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Large GI > Hepatobilary, Oral cavity/esophagus, Reticulorumen > Flashcards

Hepatobilary, Oral cavity/esophagus, Reticulorumen Flashcards

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1
Q

What is the etiology of liver abscesses?

A

Fusobacterium necrophorum

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2
Q

What causes rumenitis and how can it lead to liver abscesses?

A

Dairy/beef cattle on high concentrate diets, causes lactic acidosis. most common cause

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3
Q

What causes naval infections in neonates?

A

Umbilical vein predisposed to ascending infection, travels to liver.

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4
Q

What are clinical signs of liver abscesses?

A

Most are subclinical! Decreased rate of gain, weigh tloss, pyrexia, anorexia, abdominal pain (rolling).

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5
Q

What are 3 sequelae of liver abscesses?

A

Caudal vena caval thrombosis
Peritonitis
Occlusion of bile duct

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6
Q

What is the clinical pathology associated with liver abscesses?

A

Neutrophilia with left shift, hyperfibrinogenemia, hyperglobulinemia, hypoalbuminemia, elevations in GGT and AST, hyperbilirubinemia, anemia

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7
Q

Why do you see hypoalbuminemia with liver abscesses?

A

Hepatic insufficiency because of abscesses

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8
Q

What is the pathophysiology associated with liver abscesses?

A

Normal flora–>breakdown in rumen mucosa leads to acidosis (high grain diet)–>portal circulation–>abscesses form and encapsulate–>erosion of hepatic vessels–>emboli–>hematogenous pneumonia and caval syndrome

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9
Q

What do you treat liver abscesses with?

A

broad spectrum antibiotics but few penetrate

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10
Q

How can you prevent liver abscesses?

A

prevent rumenitis, feed additive antibiotics, prevent umbilical infections in calves

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11
Q

What leads to hepatic lipidosis?

A

sequelae of severe ketosis

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12
Q

What is typical signalment for hepatic lipidosis?

A

postpartum dairy cows, over-conditioned beef cows

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13
Q

Why are over-conditioned beef cows more at risk for hepatic lipidosis?

A

Don’t follow normal production cycle. Pregnant for 9 months, then 3 months to get pregnant again while recovering during that time. Overgraze when they can’t get pregnant right away.

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14
Q

What are clinical signs of hepatic lipidosis?

A

weakness–recumbency, pronounced anorexia, dec milk production, ketosis

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15
Q

What is the pathophysiology of hepatic lipidosis?

A

overfeeding in dry perioid, mobilization of adipose tissue fatty acids in response to negative energy balance

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16
Q

What are treatment goals for hepatic lipidosis?

A

Eliminate negative energy balance. Treat concurrent diseases. IV glucose infusion.

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17
Q

How can hepatic lipidosis be prevented?

A

Prevent obesity in late lactation, maintain weight during dry period.

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18
Q

What is the most common liver fluke in cattle?

A

Fasciola hepatica

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19
Q

What is the life cycle of a trematode?

A

indirect lifestyle–one egg can become amplified into multiple adults

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20
Q

_____(spp) more commonly have acute infections of liver flukes while ______ (spp) more commonly have chronic infections.

A

Sheep–acute

Cattle–chronic

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21
Q

What pathology will you see with acute vs chronic liver fluke infections?

A

Acute–hemorrhage tracts

Chronic–white fibrotic tracts

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22
Q

How do liver flukes cause major liver damage?

A

Migrate through liver to cause damage and insufficiency, cholangitis, and biliary obstruction and fibrosis.

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23
Q

Fascioloides magna is a liver fluke of ______ (spp). What effects does it have in cattle?

A

Deer.

Cattle–poor performance in cows, poor growth rate in calves.

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24
Q

Why are fascioloides magna eggs not found in a fecal?

A

Flukes wall themselves off in the body and do not become patent.

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25
What is treatment for liver flukes? Why is timing important?
``` Flukicides--strategically time these because they only target the adult form Snail management (but how feasible is this actually?). ```
26
Flukicide treatment is best from ______ for the SE and ______ for the Pacific NW.
SE--July thru Oct | P. NW--Nov thru Dec
27
When do you see hepatotoxicity due to plants?
Poor management, animals will resort to eating these when good forage is unavailable.
28
When will you see clinical signs from hepatotoxicity?
When 75% of functional hepatic mass has been compromised.
29
What is secondary photosensitization?
Hepatic insufficiency inhibits adequate systemic clearance of phylooerythrin, which goes into circulation. Will see lesions on dorsal midline and non-pigmented areas, sometimes on teats (cattle cool off in ponds, reflects light back onto udder area).
30
What are some causes of "broken mouth"?
Older cattle Mineral deficiencies--phosphorus, Vit D, Ca, Ricketts, osetomalasa Toxicities--Fluoride
31
Which teeth are more commonly fractured? When will you see clinical signs?
Molars/premolars>>incisors | Will be asymptomatic unless root is involved.
32
How do tooth root abscesses occur?
Infection from gingivitis or fractured teeth has spread down the tooth root.
33
What organism causes Wooden Tongue?
Actinobacillus lingieresii, normal inhabitant of oral cavity.
34
Where are wooden tongue lesions found?
SOFT TISSUE. Most often granulomas at the base of the tongue. Bacteria penetrates mucosa.
35
What is the treatment for wooden tongue?
Sodium iodide
36
What organism causes Lumpy Jaw?
Actinomycosis bovis, normal inhabitant of oral cavity.
37
Where are lumpy jaw lesions found?
Bacterium gains entrance to BONE from punctures by foreign bodies, coarse feedstuff, diseased tooth, gingivitis.
38
What is the cardinal sign of lumpy jaw?
Hard, immovable non-painful mass on mandible. Can develop fistulous tracts that have exudate and are painful.
39
What is stomatis and what are the clinical signs?
Inflammation of the oral cavity. | Anorexia, ptyalism, fetid breath, local lymphadenopathy.
40
______ is a viral cause of stomatitis and ______ is a bacterial cause.
Viral--Bovine Papular Stomatitis | Bacterial--Oral Necrobacillosis (Fusobacterium necrophorum)
41
What is the signalment for Bovine Papular Stomatitis?
Young cattle, feedlot animals within 4 weeks of arrival.
42
What is the signalment for Oral Necrobacillosis?
Young, milk-fed calves.
43
What are the hosts of Vesicular Stomatits?
Pigs, sheep, cattle, horse.
44
How does Foot and Mouth Disease (FMD) differ from other vesicular diseases?
Rapidly travels through herds.
45
What are the 3 primary hosts of FMD and what are their roles?
Sheep--maintenance hosts Pigs--amplifiers Cattle--indicators
46
Why is choke common in cattle? What is the most common cause of it?
They are indiscriminate eaters. | Rapid ingestion of grain, doesn't stimulate saliva production and causes bloat.
47
What is an indicator of true bloat?
Will see ruminal tympany with extended upper left side of abdomen, may or may not hear ping.
48
How does the chewing of cud aid in digestion?
Further breaks down feed and releases bacteria, which increases fermentation.
49
What are the four specialized contraction patterns? Which phase causes bloat?
1. primary contraction--16 steps 2. secondary contraction--occurs every 3-5 primary contractions, pushes gas forward so cattle can eructate **this phase causes bloat!** 3. rumination--chewing of cud 4. esophageal groove closure--eversion of milk to abomasum from esophagus in calves
50
What do you determine in every forestomach exam?
Rate/strength of contractions Rumen volume Nature of rumen contents Nature of feces
51
Normal ascultation of the rumen will have ____ contractions per minute.
2-3
52
What can cause hypomotility of the rumen?
Decreased Ca, bloat, increased sympathetic stimulation due to "fight or flight" reflex
53
What can cause hypermotility of the rumen?
Vagal indigestion.
54
Why is it important for there to be stratification of contents in the rumen?
Sign of a healthy rumen, keeps them eructating like they need to.
55
What are the 4 main stratifications of the rumen?
(top to bottom) | Gas--solid--slurry--liquid
56
What is normal pH of the rumen?
Depends on what is fed! Grain decreases pH, fiber/forage increase pH.
57
What happens as a result of vagal indigestion?
abdominal distention
58
Type 1 vagal indigestion
Failure to eructate--inability to handle gas, not that there was too much produced
59
Type 2 vagal indigestion
Failure of omasal transport--stenosis | **hardware disease!**
60
Type 3 vagal indigestion
Abomasal impaction
61
Type 4 vagal indigestion
Indigestion of advanced pregnancy. RARE.
62
_______ is a major cause of vagal indigestion. What species is this most common in?
Hardware disease, beef cattle.
63
What causes primary abomasal impaction?
Dry, coarse feed with restricted water access
64
What causes secondary abomasal impaction?
Decreased abomasal emptying.
65
What are the clinical signs of abomasal indigestion?
``` "Papple" contour of abdomen Intermittent bouts of indigestion and anorexia Weight loss Regurg Poor digestion--will see stems in feces Increased rumen contractions L shaped rumen on rectal palpation ```
66
What happens with chloride levels in the rumen with vagal indigestion?
Will be decreased in the blood, increased in the rumen. (Type 3 and 4)
67
What is rumen putrefaction? What is the typical signalment?
Putrefactive decompistion of forestomach contents. | Milk-fed calves.
68
Why does rumen putrefaction occur?
Poor esophageal groove function.
69
What will the pH be in calves with rumen putrefaction?
Alkaline pH>7 in older calves with necrosis. | Acidic rumen pH<5.5 in younger calves with esophageal groove dysfunction.
70
What are clinical signs of rumen putrefaction?
Recurrent bloat Intermittent diarrhea Chronic poor growth--pot belly Rumen distended with fluid
71
How does rumen tympany occur?
Failure of eructation
72
What are causes of free gas bloat?
Secondary disease, esophageal dysfunction, ruminal motility dysfunction
73
What are causes of frothy bloat?
Primary disease, relaxation of cardia does not occur
74
______ are more likely to cause frothy bloat over perennial grasses.
Legumes
75
What is treatment of frothy bloat?
Anti-foaming agents: poloxalene, mineral oil, docusate sodium
76
How do you prevent frothy bloat?
``` Feed dry, coarse forages before putting on legume grasses. Ionophores. Supplement pasture with dry grass hay. Pasture after dew has evaporated. Adapt to diet slowly. ```
77
What is the most common cause of lactic acidosis?
Ration is changed--increased rapidly fermentable carbs (aka too much grain!)
78
What is the biggest indicator on clin path of lactic acidosis?
Metabolic acidosis
79
How do you treat lactic acidosis?
Remove acid-inducing feedstuffs from the rumen by oral lavage or rumenotomy. Antacids, charcoal, fluid/electrolytes, oral thiabendazole.
80
Hardware disease is technically known as ___________.
Traumatic reticuloperitonitis
81
What occurs with hardware disease?
Perforation of reticulum by foreign body, contamination of body cavities or organs.
82
Goats or cattle more commonly have hardware disease?
Cattle--indiscriminate eaters
83
What are the outcomes of hardware disease?
Localized or diffuse peritonitis Peri-reticular abscesses, liver abscesses Vagal indigestion
84
What kind of posture will an animal with hardware disease have?
Show signs of abdominal pain; elbows abducted, arched back.
85
How do you diagnose hardware disease?
CBC (neutrophilia, leukopenia) Fibrinogen Peritoneal fluid exam U/S, rads
86
What are treatment options for hardware disease
Medical, exploratory laparotomy and rumenotomy.
87
How can you prevent hardware disease?
Magnets on feed processing, reticular magnets.

Large GI (4 decks)

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