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Farm Animal Medicine Final > Metabolic diseases in ruminants > Flashcards

Metabolic diseases in ruminants Flashcards

1
Q

Fatty Liver syndrome

A 
Contents of 30 kg milk
• Energy demand
    o Dry period: 80MJ/500kg BW
    o Lactation
        ▪ 30kg milk/day: 200 MJ
        ▪ 50kg milk/day: >350MJ
Crucial point in metabolic changes: calving
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2
Q

Fatty Liver syndrome

Metabolic characteristics of a dairy cow

A

• Factors influencing metabolism around calving
o Nutritional changes (adaptation of the ruminal flora and fauna)
o Changes in housing (stress!)
• Expected (physiological) increase of body weight (suspected BW in peak lactation: 500kg i.e. 100%)
o At start of dry period: +10%, i.e. some 550kg
o Just before calving: further 10% i.e. some 605kg
• Expected (physiological) loss of the body weight
o At calving: 60-70kg
o Due to catabolic processes in early lactation:40-60kg (mainly due to lipid mobilisation)

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3
Q

Fatty Liver syndrome

Characteristic features of the energy status in a dairy cow

A
  • Catabolic in the 1st month

* Anabolic following the 2nd month of lactation

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4
Q

Fatty Liver syndrome

Fat mobilisation (fatty liver) syndrome – development

A

• A typical “production disease” – occurs over 5000kg milk production/year
• Main cause:
o Energy demand does not meet energy supply
o Rate of morbidity depends on milk production

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5
Q

Fatty Liver syndrome

Factors influencing the energy metabolism around calving – summary

A

• Dry period
o Cause: overfeeding (concentrate!, changes in housing)
o Consequences: obesity→fat stores 
• At calving
o Cause: physiological loss of appetite housing and nutritional changes, intercurrent
diseases, obesity)
o Consequences: lipid mobilisation , fatty liver 
• Puerperium
o Cause: energy deficiency, too long catabolic period
o Consequences: loss of condition, ketone body production , fatty liver
• Lactation
o Cause: energy overload, too long anabolic state
o Consequences: disposition to obesity

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6
Q

Fatty Liver syndrome

Nomenclature

A

• During dry period/early postpartal period: Fat Cow Syndrome
• At calving/early postpartal period: Fatty Liver Syndrome, hepatic coma
• Midlactation: Thin Cow Syndrome, secondary (mainly inflammatory) diseases, reproduction
disorders

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7
Q

Fatty Liver syndrome

Forms of fatty liver/fat mobilisation syndrome

A
  • Acute/peracute
  • Subacute – during lactation
  • Subclinical (chronic disorder)
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8
Q

Fatty Liver syndrome

Forms of fatty liver/fat mobilisation syndrome

• Acute/peracute

A

o After (rarely before) calving
o Clinical signs
▪ Obesity, anorexia, sudden loss of condition, abdominal pain, hepatomegaly,
apathy, coma, death o Liver lipid >255
o Prognosis: very poor
o Differential diagnosis
▪ Ketosis, milk fever (both are easily treatable)

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9
Q

Fatty Liver syndrome

Forms of fatty liver/fat mobilisation syndrome

• Subacute – during lactation

A

o Clinical signs: “thin cow”, anorexia and apathy o Intercurrent diseases (lameness, mastitis etc.)
o Ketonuria (ketonanaemia, ketolactia is rare)
o Liver lipid: slightly elevated (around 15%)
o Course might be fatal

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10
Q

Fatty Liver syndrome

Forms of fatty liver/fat mobilisation syndrome

• Subclinical (chronic disorder)

A

o Clinical signs
▪ Not typical, poor body condition, decreased milk production, high frequency of post-parturient diseases (ketosis, mastitis, retained placenta)
▪ Ketonuria
o Liver lipid 10-12%
o Disorders in reproduction (anovulation, infertility)
o Course: not fatal

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11
Q

Fatty Liver syndrome

Consequences of fatty liver syndrome

A

• Sudden death of the cow
• Decreased milk production
• Loss of condition
• Development of secondary diseases (increase susceptibility to retained placenta, abomasal
displacement)
• Reproduction disorders (poor oestrus signs, anovulation, increase in the number of days
between two calving)

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12
Q

Fatty Liver syndrome

Diagnostic methods

A 
• Clinical signs (not typical)
• Ultrasound (rarely used)
• Liver biopsy (blind or US-guided)
    o Visual evaluation
    o Floating test 
• Laboratory tests
    o In-office (not specific – show energy deficiency)
    o Referral laboratory (too slow)
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13
Q

Fatty Liver syndrome

Laboratory diagnosis of energy deficiency

A 
• Ketone body (acetone, aceto-acetate) checking by nitroprusside-Na: o Ross-test
    o Rothera’s test
    o Test strips (urine, plasma, milk) 
• Urea determination
    o Test strips or photometric measurements: plasma, milk 
    o Physiological range: 3-6mmol/L
    o Energy deficiency: >5 mmol/L
    o (N-deficiency: <2.5mmol/L)
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14
Q

Fatty Liver syndrome

Plasma/serum parameters

A
  • FFA/NEFA
  • Total cholesterin, albumin
  • Glucose
  • Ketones: BHB
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15
Q

Fatty Liver syndrome

• Enzyme activity

A

o AST, ALT, LDH

o SDH, GLDH, OCT

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16
Q

Fatty Liver syndrome

Laboratory diagnosis in referral laboratories

A
  • Histology
  • Chemical analysis for total lipids and/or triglycerides
  • Results of these methods often arrive too late
  • Useful to monitor subclinical forms at herd level
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17
Q

Fatty Liver syndrome

Prevention and treatment

A
  • Avoid overcondition of dry cows
  • Stimulate energy supply following parturition
  • Immediate treatment of any other diseases decreasing the appetite of the cow
  • A typical condition that can be more easily prevented than treated
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18
Q

Bovine ketosis (acetonaemia of cattle)

A
  • Typical production diseases
  • Ketogenesis > ketolysis
  • Increased ketone body production→ketonaemia, ketonuria, ketolactia
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19
Q

Bovine ketosis (acetonaemia of cattle)

Occurrence

A
  • High-producing dairy cows, during postparturient period (within 60 days, average: 3 weeks after calving)
  • Little evidence for a heritable predisposition
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20
Q

Bovine ketosis (acetonaemia of cattle)

Ketone bodies

A
  • Aceto-acetate (AcAc)→3-OH-butyrate→acetone

* Na-nitroprusside: sensitive to AcAc and partially to acetone, not sensitive to 3-Oh-butyrate

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21
Q

Bovine ketosis (acetonaemia of cattle)

Ketone bodies in biological fluids

A

• Physiological ketone body ratio post partum in plasma: o 3-OH-butyrate : (AcAc + acetone) = 10:1
• Pathological ration in a ketonic cow’s plasma
o 3-OH-butyrate : (AcAc + acetone) = 3.5:1
• Ketone body distribution in biological fluids of a ketonic cow o Urine ketone : plasma ketone : milk ketone = 10:2:1
• PU/Pd deeply influences urine ketone body concentration
• Nitroprussid-Na (Rothera- and Ross-test, ketosis-strip etc.) reacts mainly with AcAC and acetone, does not react with 3-OH-butyrate

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22
Q

Bovine ketosis (acetonaemia of cattle)

Aetiology of ketosis

A

• Nutritional factors
o Low carbohydrate and high protein content in the ration
o Low propionate level, increased butyrate (poor quality silage)
• Endocrine factors
o Ketogenic hormones: thyroxin, GH, glucagon
o Antiketogenic: glucocorticoids, insulin
o Endocrine balance around calving is a predisposing factors
• Liver malfunction
o “Overload” of liver metabolic capacity
o Fatty infiltration (hepatic failure, - coma)
• Decreased muscle function
o Ketone bodies cannot be utilised (oxidised) in inactive muscles

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23
Q

Bovine ketosis (acetonaemia of cattle)

Classification of bovine ketosis

A

• Primary (production) ketosis
o Caused by high milk yield
• Secondary (starvation, deficiency) ketosis
o Caused by low energy supply or anorexia
• Nutritional
o Caused by bad quality food i.e. butyrate-containing silage

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24
Q

Bovine ketosis (acetonaemia of cattle)

Forms of primary (production) ketosis

A

• Acute nervous form
o Highly elevated (10-fold) ketone bodies increase in the blood plasma (ketonemia),
hypoglycaemia, ketonuria, ketolactia
o Signs
▪ Excitation, unconsciousness, convulsion, grinding or the teeth, apathy, ataxia, finally lateral recumbency, blindness, coma
▪ Sweet, typical smell of the expired air and urine (caused by acetone)
o Course
▪ Sometimes sudden death
▪ Quick recovery following treatment
▪ Relapses are rare
• Subacute, digestive, wasting form
o Mild ketonemia (3-5 fold increase) + hepato-steatosis, ketonuria, less severe ketolactia
o Signs
▪ Maldigestion, loss of condition, diarrhoea, abdominal pain, decreased milk production
▪ GI signs dominate with or without nervous symptoms
o Course
▪ Depending on the liver function
▪ Treatable, but the response is frequently transient
• Subclinical form
o Slight ketonemia (2-fold increase)
o Signs
▪ Not typical
▪ Drop in milk yield, loss of body condition
▪ Similar to the subacute form of fatty liver syndrome
o Course
▪ Never fatal
▪ Main consequences: reproductive disorders, secondary diseases
▪ Potential manifestation of acute form at the succeeding clave

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25
Q

Bovine ketosis (acetonaemia of cattle)

Ketonuria test (Rothera)

A
  • Comatose dairy cow with positive Rothera-test (nitrussid-Na) – a sign of energy deficiency
  • Blood and milk should be checked for ketone bodies – both were positive
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26
Q

Bovine ketosis (acetonaemia of cattle)

Treatment of ketosis

A

Acute, nervous form
• Glucose/dextrose therapy:20-40% solution, 500ml iv repeatable (attention: glucose renal threshold in ruminants is very low)
• Stimulation of GNG: dexamethasone 5-10mg iv, im
• Glucoplastic compounds per os:
o Na-propionate 100-200 g/day, propylene glycol 100-200 g/day, commercial antiketogenic medicines are available in all countries
Digestive, wasting form
• As above + proper nutritional management, glucoplastic compounds, glucose therapy (20% solution, 200-300 ml iv/day)
Subclinical form
• Adequate nutritional management

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27
Q

Bovine ketosis (acetonaemia of cattle)

Prevention

A
  • Carbohydrate-rich diet (easily fermentable) after calving. Avoid butyrate in the ration (good quality silage)
  • Appropriate N-supply
  • Exercise (stimulates ketolytic procedures in muscles)
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28
Q

Ovine ketosis (pregnancy toxaemia)

A

• Ketosis (during pregnancy) is so severe that they fall into metabolic acidosis

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29
Q

Ovine ketosis (pregnancy toxaemia)

Occurrence

A
  • Last trimester of pregnancy (twins→require much more energy that mother falls into ketosis)
  • Regularly heard-disease, prolonged outbreak
  • Typical seasonal occurrence (late autumn-winter in northern part of Europe
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30
Q

Ovine ketosis (pregnancy toxaemia)

Predisposing factors

A
  • Intensive housing

* Obesity

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31
Q

Ovine ketosis (pregnancy toxaemia)

Cause

A
  • Energy deficiency
  • Changes in nutrition and/or in housing
  • Stress (endocrine basis of the condition)
32
Q

Ovine ketosis (pregnancy toxaemia)

Symptoms

A
  • 2-6 days course
  • Similar to the nervous form of ketosis in cows
  • Apathy/lethargy, anorexia, ataxia, blindness, grinding of the teeth
  • Ketonuria, ketonaemia, hypoglycaemia, severe liver failure (fatty liver), coma, death
33
Q

Ovine ketosis (pregnancy toxaemia)

Nitroprussid-Na reaction

A

• Milk-test is not used as milk is not available before lambing

34
Q

Ovine ketosis (pregnancy toxaemia)

Treatment

A

• Regularly unsuccessful
• 100-200 ml glucose/dextrose 20% solution iv., ip.
• Treat ketosis
• Glucocorticoids → induce lambing/abortion
o Dexamethasone: large dose of 25mg/animal
• C-section has to be considered (1 week before expected lambing → okay to do C-section, but
date of mating is often unknown)

35
Q

Ovine ketosis (pregnancy toxaemia)

Prevention

A
  • More effective

* Avoid energy imbalance, stressors

36
Q

Recumbency in the periparturient period due to metabolic problems

A 
Downer cow syndrome
Atypical milk fever (downer cow)
Downer cow syndrome – musculoskeletal injury
Parturient paresis (milk fever)
Hypomagnesemic tetany
37
Q

Recumbency in the periparturient period due to metabolic problems

Downer cow syndrome

Definition:

A

• There always is a primary cause
• Animals staying recumbend ager 24 hours of calving
• Cattle cannot stand long lasting recumbency well
• After a short time (36-48h) degenerative alterations occur in the musculoskeletal system due to weight of the cow→visualisable with microscope
• Worse chance of recovery when recumbent
• Fenwick et al, 1969
o Hypocalcaemic cows treated within 6 hours, only 2% became long lasting recumbent
o Treatment after 18 hours of the occurrences 50% of the animals did not stand up
• Secondary musculoskeletal disorders can cause long lasting recumbency

38
Q

Recumbency in the periparturient period due to metabolic problems

Downer cow syndrome

Pathogenesis

A
  • Long term lateral recumbency→muscle compression, ischaemia, hypoxia, necrosis, (inflammation)
  • Compression of the nerves as well (n. ischiadicus, n. peronaeus)
  • Repeated efforts to get up→rupture of muscles, haematoma
39
Q

Recumbency in the periparturient period due to metabolic problems

Downer cow syndrome

Occurrence

A
  • Usually periparturient

* But anywhere in lactation

40
Q

Recumbency in the periparturient period due to metabolic problems

Downer cow syndrome

Incidence

A
  • 2-5% of the herd

* 20% around calving time

41
Q

Recumbency in the periparturient period due to metabolic problems

Atypical milk fever (downer cow)

Definition

A

• Primarily disorder of (hind) limb muscles (Extensors
• Due to their ischaemia myodegeneration, necrosis develops
• Ischaemia is caused by permanent compression
• Similar myodegeneration occurs in humans after long-term strangulation of the limb
(tourniquet-paralysis)

42
Q

Recumbency in the periparturient period due to metabolic problems

Atypical milk fever (downer cow)

Aetiology

A 
• Not uniform
• Any disease can be in the background causing lying of the cows.
• Always a secondary condition
• Potential background
    o Milk fever
    o Trauma (muscle, joints, bones, spinal cord)
    o Fatty liver
    o Hypomagnesaemia, hypokalaemia, hypophosphatemia o Lactacidaemia
    o Mastitis (E.coli)
    o Displaced abomasum
    o Reticulo-peritonitis
    o Infectious diseases (even BSE)
  “5 M”
• Mastitis
• Metritis
• Metabolic 
• Musculoskeletal/neurologic
• Massive sepsis (peritonitis)
→all cause recumbency
43
Q

Recumbency in the periparturient period due to metabolic problems

Atypical milk fever (downer cow)

What should you do with a recumbent cow

A

• Slaughter
• Wait (if they are able to eat and drink)
→no strict rule because we cannot estimate the amount of muscle degeneration
→based on clinical signs

44
Q

Recumbency in the periparturient period due to metabolic problems

Atypical milk fever (downer cow)

Clinical signs

A

• Sitting like a frog

45
Q

Recumbency in the periparturient period due to metabolic problems

Atypical milk fever (downer cow)

Treatment without medicaments

A
  • Pull/transport the cow to a smooth, soft surface
  • Suspension of the cow
  • Suspension with air bag
  • Aqualift water bath
  • Stimulation of circulation
46
Q

Recumbency in the periparturient period due to metabolic problems

Atypical milk fever (downer cow)

Prognosis

A

• CK (creatinine kinase)
o >1000 IU/L – guarded
o Bad – elevated for two consecutive days
• AST (aspartate aminotransferase, GOT)
o >500 IU/L – bad
• Bad sign if both are elevated for 2 days

47
Q

Recumbency in the periparturient period due to metabolic problems

Atypical milk fever (downer cow)

Laboratory findings

A

• Normal Ca-, Mg- and P-values in the blood
• Normal haematology (except when inflammation is present)
• Severe increase of enzyme activity (creatin-kinase=CK, AST=GOT,
LDH)
• Myoglobinaemia, myoglobinuria (proteinuria). Not visible

48
Q

Recumbency in the periparturient period due to metabolic problems

Atypical milk fever (downer cow)

Medical treatment

A
  • Electrolytes, vitamins, roborants
  • Iv Ca-therapy: maximum 1-2 repeated doses
  • Mg and P-therapy as well
  • Vitamin D (increases Ca- and P-levels)
  • In case of hypokalaemia K-therapy
49
Q

Recumbency in the periparturient period due to metabolic problems

Downer cow syndrome – musculoskeletal injury

Sensorium decreased/kept?

A

• Decreased
o Metabolic, (hypocalcaemia, puerperalis coma, tremor, Mg loss, neurological ketosis)
• Kept
o Good status: certain metabolic disease, muscle disease, nerve damage, psychogenic
immobility
o Bad status: acute abdomen, shock/intoxication, abdominal pain

50
Q

Recumbency in the periparturient period due to metabolic problems

Downer cow syndrome – musculoskeletal injury

Clinical examination

A
  • Hoofs (laminitis)
  • Joints
  • Tendons and muscles (effusion, temperature, pain, swelling)
  • Stifle
  • Pelvis and upper limb
  • Rectal exam
  • Spine (palpation) T2-S
  • Nerves
  • Skin
  • Anal tone/Anus-reflex
  • Corona exam
  • Patellar reflex

Secondary nerve damage due to prolonged recumbency
• Hind limb: n. ischiadicus
• Fore limb: n. radialis

51
Q

Recumbency in the periparturient period due to metabolic problems

Parturient paresis (milk fever)

Occurrence

A
  • High-producing, adult dairy cows (mainly in 5-10 years of age)
  • Immediately after calving (1-3 days)
52
Q

Recumbency in the periparturient period due to metabolic problems

Parturient paresis (milk fever)

Cause

A
  • Increased neuro-muscular irritability (hypocalcaemia, hypophosphataemia)
  • Simultaneous hypermagnesaemia (rarely normo- or hypomagnesaemia)
53
Q

Recumbency in the periparturient period due to metabolic problems

Parturient paresis (milk fever)

Pathogenesis

A

• Relative/absolute hypoparathyroidism
• Loss of mobilizable Ca-stores in bones (age!)
• Decreased Ca-absorption from the GI tract
• Increased Ca-excretion with decreased Mg-excretion in milk
• 3 phases of clinical form
Mechanism affecting the calcium level

  • 1L milk requires 1.2g Ca
  • First 4-5 days are required until the animal is able to maintain normal Ca levels
54
Q

Recumbency in the periparturient period due to metabolic problems

Parturient paresis (milk fever)

Symptoms

A
  • Sternal, later lateral recumbency
  • (tetany)
  • Opisthotonos
  • Coma
  • Frequent consequence: “downer cow” syndrome
55
Q

Recumbency in the periparturient period due to metabolic problems

Parturient paresis (milk fever)

In-office laboratory tests

A

• Ca-test, whole blood (Graeub, Switzerland)
o Semi-quantitative test
• Sulkowitch probe
o Composition
▪ 2.5 g oxalic acid
▪ 2.5 g ammonium-oxalate
▪ 5ml cc. acidum aceticum (“glacial acid”)
▪ Add 150 ml DW
o Hypothesis:
▪ Normocalcaemic cows excrete calcium via urine, precipitating in the presence
of oxalic acid
▪ Hypocalcaemic cows excrete less Ca (hypocalciuria), therefore less/no
precipitation is present
o Procedure
▪ Equal volume urine and reagent to be mixed
▪ After some 3 minutes the amount of precipitate is evaluated (+, ++, +++)
o Evaluation
▪ -/+: no Ca/hypocalciuira: most probable hypocalcaemia
▪ ++: normocalciuria, hypocalcaemia rare
▪ +++: normo/hypercalciuria, hypocalcaemia can be excluded
• Ionised calcium measurement possibilities
Measurement of blood Ca
• Total vs. ionised calcium (tCa vs. iCa)
o Ionised Ca
o Albumin bound Ca
o Other protein bound Ca
o Anioncomplex bound Ca
• Total calcium fractions in the sera
o Blood pH
o Blood albumin concentration
o Other proteins in blood
• Effecting the fractions
• The ration of ionised Ca changes 305% compared to total Ca as days go on after calving in the first five days

56
Q

Recumbency in the periparturient period due to metabolic problems

Parturient paresis (milk fever)

Course

A
  • Regularly good response to Ca-therapy

* (except: atypical from, downer cow syndrome)

57
Q

Recumbency in the periparturient period due to metabolic problems

Parturient paresis (milk fever)

Treatment

A 
• Ca-borogluconate 25% solution iv. or sc. (if Ca is not given iv not enough will be absorbed) 
    o If Calcium is given to non-hypocalcaemic cows→can be life threatening (can stop
the heart)
• 100-120ml/100kg iv. SLOWLU
• Calcium paste system
    o 2-6h: CaCl2 61%, MgCl2 2% 
    o 5-7h: Ca-propionate 88%
    o 16-20h
• Bovikalc – Ca bolus after calving
58
Q

Recumbency in the periparturient period due to metabolic problems

Parturient paresis (milk fever)

Prevention

A

• P-rich, Ca-poor diet before calving, Vitamin D3 inj. 1 million units im. before calving. This condition rarely occurs in sheep (before lambing) and in goats (after parturition)

Avoid paravenous Ca-infusion→it causes (para-)phlebitis, sever tissue necrosis

59
Q

Recumbency in the periparturient period due to metabolic problems

Hypomagnesemic tetany

Plasma MG drops from 0.8 mmol/L to 0.4 mmol/L→tetany

A
  1. Grass tetany: occurs in early spring at pasturing
    o Cause:
    ▪ Grass: decreased Mg, increased K (fertilisers)
    ▪ Decreased Mg absorption (increased ruminal N)
    ▪ Stress (changes in Mg redistribution)
    o Symptoms: weakness, anorexia, ataxia, tetany, excitation/coma
  2. Transport tetany
    o Pregnant cows are susceptible
    o Cause: transport→stress (decreased magnesium uptake)
  3. Calf tetany
    o Caused by Mg-poor milk (“whole milk tetany”)
60
Q

Recumbency in the periparturient period due to metabolic problems

Hypomagnesemic tetany

Treatment

A
  • Commercial Mg(+Ca) compounds

* 15 MgCl2 + 40g CaCl2 solved in 500 ml water iv

61
Q

Metabolic osteopathies in ruminants

A 
Rickets
Osteomalacia
Osteoporosis/-penia
Osteodystrophia fibrosa
Spastic paresis
62
Q

Metabolic osteopathies in ruminants

Rickets

Occurrence

A

• Calves, growing cattle, rare

63
Q

Metabolic osteopathies in ruminants

Rickets

Cause

A

• Ca, P and Vit D deficiency

64
Q

Metabolic osteopathies in ruminants

Rickets

Symptoms

A

• Allotriophagia (pica), ataxia, bone deformities

65
Q

Metabolic osteopathies in ruminants

Rickets

Therapy

A

• Vitamin D, balanced Ca and P intake

66
Q

Metabolic osteopathies in ruminants

Osteomalacia

Occurrence

A

• Milking cows. Endemic

67
Q

Metabolic osteopathies in ruminants

Osteomalacia

Cause

A

• P and C deficiency

68
Q

Metabolic osteopathies in ruminants

Osteomalacia

Symptoms

A

• Allotriophagia, ataxia, permanent recumbency, painful joints and bones, bone fractures, easily moveable teeth

69
Q

Metabolic osteopathies in ruminants

Osteomalacia

Therapy, prevention

A

• As for rickets

70
Q

Metabolic osteopathies in ruminants

Osteoporosis/-penia

Occurrence

A

• Mostly in sheep and in goats

71
Q

Metabolic osteopathies in ruminants

Osteoporosis/-penia

Cause

A
  • Extremely poor diet, endocrine background

* Not “pure” form of porosis (oseteoporomalacia)

72
Q

Metabolic osteopathies in ruminants

Osteodystrophia fibrosa

Occurrence

A
  • Goat (extremely rare)

* Mandible and maxilla involved

73
Q

Metabolic osteopathies in ruminants

Osteodystrophia fibrosa

Cause

A

• Not clear

74
Q

Metabolic osteopathies in ruminants

Osteodystrophia fibrosa

Symptoms

A

• Swelling and deformities of affected, rubber-like bones

75
Q

Metabolic osteopathies in ruminants

Spastic paresis

Occurrence

A

• Calves (weeks – 6 months of age)

76
Q

Metabolic osteopathies in ruminants

Spastic paresis

Cause

A

• Inherited (?) disease

77
Q

Metabolic osteopathies in ruminants

Spastic paresis

Symptoms

A
  • Increased tone of the gastrocnemius muscle, straightness of the hock, elevation of the tail
  • Progressive lameness, recumbency

Farm Animal Medicine Final (61 decks)

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