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fourth year > Production Animal ESE > Flashcards

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

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2
Q

HR for cow

A

60-80

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3
Q

Temp for cow

A

38-39

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4
Q

RR for cow

A

25

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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

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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)

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7
Q

What are clinical signs in ketosis caused by?

A

Hypoglycaemia rather than mobilisation of ketones

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8
Q

What can ketosis occur secondary to?

A

LDA, RDA, lameness, metritis

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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

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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

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11
Q

5 treatments of ketosis

A
  1. Propylene glycol -> gluconeogenesis 300ml/d
  2. Dextrose -> 500ml 40-50%. IV bolus for hypoglycaemia. Only effective short term
  3. Steroids -> dexamethasone to get hyperglycaemic state. But immunosuppressive
  4. Insulin -> used with glucocorticoids, suppress NEFA, long acting done again 24-48h later
  5. B12 -> appetite stimulant
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12
Q

Ideal treatment plan for ketosis

A
  1. 500ml dextrose 4% IV
  2. Single injection of corticosteroid
  3. Oral propylene glycol BID for 4d (200ml BID)
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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

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14
Q

Clinical signs and diagnosis of liver abscess

A

Anorexia

Ultrasound, CBC, biochem, elevated GGT, SDH, hyperbilirubinaemia, elevated serum proteins, hypoglycaemia, hypoalbuminaemia

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15
Q

Treatment of liver abscess

A

Peniciliin and macrolides, but cattle rarely treatment as recovery is rare

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16
Q

Prevention of liver abscesses

A

In feed antimicrobials
Vaccinate for fusobacterium and arcanobacterium pyogenes
Manage grain feeding to prevent acidosis

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17
Q

Gross pathology of liver abscess

A

Purulent spheres encapsulated in thick fibrotic walls
Hyperaemia around abscess
Pyogranulomatous abscesses

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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

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19
Q

Risk factors for fatty liver syndrome

A

Change to milking diet
Decreased feed intake
Low protein diets
Concurrent illness

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20
Q

Clinical signs of fatty liver syndrome

A

Obese cow, depression, anorexia, weight loss, weakness, decreased rumen motility and milk production

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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

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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

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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

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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)

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25
Q

Diagnosis of an LDA

A

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

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26
Q

Treatment of LDA

A

Abomasopexy
Ometopexy
Percutaenous tacks

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27
Q

RDA aetiology

A

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

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28
Q

RDA clinical signs

A

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

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29
Q

RDA diagnosis

A

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

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30
Q

RDA treatment

A

Omentopexy or pyloropexy

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31
Q

Abomasal ulcer formation and location

A

Greater curvature
Multifactorial - stress mainly, viral causes (BVDV)

High producing cows (stress)
Prolonged inappetance causing sustained low pH in abomasum

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32
Q

4 types of abomasal ulcers

A

non-perforating
Non-perforating with severe bloodloss
Perforating with local peritonitis
Perforating with diffuse peritonitis

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33
Q

Risk factors for abomasal ulcers

A

Stress and high grain diets

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34
Q

Clinical signs of abomasal ulcers

A

Abdominal pain
Anorexia
Decreased rumen motiity
Mild ruminal tympany
GIT haemorrhage
Decreased milk yield

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35
Q

Diagnosis of abomasal ulcers

A

Faecal occult blood
Abdominocentesis
Decreased PCV with severe bloodloss
Rarely diagnosed antemortem

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36
Q

Treatment of abomasal ulcers

A

Treatment unrealistic
Antacids limited value

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37
Q

Abomasal impaction - what, clinical signs, treatment

A

Feed poor quality and fibrous with limited water access causes blockage

Anorexia, scant faeces, distended abdomen, expiratory grunt

Treatment -> fluids, paraggin, abomasotomy

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38
Q

Haemorhagic bowel syndrome aetiology

A

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

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39
Q

Risk factors for haemorrhagic bowel syndrome

A

Management practices
Latation - first 100DIM
Feeding high energy diet and low fibre
Large herds

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40
Q

Clinical signs of haemorrhagic bowel syndrome

A

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

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41
Q

Diagnosis of haemorrhagic bowel syndrome

A

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

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42
Q

Haemorrhagic bowel syndrome gross pathology

A

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

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43
Q

Haemorrhagic bowel syndrome treatment

A

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

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44
Q

Prevention of haemorrhagic bowel syndrome

A

Feed adequate fibre length and quantity

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45
Q

Intestinal phytobezoars (intestinal obstruction) - pathogenesis and clinical signs

A

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

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46
Q

Diagnosis of intestinal phytobezoars

A

History of onion weeds
Cow suddenly off milk with yellow pasty faeces and fluid in intestines
Ex lap -> via right paralumbar fossa

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47
Q

Intestinal volvulus - types

A

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

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48
Q

Intestinal volvulus - causes

A

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

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49
Q

Clinical signs of intestinal volvulus

A

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

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50
Q

Treatment of intestinal volvulus

A

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

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51
Q

Colic aetiology - cause, signs

A

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

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52
Q

Moderate colic causes

A

Intussusception, volvulus or incarceration

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53
Q

Severe colic causes

A

Rarely observed in cattle
Torsion of mesenteric root
Extreme pain signs

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54
Q

Spasmodic colic clinical signs

A

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

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55
Q

What is paralytic ileus?

A

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

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56
Q

Pathogenesis of paralytic ileus

A

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

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57
Q

Clinical signs of paralytic ileus

A

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

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58
Q

Treatment of paralytic ileus

A

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

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59
Q

Intussuception aetiology

A

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

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60
Q

Clinical signs of intussusception

A

Sudden onset increased HR and RR, off milk and anorexic, colic + pain, rumen stasis, R abdomen enlarges from SI distention

Blood + tarry faeces, recumbency

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61
Q

Diagnosis of intuss.

A

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

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62
Q

Treatment of intussusception

A

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

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63
Q

Caecal volvulus/torsion pathogenesis

A

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

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64
Q

Clinical findings and diagnosis of caecal volvulus vs simple marked dilation

A

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.

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65
Q

Treatment options for caecal volvulus

A

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

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66
Q

Pre-operative requirements for caecal volvulus surgery

A

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

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67
Q

What does CK indicate, what increases it

A

Muscle damage
Increased with exercise or long transport
T1/2 4h = prolonged increases mean active and continuing muscle damage

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68
Q

What does AST indicate

A

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

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69
Q

What does ALP indicate

A

Sensitive indicator of cholestasis

Slightly elevated in bone disease or fractures
Neonates consuming colostrum may have increase

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70
Q

What does GGT indicate

A

Cholestasis
Increased with hepatic necrosis and indicative of ongoing hepatic damage

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71
Q

GLDH indicates:

A

Hepatic necrosis
Indicative of severe hepatocellular damage if increased

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72
Q

Bilirubin may increase due to

A

Liver failure or haemolytic anaemia (suggested with RBC conc)

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73
Q

Urea - control

A

Excreted by kidney in glomerular filtration

Excretion in ruminants governed by nitrogen intake and GIT can excrete also

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74
Q

L-Lactate increases may mean

A

Sepsis
Seen when pH is elevated and in an alkalotic state

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75
Q

BOHB increases mean:

A

ketosis

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76
Q

Hypermag and Hypomag reasons

A

Hypermag -> seen commonly in postpartum or over administration

Hypomag -> clinical when <0.4mmol/L (lactation, inappetance)

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77
Q

Causes of hypophosphataemia

A

Milk fever, post parturient decreased release from bone and increased loss in milk, and starvation

Excreted in urine and faeces

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78
Q

Causes of hyperphosphataemia

A

Seen in young aniamls
Caused by vitamin D toxicity, haemolysis, anorexia

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79
Q

Calcium is regulated by?

A

Diet, calcitonin, PTH and vitamin D

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80
Q

Hypocalcaemia is caused by?

A

Milk fever, hypomag, anorexia

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81
Q

Hypercalcaemia is caused by?

A

Excess Ca administration or hypervitaminosis D (promotes absorption of Ca and P)

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82
Q

Reasons for hypochloremia

A

Acid base disturbance
Increasees in bicarbonate

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83
Q

Reasons for hypokalaemia

A

Depletion of body stores and acute alkalosis
Adminstration of glucose or insulin - shifts potassium into the cell

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84
Q

Hyponatraemia reasons

A

Diarrhoea, renal losses
Usually seen with urea elevation

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85
Q

Displaced or torsed abomasum biochem

A

Alkalosis
Hypochloraemia
Hypokalaemia
Hyponatraemia
Dehydration (hyperproteinaemia and PCV)

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86
Q

Abomasal ulcers biochem

A

Leukocytosis - neutrophilia and hyperfibrinogenaemia if peritonitis there

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87
Q

Liver abscessation biochem

A

HYPERglobulinaemia, bilirubinaemia and fibrinogenaemia

leukocytosis

Increased GGT and SDH

Hypoalbuminaemia and hypoglycaemia

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88
Q

Ketosis biochem

A

Hypoglycaemia, high NEFA’s
Ketonuria, ketolactia

High Betahydroxybutyrate in blood

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89
Q

traumatic reticuloperitonitis biochem

A

Leukocytosis - neutrophilia with left shift
Hyperfibrinogenaemia
Hyperproteinaemia
Normal acid base - except if peritonitis = hypomotility - alkalosis

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90
Q

Vagal indigestion biochem

A

Peritonitis -> leukocytosis, increased TPP
Hypokalaemia

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91
Q

Parasitic gastoenteritis biochem

A

Eosinophilia
Hyperproteinaemia

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92
Q

Acute neonatal diarrhoea

A

Metabolic acidosis
Hyperkalaemia

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93
Q

Xylazine -> class, MOA, toxic effects

A

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
Q

Acepromazine class, MOA, route of admin

A

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
Q

Diazepam class, moA, effect

A

Benzodiazepene - enhances affinity for for GABA at GABA receptors, hyperpolarising neurons

Brief sedation in ruminants

0.25-0.5mg/kg IV

96
Q

Phenobarbital class, moa, sedation and toxic effects

A

decreases rate of dissociation of GABA from receptors
30-60min sedation

Large doses - ataxia and delirium

97
Q

Butorphanol class and MOA

A

Kappa agonist and weak Mu antagonist
Provides sedation and analgesia

IV or IM

98
Q

Dorsal approach PVRA

A

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
Q

PVRA lateral approach

A

Easier to palpate
Oblique needle and inject under and over transverse process and fan out local

More difficult - easier to get incomplete block

100
Q

When should antibiotic therapy be considered in surgery in cattle?

A

Contaminated or clean surgery where infection a risk. If contamination occurs during surgery, exteriorise and flush site, allow to drain and aftercare

101
Q

When should antibiotic therapy be given at surgery

A

IV 15 mins prior
IM 60 mins prior

102
Q

Most common prophylactic antibiotics

A

Procaine penicillin - gram positive, anaerobes and some suscpetible gram negative

Oxytetracycline - gram pos and gram neg

103
Q

When is fluid therapy used?

A

When GIT not functional or not enough time

104
Q

Fluid therapy for metabolic alkalosis

A

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
Q

Ringers lactate function

A

Iso osmotic
Crystalloid

Corrects dehydration and electrolyte imbalances as lactate metabolised to bicarb to increase blood pH when acidotic

106
Q

Ringers acetate function

A

Correct dehydration and alkalinising

107
Q

Sodium bicarbonate fluid function

A

Iso osmotic
Crystalloid
Strong alkalinising fluid for severe acidaemia

Add to sterile water

108
Q

NaCl fluid function

A

Hypertonic saline
Rapid expansion of plasma volume for severely dehydrated animals - draws water out from ICF

109
Q

Indications for ex lap

A

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
Q

Surgical approach to Ex Lap to find LDA

A
  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
Q

Considerations for surgery on farm

A

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
Q

Where is a ping in LDA?

A

9-12th rib

113
Q

Serum ca normal, subclinical and clinical hypocal

A

normal 1.9-2.6

subclinical - <1.4

Clinical <2mmol/L

114
Q

Treatment of hypocal

A

Calcium borogluconate 300ml 25-40% solution

need 8-12g IV calcium

Oral for standing cows - 50g

115
Q

Prevention of hypocal

A

TCM
Negative DCAD thorugh anionic salt feeding or cereal hays low in K

116
Q

Which cows get hypocal?

A

24h post calving but can be a few days

117
Q

Hypomagnasaemia aetiopathologenesis

A

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
Q

Hypomag treatment

A

Magnesium sulphate SC 500ml 20%

Tranq with 3-5ml pentobarbitone

Parenteral Mg 100g MgO 1-2d and 50g for next 5d

119
Q

Aetiopathogenesis of ketosis

A

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
Q

Diagnosis of ketosis

A

Blood BHB <30mg/dL

NEFAs on CBC

Ketone bodies in urine and milk - slight delay reaction

neuro signs and clinical exams

121
Q

Treatment of ketosis - wasting and neuro form

A

Wasting - propylene glycol 300g 3-5d PO

Neuro - add dextrose 500ml 50% IV

122
Q

Toxic mastitis cause

A

environmental colifroms - E.coli and pasteurella

results in endotoxic shock

123
Q

Treatment of toxic mastitis

A

NSAID
IVFT
Cephalosporin
Strip udder every 2-4h for several days

124
Q

Treatment of toxic metritis

A

IVFT
NSAID
Oxytetracycline/penicillin/cephalosporin

Precautionary calcium therapy

125
Q

Toxic metritis cause

A

Trueparella pyogenes or e.coli few days to weeks post parturition

endotoxic shock

126
Q

Bovine ephemeral fever - when, what, signs, treatment

A

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
Q

Downer cow managment

A

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
Q

Euthanasia trigger points for a downer cow

A

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
Q

Define down cow

A

A cow which is unable to stand unassisted, with any mental state and any length of recumbency

130
Q

Define downer cow

A

A cow which is unable to stand unassisted, that has been recumbent for ≥24 hours and is BAR.

131
Q

Define downer cow syndrome

A

One of the many diseases which can cause recumbency in a periparturient cow

132
Q

5 M’s of a downer cow

A
  1. Metritis
  2. Mastitis
  3. Metabolic
  4. Musculoskeletal
  5. Massive Sepsis
133
Q

Inducing parturition in a pregnancy toxaemia (ketosis)

A

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
Q

Paspalum moA and clinical signs

A

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
Q

Ryegrass staggers Moa and CLinical signs

A

Fungus neotyphoidium lolli produces tremorgen lolitrem B

Same MOA and clinical signs as paspalum

Should prevent grazing of seedheads

136
Q

Kikuyu poisoning clinical signs and problematic season

A

Unknown moA

Rumen distension, depression, muscle tremors, abdominal pain, fine muscle tremors, piloerection

Warm moist conditions

137
Q

Sorghum poisoning moA and clinical signs, when it occurs

A

Unknown, suspect cyanide toxicity

Ataxia of pelvic limbs, urinary incontinence, fetlock knuckling, recumbent, perineal muscles relaxed

138
Q

Phalaris staggers moA

A

toxicity due to dimethyl-tryptamine alkaloids

Inihbits monoamine oxidase interfering with serotonin and catecholamine synthesis

139
Q

phalaris staggers clinical signs

A

Hyperexcitable
Ataxia
Stiffness of hocks
Dragging toes
Incoordination of tongue and lips
Wide-based stance
Hypermetria
Head nodding
Muscle tremors
Aggression

140
Q

When do phalaris staggers occur?

A

Young rapid growing pasture
Late summer and autumn
>20 degrees

141
Q

Prevention of phalaris staggers

A

Introduce to pasture over several days and feed hay
Do not use N fertiliser on phalaris

142
Q

Oleaner poisoning moA and clinical signs

A

Cardiac glycosides inhibit NaKATPase

Cardiac arythmia
Sudden death
Profuse sweating
Convulsions
Paralysis

143
Q

Oleander treatment

A

Activated charcoal and anti-arrhythmic drugs
Rehydrate

144
Q

When can tachycardia be seen:

A

Pain
Fever
Inflammation
Hypocalcaemia and Mag
Metabolic disturbances causing hypovolaemia

145
Q

Causes of muffled heart sounds

A

Obesity, thick chest wall
Pericarditis - traumatic reticuloperitonitis
Lymphosarcoma
Abscess
Chronic heart failure
Emphysema

146
Q

Why are heart sounds muffled?

A

Displacement of heart from thoracic wall by fluid (pericardial effusion), a soft tissue mass or air

147
Q

Diagnosis of coxofemoral dislocation

A

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
Q

Diagnosis of spinal fracture

A

Placement and spacing of vertebrae

149
Q

Limb fracture/injury

A

Observe movement of animal
Palpate
Rads for expensive animal

150
Q

First step in neuro exam

A

Distance exam of mentation and behaviour
Head tilt, pressing, bellowing

151
Q

Lesions location that affect mentation

A

Cerebrum

Somtimes brainstem/cranial nerves

152
Q

Neural locations affecting gait

A

Cerebellum
Spinal cord/PN

Sometimes brainstem and CN

153
Q

Neural locations affecting posture

A

Cerebellum
Spinal cord and PN

Brainstem + CN (sometimes)

154
Q

Spinal reflexes problem neural location

A

Cerebrum will affect them

cerebellum, brainstem, CN, spinal cord and PN might be normal or abnormal

155
Q

Which 2 CN cannot be assessed in ruminants?

A

I - olfactory
XI - accessory

156
Q

5 units to assess cranial nerves

A
  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
Q

Menance response tests:

A

CN II and VII

Closes eyes and moves away = vision

158
Q

Pupillary reflex tests:

A

CN II and III

Miosis is normal response and small conscensual relfex in opposite eye

159
Q

Palpebral reflex tests:

A

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
Q

Strabismus directions and which nerve they suggest has a lesion

A

Ventrolateral position = CN III dysfunction

Dorsal/dorsomedial = CNIV dysfunction

Medial -> CN VI dysfunction

161
Q

If a pathologic nystagmus is present with head at rest, what does it mean?

A

Fast phase of nystagmus is directed away from side of the lesion

162
Q

What is the preyer reflex?

A

Creates auditory stimulus and assesses CN VIII

Normal = move ears towards noise

163
Q

How are CN IX, X and XII tested?

A

give food see if consumes

Pass nasopharyngeal tube to see if gag reflex initiated

CNXII also by assessing size and symmetry of tongue

164
Q

CN I

A

Olfactory - sense of smell

165
Q

CNII

A

Optic - afferent pathway for vision

166
Q

CN III

A

Oculomotor - pupil constriction, upper levator muscles

167
Q

CN IV

A

Trochlear - dorsal oblique

168
Q

CN V

A

Trigeminal - sensory to head, face, tongue

169
Q

CN VI

A

Abducens - extraocular muscles retractor oculi and lateral rectus

170
Q

CN VII

A

Facial - motor to facial muscles

171
Q

VIII

A

Vestibular Cochlear - afferent branch of vestibular system, hearing

172
Q

CN IX

A

Glossopharyngeal - swallowing

173
Q

CNX

A

Vagus - gag reflex

174
Q

CN XI

A

Accessory - cant test this in ruminants

175
Q

CN XII

A

Hypoglossal - symmetry and size of tongue

176
Q

Define paresis

A

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
Q

Define ataxia

A

Proprioceptive dysfunction causing abnormal range, rate and force of movement, and placement of the limbs
and other body parts

178
Q

Cerebellar ataxia

A

No proprioceptive deficits, strength is preserved.

179
Q

Proprioceptive ataxia

A

Secondary to damage of the afferent proprioceptive pathways
Wobliness walking and strange gait

180
Q

Vestibular ataxia

A

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
Q

The most important forelimb reflex and what it assesses

A

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
Q

Flexor withdrawal reflex procedure

A

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
Q

What does it mean if a crossed extensor reflex if seen in contralteral limb?

A

Severe central motor pathway lesion

184
Q

2 other forelimb reflex test

A

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
Q

2 hindlimb reflex tests

A

Flexor withdrawal

Extensor/patellar ligament reflex

186
Q

Hindlimb withdrawal reflex process

A

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
Q

Extensor patellar ligament reflex procedure

A

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
Q

Which reflex assesses afferent spinal nerves and efferent lateral thoracic nerve?

A

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
Q

What is flaccid paralysis of the forelimb most likely due to?

A

Brachial nerve damage -> further damaged by not being able to maintain sternal recumbancy and extra damage in lateral

190
Q

What does it mean if a cow is frog legged?

A

Femoral nerve damage

191
Q

What does it mean if a cow is knuckling and dragging limb on dorsal surface?

A

Sciatic nerve damage

192
Q

What if a cow has partial forward knuckling of the fetlock (hooves flat on ground and no dragging) and hyperflextion of hock?

A

Tibial nerve damage

193
Q

What is damaged if there is abduction of the limb with weakness and recumbency - particuarly if bilateral?

A

Obtruator nerve damage

194
Q

7 causes of ataxia in ruminants

A
  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
Q

Listeriosis causative agent and pathogenesis

A

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
Q

Listeriosis - clinical signs

A
  • 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
Q

Diagnosis of listeriosis

A

Unilateral CN deficit in depressed inappetant cow
CSF analysis (increased protein and WBC)
test silage

198
Q

Listeriosis treatment

A

Penicilin, ampicillin or tetracyclines in water for 10 days
NSAID
IVFT
Electrolytes and B-group vitamins
Nursing

199
Q

Prevention of listeriosis

A

Good quality feed and silage, reduce contamination when making silage

200
Q

Polioencephalomalacia aetiopathogenesis

A

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
Q

PEM Clinical signs

A
  • Depression
  • Apparent blindness
  • Ataxia
  • Proprioceptive deficits
  • Fine muscle tremors
  • Absence of menace
  • Nystagmus with dorsomedial strabismus
  • Recumbency
  • Seizure
  • Extensor rigidity
  • Bruxism
  • Hypermetria
  • Miosis
202
Q

Diagnosis of PEM

A

Blood thiamine <50mmol/L
response to treatment

203
Q

PEM treatment

A

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
Q

Lead poisoning aetiopathogenesis

A

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
Q

Clinical signs of acute lead poisoning

A

Staggering, tremors, ataxia
Blindness
Irritable
Bellowing, head pressing
Spastic twitching of eyelids
Frothing
Rumen atony

Absence of menace and palpebral reflexes

206
Q

Treatment of lead poisoning

A

Ca-EDTA 100 – 200mg/kg/day

IV or SC for 2 – 3 days

Thiamine to reduce deposition of lead

207
Q

Botulism pathogenesis

A

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
Q

Botulism clinical signs

A
  • 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
Q

Botulism diagnosis

A

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
Q

Treatment of botulism

A

Vaccinate
Nursing
BoNT antitoxin
Penicillin G

211
Q

Tetanus pathogenesis

A

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
Q

Diagnosis of tetanus

A

PCR assay
TeNT antigen
Clinical signs

213
Q

Treatment of tetanus

A

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
Q

Vaccine for tetanus

A

5 in 1 clostridial vaccine

215
Q

5in1 vs 7in1 vaccine

A

5in1 -> clostridial only

7in1 -> clostridial + leptospirosis

216
Q

What is meningitis?

A

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
Q

Diagnosis of meningitis

A

Lumbosacral CSF tap - increased wbc and protein

218
Q

Treatment for meningitis

A

Nurse
NSAID
Ceftiofur

219
Q

Clinical signs meningitis

A

Hyperesthesia
Stiff neck
Muscle tremor
Seizures + blindness
Pyrexia
Polyarthritis

220
Q

Thromboembolic meningoencephalitis aetiopathogenesis

A

Histophilus somni

Bacteraemia = Endothelial biofilm formation disrupting intercellular junctions = intravascular coagulation and thrombosis of small vessels in the brain

221
Q

Thromboembolic meningoencephalitis clinical signs

A

Resp disease
Pyrexia
Depressed
Fetlock knuckling
Recumbent
Muscle tremors
Swollen joints
Blindness
Tonic/clonic seizures

222
Q

Diagnosis + treatment of Thromboembolic meningoencephalitis clinical signs

A

CS and history
CSF -> protein, wbc, rbc

Penicillin, oxytet or florfenicol

223
Q

Aetiopathogenesis of nitrate/nitrite poisoning

A
  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
Q

Epidemiology of nitrate/nitrite poisoning

A

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
Q

Diagnosis of nitrate/nitrite

A

Blood test for methaem. in heparin tube

Test for nitrate in urine

aqueous humour of eye or CSF if dead >24h

226
Q

Treatment of N/N poisoning

A

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
Q

Which analytes are increased/decreased with haemolysis?

A

Increased -> K, P, AST, PO4, Mg, CK

Decreased -> GGT and ALP

228
Q

Which analytes are collected in a clot tube?

A

Mg, Ca, K and P

229
Q

What is glucose collected in?

A

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
Q

4 aims of TCM

A

Reduce ruminal disruption
Minimise micronutrient deficiencies
Minimise lipid mobilisation disorders
Avoid immune suppression

fourth year (8 decks)

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