Brainscape's Knowledge GenomeTM

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


See full index

Farm Animal Medicine Final > Diagnostics and treatment of liver diseases in ruminants. > Flashcards

Diagnostics and treatment of liver diseases in ruminants. Flashcards

1
Q

Liver diseases of cattle and sheep

A

Measurement on insulin resistance
• Gold standard is hyperinsulinemic eughlycemic (HEC) test (the gluconeogenesis if the liver can be suppressed at 100-120 uU/mL insulin concentration)
• Intravenous glucose tolerance test (IVGTT)
• Intravenous insulin tolerance test (IVITT
• Indexes
o HOMA-IR
o QUICKI
o RQUICKI*
o QUICKIGLycerol o RQUICKIBHB

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

Diagnosis of liver diseases in ruminants

A
  • Often subclinical with no specific clinical signs
  • Often secondary
  • Classical clinical examinations do not give guideline
  • Laboratory findings not always correlate with functional severity
  • Increasing importance of instrumental diagnosis (ultrasonography)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diagnosis of liver diseases in ruminants

Jaundice

A

Rare compared to monogastric animals but still a sign of liver disease
• Haemolytic icterus
o Leptospirosis (calf), babesiosis, anaplasmosis o Food (cabbage, onion etc)
o Copper-toxicosis (sheep)
• Hepatic icterus
o The icterus of hepatic origin is rare in cattle, common in sheep (toxic hepatopathies)
• Obstructive icterus
o Obstruction of the bile duct (extrahepatic) - very rare
o Intrahepatic bile capillary compression (ex. Fatty liver) – more frequent

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

Diagnosis of liver diseases in ruminants

Clinical signs

A
  • Yellow colour of sclera, mucous membranes, skin
  • Dark urine (bilirubinuria and/or hemoglobinuria)
  • Increase in plasma Br rarely results in clinical icterus in ruminants
  • TBr > 3 mg/dl
  • Yellow plasma → β-carotene (cattle)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diagnosis of liver diseases in ruminants

Cattle liver enzymes

A

(AST) - ↑ hepatocellular necrosis, acute and chronic liver necrosis, (T1/2 time ~2 days) But also muscular injury, haemolysis!

(ALT) - ↓ sensitivity, not measured in ruminants

(SDH) - specific
quick T1/2 time(~4 hours)→ acute liver injury (labile in sample, must be measured within 4 hours!)

(GLDH) - specific
quick T1/2 time(~14 hours)→ acute liver injury

(OCT) - Sensitive, specific, but difficult to measure

(GGT) - Hepatobiliary diseases, slow T1/2 time ex. Fasciolosis → chronic cholangitis

(ALP) - Hepatobiliary diseases, but low sensitivity, wide reference range for ruminants

(LDH) - Low specificity, isoenzymes: RBCs, muscle

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

Diagnosis of liver diseases in ruminants

Total bile acids (TBA)

A
  • Normal: < 90 μmol/l
  • Fatty liver 1.5-2-fold increase
  • High variability between individuals
  • No importance of pre-and postprandial levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Diagnosis of liver diseases in ruminants

Dry chemistry NH3-analyzer (Blood Ammonia Checker)

A
  • Reference value: 25-50 μmol/l
  • Energy deficiency, protein overload 50 - 80 μmol/l
  • Severe fatty liver, coma hepaticum: > 100 μmol/l)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diagnosis of liver diseases in ruminants

Summary of clinical diagnostics in liver diseases

A 
• Plasma/Serum: AST, ALT, ALKP, GLDH, bilirubin, ammonia, BHB, NEFA
• Urine: Acetic acid, acetone
• Ultrasound
• Biopsy:
o TL, TAG,
o Gene expression: ACLS-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diagnosis of subclinical and clinical ketosis

A
  1. Urine diagnostics

2. Blood ketone body measurement - Beta-hydroxy butyrate (BHB) (on farm ketone body measurement)

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

Diagnosis of subclinical and clinical ketosis

Urine diagnostics

A
  • Acetic acid/acetone: In urine and milk (colour changes to purple)
  • KetoCheck powder (Milk, acetic acid)
  • Ketostix strip (urine, acetic acid)
  • KetoTest strip (Milk, BHB)
  • NEFA: > 0.6 mmol/l (only lab)
  • Glucose: 2.3-3.3 mmol/l
  • Milk yield: Fat:Protein ratio (F:P) > 1.5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diagnosis of subclinical and clinical ketosis

Blood ketone body measurement - Beta-hydroxy butyrate (BHB) (on farm ketone body measurement)

A

• Beta-hydroxybutyrate (BHB)
o Blood: (“Gold standard”: spectrophotometry)
▪ Clinical ketosis: > 2.5-3 mmol/l
▪ Subclinical ketosis: > 1.2-1.4 mmol/l
▪ Electronic device (Precision Xtra)
o Change rate
▪ Clinical: 3 mmol/l = 31.1 mg/dl = 311 mg/l
▪ Subclinical: 1.4 mmol/l = 14.5 mg/dl = 145 mg/l
o Collect about 2 ml blood via v. jugularis, v. coccygea
o Do not collect from milk vein because comes out from udder and lots of metabolism is
happening here
o Fast approach
o One droplet of blood is enough for accurate measurement

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

Clinical disease of the liver

A

Hepatosis et hepatitis non purulenta

Infectious necrotic hepatitis (Black disease)

Hepatic abscess, purulent hepatitis

Chronic rumen acidosis leading to purulent hepatitis (most common cause)

Hepatitis (necrobacillosis) caused by Fusobacterium necrophorum

Liver abscess ultrasound and pathology

Panaritium, Foot rot, Interdigital necrobacillosis as a causative factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical disease of the liver

Hepatosis et hepatitis non purulenta

Causes

A

• Metabolic
o Energy deficiency→fatty liver
• Toxic
o Toxic compounds: Cu, P, As, CCl4 etc.
o Foodstuffs: cabbage
o Lupinosis: phomopsin (a mycotoxin is responsible)
o Plant toxins: pyrrolizidine alkaloids (Senecio, Crotalaria, Amsinckia spp.)
o Poor quality silage, mycotoxins
• Infectious
o Bacteria, bacterial toxins (Cl. novyi, Salmonella enteriditis)
o Hepatic fascioliasis (acute hepatitis, cholangitis)
• Predisposing factors: energy deficiency, acidosis, Co deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clinical disease of the liver

Hepatosis et hepatitis non purulenta

Clinical signs

A
  1. Subclinical disease
    o Few/no clinical signs
    →decreased meat and milk production
    →reproductive disorders
  2. Secondary hepatopathies
    o Clinical signs of the underlying disease
  3. Clinical signs indicating hepatic disease
    o Anorexia, ruminal atony, weight loss, jaundice (?)
    o Hepatomegaly, photodermatitis, watery-yellow diarrhoea (sheep) o Recumbency, hepatic coma
    o Laboratory examination important
    o Often heard problem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical disease of the liver

Hepatosis et hepatitis non purulenta

Therapy

A
  • Find and eliminate underlying cause

* Optimal nutrition, supportive therapy

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

Clinical disease of the liver

Infectious necrotic hepatitis (Black disease)

Cause

A

• Histotoxic Clostridium novyi type B (exotoxin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clinical disease of the liver

Infectious necrotic hepatitis (Black disease)

Occurrence

A

• Frequent in sheep, less common in cattle

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

Clinical disease of the liver

Infectious necrotic hepatitis (Black disease)

Pathophysiology

A

• Fasciolosis triggers the disease, then tissue damage near spores triggers Cl. growth and production of toxins

19
Q

Clinical disease of the liver

Fasciolosis

A

Acute

Chronic

  • Cirrhosis
  • Chronic billiary cirrhosis)
20
Q

Clinical disease of the liver

Hepatic abscess, purulent hepatitis

Occurrence

A

• Sporadic, but 5-10% of slaughtered animas, 45-50% of feedlot animals (baby beef)

21
Q

Clinical disease of the liver

Hepatic abscess, purulent hepatitis

Cause

A
  1. Rumen acidosis (chronic)→rumen paraketosis + pyogenic bacteria via portal circulation (Fusobacterium necrophorum, Corynebacterium pyogenes, Stapylococcus aureus, Streptococcus equi,)
  2. Systemic infection (umbilicus, udder, uterus)
  3. Direct bacterial effect (traumatic hepatitis)
22
Q

Clinical disease of the liver

Hepatic abscess, purulent hepatitis

Clinical signs

A
  1. Without clinical signs (decreased performance?)
  2. Fever, septicemia, peritonitis, shock
  3. Chronic disease
23
Q

Clinical disease of the liver

Hepatic abscess, purulent hepatitis

Diagnosis

A

• Hemogram, glutaraldehyde test, other acute phase proteins

24
Q

Clinical disease of the liver

Hepatic abscess, purulent hepatitis

Prevention

A

• Prevention of conditions leading to
o Chronic rumen acidosis
o Infection at calving/lambing
o Mastitis, metritis, laminitis

25
Q

Clinical disease of the liver

Chronic rumen acidosis leading to purulent hepatitis (most common cause)

A

Consequence is parakeratosis (liver abscess syndrome)

26
Q

Clinical disease of the liver

Hepatitis (necrobacillosis) caused by Fusobacterium necrophorum

Occurrence

A

• Sheep, roe-deer, deer (cattle)

27
Q

Clinical disease of the liver

Hepatitis (necrobacillosis) caused by Fusobacterium necrophorum

Cause

A
  • Enteritis/rumenitis)→Fusobacterium necrophorum entering portal vein (other hepatopathies, impaired hepatic blood flow, anaerobic conditions)
  • Infection via systemic circulation: panaritium, diseases of the distal extremities, necrotic stomatitis (lamb), umbilical infection
28
Q

Clinical disease of the liver

Hepatitis (necrobacillosis) caused by Fusobacterium necrophorum

Clinical signs

A

• Large number of acute diseases in certain flocks
o Fever, anorexia, lethargy
o Jaundice
o Death after 4-5 days or chronic weight loss

29
Q

Clinical disease of the liver

Hepatitis (necrobacillosis) caused by Fusobacterium necrophorum

Treatment

A

• Antibiotic treatment in infected flocks (?)

30
Q

Fatty liver syndrome

A

• Rare disease but involved the absolute dysfunction of the liver

31
Q

Fatty liver syndrome

Occurrence

A

• High-producing dairy cattle, postpartum period, older cows, herd disease
• Lipid (mainly triglyceride, TG) content of the liver
o Dry period: < 50 g/kg
o Early postpartum period: 80-100 g/kg
o 4 weeks postpartum: 40-60 g/kg
o Fatty liver >150 g/kg to 300 g kg

32
Q

Fatty liver syndrome

Cause

A

• Energy deficit after parturition
• Increased lipid mobilization
• Obesity during the dry period, lipid stores 
• Anorexia after parturition
• Diseases/conditions causing anorexia
• Nutritional anomalies
• Stress →catecholamines, glucocorticoid, insulin  → lipid mobilization 
• Relative deficiency in lipotropic factors (methionine, choline)
Hepatocyte-TG →liver dysfunction
Lipoprotein synthesis →lipid export →increased hepatocyte-TG

33
Q

Fatty liver syndrome

Clinical signs

A
  1. Acute (peracute disease)
    o Anorexia after parturition, lethargy, fast progress to recumbency, behavioral disorders→
    coma
  2. Subacute disease
    o Slow progression of the disease, gradual worsening, anorexia, weight loss, ketonuria (same as in the digestive form of ketosis)
  3. Subclinical fatty liver
    o Decreased resistance → secondary diseases
    o Reproductive disorders
    o Predisposition to fatty liver disease at next calving
34
Q

Fatty liver syndrome

Diagnosis

A
  • Ultrasonography shows: diffuse increased echogenicity
  • Liver biopsy and floating test, total lipid det.
  • Increased serum AST, bile acids, blood ammonia
  • Ketonuria
  • Cholesterol, urea , NEFA 
35
Q

Fatty liver syndrome

Therapy

A

• No specific therapy exists
• Support liver function with
o Fluid and electrolyte therapy, glucose IV
o Gluconeogenetic substances: propylene glycol drench, glycerol, propionate (Na, Ca) salts
o Glucocorticoids: dexamethasone, prednisolone IM
o Insulin (retard): 100 IU/animal IM
o Lipotropic factors: methionine, choline
o Transfaunation

36
Q

Fatty liver syndrome

Prevention

A
  • A typical condition that can be more easily prevented than treated!
  • Avoid over conditioning around calving: BCS 3.5-4
  • Feeding according to production levels
  • Progressive adaptation to concentrates (2-3 weeks) before calving
  • Walking
37
Q

Therapeutic approach to liver diseases

Ketosis treatment

A
  1. Gluconeoplastic materials
  2. Glucocorticoids
  3. Glucose/dextrose infusion
  4. Niacin (B3 vitamin, nicotinic acid)
  5. B12 vitamin/Butafosfane
  6. Insulin
  7. Further additives PO
38
Q

Therapeutic approach to liver diseases

  1. Gluconeoplastic materials
A

• Propylene glycol (1,2 propane-diol)
o Slight metabolization in the rumen: propionate Mostly absorbing in small intestine
o Metabolization in the liver
▪ 300 ml/cow/day 5-10 days PO
▪ Small ruminant 60ml/animal/day PO
• Glycerin (1,2,3 – propane-triol)
o Same dose as propylene glycol
o Industrial glycerin– toxicity issues
• Na-propionate, Ca-propionate
o Hardly soluble, mostly powders in form
o Palatability problems, refusal can occur
o 100-120 g/animal/day PO

39
Q

Therapeutic approach to liver diseases

  1. Glucocorticoids
A

• The usage of steroids results hyperglycemia because they inhibit insulin, fat and protein storages catabolic processes are starting to act, in order to help glucose production in the liver
o Decreases milk yield
o Increases appetite)
• Dexamethasone (Dexadreson A.U.V): 12-14 mg/animal (0.02-0.03 mg/kg im.) once in 3-4 days
• Flumetasone: 20 mg/animal (0.03 mg/kg im.)
• Isoflupredon-acetate: 30-40 mg/animal (0.05-0.06 mg/kg im.)
• Unwanted effects 0,04-0,05 mg/ttkg can be immunosuppressive so infections can exacerbate
• Can induce clinical hypokalemia (isoflupredone-acetate)

40
Q

Therapeutic approach to liver diseases

  1. Glucose/dextrose infusion
A

• 50-70 g glucose/hour maintenance, 200 g glucose/hour milk production, not so many in blood, <40 g. Effecting some hours, excretion in kidney, after 2-4 hours blood concentration tends to baseline
• Short term consequences of intravenous glucose:
o Hyperglycaemia → ↓ ruminal contractions AND ↓ abomasal emptying rate
o Hyperglycaemia → insulin ↑ → downregulation of hepatic glucose production
o Because of the insulin peak the blood glucose → excretes through the kidney (electrolyte
imbalance; hypokalemia)
• Therefore therapeutic advise:
• Max 250 ml 50% dextrose/glucose (125 g glucose) PO propylene glycol continues
• In case of clinical ketosis (neurogenic form, etc.) IV (250-500ml)
• Can be given daily more times, but have to consider the consequences

41
Q

Therapeutic approach to liver diseases

  1. Niacin (B3 vitamin, nicotinic acid)
A

• Peroral niacin degrades in rumen, rumen protection is needed Normally ruminal microflora is producing it
• Effects
o Anti-lipolytic effect
o Slight increase in milk production
o Low dosage PO 6-12 g/day/animal (questioned effect) or 49-98 g/day/animal (positive
effect)
o Effect of niacin supplementation on blood BHB and NEFA

42
Q

Therapeutic approach to liver diseases

  1. Insulin
A

• Two sided problem of peripartial period low insulin blood concentrations and insulin resistance
• Insulin has mostly anabolic effects: slows down lipolysis, fat synthesis improves, improves the utilisation of ketone bodies
• We do not use it alone, adjuvant therapy, the effect is questioned
o Protamine zinc (not available, of animal origin)
o Recombinant insulins: GMO in Europe, questioned effect
o Lente insuline: 200 IU, together with glucose therapy
• In case of fatty liver syndrome can be an option

43
Q

Therapeutic approach to liver diseases

  1. Further additives PO
A

• Choline (trimetile-ethanolamine) gives rumen protection, improves TCA cycle in the liver, 40- 70 g/animal/day PO
• Chromic acids at 4g/day/animal (decreasing insulin resistance)
• Methionine: two enantiomers (D,L), L-Met active, should be rumen protected
(encapsularisation/polymerisation) improves liver amino acid synthesis: 20-30g/animal/day
• Polyunsaturated Fatty Acids(PUFA): Omega 3 and omega 6 at 5-10g/animal/day, excrete with
milk fat, alter fat profile, Linoleic acid, retinol palmitate, Sterculia oil. Can decrease appetite
• Non-fibre carbohydrates (NFC) like molasses
• Ionophore antibiotics like Monensin (forbidden in EU)

Farm Animal Medicine Final (61 decks)

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