Production Animal ESE Flashcards
1
Q
Describe the steps for physical exam (areas of the cow)
A
Tail -> urine, blood, temp, RR, BCS
Right Side
Head
Left side
Tail - repro/MM
2
Q
HR for cow
A
60-80
3
Q
Temp for cow
A
38-39
4
Q
RR for cow
A
25
5
Q
How is ketosis diagnosed? What are the ketone bodies?
A
Ketone bodies in blood plasma, milk and urine. Milk and urine are diagnosed 2d later than blood
Beta hydroxybutyrate - blood
Acetoacetate - urine
6
Q
Pathophysiology of ketosis - cause, results in
A
Cause -> inadequate nutrient supply for fat and carb metabolism needed for lactation
Results in -> Hypoglycaemia, reduced milk yield, low BW, ketone bodies in fluids
May be clinical or subclinical (ketonuria or ketonemia without clinical signs)
7
Q
What are clinical signs in ketosis caused by?
A
Hypoglycaemia rather than mobilisation of ketones
8
Q
What can ketosis occur secondary to?
A
LDA, RDA, lameness, metritis
9
Q
2 types of ketosis
A
type 1 -> high yielding dairy cows 2-8wks post calving due to inad. intake
Type 2 -> occurs within 2 wks of calving due to excess fat deposition into the liver in late pregnancy resulting in insulin resistance
10
Q
6 risk factors for ketosis
A
Feeding poor quality silage with high butyrate concentrations
Poor rumen function
SARA
Cows with BCS >3.5 at calving
High protein diet
High milk production demands
11
Q
5 treatments of ketosis
A
- Propylene glycol -> gluconeogenesis 300ml/d
- Dextrose -> 500ml 40-50%. IV bolus for hypoglycaemia. Only effective short term
- Steroids -> dexamethasone to get hyperglycaemic state. But immunosuppressive
- Insulin -> used with glucocorticoids, suppress NEFA, long acting done again 24-48h later
- B12 -> appetite stimulant
12
Q
Ideal treatment plan for ketosis
A
- 500ml dextrose 4% IV
- Single injection of corticosteroid
- Oral propylene glycol BID for 4d (200ml BID)
13
Q
Liver abscess formation - how, why, where can they go?
A
Cattle fed high grain diets are at risk, generally form from infection with anaerobic bacteria (fusobacterium, truperella) that contain leukotoxins
Enter liver in portal vein, hepatic artery or bile duct, or from site of trauma
Occur following ruminitis (after acidosis)
Caudal vena cava syndrome -> gut infected, to liver, to lungs
14
Q
Clinical signs and diagnosis of liver abscess
A
Anorexia
Ultrasound, CBC, biochem, elevated GGT, SDH, hyperbilirubinaemia, elevated serum proteins, hypoglycaemia, hypoalbuminaemia
15
Q
Treatment of liver abscess
A
Peniciliin and macrolides, but cattle rarely treatment as recovery is rare
16
Q
Prevention of liver abscesses
A
In feed antimicrobials
Vaccinate for fusobacterium and arcanobacterium pyogenes
Manage grain feeding to prevent acidosis
17
Q
Gross pathology of liver abscess
A
Purulent spheres encapsulated in thick fibrotic walls
Hyperaemia around abscess
Pyogranulomatous abscesses
18
Q
Aetiology of fatty liver syndrome - who, risk factors
A
Occurs in high producing dairy cows (month after parturition)
Risk factors -> increased BCS, NEB due to fetal growth lactation, feed consumption, disease
Hypoglycaemia = decreased insulin and glucagon which converts tissue fat to FFAs, NEFAs and glycerol. Glycerol has role in oxaloecetate which if deficient, we get ketone production
Large amounts of body fat mobilised, liver overwhelmed and stores TG in hepatocytes
19
Q
Risk factors for fatty liver syndrome
A
Change to milking diet
Decreased feed intake
Low protein diets
Concurrent illness
20
Q
Clinical signs of fatty liver syndrome
A
Obese cow, depression, anorexia, weight loss, weakness, decreased rumen motility and milk production
21
Q
Diagnosis of fatty liver syndrome
A
Liver biopsy
CBC, biochem -> increased liver enxymes, leukopaenia, degen. left shift, NEFA increased, decreased TG and cholesterol
22
Q
Treatment of fatty liver syndrome
A
IV glucose -> 100-200mg/kg/h to induce insulin
Insulin
Glucagon (too spenny)
Corticosteroids
Polypropylene glycol
Make them eat
Transaunation of ruminal fluid
23
Q
Reasons for an LDA occuring and how
A
Pregnancy -> pushes rumen cranially and dorsally allowing abomasum to shift to the left
Decreased feed intake -> lack of rumen fill
Following birth -> rumen fails to fill void, omentum on abomasum is stretched, abomasal atony allowing gas to fill
Feed low in fibre increase VFA = atony and gas
Risk factors -> ketosis, feed intake, grain, hypocalcaemia, excess BCS
24
Q
Clinical signs of a LDA
A
Anorexia, abdominal pain, abscense of rumination
Decline in milk
Calving in last month
Reduced feed intake
Soft faeces, sunken paralumbar fossa, OR
Buldge in upper left PLF (severe cases)
25
Diagnosis of an LDA
Ping over 9-12th rib on LHS
Rumen tinkle on ballottment of lower abdomen behind last rib
Biochem-> hypochloraemia, hypokalaemia, metabolic alkalosis
Abomasal fluid sample no protozoa, pH <4
26
Treatment of LDA
Abomasopexy
Ometopexy
Percutaenous tacks
27
RDA aetiology
Unknown - more likely atony
Gas, feed and liquid causes it to swell and go dorsal
Occurs 3-6 weeks post calving
Same risk factors as LDA
28
RDA clinical signs
SAme as LDA
Reduced amount of diarrhoea faeces, may be melena
Elevated HR - volvulus can be up to 140
Dehydration
DDx volvulus -> decreased peripjheral circulation, pale MM, auscultation large gas fill in upper right quadrant of abdomen
29
RDA diagnosis
Metabolic alkalosis - hypochloraemia, hypokalaemia
Percussion and auscultation over right middle to upper 1/3 of abdomen gets ping
Tinkles under last 5 ribs - rarely extends to paralumbar fossa
Volvulus we get haemoconcentration
30
RDA treatment
Omentopexy or pyloropexy
31
Abomasal ulcer formation and location
Greater curvature
Multifactorial - stress mainly, viral causes (BVDV)
High producing cows (stress)
Prolonged inappetance causing sustained low pH in abomasum
32
4 types of abomasal ulcers
non-perforating
Non-perforating with severe bloodloss
Perforating with local peritonitis
Perforating with diffuse peritonitis
33
Risk factors for abomasal ulcers
Stress and high grain diets
34
Clinical signs of abomasal ulcers
Abdominal pain
Anorexia
Decreased rumen motiity
Mild ruminal tympany
GIT haemorrhage
Decreased milk yield
35
Diagnosis of abomasal ulcers
Faecal occult blood
Abdominocentesis
Decreased PCV with severe bloodloss
Rarely diagnosed antemortem
36
Treatment of abomasal ulcers
Treatment unrealistic
Antacids limited value
37
Abomasal impaction - what, clinical signs, treatment
Feed poor quality and fibrous with limited water access causes blockage
Anorexia, scant faeces, distended abdomen, expiratory grunt
Treatment -> fluids, paraggin, abomasotomy
38
Haemorhagic bowel syndrome aetiology
Acute segmental intraluminal haemorrhage with secondary obstruction to the SI due to clots and sloughing of the jejunum
Pathgenesis unknown
Multifactorial -> feed intake, density, pH of GIT, parity, clostridium perfringens type A is normal commensal, isolated in cases but not primary cause
39
Risk factors for haemorrhagic bowel syndrome
Management practices
Latation - first 100DIM
Feeding high energy diet and low fibre
Large herds
40
Clinical signs of haemorrhagic bowel syndrome
Affected animals may be found dead, recumbant or in systemic collapse, still standing but weak and depressed
Decline in production, anorexia, sunken eyes, shock
Rapid progression
MM pale or congested, hypovolaemic shock
Teeth grinding, ruminal distention, dec contractions, dec faecal output, melena, constipation or diarrhoea with clots
Ballottment of lower R abdomen = splashing sound from backed up ingesta
41
Diagnosis of haemorrhagic bowel syndrome
Laparotomy or PM
Transabdominal ultrasound has intestinal obstruction - distended intestinal loops, blood clots, appear and hyperechoic structures in the lumen
DDx - salmonellosis, intussusception, abomasal haemorrhage + ulceration or volvulus
Bloods -> neutropaenia with marked left shift, hypocal, hyponat, hypokal
42
Haemorrhagic bowel syndrome gross pathology
May not have time for clinical pathology as disease is acute
Distinct section of jejunum distended by large clots occluding lumen
Necrosis of mucosa maybe
43
Haemorrhagic bowel syndrome treatment
Medical emergency, antibiotics ineffective
IV fluids + calcium, NSAID and corticosteroids for pain and shock
Surgery -> poor prognosis. Remove clot via enterotomy or intestinal resection or manual massage of affected area to break clot
44
Prevention of haemorrhagic bowel syndrome
Feed adequate fibre length and quantity
45
Intestinal phytobezoars (intestinal obstruction) - pathogenesis and clinical signs
Pastures with onion grass
Obstruction due to phytobezoars occurs spring/summer after they dominate in autumn
Large ones lodge in abomasum, smaller in SI
Signs -> fluid + electrolyte loss into lumen proximal to obstruction. Abdominal pain, HR and temp normal but increase with dehydration, sudden and severe decline in milk.
Ballottment of right side fluid splashing. Grey/yellow pasty faeces with foul smell. May have nasal discharge
46
Diagnosis of intestinal phytobezoars
History of onion weeds
Cow suddenly off milk with yellow pasty faeces and fluid in intestines
Ex lap -> via right paralumbar fossa
47
Intestinal volvulus - types
Physical obstruction of intestinal lumen - twisting of segment causing strangulation of blood supply
Two types:
1. Segmental volvulus of jejuno-ileum
2. Volvulus up to 360 degrees of small and large intestine around root of mesentery
48
Intestinal volvulus - causes
Unknown
Rolling of cow to correct uterine torsion or LDA
Calves -> excessive feeding of reconstituted milk replacer. Excess flow out of abomasum into SI, rapid lactose fermentation and gas production
49
Clinical signs of intestinal volvulus
Sudden onset
Severe colic
Bilateral ab. distenstion, multiple areas of tympanic resonsance over R abdomen at paralumbar fossa and extending over the ribs
Faeces nromal then scant/absent
Elevated rectal temo, HR, rapid dehydration and recumancy
Multiple gas distended loops in SI on rectal exam
Death in 12 hours
50
Treatment of intestinal volvulus
Courageous surgery but may recover
R paralumbar fossa approach standing -> liberal vertical incision , see distended SI, follow mesentery to root and find site and direction of twist to reposition.
IV fluids and antibiotics after
Death post surgery due to release of toxins sequestered in occluded bowel
51
Colic aetiology - cause, signs
Severe paraoxsymal pain due to abdominal organ
Discomfort, kicking, lying down, up and down,
Less likely than horses to develop intestinal ischaemia due to thick mesenteric fat layer
Mild, moderate or severe
52
Moderate colic causes
Intussusception, volvulus or incarceration
53
Severe colic causes
Rarely observed in cattle
Torsion of mesenteric root
Extreme pain signs
54
Spasmodic colic clinical signs
Severe and sudden onset with intesne pain
Cardinal signs normal, abdominal sounds increased
Treatment -> Spasmolytic drug and/or sedative like xylazine. Should recover in 4-6h if not needs re-exam
55
What is paralytic ileus?
A state of functional obstruction of intestines or failure of peristalsis mimicking complete physical intestinal obstruction
May be localised or affect whole small and large intestines. Common cause of failure to pass faeces in dairy cattle
56
Pathogenesis of paralytic ileus
loss of intestinal tone and motility due to reflex inhibition
Causes -> acute peritonitis, prolonged distension from enteritis, surgery outcome, Severe toxaemia, electrolyte disturbances, dehydration
Pain amd can predispose to secondary torsion of mesentery
57
Clinical signs of paralytic ileus
Intestinal distention, abdominal pain, dehydration, scant faeces
R abdominal distension and ausculatated pings, splashing and tinkling
Rectal exam -> distended spiral colon, caecum or SI. No faeces passed but rectal glove may be coated with sticky mucus
Diagnose with clinical signs
58
Treatment of paralytic ileus
Resolve without
Cause dependent -> electrolytes, fluid therapy, IV or SC calcium solution and oral laxative antacids like magnesium hydroxide 0.5-1g/kg repeated daily
NSAIDs for pain control
Surgical decompression of bowel may be required
59
Intussuception aetiology
Strong peristalsis (calves with diarrhoea) or tumour/inflammatory growth in lumen
Mesentery drawn in occluding blood flow. Dehydration + electrolyte imbalances with toxaemia from sichaemia and necrosis of the bowel
60
Clinical signs of intussusception
Sudden onset increased HR and RR, off milk and anorexic, colic + pain, rumen stasis, R abdomen enlarges from SI distention
Blood + tarry faeces, recumbency
61
Diagnosis of intuss.
Dehydration = GI secretions accumulate in gut lumen and hypochloraemia, hypokalaemia, metabolic alkalosis develops
Tarry faeces very indicative
Voluminous peritoneal fluid with high conc. of protein
WBC normal-high depending on degree of peritonitis
Confirmed with ex-lap of R paralumbar fossa
62
Treatment of intussusception
Surgery -> proximal gut always dilated, fluid filled and distal narrow and empty
Intuss. will be spongy-solid, painful coiled part
Hard to maintain good analgesia and animal will kick and lie down once manipulated
63
Caecal volvulus/torsion pathogenesis
Atony/hypotony affected caecum starts the disease
Caecum and colon main sites of microbial digestion, so starch escaping forestomach are metabolised here into VFA's which lower pH of caecal contens and inhibit caecal motility = caecal dilation due to gas = displacement
Diets rich in rumen resistant starches are factor
Apex or posterior 1/3 of caecum is free from mesenteric attachment and most likely involved in torsion
64
Clinical findings and diagnosis of caecal volvulus vs simple marked dilation
Simple marked dilation -> reduced milk yield, reduced appetite, mild abdominal discomfort, dec faecal output, upper right abdomen near flank distended
- R dorsal area of tympanic resonance from tuber coxae to 11th/12th rib
- Rectal palpation - distended with apex in pelvic cavity
Caecal volvulus -> R abdomen marked distended, varying degrees of dehydration, scant faeces, ping in right paralumbar fossa extending in greater area than simple marked dilation.
Ping more caudal than right RDA/torsion. R flank ballott shows fluid splashing
Rectal -> distneded body of caecum palpable at entrance to pelvic cavity and apex displaced cranially/medially or laterally.
65
Treatment options for caecal volvulus
Medical management -> good hay 2-4d recovery. used for simple caecal dilation. Instant coffee 0.5kg oral or parrafin oil. Metamizole IV, bethanechol SC
Surgery -> for severe cases. Indicated with tachycardia >90, marked abdominal pain and scant faeces
66
Pre-operative requirements for caecal volvulus surgery
Analgesia
Should be eating and pooing in 24h normally
Long term recurrance 10-20%. Can remove apex (free mobile part) so remainder can be more firmly attached to adjacent structures
67
What does CK indicate, what increases it
Muscle damage
Increased with exercise or long transport
T1/2 4h = prolonged increases mean active and continuing muscle damage
68
What does AST indicate
Found in high concentrations in muscle (skeletal and cardiac), liver, RBC's and kidney
Elevations may persist for weeks, useful when compared to more specific tissue enzymes
69
What does ALP indicate
Sensitive indicator of cholestasis
Slightly elevated in bone disease or fractures
Neonates consuming colostrum may have increase
70
What does GGT indicate
Cholestasis
Increased with hepatic necrosis and indicative of ongoing hepatic damage
71
GLDH indicates:
Hepatic necrosis
Indicative of severe hepatocellular damage if increased
72
Bilirubin may increase due to
Liver failure or haemolytic anaemia (suggested with RBC conc)
73
Urea - control
Excreted by kidney in glomerular filtration
Excretion in ruminants governed by nitrogen intake and GIT can excrete also
74
L-Lactate increases may mean
Sepsis
Seen when pH is elevated and in an alkalotic state
75
BOHB increases mean:
ketosis
76
Hypermag and Hypomag reasons
Hypermag -> seen commonly in postpartum or over administration
Hypomag -> clinical when <0.4mmol/L (lactation, inappetance)
77
Causes of hypophosphataemia
Milk fever, post parturient decreased release from bone and increased loss in milk, and starvation
Excreted in urine and faeces
78
Causes of hyperphosphataemia
Seen in young aniamls
Caused by vitamin D toxicity, haemolysis, anorexia
79
Calcium is regulated by?
Diet, calcitonin, PTH and vitamin D
80
Hypocalcaemia is caused by?
Milk fever, hypomag, anorexia
81
Hypercalcaemia is caused by?
Excess Ca administration or hypervitaminosis D (promotes absorption of Ca and P)
82
Reasons for hypochloremia
Acid base disturbance
Increasees in bicarbonate
83
Reasons for hypokalaemia
Depletion of body stores and acute alkalosis
Adminstration of glucose or insulin - shifts potassium into the cell
84
Hyponatraemia reasons
Diarrhoea, renal losses
Usually seen with urea elevation
85
Displaced or torsed abomasum biochem
Alkalosis
Hypochloraemia
Hypokalaemia
Hyponatraemia
Dehydration (hyperproteinaemia and PCV)
86
Abomasal ulcers biochem
Leukocytosis - neutrophilia and hyperfibrinogenaemia if peritonitis there
87
Liver abscessation biochem
HYPERglobulinaemia, bilirubinaemia and fibrinogenaemia
leukocytosis
Increased GGT and SDH
Hypoalbuminaemia and hypoglycaemia
88
Ketosis biochem
Hypoglycaemia, high NEFA's
Ketonuria, ketolactia
High Betahydroxybutyrate in blood
89
traumatic reticuloperitonitis biochem
Leukocytosis - neutrophilia with left shift
Hyperfibrinogenaemia
Hyperproteinaemia
Normal acid base - except if peritonitis = hypomotility - alkalosis
90
Vagal indigestion biochem
Peritonitis -> leukocytosis, increased TPP
Hypokalaemia
91
Parasitic gastoenteritis biochem
Eosinophilia
Hyperproteinaemia
92
Acute neonatal diarrhoea
Metabolic acidosis
Hyperkalaemia
93
Xylazine -> class, MOA, toxic effects
Alpha-2 agonist
Binds presynaptic receptors to reduce release of noradrenaline
Give IV or IM
Causes sedation, analgesia and muscle relaxation
High doses 0.1-0.2mg/kg = recumbency, CNS and respiratory depression
94
Acepromazine class, MOA, route of admin
Phenothiazine - inhibits dopamine receptors
Barely used in cattle due to long WHP and DOA
Causes sedation with no analgesia
0.02-0.05mg/kg IV (IM painful)
95
Diazepam class, moA, effect
Benzodiazepene - enhances affinity for for GABA at GABA receptors, hyperpolarising neurons
Brief sedation in ruminants
0.25-0.5mg/kg IV
96
Phenobarbital class, moa, sedation and toxic effects
decreases rate of dissociation of GABA from receptors
30-60min sedation
Large doses - ataxia and delirium
97
Butorphanol class and MOA
Kappa agonist and weak Mu antagonist
Provides sedation and analgesia
IV or IM
98
Dorsal approach PVRA
Nerves branch above and below transverse process along caudal edge of rib
Nerves L1-L3
Walk off cranial edge of transverse process inject cranial and above
99
PVRA lateral approach
Easier to palpate
Oblique needle and inject under and over transverse process and fan out local
More difficult - easier to get incomplete block
100
When should antibiotic therapy be considered in surgery in cattle?
Contaminated or clean surgery where infection a risk. If contamination occurs during surgery, exteriorise and flush site, allow to drain and aftercare
101
When should antibiotic therapy be given at surgery
IV 15 mins prior
IM 60 mins prior
102
Most common prophylactic antibiotics
Procaine penicillin - gram positive, anaerobes and some suscpetible gram negative
Oxytetracycline - gram pos and gram neg
103
When is fluid therapy used?
When GIT not functional or not enough time
104
Fluid therapy for metabolic alkalosis
Isotonic saline (0.9%) NaCl -> iso-osmotic solution
Ringers solution (Na, Cl, Ca, K) - iso-osmotic crystalloid. Given to lactating dairy cows requiring surgery for GIT disease
Glucose and calcium added to these bases for cows with surgical diseases (LDA)
Hypertonic -> 4-5ml/kg IV over 5min and 20L oral water if they do not drink afterwards
105
Ringers lactate function
Iso osmotic
Crystalloid
Corrects dehydration and electrolyte imbalances as lactate metabolised to bicarb to increase blood pH when acidotic
106
Ringers acetate function
Correct dehydration and alkalinising
107
Sodium bicarbonate fluid function
Iso osmotic
Crystalloid
Strong alkalinising fluid for severe acidaemia
Add to sterile water
108
NaCl fluid function
Hypertonic saline
Rapid expansion of plasma volume for severely dehydrated animals - draws water out from ICF
109
Indications for ex lap
Acute surgically correctable condition
Distension of abdomen due to abomasum, caecum or intestines with fluid and gas
Scant of absent faeces for 36-48h indicating obstruction
Presence of grunt on deep palpation - inflammation or stretching of peritoneum
HR >100
Hypomotile GIT
Abdominal pain >8h no relief
Pings or gas caps
110
Surgical approach to Ex Lap to find LDA
1. Clip and shave
2. Caudal epidural with 5ml 2% lignocaine
3. Proximal PV block with 90ml 2% lignocaine
4. Scrub
5. 15-20cm incision 2cm caudal to caudal border 13th rib
6. Left arm around back of omental sheet behind rumen to left body wall
7. Feel gas cap of displaced abomasum to confirm LDA
8. Decompress
9. Push abomasum ventral under rumen
10. Identify sows ear of omentum for suturing. Include into peritoneum and transverse abdominal layer for pexy
close
111
Considerations for surgery on farm
Restraint
Cleaning surgical area - scrub inside to outside, paper towel inside to outside, regional anaesthesia and then second wash and alcohol spray
soak rectal sleeve in chlorhex and sterile surgery gloves
112
Where is a ping in LDA?
9-12th rib
113
Serum ca normal, subclinical and clinical hypocal
normal 1.9-2.6
subclinical - <1.4
Clinical <2mmol/L
114
Treatment of hypocal
Calcium borogluconate 300ml 25-40% solution
need 8-12g IV calcium
Oral for standing cows - 50g
115
Prevention of hypocal
TCM
Negative DCAD thorugh anionic salt feeding or cereal hays low in K
116
Which cows get hypocal?
24h post calving but can be a few days
117
Hypomagnasaemia aetiopathologenesis
Low mG CSF
Ach accumulates at NMJ resulting in excitability
Associated with hypocal (PTH) and decreased milk production
<0.4mmol/L = tetany
<0.75mmol/L = low
118
Hypomag treatment
Magnesium sulphate SC 500ml 20%
Tranq with 3-5ml pentobarbitone
Parenteral Mg 100g MgO 1-2d and 50g for next 5d
119
Aetiopathogenesis of ketosis
NEB from high glucose demand and liimted supply
Diets with high protein and poor feed intake at risk
Body fat -> NEFA -> (energy or ketone bodies or fatty acids again) -
ketone bodies - butyhydroxybutyrate, acetate, acetoacetate
120
Diagnosis of ketosis
Blood BHB <30mg/dL
NEFAs on CBC
Ketone bodies in urine and milk - slight delay reaction
neuro signs and clinical exams
121
Treatment of ketosis - wasting and neuro form
Wasting - propylene glycol 300g 3-5d PO
Neuro - add dextrose 500ml 50% IV
122
Toxic mastitis cause
environmental colifroms - E.coli and pasteurella
results in endotoxic shock
123
Treatment of toxic mastitis
NSAID
IVFT
Cephalosporin
Strip udder every 2-4h for several days
124
Treatment of toxic metritis
IVFT
NSAID
Oxytetracycline/penicillin/cephalosporin
Precautionary calcium therapy
125
Toxic metritis cause
Trueparella pyogenes or e.coli few days to weeks post parturition
endotoxic shock
126
Bovine ephemeral fever - when, what, signs, treatment
Seasonal incidence "called 3 day sickness"
Arbovirus, Rhabdovirus - IV inoculation (vector mosquito or midgey)
Serious in older, fatter animals
Vasculitis, ocular discharge, hypocal, neutrophilic leucocytosis, pyrexia, stiffness, shivering, depression, severe lameness
Nurse, water, NSAID, treat hypocal
Vaccinate bulls
127
Downer cow managment
Treat primary cause
Nursing -> lifted 1-2x/d, 50cm hay, protected from weather, constricted to 4m, prevent crawling off bedding
Roll off affected leg
Clean and dry, clean often, food and water
Disinfect teats 2x a day
128
Euthanasia trigger points for a downer cow
Poor prognosis
Non-responsive pain and suffering
Non-alert cow not responding in suitable time
Not eating
Persistent lateral recumbency
Detiorates despite treatment
Unwilling to nurse
129
Define down cow
A cow which is unable to stand unassisted, with any mental state and any length of recumbency
130
Define downer cow
A cow which is unable to stand unassisted, that has been recumbent for ≥24 hours and is BAR.
131
Define downer cow syndrome
One of the many diseases which can cause recumbency in a periparturient cow
132
5 M's of a downer cow
1. Metritis
2. Mastitis
3. Metabolic
4. Musculoskeletal
5. Massive Sepsis
133
Inducing parturition in a pregnancy toxaemia (ketosis)
In cattle with pregnancy toxaemia, termination of pregnancy eliminates the energy drain of the fetoplacental unit.
* Corticosteroid: 20 – 30 mg dexamethasone or 25 mg triamcinolone
* Prostaglandin: 25 mg
134
Paspalum moA and clinical signs
Ergot producing claviceps paspali produce indole diterpenoid tremorgen "Paspalanine"
Block Ca activated K channels
Anxiety, hypersensitive, fine muscle tremors continuously and spontaneously, ataxia, paddling, paralysis
135
Ryegrass staggers Moa and CLinical signs
Fungus neotyphoidium lolli produces tremorgen lolitrem B
Same MOA and clinical signs as paspalum
Should prevent grazing of seedheads
136
Kikuyu poisoning clinical signs and problematic season
Unknown moA
Rumen distension, depression, muscle tremors, abdominal pain, fine muscle tremors, piloerection
Warm moist conditions
137
Sorghum poisoning moA and clinical signs, when it occurs
Unknown, suspect cyanide toxicity
Ataxia of pelvic limbs, urinary incontinence, fetlock knuckling, recumbent, perineal muscles relaxed
138
Phalaris staggers moA
toxicity due to dimethyl-tryptamine alkaloids
Inihbits monoamine oxidase interfering with serotonin and catecholamine synthesis
139
phalaris staggers clinical signs
Hyperexcitable
Ataxia
Stiffness of hocks
Dragging toes
Incoordination of tongue and lips
Wide-based stance
Hypermetria
Head nodding
Muscle tremors
Aggression
140
When do phalaris staggers occur?
Young rapid growing pasture
Late summer and autumn
>20 degrees
141
Prevention of phalaris staggers
Introduce to pasture over several days and feed hay
Do not use N fertiliser on phalaris
142
Oleaner poisoning moA and clinical signs
Cardiac glycosides inhibit NaKATPase
Cardiac arythmia
Sudden death
Profuse sweating
Convulsions
Paralysis
143
Oleander treatment
Activated charcoal and anti-arrhythmic drugs
Rehydrate
144
When can tachycardia be seen:
Pain
Fever
Inflammation
Hypocalcaemia and Mag
Metabolic disturbances causing hypovolaemia
145
Causes of muffled heart sounds
Obesity, thick chest wall
Pericarditis - traumatic reticuloperitonitis
Lymphosarcoma
Abscess
Chronic heart failure
Emphysema
146
Why are heart sounds muffled?
Displacement of heart from thoracic wall by fluid (pericardial effusion), a soft tissue mass or air
147
Diagnosis of coxofemoral dislocation
Displacement of coxofemoral head outside acetabulum, cranial and dorsal
Palpate greater trochanter in relation to pelvis
Affected limb held forwards, backwards and rotated out looking for crepitus on rotation and abduction of femur
148
Diagnosis of spinal fracture
Placement and spacing of vertebrae
149
Limb fracture/injury
Observe movement of animal
Palpate
Rads for expensive animal
150
First step in neuro exam
Distance exam of mentation and behaviour
Head tilt, pressing, bellowing
151
Lesions location that affect mentation
Cerebrum
Somtimes brainstem/cranial nerves
152
Neural locations affecting gait
Cerebellum
Spinal cord/PN
Sometimes brainstem and CN
153
Neural locations affecting posture
Cerebellum
Spinal cord and PN
Brainstem + CN (sometimes)
154
Spinal reflexes problem neural location
Cerebrum will affect them
cerebellum, brainstem, CN, spinal cord and PN might be normal or abnormal
155
Which 2 CN cannot be assessed in ruminants?
I - olfactory
XI - accessory
156
5 units to assess cranial nerves
1. Visual ability = II
2. eye symmetry = III, IV, VI
3. Face symmetry = V, VII
4. Horizontality of eyes = CN VIII
5. Swallowing reflex = IX, X, XII
157
Menance response tests:
CN II and VII
Closes eyes and moves away = vision
158
Pupillary reflex tests:
CN II and III
Miosis is normal response and small conscensual relfex in opposite eye
159
Palpebral reflex tests:
CN V and VII
Skin eye touched should close, retract eye and move head away
Touch medial canthus -> opthalmic branch of CNV
Touch lateral canthus -> maxillary branch
160
Strabismus directions and which nerve they suggest has a lesion
Ventrolateral position = CN III dysfunction
Dorsal/dorsomedial = CNIV dysfunction
Medial -> CN VI dysfunction
161
If a pathologic nystagmus is present with head at rest, what does it mean?
Fast phase of nystagmus is directed away from side of the lesion
162
What is the preyer reflex?
Creates auditory stimulus and assesses CN VIII
Normal = move ears towards noise
163
How are CN IX, X and XII tested?
give food see if consumes
Pass nasopharyngeal tube to see if gag reflex initiated
CNXII also by assessing size and symmetry of tongue
164
CN I
Olfactory - sense of smell
165
CNII
Optic - afferent pathway for vision
166
CN III
Oculomotor - pupil constriction, upper levator muscles
167
CN IV
Trochlear - dorsal oblique
168
CN V
Trigeminal - sensory to head, face, tongue
169
CN VI
Abducens - extraocular muscles retractor oculi and lateral rectus
170
CN VII
Facial - motor to facial muscles
171
VIII
Vestibular Cochlear - afferent branch of vestibular system, hearing
172
CN IX
Glossopharyngeal - swallowing
173
CNX
Vagus - gag reflex
174
CN XI
Accessory - cant test this in ruminants
175
CN XII
Hypoglossal - symmetry and size of tongue
176
Define paresis
Weakness, poor ability to initiate a gait, to maintain a posture, to support weight of the body and its parts, and to resist gravity
177
Define ataxia
Proprioceptive dysfunction causing abnormal range, rate and force of movement, and placement of the limbs
and other body parts
178
Cerebellar ataxia
No proprioceptive deficits, strength is preserved.
179
Proprioceptive ataxia
Secondary to damage of the afferent proprioceptive pathways
Wobliness walking and strange gait
180
Vestibular ataxia
Associated with head tilt, hypermetria, and hypotonia
The animal can have a unilateral lesion and falls towards the side of the lesion, or bilateral with a milder head tilt to the more severely affected side with intentional head tremor
No knuckling or weakness.
181
The most important forelimb reflex and what it assesses
Flexor withdrawal reflex
Sensory fibres in median and ulnar nerves, C6-T2 and motor fibres in median and ulnar nerves, axillary and musculocutaneous nerves.
182
Flexor withdrawal reflex procedure
The skin of the distal limb is pinched with needle holders, and in a normal animal the fetlock, knee, elbow, and shoulder should occur.
183
What does it mean if a crossed extensor reflex if seen in contralteral limb?
Severe central motor pathway lesion
184
2 other forelimb reflex test
Triceps reflex - ballot slightly flexed long head of tricep and watch from contraction of tricep and extension of elbow. Radial nerve and c7-T2
Extensor carpi radialis -> radial nerve. Observe weightbearing of forelimb or extension of knee. May not be present in normal animals
185
2 hindlimb reflex tests
Flexor withdrawal
Extensor/patellar ligament reflex
186
Hindlimb withdrawal reflex process
Afferent and efferent branches of sciatic nerve and L5-S3. Pinch skin of distal limb with needle holders and watch for flexion of limb
187
Extensor patellar ligament reflex procedure
Sensory and motor innervation of femoral nerve and L4-L5
Support limb in mildly flexed position and tap patellar ligament which causes contraction of quads and extension of stifle
188
Which reflex assesses afferent spinal nerves and efferent lateral thoracic nerve?
Cutaneous trunci
Should cause skin to flinch
Start at wing of ilium and if there is a response then do not continue
Lesion is 1-4 vertebrae above site with reflex returns
189
What is flaccid paralysis of the forelimb most likely due to?
Brachial nerve damage -> further damaged by not being able to maintain sternal recumbancy and extra damage in lateral
190
What does it mean if a cow is frog legged?
Femoral nerve damage
191
What does it mean if a cow is knuckling and dragging limb on dorsal surface?
Sciatic nerve damage
192
What if a cow has partial forward knuckling of the fetlock (hooves flat on ground and no dragging) and hyperflextion of hock?
Tibial nerve damage
193
What is damaged if there is abduction of the limb with weakness and recumbency - particuarly if bilateral?
Obtruator nerve damage
194
7 causes of ataxia in ruminants
1. Vascular
2. Infectious/inflamm = encephalitis, listeriosis
3. Trauma - femoral nerve paralysis, dislocated hip, sciatic nerve damage
4. Congenital defect
5. Metabolic/toxic = plants, botulism
6. Idiopathic
7. Degenerative = spastic paralysis
195
Listeriosis causative agent and pathogenesis
Listeria monocytogenes
gram-positive, nonsporulating
coccobacillary rods
Silage contaminated with
soil, faeces, or infected
material prior to
fermentation
* Enters via MM, wounds
etc.
* Enters via cranial nerve
(V, VII, VIII, IX) and
migrates to the
brainstem, causing
neuritis, meningitis and
encephalitis
196
Listeriosis - clinical signs
* Depends on CN affected
* Depressed
* Inappetant
* Mania
* Head tilt
* Moderate pyrexia in early stages
* Facial paralysis
* Ataxia
* Circling
* Dysphagia
* Tremor
* Rumen hypermotility
Poor prognosis if absent menace
197
Diagnosis of listeriosis
Unilateral CN deficit in depressed inappetant cow
CSF analysis (increased protein and WBC)
test silage
198
Listeriosis treatment
Penicilin, ampicillin or tetracyclines in water for 10 days
NSAID
IVFT
Electrolytes and B-group vitamins
Nursing
199
Prevention of listeriosis
Good quality feed and silage, reduce contamination when making silage
200
Polioencephalomalacia aetiopathogenesis
Functional deficiency of
thiamine
Other causes: production
of poorly absorbable
thiamine, inhibition of
phosphorylation, or
inhibition of absorption, lead poisoning or excess sulphur
Reduced thiamine ->
decreased transketolase -> less ATP for nervous tissue -> Decreased function of
ATP dependent Na/K
pump -> increased intracellular
Na and H20 -> swelling of brain
cells -> necrose under pressure against the skull
201
PEM Clinical signs
* Depression
* Apparent blindness
* Ataxia
* Proprioceptive deficits
* Fine muscle tremors
* Absence of menace
* Nystagmus with dorsomedial strabismus
* Recumbency
* Seizure
* Extensor rigidity
* Bruxism
* Hypermetria
* Miosis
202
Diagnosis of PEM
Blood thiamine <50mmol/L
response to treatment
203
PEM treatment
Thiamine hydrochloride IV 10 –
15 mg/kg
If there is a response, repeated twice in next 12 hours
Continue twice daily for 3 days
IV dexamethasone 1-2mg/kg
Mannitol 1– 2 mg/kg in 20% solution
204
Lead poisoning aetiopathogenesis
Lead enters through GIT,
and is converted to
soluble lead acetate
which is distributed to
tissues but most binds to
RBC proteins
Effects sulphhydryl containing enzymes, and tissues rich in mitochondria
Capillary damage -> cerebellar haemorrhage and oedema
205
Clinical signs of acute lead poisoning
Staggering, tremors, ataxia
Blindness
Irritable
Bellowing, head pressing
Spastic twitching of eyelids
Frothing
Rumen atony
Absence of menace and palpebral reflexes
206
Treatment of lead poisoning
Ca-EDTA 100 – 200mg/kg/day
IV or SC for 2 – 3 days
Thiamine to reduce deposition of lead
207
Botulism pathogenesis
Ascending motor neuroparalytic disease caused by toxins released
by Clostridium botulinum
→ proliferates in decomposing animal carcasses (sometimes plant material)
Ingestion is route of entry - inactivated in rumen but some makes it to SI where it is activated by endogenous proteases. Can rarely be through a wound.
At NMJ it inhibits vesicular release of ACh resulting in flaccid paralysis of striated muscles
No effect on CNS
208
Botulism clinical signs
* Tongue weakness
* Miosis
* Isolated
* Unable to eat or drink
* Restlessness, stumbling, knuckling over
* Shallow abdominal breathing
* Constipation
* Bradycardia (40-50 bpm)
* Sluggish rumen contractions
* Significant dehydration
* Sternal recumbency
* Death due to cardiac or respiratory failure
209
Botulism diagnosis
Clinical signs and elimination of ddx -> Presence of botulinum bacteria or spores in viscera on PM does not mean it died from it
ELISA, PCR
Detect toxin, antibodies or spores
210
Treatment of botulism
Vaccinate
Nursing
BoNT antitoxin
Penicillin G
211
Tetanus pathogenesis
Tetanospasmin exotoxin causes clinical signs - produced by anaerobic spore forming gram positive Clostridium Tetani
Other toxin is Tetanolysin -> damages viable tissue
Tetanospasmin -> travels retrograde to reach CNS where it enters neuronal bodies and binds presynaptic inhibitory interneurons preventing release of glycine and GABA
Most common route -> inoculation of wounds with C. tetani spores or infection of uterus post partum
Bacterial growth enhanced by necrotic tissue, pus, foreign bodies
212
Diagnosis of tetanus
PCR assay
TeNT antigen
Clinical signs
213
Treatment of tetanus
Antitoxin - only binds toxins that havent bound to the neuron
Keep animal sedated and give muscle relaxant (pentobarbitone and acepromazine)
Debride wound and give pen G
214
Vaccine for tetanus
5 in 1 clostridial vaccine
215
5in1 vs 7in1 vaccine
5in1 -> clostridial only
7in1 -> clostridial + leptospirosis
216
What is meningitis?
Inflammation of the meninges as a result of bacterial (suppurative) infection
Follows septicaemia and bacteraemia, infected
mononuclear cells enter CNS
Most commonly gram negative bacteria (E.coli) -> Enter via umbilicus
217
Diagnosis of meningitis
Lumbosacral CSF tap - increased wbc and protein
218
Treatment for meningitis
Nurse
NSAID
Ceftiofur
219
Clinical signs meningitis
Hyperesthesia
Stiff neck
Muscle tremor
Seizures + blindness
Pyrexia
Polyarthritis
220
Thromboembolic meningoencephalitis aetiopathogenesis
Histophilus somni
Bacteraemia = Endothelial biofilm formation disrupting intercellular junctions = intravascular coagulation and thrombosis of small vessels in the brain
221
Thromboembolic meningoencephalitis clinical signs
Resp disease
Pyrexia
Depressed
Fetlock knuckling
Recumbent
Muscle tremors
Swollen joints
Blindness
Tonic/clonic seizures
222
Diagnosis + treatment of Thromboembolic meningoencephalitis clinical signs
CS and history
CSF -> protein, wbc, rbc
Penicillin, oxytet or florfenicol
223
Aetiopathogenesis of nitrate/nitrite poisoning
1. Nitrate ingested from heavily fertilised pasture
2. Rumen microflora reduce nitrate to nitrite, can become too much to convert all to ammonia so blood conc increases (but not in excess or this can cause toxicity too)
3. Nitrite converts ferrous Fe to ferric Fe to form methaemoglobin which binds o2 preferentially to haemoglobin leading to hypoxia when 20-30% haemoglobin converted.
Death at 70-80% conversion
224
Epidemiology of nitrate/nitrite poisoning
overcast - plant cannot convert nitrate to ammonia
Stress on plant - during drought nitrate accumulates
stark changes in diet, lush new fertilised pasture - ryegrass or brassicas
225
Diagnosis of nitrate/nitrite
Blood test for methaem. in heparin tube
Test for nitrate in urine
aqueous humour of eye or CSF if dead >24h
226
Treatment of N/N poisoning
IV methylene blue 5mg/kg as 3% aqueous solution - returns iron to ferrous state -> not approved in food producing animals
Remove from pasture and feed high quality hay
Rest pastures for 6 weeks after application of fertilisers
227
Which analytes are increased/decreased with haemolysis?
Increased -> K, P, AST, PO4, Mg, CK
Decreased -> GGT and ALP
228
Which analytes are collected in a clot tube?
Mg, Ca, K and P
229
What is glucose collected in?
EDTA (purple), heparin (green) or citrate tube (blue) and it halts glycolysis by RBC to precent depletion of sample. 5-10% decrease per hour
Separate plasma ASAP to prevent artefact
Store at 4 degrees
230
4 aims of TCM
Reduce ruminal disruption
Minimise micronutrient deficiencies
Minimise lipid mobilisation disorders
Avoid immune suppression
