
Q

Why can hemorrhage occur with liver disease?

A

When clotting factors are not synthesized in adequate amounts, such as factor I, II, V, VII, IX, X
- terminal hemolytic crisis caused by RBC fragility
**advanced liver disease

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13
Q

Why is tenesmus (+/- rectal prolapse) seen in some cattle with liver disease?

A
  • assoc with diarrhea
    -hepatic encephalopathy
    -aggrevated by edema of the bowel secondary to portal hypertension
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14
Q

Define hepatic encephalopathy

A

syndrome caused by hepatic dysfunction or portosystemic shunting of intestinal blood
- potentially reversible metabolic or neurotransmitter disorder
-characteristic lesions in the CNS (altered astrocytes)

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15
Q

Clinical signs of hepatic encephalopathy

A

-behavioral changes
-depression & incoordination
-walk aimlessly
-head pressing
-apparent blindness
-foot stomping

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16
Q

What product in the brain is correlated with severity of hepatic encephalopathy?

A

glutamine

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17
Q

Blood ammonia is associated with hepatic encephalopathy, which is believed to be through which mechanism?

A

Ammonia not being metabolized by liver to urea
–> astrocytes contain the enzyme glutamine synthase, which adds a molecule of glutamate to ammonia to form glutamine

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18
Q

Besides ammonia what other substances have been implicated in the clinical signs of hepatic encephalopathy?

A

-manganese deposits in brain
-imbalance of inhibitory & excitotary neurotransmission (GABA)
-false neurotransmitters
-INC tryptophan, phenylalanine, tyrosine
-aromatic amino acids

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19
Q

Besides liver, GGT is present in what other organs?

A

kidney
pancreas
**high levels in young animals from colostrum

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20
Q

Which enzyme is the most sensitive indicator of disease in the horse?

A

GGT
**will remain elevated for weeks

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21
Q

Besides liver, ALP is present in what other organs?

A

bone
intestine
macrophages
placenta

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22
Q

Which liver enzymes are increased in cholestasis?

A

ALP
GGT

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23
Q

Which liver enzymes are increased d/t hepatocellular damage?

A

AST
LDH, SDH, GDH

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24
Q

SDH in horses should be interpreted with other liver enzymes because it can increase d/t

A

decreased tissue perfusion–> hypoxia or dehydration

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25
Q

Where is ammonia produced from?

A

GI tract from digestion of proteins and amino acids, absorbed by GIT into blood and carried to liver in portal circulation

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26
Q

What is ammonia converted to?

A

urea in the hepatic urea cycle

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27
Q

Why in ruminants is serum urea nitrogen low and ammonia is often high?

A

because rumen bacteria synthesize protein from urea, ruminants have been off feed

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28
Q

What is the albumin half-life in the following species:
cattle
horse
sheep

A

Horse: 19.4 days
cattle: 16.5 days
sheep: 14 days

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29
Q

Is hypoalbuminemia/hypoproteinemia a common feature of liver disease in horses?

A

not common/rare in horses

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30
Q

Amino acid ratios are altered in liver disease to what ratio?

A

short branched chain amino acids are decreased
aromatic amino acids increased

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31
Q

Increased total bilirubin is caused by:

A

liver failure
bile blockage
excess production d/t hemolysis
fasting animals (esp horses)

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32
Q

direct bilirubin to total bilirubin ratio in horse & cattle

A

horse: direct: total= 0.3
cattle: direct: total = 0.5

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33
Q

what is the primary bile pigment?

A

bilirubin– produced from heme

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34
Q

breakdown of erythrocytes (rbcs), then

A

heme converted to bilverdin
–> bilirubin

**in macrophage system

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35
Q

Unconjugated bilirubin is bound to?

A

albumin

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36
Q

Within the hepatocyte bilirubin is conjugated to

A

diglucuronide or glucose (horse)

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37
Q

Will the kidneys filter conjugated vs unconjugated bilirubin?

A

conjugated bilirubin

**when concentrations are high enough

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38
Q

IN the GIT bilirubin is convered to what compound?

A

urobilinogen by anaerobic bacteria

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39
Q

What is the pathway for urobilinogen?

A

– absorbed by GIT & re-excreted by liver
–excreted in urine

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40
Q

What is the benefits of measuring urobilinogen in urine?

A

If complete biliary blockage– no urobilinogen in urine
If hemolysis– increased urobilinogen in urine

**must be measured within 1-2 hours or amount detected will be erroneously low

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41
Q

Increased serum bile acid concentrations in horses can be caused by:

A

hepatocyte damage
blockage of bile flow
shunting of portal blood to systemic circulation (bypassing liver)

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42
Q

What does the liver synthesize bile acids from?

A

cholesterol

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43
Q

What are the primary bile acids connugated with amino acids before excretion into the bile?

A

cholic
chenodeoxycholic acids

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44
Q

Which form of bile acids are present within the intestine?

A

conjugated
**they are soluble & form micelles with fat b/c detergent properties

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45
Q

Where are bile acids resorbed?

A

w/in the ileum
– enterohepatic ciruclation 95% of bile acids

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46
Q

What is the difference between cattle and horses when measuring serum bile acid concentrations?

A

cattle have hourly fluctuation in bile acid concentrations

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47
Q

Liver biopsy is most beneficial in which group of diseases?

A

diffuse or zonal lesions: toxic, infectious, & metbaolic liver dzes

**focal lesions are easily missed on biopsy

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48
Q

What is the difference in location for liver biopsy among sp:
cattle
horse
sm ruminant

A

cattle: 11th ICS
horse: 12-14th (ideally 14th)
sm rum: 9th or 10th

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49
Q

What are indicators of a poor prognosis for liver disease?

A

albumin: less than 2.6 g/dL in horses
INC globulin
prothrombin time (PT) > than 30% normal
INC GGT, ALP (esp if SDH/LDH normal to dec)
Severe histopath abnromalities )PA tox

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50
Q

What are terminal clinical signs of liver disease?

A

development of hemolytic crisis in the horse
marked hepatic encephalopathy in patient with fibrotic liver

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51
Q

What is the most common cause of acute hepatitis and hepatic failure in N. America?

A

Theilers disease

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52
Q

What are the 2 forms of Theilers disease?

A
  1. complication of equine origin biologic product (serum/plasma)
  2. recent equine origin biology product administration
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53
Q

Which population of horses is at most risk for development of Theilers disease?

A

Disease of adult horses
- post foaling mares & post castration geldings at increased risk d/t freq us of prophylactic tetanus antitoxin in those horses

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54
Q

Which viruses have been implicated as the etx agent of Theilers disease?

A

Theilers dz associated virus
Equine parvovirus hepatitis
Equine hepacivirus

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55
Q

Clinical signs of Theilers disease arise typically after what time frame of administration of blood products?

A

1 to 3 months

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56
Q

Theilers disease can be diagnosed via histopath/necropsy, what are the lesions

A

liver is small, “dish rag appearance”

Histo: widespread necrosis of hepatocytes– most severe in the centrilobular and midzonal areas; eosinophilic granular mass around normal architecture in which ghost out lines of necrotic hepatocytes are present

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57
Q

Differentials for Theilers disease (acute hepatitis)

A

heavy metal and organic hepatotoxins (PA)

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58
Q

Diets containing what protein source are beneficial in preventing worsening signs of hepatoencephalopathy?

A

Diets high in branched chain amino acids
-sorghum, milo or beet pulp

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59
Q

Which medications can be administered to reduce ammonia production and absorption from the GI tract?

A

oral neomycin, lactulos and mineral oil

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60
Q

Which sedatives should be avoided in horses with hepatoencephalopathy?

A

benzodiazepines (midazolam/diazepam)

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61
Q

Why are IV fluids (+/-dextrose) recommended in treatment of liver disease?

A

to reduce hepatic work load and maintain plasma volume

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62
Q

Black disease is also named

A

infectious necrotic hepatitis
**highly fatal disease occurs worldwide

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63
Q

What is black disease caused by?

A

Clostridium novyi type B

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64
Q

When does black disease occur?

A

require an anaerobic environment for growth, so black dz occurs only when there has been enough damage to liver to provide anaerobic environment for bug to grow

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65
Q

What parasite is associated with black disease?

A

liver flukes: fasciola hepatica, but also Fascioloides magna or Dicrocelium dendriticum (france)

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66
Q

The C. novyi strainst hat cause black disease produce which two exotoxins?

A

alpha toxin and beta toxin

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67
Q

How does C. novyi alpha toxin enter cells

A

by receptor mediated endocytosis & inhibits ras and rho guanosin triphosphates by glycosylation

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68
Q

How does C. novyi beta toxin enter cells

A

necrotizing and hemolytic phospholypase C (lecithinase)

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69
Q

C. novyi type B is widely distributed in soils and its spores are continuously ingested and shed in feces of grazing animals. How does black disease occur?

A

C. novyi spores enter macrophage system– particularly Kupffer cells of liver
–anaerobic conditions develop– resident spores geminate & enter a vegetative state–> exotoxins produced by the bacteria then damage neurons, vascular endothelium and other tissues–> death

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70
Q

What is the most common clinical presentation associated with black disease?

A

peracute death

** c/s prior to death are nonspecfic

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71
Q

How does black disease get its name?

A

Venous congestion darkens the skin– which gives the disease its common name

**affected animals do not show red urine or bleeding from the nose or rectum

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72
Q

What are the primary necropsy lesions of Black disease?

A

single or multiple areas of hepatic necrosis that appear yellow to white in color and are surrounded by a broad zone of hyperemia

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73
Q

What sample is ideal for fluorescent antibody identification of C. novyi type B?

A

impression smears from the liver lesions

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74
Q

Prevention of black disease

A

fluke control–> pasture or range management, control of water sources, strategic tx of animals with appropriate anthelmintics, limiting access to streams/ponds/marshes

clostridial bacterins (vaccines)

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75
Q

Bacillary hemoglobinuria or “Redwater” disease is caused by whic organism?

A

Clostridium haemolyticum

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76
Q

What is the major toxin of C. haemolyticum?

A

beta toxin– phospholipase C that causes hetpaocyte necrosis, hemolysis and dmage to capillary endothelium

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77
Q

What is the primary action of C. haemolyticum beta toxin

A

induce localized hepatic necrosis & intravascular hemolysis

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78
Q

Like C. novyi, C. haemolyticum is also found in teh soil. When does disease occur?

A

when insult to the liver providdes an anaeorbic condition required fo rabcterial growth and toxin production

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79
Q

Bacillary hemoglobinuria is a regionalized disease, to which locations?

A

limited to alkaline soils (but can be endemic in regions with acid soils)
outbreaks tend to follow flooding
distribution tends to be erradic

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80
Q

Bacillary hemoglobinuria can be present with peracute death, but reports of what clinical signs are observed?

A

rectal bleeding or bloody feces

severe hemoglobinuria– dk red, port-wine colored urine reported

blood is thin and coagulates slowly

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81
Q

What is the pathognomonic lesions of bacillary hemoglobinuria?

A

ischemic hepatic infarct– zone of hyperemia at its interface with viable liver titsue

**unlike a classic infarct– bacillary hemoglobinuria results form progressive nelargement of focus of coagulative necrosis caused by bacterial toxins

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82
Q

Laboratory confirmation of Bacillary hemoglobinuria is performed through:

A

identification of both the causative bacteria and the toxin

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83
Q

When vaccinating for prevention of bacillary hemoglobinuria or prevention of black disease, what is the timing?

A

timing of vaccination must be determiend by local climate and liver fluke season
–short liver fluke season– vaccinate once
–long liver fluke season– vaccinate twice

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84
Q

liver enzymes in neonatal foals tend to be significantly more elevated in comparison to adults. What of serum bile acids?

A

serum bile acids greater in foals than adults for first 5 weeks of life

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85
Q

What is Tyzzer’s disease? and which age range does it affect?

A

acute hepatitis

foals: 7-42 days of age

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86
Q

What is the causative organism of Tyzzer’s disease?

A

Clostridium piliforme : gram negative, flagellated, spore-forming intracellular obligate anaerobc

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87
Q

Multiple strains can infect horses, which two distinct strains?

A

E and R1

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88
Q

What are predisposing factors to the development of Tyzzers disease?

A

-bacterial spores shed in feces of carrier horses
-high-protein & nitrogenous diets fed to nursing mares
-time of year, age, resident statu sof mare, heavy rain fall in spring
-foals born between march and may more likely to develop disease
-foals from younger mares
-immunocompromised foals

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89
Q

Diagnosis of Tyzzers disease

A

PM: acute, widespread multifocal areas of necorsis and hepatitis, with intrahepatocellular filamentous bacteria present ath tpierphery of the lesion

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90
Q

Prognosis of Tyzzers disease?

A

Poor- high fatal, foals die within 2 to 48 hours of showing clinical signs

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91
Q

Other possible bacterial causes of hepatitis/abscess formation in foals (besides tyzzers)

A

leptospirosis
actinobacillus equuli
streptococcus zooepidemicus
listeria moncytogenes
bartonella henselae
others

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92
Q

In blood transfusions in foals, what volume of blood products are foals likely to develop liver failure?

A

4L or more
**19.5 times more likely to develop liver failure than foals receiving a lower volume

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93
Q

Deferoxamine

A

iron chelator
enhances urinary iron elimination & decreases hepatic iron accumluation after blood trasnfusion in healthy foals

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94
Q

Kernicterus is mroe likely to develop in foals with total bilirbin of what level?

A

tbili of 27 mg/dL or greater

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95
Q

Iron toxicity in foals usually manifests when?

A

Foals given iron prior to receiving colostrum, colostral acquired glutahtion or other susbtances may be protective against hepatotoxicity

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96
Q

When do C/S of iron toxicity occur after supplementation in foals?

A

2 to 5 days post admin

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97
Q

When do signs of a congenital portosystemic shunt in foals usually occur?

A

at age of 2 to 3 months of age
**when start ingesting grass

98
Q

Hepatic failure syndrome can be seen in what breed of horses? and pathogenesis?

A

Morgan foals

micro exam: bridging fibrosis, bile duct hyperplasia, karyomegaly, cytomegaly

unknown cause, though to be inherited defect in mitrochondrial tarsnporter proteins

99
Q

Glycogen branching enzyme deficiency is a fatal inherted disease of what breeds?

A

autosomal recessive dz
Quarterhorses and Paint horses

100
Q

GBED is a result of

A

mutation of glycogen branching enzyme 1 (GBE1) gene that drastically decreases the amount of GBE protein in homozygotes

**dzed foals cannot store and use glycogen to maintain normal glucose homeostasis

101
Q

Chronic active hepatitis is

A

an idiopathic progressive hepatophaty with insious onset
**etx and pathogeneiss unkonwn

102
Q

DDx for chronic active hepatitis

A

pyrrolizidine alkaloid toxicity
bile stones
abdominal abscesses
other chronic wasting diseases

103
Q

Histopath of chronic active hepatitis

A
  • localized portal or periportal areas
    -infiltration of inflammatory cells, biliary hyperplasia and fibrosis or cirrhosis
    -mononuclear cell infiltration often predominants, but neutrophilic component may be present wiht a primary ro secondary infecitou sprocess
104
Q

in chronic active hepatitis, when are corticosteroids beneficial?

A

when lymphocytes orplasma cells are predominant cell type

105
Q

What are common plants that contain pyrrolizidine alkaloids?

A

Senecio jocaboae- tansy ragwort or stinking willie
Senecio vulgaris- common groundsel
Senecio douglasii var longilobus—threadleaf groundsel
Senecio riddelli00 Riddell’s groundsel
Senecio triangularis— Arrowleaf groundsel or tarweed
Senecio alpinus— Alpen-Kreuzkraut (EU)
Amsinckia intermedia—Fiddleneck
Crotalaria spp.—Rattlebox
Echium plantagineum, Echium lycopsis— Patterson’s curse, Salvation Jane or vipers bugloss
Heliotropium europaeum—Common heliotrope
Symphytum officinale—Comfrey
Cynoglossum officinale-Houndstongue
Eupatrium maculatum— Joe Pye weed or Bruner’s trumpet
Baccharis pteronioides— Yerba depasmo
Borago officinalis— Borage or starflower
Erechitites spp.
Trichodesma spp.

106
Q

What is the approximate toxic dose of dried Senecio as a percentage of body weight for each spp:
Horses
Cattle
Goats
Sheep

A

Horses: 5%
Cattle: 2-5%
Goats: 125%-400%
Sheep: >150%

107
Q

Why are clinical signs of PA toxicity delayed?

A

The effects of PA toxicity are cumulative

108
Q

Are pyrrolizidien alkaloids directly toxic?

A

No— they must be bioactivated to toxic alkaloids (pyrroles) in the liver

109
Q

The pyrroles that are metabolized from pyrrolizidine akaloid results in:

A

-pyrroles crosslink double-strand DNA in a dose-dependent manner
— crosslinking of DNA produces an anti-mitotic effect

110
Q

Because hepatocytes cannot divide once pyrroles cause antimitosis. What is the effect?

A
  • hepatocytes becomes megalocytes (large hepatocytes and large nuclei)
  • as cells die they are replaced by connective tissue
111
Q

PA toxicity is a veno-occlussive disease that result in marked portal hypertension. What clinical signs can this result in ruminants?

A

Diarrhea
Ascites

112
Q

What are differential diagnosis for PA toxicity?

A

Dzes that cause liver failure (eg, alfatoxicosis or liver flukes)
Chronic debilitating dzes: GI parasites, Johnes disease

113
Q

Why are sheep and goats more resistant to PA toxicity?

A

Because a consortium of ruminal micorbes from sheep degrades PAs found in Senecio jacobaea to less toxic metabolites
- sheep liver microsomal enzymes play a role in detoxifying PAs

114
Q

What are the characteristic changes on histopathology for PA toxicity?

A

Fibrosis
Bile duct proliferation
Megalocytosis

115
Q

When is PA toxicity fatal?

A

Once bridging of connective tissue between portal areas

116
Q

What is a possible control measure that can be implemented into prevent PA toxicity?

A

To have sheep graze Senecio infested pastures to control the weed
**b/c they are less susceptible

117
Q

Why is the liver most vulnerable to toxins?

A

B/c the liver is the first organ to receive toxins absorbed from the GIT

118
Q

Hepatic abscesses are most common in which animals?

A

Cattle fed high grain diets
**especially feedlot cattle

119
Q

Hepatic abscesses in cattle are geernally polymicorbial infections— what is the primary etiologic agent?

A

Fusobacterium necrophorum — gram negative pleomorphically rod shaped anaerobe

120
Q

What are virulence factors of Fusobacterium necrophorum in the pathogenesis of hepatic abscesses?

A

Luekotoxin— cytotoxic to polymorphonuclear neutrophil leukocytes (PMN), macros, hepatocytes & ruminal epithelial cells
**allows bact to surivve, proliferate & establish to set up infection

121
Q

What is the second most frequent pathogen isolated from liver abscesses?

A

Trueperella pyogenes

122
Q

Why is Trueperella pyogenes so easily cause liver abscesses?

A

B/c ruminal wall appears to be the niche for T. Pyogenes
** the wall provides an aerobic microenvironment in an otherwise anaerobic environment of the rumen

123
Q

Abscesses in the liver result from entry and establishment of F. Necrophorum alone or with other bacteria. What are rouched by which other bacteria can gain access to the liver?

A

Lportal vein, hepatic artery, umbilical vein (newborns with omphalophlebitis), bile duct system, and direct extension

124
Q

Liver abscesses caused from direct extension of infection from adjacent tissues and organs, is most commonly seen in what population of animals?

A

DAIRY COWS
**traumatic reticuloperitonitis

125
Q

Rumenitis liver abscess complex is caused by:

A

Ruminal lesions results from acidossi that predipose to hepatic abscesses

126
Q

Pathology of liver abscess formation?

A

F. Necrophorum forms an embolus in the sinusoid
—> progresses to coagulative necrosis by involving adjdacen thepatocytes
—> progressively changes into a pus filled, encapsulated, true abscess

127
Q

What antibiotics are used for the prevention of liver abscesses in feedlot cattle?

A

Chlortetracycline, oxytetracycline and tylosin used for prevention

128
Q

What is teh most effective antibiotic and most commonly used feed additive in feedlot cattle for liver abscesses?

A

Tylosin

129
Q

What management recommendations are there for control and prevention of liver abscesses?

A

Antimicrobial compounds in feed or vaccination
Prudent bunk mgmt to minimize fluctuations in intake & ruminal acidosis
Gradual adaptation to high-grain diets
Avoiding either underfeeding or overfeeding
Increasing feeding freqency to spread otu intake
Increasing roughage content of the feed
Inclusion of grain by-products like distsiller’s grains
Imposing quality control in mixing feeds
Providing adequate bunk space and fresh clean water

130
Q

What are possible sequelae to liver abscess formation?

A

Septic cardiac and pulmonary emboli

131
Q

Liver abscesses can spread to septic cardiac and pulmonary emboli, how does the condition lead to sudden death?

A

Phlebitis caused by extension of liver abscess involving the caudal vena cava
— leads to thrombus formation anywhere between liver & right atrium

—Then lead sto rupture of caudal vena cava, pneumonia, infarction, endocarditis, hemopytysis and epsitaxis

132
Q

Why do liver abscess have a major economic liability to the producer, packer and consumer of beef?

A

From reduce animal performance and reduction in carcass yield d/t reduced feed intake, reduced weight gain, decreased feed efficiency, and decreased carcass dressing percentage

133
Q

Hepatic abscess in horses are usually associated with:

A

Gastrointestinal diseases: proximal enteritis, inflammatory bowel disease, or ileal diverticulitis and may develop as a sequel to abdominal exploratory surgery

134
Q

What are the most frequent bacteria isolated from liver abscesses in horses?

A

Streptococcus equi
E. Coli
Bacteroides fragilis
Coryndebacterium pseudotuberculosis
F. Necrophorum
Peptostreptococcus spp

135
Q

What is the prognosis for liver abscesses in horses?

A

Generally poor bc/c failure to respond to antimicrobial therapy

136
Q

Hepatic lipidosis (fat cow syndrome) occurs in what population of cattle?

A

Dairy cows after parturition—> d/t excessive mobilization of fat to the liver in well condition or overconditioned cows

137
Q

Mobilization of fat that results in hepatic lipidosis is induced by

A

By negative energy balance and hormonal changes that occur around the time of calving
— negative energy balance is aggravated by concurrent periparturient diseases tha treduce feed intake and icnrease energy needs

138
Q

Clinical disease of hepatic lipidosis can be prevented how?

A

Controlling the cows diets to meet National Research Council (NRC) requirement and preventing milk fever

139
Q

What other concurrent diseases are associated with hepatic lipidosis?

A

Metritis
Retained fetal membranes
Mastitis
Parturient paresis
Displaced abomasum

140
Q

What are common abnormalities on bloodwork for hepatic lipidosis?

A

Most consistently elevated: OCT, total bilirubin, AST
Leukopenia and degenerative left shift
NEFA (non-esterified fatty acid levels increased
Triglycerides & cholesterol decrased

141
Q

Clinical chemistry and ultrasound findings may be helpful in the diagnosis of hepatic lipidosis in cows, what is the gold standard diagnostic?

A

Liver biopsy

142
Q

What remains the gold standard for the laboratory diagnosis of hepatic lipidosis in cattle?

A

Total hepatic fat concentrations

143
Q

Necropsy and Histologic changes of hepatic lipidosis

A

Enlarged with swollen and rounded edges, pale yellow in color and may float inw ater
Histo: fatty infiltration of hepatocytes, esp in centrilobular & intermediate areas

** these findings are sometimes not much different from those of healthy, high-producing dairy cows in early lactation

144
Q

What occurs in the negative energy balance that leads to hepatic lipidosis in cattle?

A
  1. Negative energy balance induced by lactation, fetal growth , exercise, etc.
  2. Blood glucose decreases, hormone sensitive lipases activated to convert fat to FFAs and NEFAs and glycerol
  3. In liver glycerol used to produce glucose or combine with FFAs to make triglycerides
  4. Fatty acids may be degraded through beta oxidation and two carbon fatty acids converted to acteyl coenzyme A (coA)— combines with oxaloacetate to ener the Krebs cycle for production of energy
145
Q

In the negative energy balance pathway (that leads to hepatic lipidosis), if there is not enough oxaloacetate available, acetl CoA is converted to

A

Ketone bodies
**high concentration can reduce feed consumption perpetuates the negaative energy balance

146
Q

When triglycerides elave the liver, they are very low-density lipoproteins (VLDLs), which contain:

A

Phospholipid
Cholesterol
Triglycerides
Apolipoprotein A

147
Q

When liver is producing more circulating VLDL’s why does the body send it back to the tissues for storage?

A

Because the same endocrine hormones that activate hormone-sensitive lipase and inhibit lipogenesis and glycogen synthesis may also inhibit production of VLDLs

148
Q

In hepatic lipidosis, why is fat accumulation in the liver bad?

A

It impairs function of liver

** hepatic lipidosis is reversible if the cause is removed and energy balance becomes positive

149
Q

IN which population of cattle is hepatic lipidosis occur naturally?

A

All high-producing dairy cows have increased amounts of fat (15-32% by weight) in liver before calving and during the first few weeks after parturition

150
Q

The treatment of midl to moderately fatty liver involves

A

Elimination of negative energy balance
—IV glucose
-insluin to alter ratio
-glucagon
-glucocorticoid injections
0choline subcu

151
Q

What is the prognosis for hepatic lipidosis in cows?

A

Guarded— unless the concurrent dzes can be treated succesffuly and liver fat mobilized
**important to treat the primary disease

152
Q

Prevention for hepatic lipidosis involves minimizing or eliminating what primary risk factors? **Prepartum

A

Obesity (BCS >4)
Severe feed restriciton
Feeding excess energy
Long calving interval

153
Q

Prevention for hepatic lipidosis involves minimizing or eliminating what primary risk factors? **Postpartum

A

Concurrent diseases
Anorexia or fasting
Feed restriction
Sudden feed changes

154
Q

What are factors to consider in the dry cow ration to prevent periparturient diseases?

A

Feed higher protein diets during the dry period
Feeding good quality roughages
Additional grain 2-4 weeks before parturition
Limit dry matter consumption to 2% of body weight

155
Q

What are other periparturient diseases to consider, along with hepatic lipidosis when developing a dry matter ration for cows?

A

Milk fever
Displaced absomasum
Mastitis
Metritis
Ketosis
Ruminal lactic acidosis
Retained placenta

156
Q

Why is it beneficial to supplement the dry matter ration of cattle with cobalt?

A

Because it is a precursor of vitamin B12 that is a cofactor int he rate limiting step in conversion of proprionate (the primary glucose precursor) to succinyl coA

157
Q

The protein energy malnutrition and pregnancy of beef cows occurs in what months (typically) and is characterized by?

A

**usually occuring in the winter
**characterized by weight loss, weakness, depression & sometimes inability to rise

158
Q

What are potential predisposing factors to beef cows developing protein-energy malnutrition/pregnancy toxemia?

A

Negative energy balance: decreased quality & quantity of feed when caloric requirements are increased by fetal development & cold weather
Growing, pregnant heifers especially suscepible
Unaplatable feed
Snow cover
Diseases

159
Q

Different from hepatic lipidosis seen in dairy cattle, protein energy malnutrition/pregnancy toxemia of beef cattle, diagnosis and presentation is ddifferent in which ways

A

Necropsy: liver is small\
Ketonuria- not typical
Muscle mass decreased
Serous (brown) atrophy of fat is often present (esp in coronary groove, bone marrow & perirenal areas)
+/- fatty yellow liver

160
Q

When treating protein energy malnutrition/pregnancy toxemia treatment?

A

**usual unrewarding, d/t reversing an advanced catabolic state—> 454 kg cow requires 13 mCal of metabolizable enrgy daily

  1. IV fluids
  2. Improve energy balance
    3 Treat concurrent dzes
161
Q

What role does environmental temperature play a role in protein energy malnturition and pregnancy toxemia of beef cows?

A

Envrionmental temperature can increase energy needs for beef cattle on pasture or range, as temperature falls from 20C to 10C, roughly 10% more energy is necessary for maintenance and at freezing temperature 0C, 20% additional energy is required

162
Q

What are the keys in prevention of protein-energy malnutrition and pregnancy of beef cows?

A

Adequate body condition (scores 5 to 7) entering the third trimesteer
Availability of good quality to excellent quality forage in adequate amounts

163
Q

When does pregnancy toxemia occur in ewes and does?

A

During the last 2 to 4 weeks of gestation

164
Q

Why does pregnancy toxemia occur in the last 2 to 4 weeks of gestation?

A

Nearly 80% of fetal growth occurs in the last 6 weeks of gestation- can result in negative energy balance occurring from increased energy demands of rapid fetal growth in late gestation and insufficient feed intake

165
Q

Predisposing factors to the development of pregnancy toxemia in ewes and does?

A

Poor quality feed
Cold weather
Lack of exercise
Stress of movement
Greater than one fetus
Over weight animals

166
Q

Clinical signs of pregnancy toxemia in ewes and does

A

Anorexia
Separation from herd/flock
Depression
Recumbency
Neurologic signs: tremors, star-gazing, incoordination, circling, blindness, grinding the teeth
Comatose/lateral recumbency

167
Q

Differential diagnosis for pregnancy toxemia in ewes and does **other periparturient dzes

A

Mastitis
Hypocalcemia
Polioencephalomalacia
Enterotoxemia type D
Toxicosis

168
Q

What are the 2 main principles of treatment of pregnancy toxemia in ewes and does?

A
  1. Administering exogenous energy sources
  2. Removing facotrs increasing the anergy demand
169
Q

Parturition can be induced in does or ewes using:

A

Ewes: 15-20 mg dexamethasone
Does: 10 mgdexamethasone or 10 microg of prostaglandin F2 alpha

170
Q

Antibiotics would be indicated in the treatment of pregnancy toxemia in ewes and does?

A

Concurrent diseases
Post C-section
Prevention of metritis

171
Q

What parameters could be early indicators of disease in pregnant sheep and goats (PREGNANCY TOXEMIA)?

A

Decrase blood pH, bicarb, and base excess values
**well in advance of clinical signs

172
Q

What are suggested predisposing factors to hyperlipemia and hypertriglyceridemia in ponies?

A

Hypophagia
Pegnancy
Lactation

**obese ponies, American miniature horses or donkeys

173
Q

Define hyperlipidemia (in ponies and horses)

A

Mildly elevated triglyceride concentrations: 1000-500 mg/dL
Clear palsma
No evidence of hepatic dysfunction

174
Q

Define hyperlipemia (of ponies and horses)

A

Fatty liver
Serum that is cloudy with lipids
Triglycerides >500 mg/dL

175
Q

Equine hyperlipemia is charactered by (pathogenesis)

A

Production of abnormal VLDL fraction that has reduced content of apolipoprotein B0199 and increased content of apoliporotein B-48

176
Q

PM exam of ponies with hyperlipemia

A

Fatty infiltraiton of liver and kdienys: pale swollen, greasy texture
Liver rupture— intraabdominal hemorrhage. Death

177
Q

Why is heparin indicated in treatment of hyperlipemia?

A

Used to alter lipoprotein lipase activity and inhibit hormone-sensitive lipase of adipose tissue— it may later coagulation enough to cause hemorrhage

178
Q

Mortality rates reported for hyperlipemic ponies

A

22 to 80%

179
Q

What are diseases to cause congenital hyperbilirubinemia?

A

Gilberts syndrome
Dubin johnson syndrome
Persistent hyperbilirubinemia in thoroughbreds

180
Q

Gilberts syndrome is described in what species? And what is the disease

A

An unconjugated hyperbilirubinemia in the presence of normal erythrocyte life span
**Southdown sheep

181
Q

Pathogenesis of Gilbert’s syndrome

A

Failure of unconjugated bilirubin to cross the liver cell membrane and be oncjungated
**most likely d/t defect in carrier proteins or the conjugating enzyme
**clearance is 30% of normal when tested

182
Q

What is Dubin-Johnson syndrome? And is described in what spp?

A

Failure of conjugated bilirubin to enter the bile canaliculi
**Corriedale sheep

183
Q

Pathogenesis of Dubin Johnson syndrome

A

Impairment not only in bilirubin but also in excretoin of other conjugated organic anions
— conjugated and unconugated bilirubin increased
—delayed BSP clearance

184
Q

Histologically what is seen in Dubin Johnson syndrome?

A

Hepatocytes contain a black, melanin like pigment

185
Q

What is persistent hyperbilirubinemia in thoroughbreds?

A

Reported in a thoroughbred racehorse that had no evidence of liver damage, choelstasis or hemolysis and was not fasting
**horse was persistently icteru and high total bilirubin
**horse acted clinically normal

186
Q

Rift Valley fever is a disease of:

A

Acute febrile athropod borne disease of hseep, goats, cattle and humanns present in most countries of sub-Saharan AFrica

187
Q

Rift valley fever causative agent?

A

Virus of genus Phlebovirus

188
Q

Rift valley fever proposed vector

A

Mosquitoes

189
Q

C/S of rift valley fever

A

Abortion in pregnant females
Febrile condition with rapid death- lambs, kids and calves
Fever, anorexia, weakness, salivartion, dairrhea, abdominal pain

190
Q

Rift valley fever mortality rate

A

Young animals: close to 100%
Adults: 20-30%

191
Q

Lesions on necropsy indicating rift valley fever

A

Primary gross lesion: hepatomegaly and hemorrhage
Histo: focal hepatic necrosis, eosinophilic intranuclear inclusion biopsies

192
Q

Telangiectasia is commonly known as what layman’s term and for what lesion?

A

Sawdust livers (known as in packing houses)
**focal degneration in liver lobular circulation characterized by red-brown foci 1 to 5 mm in dimeter— account for more than 10% of bovine liver condemnation, but do not result in clinical signs

193
Q

Clinical signs of Telangiectasia

A

No C/S

194
Q

Cause of Telangiectasia

A

Hypothesis proproes:
-necrotizing hepatits
Ischemia induced by emboli or other vascular pathogies
Dilation of Isse spaces
Redcued density of the reticulin framework
Vit E/selenium defiency
Alteration of sinusoidal barrier
Immune mediated disease

195
Q

Chronic passive congestion of liver causes:

A

Grossly visible “nutmeg liver” caused by distention of sinusoids and central veins with blood

196
Q

ISChemia/hypoxia lesions in the liver

A

**more apparent in centrilobular areas, which are last to reive blood an oxygen

197
Q

Example of disease that causes fetal liver damage in horses?

A

Equine herpesvirus infection of fetus— hepatocyte necrosis with acidophilic intranuclear inclusion bodies in more than 50% of the hepatocytes

198
Q

Example of disease that causes fetal liver damage in cattle?

A

Infectious bovine rhinotracheitis: some focal necrosis of liver, but this is not enough to be diagnostic

199
Q

What are factors that influence hepatic drug metabolism and clearance?

A

Hepatic blood flow
Hepatic metabolism
Protein binding

200
Q

Drugs are classified in relation to the liver into what 2 groups?

A

High hepatic extraction ratios (flow-limited drugs)
Low hepatic extraction ratios (capacity-limited ddrugs)

201
Q

Flow-limited drugs hepatic metabolism

A

Quickly and efficiecntly extract by the liver
Rate of elimination is limited only by hepatic blood flow

202
Q

In relation to chronic liver disease, how does it effect flow-llimited drugs?

A

Morphine, verapamil, lidocaine
Decreased parenchymal blood flow or hepatic shunts shunts can decreased blood flow in the liver & compromise clearance of flow-limited drugs
**decrease dosage of these drugs up to 50% in patients with liver disease

203
Q

Capacity limited drugs in relation to hepatic metabolism

A

Slowly extracted by liver & their elimination is independent of blood flow but is highly dependent on hepatocellular uptake and metabolism

204
Q

What is the effect of liver disease on drug metabolism of capacity limited drugs

A

Variable
— drug clearance increased: atenolol
—Decreased: diazepam & chloramphenicol

205
Q

Drug metabolism (in relation to phases) that occur in the liver:

A

Phase I: oxidation-reduction
Phase II: glucuronidation

**take place in hepatocytes

206
Q

What is the purpose of phase 1 and 2 reactions in drug metabolism?

A

Make compounds more water-solubel and prepare them for excretion via the kidney

207
Q

Decreased biliary clearance can be used as an advantage when treating?

A

Biliary tract disease— to attain higher concentrations of the drug in the bile ducts
**as long as the drug has large therapeutic index

208
Q

What are most common metastatic neoplasia of the liver in cattle?

A

Lymphosarcoma

209
Q

What are most common metastatic neoplasia of the liver in horses?

A

Lymphosarcomas and carcinomas

210
Q

Although uncommon, what primary hepatic neoplasia have been reported in horses

A

Hepatoblastoma (foals/young horses)
Hepatocellular carcinoma (old and young horses)
Cholangiocarcinoma or cholagniocellular carcinoma (old horses)

211
Q

Define hemochromatosis

A

Disorder caused by deposition of hemosiderrin in the parenchymal cells, resulting in tissue damage and dysfunction of the liver and other tissue

212
Q

Hemochromatosis is described in humans and which large animal spp and breed?

A

Salers cattle
Horses

213
Q

Difference between hemochromatosis and hemosiderosis?

A

Hemosiderosis: iron accumulates in the reticuloendothelial system and not hepatocytes, and which can be caused by hemolysis and other conditions

214
Q

When should hemochromatosis be suspected?

A

With emaciation or elevated liver enzymes in Salers cattle with greater than 60% saturation of transferrin

215
Q

Intrahepatic causes of cholestasis include:

A

Cholangitis
Cholecystitis
Choledocholithiasis
Foreign body

216
Q

Extrahepatic causes of cholestasis

A

Abscess formation
Obstruction or inflammatory intestinal disease
Neoplasia

217
Q

Define cholelithiasis

A

Presence of biliary calculi in either the bile ductrs or the gall bladder

218
Q

Define choledocholithiasis

A

Stones found in the common bile duct

219
Q

Define hepatolithiasis

A

Indicates the presence of calculi in the intrahepatic bile ducts above the right adn elft ehpatic ducts
**variation of cholelithiasis

220
Q

Billiary stone formation involves:

A

-precipitation or aggregation of normally soluble ocmponent of bile
-other mech: ascariasis, ascending biliary infection or inflammation, biliary stasis, changes in bile composition and presence of a foreign body

221
Q

Cholelith composition

A

Mixed composition: bilirubin, bile pigments, cholesterol esters, esters of cholic and carboxylic acid, calcium phosphate, sodium taurodeoxylcholate

222
Q

Cholelithiasis should be suspected in horses with what clinical signs?

A

Recurrent abdominal pain
Intermittent pyrexia
Icterus

223
Q

What is the parallel channel sign on ultrasound?

A

Dilation of interhepatic biliary radicals adjacent to the portal vein

224
Q

Differentials for clinical signs associated with cholelithiasis?

A

Othr casues of liver disease
Mildl recurrent abdominal discomfort

-verminous areritis
-mesenteric abscesses
-sand enteropathy
-enterolithiasis
-abdominal neoplasia
-urolithiasis

225
Q

Antibiotic therapy for cholelithiasis should be directed towards

A

Gram negative enteric bacteria or anaerobes
- potentiated sulfonamides
-enrofloxacin
-chloramphenicol— don’t use if hepatic function.compromised

Tx for 6 wks past the time when GGT values return to normal

226
Q

Reported survival rate for cholelithiasis

A

75 to 80% survival rate with medical or medical plus surgical therapy

227
Q

Cholangitis and cholangiohepatitis may be primary or secondary, and can rsult from:

A

Choleithiasis
Duodenal inflammation
Inestinal obstruction
Neoplasia
Parasitism
Certain toxins

228
Q

Clinical disease of the bovine gall bladder is rare, but obstructive gallbladder disase has been associated with:

A

Abdominal fat necrosis
Choleliths
Fascioliasis
Foreign bodies
Hepatic abscesses
Neoplasia
Suppurative cholecystitis

229
Q

What is the most common tumor found in the gallbladder?

A

Adenocarcinomas

230
Q

Why should benzodizepines not be used in liver disease?

A

They enhance the effect of GABA on inhibitory neurons, worsening hepatic encephlopathy

231
Q

What dietary management changes should be made in liver failure?

A

Low protein diet with a high BCAA (branched chain amino acids)/ AAA ratio recommended
— low protein, high starch feeds include grass or oat hays, beet pulp, racked corn, milo, sorghum

232
Q

Drugs used to reduce intestinal ammonia absorption

A

Neomycine
Oral metronidazole
Lactulose
Acetic acid, mineral oil and magnesium sulfate— avoid nasogastric intubation nose bleeds as blood swallowed increase enteric ammonia production

233
Q

In regards to protein metabolism in liver failure, why is dietary management important?

A

Aromati camino acids (AAAs) metabolism is reduced and accumulation occurs, wherease muscle and adipose tissue can metabolize branched chain amino acids (BCAAs) resulting in less accumulation

AAA cross the blood brain barrier and can act as false neurotransmitters— aggravating signs of HE

234
Q

Treatmetns to reduce cerebral edema

A

Furosemide
Mannitol
Hypertonic saline

235
Q

When correcting dehydration and maintained IV fluids therapy, what should the fluids not contain?

A

Lactate—- normally metabolized ot bicabronate in teh liver and has an alkalizign effect

Use acetate buffer solutions as an alternative (0.9% sodium chlride, dextrose 2.5-5%, otassium: 20 to 40 mEq/L)

236
Q

Benefits of dextrose supplementation in intravenous fluids?

A

Redcues the relaince on catabolic gluconeogenesis
Decreases protein cataolism
Spares hepatic energy coonsumedi n hepatic gluconeogenesis

237
Q

Benefits of fresh or fresh frozen plasma

A

Increase colloidal oncotic pressure
Clotting factor transpoort proteins
Antiproteases

238
Q

Why should stored whole blood not be used in cases of liver failure?

A

Because ammonai levels may be high

239
Q

Why should PCV not be used to judge fluid therapy in cases of liver failure?

A

Because polycythemia may be relatively unresponsive in some cases of hepatic failure and should not be used as the primary guide for judging adequate fluid therapy

240
Q

Pentoxifylline MOA

A

Methylxanthine derivative
Nonselective phosphodiesterase inhibitor— results in weak inhibition of hte inflammaotry cytokines TNF alphl and IL-6

241
Q

N-acetylcysteine MOA

A

Cysteine donor thought to be cytoprotective
— may improve hepatic microcirculation and oxygen delivery, enahnce hepatic metabolic functions by restoring glutathione levels, block TNFalpha release and act as a free radical scavenger

242
Q

What are laboratory tests that may be of value in teh diagnosis of pancreatitis int he horse?

A

Measuring serum amylase and lipase activity
Peritoneal fluid amylase concentrations
Fractional excretion of amylase
Plasma trypsin levels

G.I. (7 decks)

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