Digestion & Metabolism 2: Ruminant Hepatic Dz Flashcards

1
Q

HEPATIC LIPIDOSIS in RUMINANTS…

uniquely in cattle, this can be a ___ dz due to a ____ ____ ____

usually seen during (2)…

4 causes?

A

PRIMARY, NEGATIVE ENERGY BALANCE

usually seen during…
1. FIRST FEW WEEKS OF LACTATION
2. or LATE GESTATION

4 causes?
1. FETUS INCREASED DEMAND for GLUCOSE
2. LARGE mammary gland (producing a lot of milk)
3. CONCURRENT DZ
4. if cow is OVERCONDITIONED so MORE FAT TO MOBILIZE

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2
Q

PATHOGENESIS HEPATIC LIPIDOSIS in RUMINANTS (5)

A
  1. go OFF FEED & not eating enough to support LACTATION or PREGNANCY
  2. causes MOBILIZATION of FAT TISSUE to provide ENERGY & GLUCOSE
  3. more fat tissue mobilized increases NON-ESTERIFIED FATTY ACIDS
  4. the liver CANNOT handle EXPORTING/OXIDIZING all of these fats
  5. EXCESS fats accumulate IN LIVER as TRIGLYCERIDES
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3
Q

TREATMENT options for HEPATIC LIPIDOSIS in ruminants? (5)

A
  1. correct UNDERLYING PROBLEM & give SUPPORTIVE CARE +/- antimicrobials if needed
  2. give DEXTROSE SUPPLEMENTATION so they don’t have to rely on MOBILIZATION OF FAT
  3. other GLUCOSE PRECUSORS (propylene glycol) = MAKE MORE GLUCOSE
  4. GCCs = ENHANCE mobilization of GLUCOSE PRECURSORS & stimulate GLUCONEOGENESIS
  5. INSULIN = DECREASE LIPID MOBILIZATION from ADIPOSE TISSUE
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4
Q

TRANSFAUNATION in RUMINANT HEPATIC LIPIDOSIS…

when/why is this performed?

how MUCH can be given?

what 3 nutritional components are we adding by doing this procedure?

A

when/why is this performed?
–> once animal GOES OFF FEED, NORMAL RUMEN MICROFLORA is DESTROYED so needs TRANSFAUNATION (rumen transplant)

can give usually UP TO 10 LITERS

what 3 nutritional components?
1. ESSENTIAL FATTY ACIDS
2. VOLATILE FATTY ACIDS
3. APPETITE STIMULANT

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5
Q

2 RISKS of giving GLUCOSE PRECURSORS?

what DZ is this used to treat?

A

2 risks?
1. can IMPACT RUMEN FUNCTION
2. NEUROLOGIC SIDE EFFECTS

used to treat HEPATIC LIPIDOSIS

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6
Q

how do we PREVENT hepatic lips

A
  1. AVOID OBESITY in DRY COWS so that they can’t mobilize a ton of fat
  2. IMPROVE DRY MATTER INTAKE/ENERGY-HEAVY GRAINS via TRANSITION DIET
    –> 2-3 weeks BEFORE calving & 2-3 weeks POSTPARTUM
  3. PREVENT PERIPARTURIENT ILLNESSES like mastitis, metritis, etc.
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7
Q

LIVER ABSCESSES

ruminants vs. horses

common management cause?

common in WHAT type of cattle?

etiology? (4)

A

RUMINANTS > HORSES

common management cause = HIGH-GRAIN DIETS

common in FEEDLOT cattle

etiology?
1. HIGH-GRAIN DIETS cause ACIDIC RUMEN ENVIRONMENT

  1. high acid causes EROSION of rumen wall
  2. allows FUSOBACTERIUM NECROPHORUM (normal ruminal flora) to GET INTO PORTAL CIRCULATION
  3. colonizes in liver & causes ABSCESSES
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7
Q

if an cow is NOT EATING, what drug should we NOT give if trying to treat HEPATIC LIPIDOSIS?

A

DO NOT GIVE INSULIN bc can cause HYPOGLYCEMIA

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8
Q

ID LESION

A

LIVER ABSCESSES

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9
Q

what 2 US findings can help with LIVER ABSCESS DIAGNOSIS?

A
  1. BILIARY DISTENTION
  2. CAVITARY LESIONS
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10
Q

TREATMENT for LIVER ABSCESSES…

usually reserved for WHAT ruminant patients? (2)

MAIN treatment & 2 specific options?

other treatment?

A

usually reserved for…
1. HIGHLY VALUABLE ANIMALS or PETS
2. ONLY IF DIAGNOSED EARLY

MAIN tx = LONG-TERM ANTIMICROBIAL THERAPY
1. PENICILLIN
2. FLORFENICOL

other treatment = SUPPORTIVE CARE (nutritional, hydration)

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11
Q

LIVER ABSCESS PREVENTION in ruminants? (2)

what is a BIG complication of LIVER ABSCESSES?

A
  1. SLOWLY increase grain over 3-4 WEEKS so that RUMEN CAN ADAPT to HIGH ENERGY DIET
  2. AVOID ACUTE GRAIN OVERLOAD SCENARIOS! Do not let animals get into grain bags & eat a ton of grain all at once

BIG COMPLICATION = CAUDAL VENA CAVA THROMBOSIS

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12
Q

3 treatments for ACUTE GRAIN OVERLOAD SCENARIO

what DISEASE are we trying to PREVENT?

A

3 treatments?
1. RUMENOTOMY
2. remove GRAIN & CLEAN rumen
3. treat with ANTIBIOTICS for 2-3 WEEKS

trying to prevent LIVER ABSCESSES

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13
Q

CAUDAL VENA CAVA THROMBOSIS…

common sequelae of ____ ____ that are located

pathogenesis? (6)

define ANEURYSM here

GROSS clinical sign?

prognosis?

A

LIVER ABSCESS that are located NEAR THE HEPATIC VEIN

pathogenesis?
1. LIVER abscesses ERODE WALL OF HEPATIC VEIN
2. THROMBUS formation in VEIN
3. throws EMBOLIS to the LUNGS
4. HEMATOGENOUS PNEUMONIA then causes PULMONARY THROMBOEMBOLISM
5. ANEURYSM of PULMONARY VESSEL occurs
6. causes AIRWAY RUPTURE

ANEURYSM = weakening of the HEPATIC VEIN’S WALL due to LIVER ABSCESSES causing EROSIONS

GROSS clinical sign = HEMORRHAGE OUT OF THE MOUTH

prognosis = GRAVE, NEED TO EUTHANIZE

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14
Q

PYRROLIZIDINE ALKALOID TOXICITY…

cattle are MORE likely to have this than horses because…

more commonly get WHAT 2 clinical signs than horses?

what clinical sign is LESS likely in cattle than horses?

what 2 species are more RESISTANT to PYRROLIZIDINE ALKALOIDS?

A

MORE likely to eat ALKALOIDS bc INDISCRIMINATE EATERS

more commonly get 2 clinical signs…
1. DIARRHEA
2. ASCITES

ICTERUS HORSES > RUMINANTS

what 2 species are more RESISTANT to PYRROLIZIDINE ALKALOIDS?
1. SHEEP
2. GOATS

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15
Q

FASCIOLA HEPATICA…

“common name?”

has a ___ ___ transmission

this parasite migrates through the ____ & ____ of ____ determines SEVERITY of dz

what 2 species are MORE SUSCEPTIBLE?

A

“LIVER FLUKE”

has DISTINCT SEASONAL transmission

this parasite migrates through the LIVER & NUMBER of FLUKES determines SEVERITY of dz

2 species MORE SUSCEPTIBLE?
1. SHEEP
2. GOATS

15
Q

FASCIOLA HEPATICA…

DEFINITIVE diagnosis & what 2 things do we see?

what other diagnostic can we use?

what is KEY for managing this dz? how do we do this?

A

DEFINITIVE diagnosis = NECROPSY
1. TORTUROUS TUNNELS or COAGULATIVE NECROSIS & FIBROSIS
2. fluke SPINES & SUCKERS erode & denude BILE DUCT EPITHELIUM

we can also use FECAL SEDIMENTATION

KEY = PREVENTION!
–> perform FALL or LATE-FALL Tx with ALBENDAZOLE to REMOVE ADULT FLUKES BEFORE WINTER STRESS

16
Q

BLACK DISEASE…

what is the clinical name for the dz? (3 words)

can be secondary to ____ _____ infection which can…

etiologic agent? how are they spread?

5 species that can get this? which is MOST COMMON?

A

INFECTIOUS NECROTIC HEPATITIS

can be secondary to LIVER FLUKE infection which can DAMAGE LIVER & make animal SUSCEPTIBLE

etiologic agent = CLOSTRIDIUM NOVYI TYPE B EXOTOXINS
–> spread via ENVIRONMENTAL CONTAMINATION

5 species?
1. SHEEP –> MOST COMMON
2. CATTLE
3. HORSES
4. GOATS
5. PIGS

17
Q

BLACK DISEASE can cause DOWNSTREAM DAMAGE via ____ to cause damage to… (3)

BLACK DISEASE is CHRONIC/ACUTE & can cause CHRONIC/ACUTE ___

A

EXOTOXINS from CLOSTRIDIUM NOVYI TYPE B, causes damage to…
1. NEURONS
2. VASCULAR ENDOTHELIUM
3. TISSUES

this is an ACUTE DISEASE & can cause ACUTE DEATH

18
Q

BLACK DISEASE…

diagnosis based on… (2)

effect on liver?

on NECROPSY, see ___ because of _____ _____

can also isolate ____ ____ from the LIVER

A

diagnosis?
1. CLINICAL SIGNS
2. HISTORY

LIVER = has PROFOUND VENOUS CONGESTION

on NECROPSY, see AUTOLYSIS because of COAGULATIVE NECROSIS

can also ISOLATE CLOSTRIDIUM NOVYI from the LIVER

19
Q

the best way to MANAGE BLACK DISEASE IS BY…

2 medications we can use? dosage?

A

CONTROLLING/PREVENTING LIVER FLUKE in ENVIRONMENT & INDIVIDUAL CASES

2 medications? = HIGH DOSE of…
1. PENCILLIN
2. OXYTETRACYCLINE

20
Q

BACILIARY HEMOGLOBINURIA

“common name?”

etiologic agent?

secondary to ___ ____

what 4 kinds of damage does it cause?

3 clinical signs?

on necropsy, might see…

A

“REDWATER”

etiologic agent = CLOSTRIDIUM HEMOLYTICUM BETA TOXIN

secondary to LIVER FLUKE

4 kinds of DAMAGE?
1. HEPATOCYTE NECROSIS
2. HEMOLYSIS
3. INTRAVASCULAR HEMOLYSIS
4. CAPILLARY DAMAGE

clinical signs?
1. SUDDEN DEATH
2. NON-SPECIFIC signs = pale, ICTERUS, FEVER
3. BLOOD from NOSTRIL & in FECES/URINE

on necropsy, might see RAPID AUTOLYSIS

21
Q

BACILLARY HEMOGLOBINURIA…

diagnosis? (3)

treatment is RARELY ___, but can include… (2)

A

diagnosis?
1. LIVER IMPRESSION SMEAR
2. LIVER CULTURE
3. PCR

treatment is RARELY UNDERTAKEN, but can include…
1. HIGH DOSE PENICILLIN/OXYTETRACYCLINE
2. COMMON BACTERIN TOXOIDS