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Cattle II > Non-infectious disease of GI tract > Flashcards

Non-infectious disease of GI tract Flashcards

1
Q

Aetiology of congenital cleft lip and cleft palate

A

congenital defects caused by failure of midline fusion of palatal folds during foetal development.

Cleft palate can also be an inherited condition in Charolais and Hereford calves.

Ingestion of teratogenic substances

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2
Q

Scientific name of cleft lip

A

cheilognathoschisis

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3
Q

Scientific name of cleft palate

A

palatoschisis

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4
Q

Clinical signs of cleft lip

A

Deep groove on the upper lip and nasolabial palate that can also involve the bone of maxilla;

extreme difficulties in sucking milk;

loss of the milk during feeding through regurgitation

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5
Q

Clinical signs of cleft palate

A

fissure of varying width in both the hard and soft palates;

exposure of the nasal turbinates;

nasal regurgitation of milk;

signs of aspiration pneumonia can develop early in life;

failure to thrive;

small defects can only show signs when calf starts solid feed.

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6
Q

Treatment of cleft lip and cleft palate

A

mandibular symphysiotomy (only if there are no other malformations)

Post op:
systemic antibiotic for at least 5 days or until resolution of aspiration pneumonia, NSAIDs and milk feeding

May not be worth it, consider euthanasia

High failure rate of repair (30% success rate)

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7
Q

Aetiology of oral lacerations

A

indiscriminate eating behaviour and iatrogenic causes

more frequent in calves

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8
Q

Clinical signs of oral laceration

A

excessive salivation;

saliva mixed with blood;

decreased feed intake;

decreased appetite;

dysphagia (varies with severity of the laceration);

protrusion of the tongue;

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9
Q

Signs of soft palate lacerations

A

nasal regurgitation of water and feed as well as signs related to tracheal aspiration of water and feed;

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10
Q

Signs of buccal fistulae

A

loss of saliva and feed via defect;

the cud may drop during rumination;

cosmetic defect;

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11
Q

Signs of oropharyngeal trauma

A

retropharyngeal cellulitis;

dysphagia;

anorexia;

decreased milk production;

fever;

cervical swelling and sometimes crepitus;

extended head and neck to straighten the upper airway to improve breathing;

foul-smelling odour;

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12
Q

Treatment of oral lacerations

A

Most lacerations heal without surgical repair

daily mouth lavage, systemic antibiotics, NSAIDs and by feeding a soft diet for 10-14 days.

May require surgery

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13
Q

Aetiology of mandibular fractures

A

Traumatic injuries

In young calves, fractures are often secondary to obstetric manipulation

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14
Q

Clinical signs of mandibular fractures

A

difficulty or inability to eat;

dropping saliva;

prolapse of tongue;

tooth integrity might be affected (if fracture involves an alveolus);

mal alignment of dental arcade;

swollen around the fracture site;

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15
Q

Treatment of mandibular fractures

A

Stabilisation using external holding tools

May need reduction and immobilisation

Dental care

postoperative systemic antibiotic (7 to 10 days), NSAIDs, daily mouth lavage with mild antiseptic solution and soft diet (10 to 14 days)

Healing usually takes 1-2 months after surgery

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16
Q

Aetiology of tooth root abscess

A

Uncommon in cattle

Injury to the gingiva predisposes to infection

Trueperella pyogenes is the most common isolated bacteria.

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17
Q

Clinical signs of tooth root abscess

A

may be asymptomatic until soft swelling develops, firm mass can develop;

tooth may be loose or fractured;

cemental cavities with secondary feed impaction;

malodours breath;

unilateral purulent nasal discharge (maxillary teeth);

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18
Q

Treatment of tooth root abscess

A

Surgical drainage of the abscess, removal of any loose or fractured tooth, NSAIDs and systemic antibiotic (e.g., penicillin)

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19
Q

Common tumours of oral cavity

A

odontoma,

odontogenic myxomas,

ameloblastoma,

adamantinoma

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20
Q

Amenoblastomas

A

locally invasive and highly destructive tumours

mass firmly attached to the mandible distorting the mandible and making prehension extremely difficult.

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21
Q

Hamartoma

A

not considered a true neoplasm, instead it is thought to be a developmental abnormality of poorly organised tissue

generally seen in animals younger than 3-year-old and can interfere with mastication

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22
Q

Osteosarcomas and lymphosarcomas

A

present as a hard swelling either on the mandible or maxilla

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23
Q

Treatment of oral neoplasias

A

Better chance of success if surgical resection is performed early and the lesion is entirely removed without significant mandibular loss.

Euthanasia should be considered if surgical resection is impossible.

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24
Q

Aetiology of oesophageal obstruction

A

Also known as choke

Acute and complete oesophageal obstruction is an emergency

foreign bodies, occasionally, sharp foreign bodies

Most common sites of obstruction: just dorsal to larynx; thoracic inlet.

Extraoesophageal masses

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25
Q

Clinical signs of oesophageal obstruction

A

anxious or very agitated;

extension of the head and neck;

drooling saliva;

inability to swallow saliva;

absence of eructation;

ruminal bloat (free-gas);

dyspnoea;

occasional coughing and chew movements;

inability to eat;

tongue protrusion;

dehydration signs;

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26
Q

Treatment of oesophageal obstruction

A

Hold off feed and water

Resolve ruminal bloat by using needle and suction, trocar or cannula

Resolve obstruction, failure may lead to oesophagostomy which is risky

correction of dehydration and metabolic acidosis

treat aspiration pneumonia

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27
Q

Aetiology of oesophageal trauma

A

often the result of overzealous use of instruments to dislodge an obstruction

can also occur during the downward movement of an ingested foreign body

can also result from the use of stomach tubes, oesophageal feeders, ingestion of chemical products.

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28
Q

Clinical signs of oesophageal trauma

A

impressive subcutaneous emphysema;

anorexia;

depression;

swelling at the site of the rupture;

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29
Q

Treatment of oesophageal trauma

A

might heal with systemic antibiotics

Larger perforations that leak feed material need surgical repair

Feeding can be done via rumen fistula

Grave prognosis

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30
Q

Aetiology of oesophageal diverticulum

A

acquired condition

Traction (true) diverticula: results from contraction of periesophageal fibrous scar tissue, frequently secondary to wound or surgery

Pulsation (false) diverticula: results from protrusion of mucosa and submucosa through a defect in the musculature of the oesophagus; the defect in the muscular layer may result from external trauma, fluctuation in intraluminal pressure of the oesophagus and overstretch damage by impacted food;

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31
Q

Clinical signs of oesophageal diverticulum

A

Traction diverticula: usually asymptomatic;

Pulsation diverticula: dysphagia but retain the ability to drink; cough; salivation; ruminal distention; the diverticulum can enlarge enough to become evident in the neck as a large swelling;

Regurgitation is the most common clinical sign when diverticula are in the thoracic region;

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32
Q

Treatment of oesophageal diverticula

A

Surgical repair: mucosal inversion with reconstruction of the muscular layer or diverticulectomy

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33
Q

Aetiology of megaoesophagus

A

sporadic and uncommon disorder in cattle

can be segmental or generalized

chronic dilatation and atony of the oesophagus

usually is congenital but may occur secondary to infections or trauma

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34
Q

Clinical signs of megaoesophagus

A

regurgitation;

dysphagia;

salivation;

cough;

signs of aspiration pneumonia;

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35
Q

Treatment of megaoesophagus

A

Only supportive treatment is available.

Treatment of aspiration pneumonia.

Poor prognosis

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36
Q

Aetiology of simple ruminal indigestion

A

common in hand-fed dairy cattle, and beef cattle

minor disturbance in the gastrointestinal function

typically associated with abrupt change in the quantity and quality of the diet

Sudden change in the pH ruminal contents

Physical impairment ruminal function caused by accumulation of excessive quantities of relatively indigestible feed

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37
Q

Clinical signs of simple ruminal indigestion

A

Caused by excessive grain feeding:
- anorexia;
- ruminal hypomotility or atony;
- excessive fluid content in the rumen;
- faeces watery or soft with foul smelling;
- animal bright and alert;
- animals generally begin to eat within 24 hours;

Caused by excessive silage feeding:
- anorexia;
- moderate drop in milk production;
- rumen full, firm, and doughy;
- primary rumen contractions are less frequent or absent;
- secondary rumen contractions may be present but with reduced strength;
- faeces normal to firm but reduced in quantity;
- recovery generally spontaneous within 24-48 hours;

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38
Q

Rumen fluid analysis - normal rumen pH

A

6-7

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39
Q

Treatment of simple ruminal indigestion

A

Stopping feeding the abnormal diet and restitution of an adequate ruminal diet can sometimes lead to spontaneous recovery without additional treatment.

administration of oral laxative and/or antiacid rumen stimulant e.g. Magnesium hydroxide

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40
Q

Two major types of ruminal acidosis

A

Subacute ruminal acidosis

Acute ruminal acidosis

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41
Q

Aetiology of subacute ruminal acidosis

A

Dairy cows, feedlot cattle and cattle grazing lush grass from intensively managed pasture alone

Results from feeding excessive amounts of rapidly fermentable carbohydrates

lead to excessive accumulation of volatile fatty acids (VFAs), without persistent lactic acid accumulation

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42
Q

Diagnosis of subacute ruminal acidosis

A

intermittent periods of low ruminal pH, between 5.6 and 5.2

Individual cows do not exhibit clinical signs while their ruminal pH is low

Herd clinical signs and performance:
- decreased or cyclic feed intake;
- decreased milk production, poor body condition score despite adequate feed intake;
- unexplained diarrhoea;
- sporadic cases of caudal vena cava;
- high culling rates or unexplained deaths;

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43
Q

Treatment of subacute ruminal acidosis

A

Because SARA is not detected at the time of decreased ruminal pH, there is no specific treatment.

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44
Q

Prevention of subacute ruminal acidosis

A

gradual adaption of the rumen to diets with high-grain and limiting the ingestion of rapidly fermentable carbohydrates.

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45
Q

Aetiology of acute ruminal acidosis

A

mostly seen in feedlots but can happen in other circumstances such as inadequately mixed rations or accidently events of cattle getting loose in the feed room.

characterized by a sudden and uncompensated drop in the ruminal pH

ingestion of large amounts or sudden change to feed with rapidly fermentable carbohydrates

change in the ruminal microbiome within 2-6 hours

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46
Q

Clinical signs of ruminal acidosis

A

clinical signs often develop within 6-8 hours after ingestion;

Rumen distension;
rumen hypomotility to atony;
anorexia;
dehydration;
abdominal pain (e.g., treading of hind limbs);
diarrhoea (profuse and malodorous/sweet-sour odour;
anuria;
depression;
incoordination;
palpebral reflex sluggish or absent (positively associated with severity of plasma D-lactate);
muscular weakness; recumbency (within 24-48h of the onset in severe cases);
heart rate increases with severity of the acidaemia; collapse;
shock;
death in severe cases (within 24-72 hours);

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47
Q

Treatment of acute ruminal acidosis

A

Cattle just found during the accidental ingestion or shortly after: : close monitoring; no more access to any concentrate; ad libitum good hay

Moderate cases: Require supplementation with alkalinizing products,
Palatable, good-quality hay feeding should be available for 2 to 4 days

Severe cases: Require immediate surgery to remove of all rumen contents

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48
Q

Aetiology of ruminal drinkers

A

Also known as D-Lactic acidosis

a condition of calves on a liquid diet

presents as primary chronic disease (ruminal drinking syndrome) in veal calves or as acute condition secondary to other neonatal diseases

Failure of the reticular groove reflex

Low ruminal pH leads to variable extents of inflammation of the ruminal mucosa

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49
Q

Clinical signs of ruminal drinkers

A

Primary chronic cases:
§ Usually occur some weeks after stressful situation;
§ Inappetence, lethargy, poor growth, hair loss, recurrent bloat, ventral abdominal distention (more obvious on the left side), claylike faeces;

Acute cases:
§ Lethargy, ataxia, general weakness;
§ Teeth grinding, arched back and slight abdominal distention (in cases with severe ruminitis);
§ Predominant signs are related with underlying disease;

Ballottement and simultaneous auscultation: fluid-splashing sounds at the left flank;

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50
Q

Treatment of ruminal drinkers

A

Feeding small volumes of milk from a nipple bottle or bucket

Older calves that can be weaned

In acute cases appropriate treatment of underlying disease is key

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51
Q

Aetiology of acute ruminal bloat

A

Frothy bloat
- caused by entrapment of normal gases of fermentation in stable form
- grazing, legume dominant pastures, high quality leguminous hay, high grain diets

Free gas bloat
- results from physical obstruction of eructation

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52
Q

Clinical signs of frothy ruminal bloat

A

Sudden and obvious rumen distention; skin over left flank progressively tauter; marked dyspnoea, with mouth breathing, extended neck, and protrusion of tongue; grunting; frequent urination; rumen motility present and not decreased until severe bloat; collapse;

Death usually ~3-4 hours after onset of signs, but can occur within 1 hour after access to bloat-producing pasture;

If affects a group, commonly several animals affected with variable severity of ruminal bloat; mortality rates can reach 20%.

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53
Q

Clinical signs of gas-free ruminal bloat

A

Transabdominal palpation of the rumen: excess gas usually free on top of the solid and fluid ruminal contents;

Percussion and auscultation: tympanic resonance over the dorsal abdomen on the left flank; higher pitched ping than in frothy ruminal bloat;

Transrectal palpation: distention of the rumen;

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54
Q

Treatment of frothy ruminal bloat

A

not relieved by the passage of the tube; presence of stable foam can be present in the tube after removal;

emergency rumenotomy may be necessary

Emergency relief of free-gas ruminal bloat can be accomplished by rumen trocarisation/cannulation

Antifoaming agents e.g. vegetable oils administered via large bore stomach tube

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55
Q

Treatment of free-gas bloat

A

bloat is immediately relieved by the passage of the tube (rumen trocarisation can be used for gas-free release too)

Removal of oesophageal obstruction if the cause of the bloat

Passage of a large bore stomach tube

Placement of temporary rumen fistula

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56
Q

Chronic ruminal bloat

A

Relatively frequent in calves up to 6-month-old.

Usually resolves spontaneously in time and in most cases the cause is indetermined.

Necropsy examination failed to detect any physical abnormality, although a developmental defect appears to be likely due to the age at which it occurs.

Chronic ruminal bloat can also occur secondarily to other diseases.

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57
Q

Aetiology void syndrome

A

also called rumen collapse

poorly understood syndrome

Sporadically observed in cattle suffering from severe inflammatory diseases such as septic mastitis, septic metritis or severe pneumonia that led to several days of complete anorexia.

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58
Q

Clinical signs of rumen void syndrome

A

large area of tympanic resonance in the left upper quadrant of the abdomen;

no abdominal distension;

rumen not palpable in the left paralumbar fossa;

left paralumbar fossa appeared sunken;

no fluid detected at abdomen ballottement or succussion.

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59
Q

Treatment of rumen void syndrome

A

correction of dehydration and electrolytes abnormalities, correction of rumen stasis with ruminotoric or rumen transfaunates

Prognosis is excellent if primary disease is successfully managed

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60
Q

Aetiology of ruminal impaction due to indigestible foreign bodies

A

Ingestion on non-metallic foreign bodies

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61
Q

Clinical signs of Ruminal impaction due to indigestible foreign bodies

A

decreased feed intake;

weight loss, thinner that cattle without foreign bodies;

ruminal tympany;

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62
Q

Treatment of Ruminal impaction due to indigestible foreign bodies

A

Rumenotomy to retrieve foreign body.

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63
Q

Aetiology of ruminal parakeratosis

A

hardening and enlargement of papillae of the rumen. Papillae have also a dark in colour aspect and often several adhere together forming bundles

Thought to be caused by decrease of ruminal pH and increase concentration of volatile fatty acids in the ruminal fluid

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64
Q

Clinical signs of ruminal parakeratosis

A

might present reduced weight gain and productivity; ruminal tympany (if parakeratosis severe in the cardia region)

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65
Q

Ruminal and reticular neoplasia

A

Fibropapillomas

Carcinomas or SCCs

Lymphosarcomas

66
Q

Fibropapillomas

A

Alimentary tract fibropapillomas are caused by Bovine Papillomaviruses

Relatively common in the reticulum and rumen of young cattle

can interfere with eructation and result in intermittent or chronic bloat.

Rumenotomy allows diagnosis and surgical removal

67
Q

Carcinomas or squamous cell carcinomas

A

Can result from malignant transformation of fibropapillomas in cattle ingesting bracken fern

68
Q

Lymphosarcoma

A

Can arise spontaneously or result from Bovine Leukaemia Virus

Singular or multiple lesions in the wall of the forestomach compartments

Signs of bloat and vagal indigestion may be present

69
Q

Traumatic reticuloperitonitis

A

also referred to as traumatic reticulitis, hardware disease, and wire disease.

caused by ingested sharp objects

Pica behaviour has also been implicated in the pathogenesis of TRP

70
Q

Common clinical signs of Traumatic reticuloperitonitis

A

Anorexia;

fever;

drop in milk production;

rumen hypomotility or atony, and mild to moderate tympany;

reduced rumen fill;

cranial abdominal pain;

arched back;

tucked up and “guarded” abdomen (tense abdomen);

abducted elbows;

difficulty in rising and lying down;

spontaneous grunting to reticular contractions or changes in posture (might be obscured or absent in chronic cases); bruxism;

abnormal demeanour and general condition;

Clinical signs in chronic disease are often less apparent;

71
Q

Treatment of Traumatic reticuloperitonitis

A

conservative or surgical

first approach in acute cases is conservative treatment with the oral administration of a magnet, antibiotic

confinement/stall rest should be considered to prevent migration of the sharp foreign body cranially

surgical treatment such as left flank laparotomy and rumenotomy, left flank laparotomy and rumenostomy (less commonly applied), or euthanasia

72
Q

Complications of traumatic reticuloperitonitis

A

traumatic pericarditis (septic pericarditis), hepatic inflammation or abscesses, splenic inflammation or abscesses, pleuropneumonia, reticular abscesses, vagal indigestion, and generalised peritonitis.

73
Q

Prevention of traumatic reticuloperitonitis

A

administration of reticulum-ruminal magnets to all cows, all breading heifers or heifers over 1 year-old, and young and mature bulls

74
Q

Aetiology of reticular abscesses

A

Frequent complication of traumatic reticuloperitonitis

75
Q

Clinical signs of reticular abscesses

A

vague signs of chronic indigestion;

chronic weight loss, fever, decreased appetite, impaired rumination, and reduced rumen motility

76
Q

Treatment of reticular abscesses

A

Ultrasound-guided transcutaneous incision and drainage, if abscess adjacent to body wall (cannot be ensured that catheter

77
Q

Aetiology of traumatic retiluosplenitis and reticulohepatitis

A

a relatively uncommon complication of traumatic reticuloperitonitis.

78
Q

Clinical signs of traumatic reticulosplenitis and reticulohepatitis

A

fever;
tachycardia;
gradual decrease of milk production and feed intake;
ruminal contractions may be present and normal;

Deep and forceful palpation of abdomen: may elicit a mild grunt on the left side if spleen affected or right side if liver involved;

79
Q

Treatment of traumatic reticulosplenitis and reticulohepatitis

A

Antibacterial drugs

Exploratory laparotomy and rumenotomy are not usually performed, except to remove a penetrating wire that is still present.

80
Q

Aetiology of omasal impaction

A

thought to result from feeding tough and fibrous feed, particularly wheat straw.

Lucerne stalks and branches from fodder trees can also be implicated.

81
Q

Clinical signs of omasal impaction

A

recurrent bouts of indigestion signs, e.g., decreased ruminal motility, infrequent and scant faeces, and refusal to eat grain;

complete anorexia;

empty rectum;

subacute abdominal pain with disinclination to move or lie down;

Abdominal deep palpation: hard distended omasum may be palpated;

82
Q

Treatment of omasal impaction

A

flexible tube can be passed through the reticulo-omasal orifice for omasal flush with warm water to soften and break up the impacted feed

Repeated mineral oil administration

83
Q

Aetiology of vagal indigestion

A

characterized by impaired emptying of the forestomach, abomasum, or both

result of functional or mechanical disorders of the bovine stomachs that impair the gastrointestinal transit

Many different causes

84
Q

Different classifications of vagal indigestion

A

Hoflund’s classification

Ferrante and Whitlock’s classification

Cornell classification

85
Q

Hoflund’s classification of vagal indigestion

A

· Type 1 – functional stenosis between reticulum and omasum with atony of the rumen and reticulum;

· Type 2 – functional stenosis between reticulum and omasum with normal or hypermotile rumen and reticulum;

· Type 3 – permanent functional stenosis of the pylorus with atony or retained activity of the reticulum;

· Type 4 – incomplete pyloric stenosis.

86
Q

Ferrante and Whitlock’s classification of vagal indigestion

A

· Type 1 – failure of eructation or free-gas bloat;

· Type 2 – omasal transport failure;

· Type 3 – abomasal impaction;

· Type 4 – partial obstruction of the stomach.

87
Q

Cornell classification of vagal indigestion

A

· Type I – failure of eructation resulting in gaseous distension of the rumen;

· Type II – failure of the omasal transport, which results in distension of the reticulum and rumen with gas and well-mixed feed and fluid;

· Type III – failure of normal abomasal outflow resulting in dilation of forestomaches with fluid and ingesta. The abomasum is filled with fluid or firm ingesta.

88
Q

Clinical signs of vagal indigestion

A

Poor appetite to anorexia, weight loss;

abdominal and ruminal distension;

recurring tympany;

reduced faecal output;

bradycardia (absence does not rule out vagal indigestion);

markedly reduced or absent rumination;

rectal temperature is normal or slightly below normal;

Unresponsiveness to conventional treatments;

89
Q

Atropine test for vagal indigestion

A

Indicated for cattle with chronic indigestion and bradycardia (<60 bpm);

Helps to determine whether bradycardia is vagal nerve mediated or due to cardiac disease;

The administration of 40 mg atropine sulphate (as a 1% solution), SC, should result in an increase of >16% in heart rate after 15 minutes of the administration, strongly suggesting vagal nerve mediated bradycardia;

Vagal indigestion caused by vagus nerve lesion are stronger affected by atropine test than in other cases of vagally mediated bradycardia;

This test has a diagnostic certainty of 98% for permanent vagal nerve lesion;

Bradycardia that is abolished by atropine test does not prove vagal nerve damage as cause of indigestion.

90
Q

Treatment of vagal indigestion

A

indicated, but with guarded prognosis, in animals:
· With mechanical obstruction of the reticulo-omasal orifice (e.g., by ropes or placenta);
· With reticuloperitonitis, abscesses involving reticulum and liver;
· With bronchopneumonia (with lesion or mediastinal lymph nodes compressing of the vagal nerve);
· In late pregnancy.

91
Q

Types of abomasal diseases

A

No change in abomasal position
Abomasal displacement syndromes
Abomasal fistula
Abomasal ulceration

92
Q

Aetiology of abomasal impaction

A

the presence of an enlarged abomasum due to the accumulation of drier than normal abomasal contents

primary impaction (dietary causes)
· Consumption of excess poor-quality roughage
· Impaction with sand or gravel

secondary impaction (nondietary causes)
· Abomasal hypomotility and decreased abomasal emptying;
· Decreased abomasal motility and emptying caused by vagal indigestion;
· Neurogenic or mechanical abomasal outflow disturbances
· Pyloric outflow disturbances

93
Q

Clinical signs of abomasal impaction

A

Primary impaction (dietary causes) initial signs: complete anorexia; scant faeces; moderate distention of the abdomen; weight loss; weakness. Heart rate may be increased; mild dehydration is common; muzzle is usually dry and cracked.

Sand impaction: weight loss; chronic diarrhoea with sand in the faeces; weakness; recumbency; death can occur within a few weeks.

Rumen:
§ Most often is atonic and distended with dry contents;
§ In cattle fed finely ground feed it may contain excess fluid;
§ pH of ruminal fluid usually normal;
§ Protozoal activity: normal to marked reduction in numbers and activity.

Severely affected animals die 3-6 days after the onset of clinical signs; the abomasum can rupture, and death occurs from acute, diffuse peritonitis and shock.

94
Q

Treatment of abomasal impaction

A

facilitating abomasal emptying

Correction of metabolic alkalosis, hypochloraemia, hypokalaemia, and dehydration

Lubricants can be used to try to move the impacted material

Medical + standing right-side laparotomy with abomasum massage

Medical treatment + standing right-side laparotomy + abomasotomy (or pyloromyotomy)

Guarded to poor prognosis

95
Q

Aetiology of abomasal intraluminal obstructions

A

Baling twine, gravel, placenta and trichobezoars occasionally cause obstruction of the pyloric region in adult cattle.

96
Q

Clinical signs of abomasal intraluminal obstructions

A

Clinical signs of peritoneal inflammation and possible infection may occur when intraluminal material penetrates the wall or causes pressure necrosis.

97
Q

Treatment of abomasal intraluminal obstructions

A

Surgical removal of the obstructing object, correction of fluid and electrolyte abnormalities, management of inflammation and/or any infection.

98
Q

Aetiology of abomasal mural lesions

A

· Abscesses: commonly resulting from ulcers;
· Fibrosis: commonly resulting from ulcers; from intraluminal obstruction that creates pressure necrosis and loss of mucosal barrier;
· Tumours: lymphosarcoma, adenocarcinoma.

99
Q

Treatment of abomasal mural lesions

A

Mural tumours have very poor prognosis and treatment is not generally recommended.

100
Q

Abomasal extramural masses

A

Any extraluminal mass adjacent to the pyloric antrum or proximal duodenum can compress the lumen and create partial or complete obstruction.

Most commonly omental fat necrosis or abscesses.

101
Q

Treatment of abomasal extramural masses

A

Drainage and marsupialization of abscesses. The normal anatomic relation of the abomasum and duodenum needs to be maintained in case of marsupialization.

In cases of fat necrosis, the obstruction might be relieved with a bypass between pylorus and duodenum.

102
Q

Aetiology of abomasal displacement syndromes

A

Displacement of the abomasum (DA) is an abnormal position of the abomasum in the abdominal cavity. DA is the most common abdominal disorder and reason for abdominal surgery in dairy cattle.

multifactorial aetiology

reduction of the abomasal emptying by abomasal hypomotility or atony and/or dysfunction of the intrinsic nervous system

103
Q

Predisposing factors of abomasal displacement

A

Higher incidence of LDA early in the lactation

RDA and AV cases are also most seen in the postparturient period

Periparturient diseases

Hypokalaemia in lactating cattle

Inadequate dry and transition period nutrition

inadequate feed management and hygiene

excess loss of condition

prepartum NEB

postpartum ketosis

anatomical space arrangement after birth

genetic influence

abomasal ulcers etc.

104
Q

Prevention of abomasal displacement

A

limit energy intake in dry period and maximise DMI

avoid NEB

basically just prevent disease

105
Q

Clinical signs of LDA

A

the abomasum is usually mildly to moderately distended, and the animals is not colicky;

Decrease milk production (30% to 50% reduction or more is common); decrease feed intake; mild dehydration; depression; loose or pasty faeces; rumen often reduced in frequency and strength of contraction; “sprung” rib cage on the left may be present in a large LDA and distended abomasum can appear caudal to the 13th rib;

106
Q

Blood biochemistry of LDA

A

Mild metabolic alkalosis with hypochloraemia and hypokalaemia is common;

Ketonemia - secondary ketosis is common (may be complicated by development of fatty liver disease);

107
Q

Treatment of LDA

A

Medical:
analgesic drugs, spasmolytic, calcium, oral potassium chloride + casting and rolling the cow through a 180° arc; recurrence is very likely

Surgical correction, generally good prognosis

108
Q

Clinical signs of RDA

A

Inappetence to anorexia; depression; scant abnormal faeces; right abdomen may be distended; decrease in milk production (30% to 50% reduction or more is common); mild dehydration;

109
Q

Treatment of RDA

A

not regarded as a disorder that needs emergency surgery, but due to the difficulty in distinguishing preoperatively cattle with RDA and early AV based on the physical examination, it is advised that surgery should be taken immediately. The time between diagnosis and start of treatment is highly relevant to the outcome.

110
Q

Aetiology of abomasal volvulus (AV)

A

results from abomasal movement involving rotation of structures around the axis through the lesser omentum

abomasal movements can also involve the omasum forming an omasal abomasal volvulus (OAV).

111
Q

Clinical signs of abomasal volvulus

A

clinical deterioration is rapid;

Abomasum is typically severely distended;

may cause “sprung rib cage” as viewed from the rear of the cow; a large AV may be visible and palpable in the right paralumbar fossa behind the 13th rib;

Moderate to severe dehydration (occurs very early); often very sunken eyes;

Moderate to severe depression; weakness; complete anorexia; absence of faeces; acute and marked reduction of milk production; anxious expression; cold extremities;

Signs of colic are common with tachycardia (proportional to the severity of the condition) and tachypnoea;

Signs of shock and endotoxemia can occur due to decrease of abomasal perfusion (ischemia), total devitalized abomasal tissue leading to abomasal wall necrosis;

112
Q

How to differentiate between RDA and AV

A

Blood L-lactate

with progression of AV, circulatory failures progresses and a metabolic acidosis due to hyper-L-lactatemia and azotaemia can develop overwhelming the previous metabolic alkalosis, masking the severity of the metabolic disorder

113
Q

Treatment of abomasal volvulus

A

requires emergency surgery

114
Q

Differences of abomasal displacement in calves

A

typically location of the displaced abomasum is caudal to the rib cage and extends dorsally into the paralumbar fossa;

generally, these calves present chronic or intermittent bloating;

LDA and rumen pings can coexist causing a more cranial position of the abomasum, but the ruminal pings should not extend as much ventrally as LDA pings and do not have the fluid succussion neither high-pitched tympanic resonance of a typical from LDA.

115
Q

Aetiology of abomasal fistula

A

sometimes develop after ventral surgical abomasopexies or blind abomasopexy procedures

Penetration of the abomasal lumen allows abomasal contents to follow the non-absorbable sutures through the body wall

Failure to remove the abomasopexy suture in a timely manner

116
Q

Clinical signs of abomasal fistula

A

Drainage of abomasal fluid and/or blood from the centre of an area of cellulitis;

Abomasal mucosa prolapse from fistula: haemorrhagic, oedematous, or necrotic;

Tachycardia; hypovolemia;

117
Q

Treatment of abomasal fistula

A

stabilization of the cow previously to surgery to resect the fistulous tract and close the abomasum

118
Q

Aetiology of abomasal ulcers

A

assumed that the underlying cause is the disturbance of the equilibrium of protective and aggressive mechanisms on the gastric mucosa

119
Q

Classification of abomasal ulcers

A

U1 – Non-perforated ulcer of the abomasal mucosa associated with minimal haemorrhage;
o U1a – erosion with minimal mucosal defects and loss of mucosal rugae, sometimes mucosal discolouration only (often reddish-violet or green-brown);
o U1b – deeper erosions with mucosal haemorrhage, sharply demarcated with a depressed centre;
o U1c – craters with coating of detritus of fibrin, depressed centre, and bulging margins;
o U1d – radial wrinkles with a central point, affecting gastric folds only;

U2 – Non-perforated ulcer of abomasal mucosa accompanied by erosion of a large blood vessel and associated massive intraluminal haemorrhage;

U3 – Perforated ulcer accompanied by localised peritonitis;

U4 – Perforated ulcer accompanied by general peritonitis;

U5 – Perforated ulcer into the omental bursa causing omental bursitis;

120
Q

Clinical signs of abomasal ulcer (U1)

A

Non-perforated abomasal ulcers associated with minimal haemorrhage (U1):

§ Most difficult to diagnose

§ Animals may be asymptomatic or have mild clinical signs;

§ Partial anorexia; capricious appetite; interested in feed but stop eating after a few mouthfuls as if causes/increases abdominal discomfort; decreased rumen motility; may have melena; periodic bruxism; decreased milk production;

121
Q

Clinical signs of abomasal ulcer (U2)

A

Non-perforated abomasal ulcers accompanied by erosion of a large blood vessel and massive intraluminal haemorrhage (U2):

partial or complete anorexia; decreased or absent rumen motility; haemorrhagic shock signs (pale mucous membranes, weakness, cold extremities, tachycardia (100-140 bpm), and some will show tachypnoea); obvious melena; fever; depression; bruxism;

122
Q

Clinical signs of abomasal ulcer (U3)

A

Perforated abomasal ulcers accompanied by localised peritonitis (U3):

§ Clinical signs similar to reticuloperitonitis signs;
§ Partial or complete appetite; obtunded demeanour; decreased skin surface temperature; congested scleral vessels; abdominal guarding; tachypnoea; fever; tachycardia; rumen hypomotility or atony; painful abdomen (at deep ventral palpation usually midventral to the right of the midline) and reluctance to move); occasional bruxism of pressing the nose against objects;
§ Melena is not a typical feature;
§ Rumen and abomasum tympany can also happen in calves;

123
Q

Clinical signs of abomasal ulcer (U4)

A

Perforated abomasal ulcers with massive leakage with diffuse peritonitis (U4):

§ Acute complete anorexia; abdominal guarding; congested scleral vessels; tachycardia (100 -140 bpm); tachypnoea; cold extremities and skin surface; fever; rumen and intestinal atony; distention of rumen secondary to atony; scant manure; reluctant to move and audible grunt or groan when forced to move or rise; severe depression; ventral abdomen distention with or without fluid wave at ballottement; positive foreign body tests; at rectal examination can be detected pneumoperitoneum with or without crepitation on visceral surfaces;
§ Calves often are found dead or recumbent, with abdominal distension and respiratory distress; dipping the mouth into water without drinking (wet chin), painful facial expression (empty look), abnormal posture (arched back, head low, ears drooping, and sometimes colic sings may be observed;

124
Q

Clinical signs of abomasal ulcer (U5)

A

Perforated abomasal ulcers with leakage into an omental bursa (U5):

more chronic disease; decreased appetite; weight loss; progressive abdominal distention bilaterally due to rumen stasis and accumulation of fluid in the omental bursa;

125
Q

Treatment of abomasal ulcers

A

Early treatment is essential

most important treatment is making the animal to begin to eat again

Antiacids

Broad-spectrum antimicrobial therapy for at least 5 day

Surgical treatment indicated when abomasal ulcers are concomitant with abomasal displacement

126
Q

Aetiology of abomasal tympany syndrome in calves

A

occurs in calves in milk feeding, often 2 to 6 weeks of age

Related to:
· Increased use of whey-based milk replacers that have high levels of salt and high osmolality, which decrease abomasal emptying;
· Feeding systems that allow the intake of large amounts of milk at infrequent intervals;
· Administration of high glucose and high osmolality solutions, which decrease abomasal emptying rate;

127
Q

Clinical signs of abomasal tympany syndrome in calves

A

o Severe acute abomasal distension within 1 hour after feeding; colic signs (e.g., stretching of hind legs); diarrhoea may be present; anorexia; rapidly progressive depression leading to recumbency; shock (e.g., tachycardia, cold extremities);

o Asphyxia, acute circulatory failure (due to compression of thoracic and abdominal viscera, and their blood vessels, resulting in lack of venous return), and death often occur within 6 to 48 hours after obvious clinicals signs;

128
Q

Treatment of abomasal tympany syndrome in calves

A

Parenteral antibiotics with good efficacy against clostridium bacteria

Relieve the abomasal bloat via percutaneous deflation using a large-diameter needle

IV fluid therapy to correct electrolyte abnormalities

Guarded prognosis

129
Q

Aetiology of abomasal trichobezoars in calves

A

frequently found in calves 2 to 3 months-old, they are usually of no clinical significance

originate from ingestion of hair during periods of excessive licking of their own or other animals’ hair coats

more common in calves fed only milk, as the case of veal calves.

130
Q

Clinical signs of abomasal trichobezoars

A

most commonly non-specific signs with inappetence and weight loss;

131
Q

Treatment of abomasal trichobezoars

A

Surgery to remove the trichobezoar.
Correct the diet, particularly introducing fibre

132
Q

Aetiology of intestinal volvulus

A

can affect cattle of any breed, age, or sex at any time during the year.

The apparent higher risk of developing intestinal volvulus in dairy cattle was attributed to differences in management.

133
Q

Volvulus or torsion of the mesenteric root

A

Most severe forms of intestinal volvulus. It causes dramatic illness because much of the intestine and mesenteries are involved, with exception of part of duodenum and descending colon

134
Q

Clinical signs of intestinal volvulus

A

Acute and severe signs of abdominal pain (animals can even throw themselves to the ground, lying down and getting up with frequency, kicking the abdomen, rolling, grunting); bilateral abdominal distension; marked tachycardia (>120 bpm); marked tachypnoea (>80 rpm);

Cardiovascular shock is usually present, dehydration usually is precluded by rapid progression of the disease;

May be found dead with abdominal distention;

135
Q

Treatment of volvulus or torsion of the mesenteric root

A

Affected cattle rapidly deteriorated and die due to extensive intestinal involvement, therefore immediate surgical treatment is required.

136
Q

Volvulus of the jejunal flange

A

volvulus of the mid-to-distal jejunum and proximal ileum with the associated long mesentery. The rotation of this structures may occur without involving the remain small intestine.

137
Q

Clinical signs of volvulus of the jejunoileal flange

A

Similar signs to volvulus at the root of the mesentery, but often demonstrate signs of acute intestinal obstruction rather than cardiovascular shock;

Signs of abdominal pain; tachycardia (80-120 bpm); pass minimal faeces quantity; can be dehydrated at time of examination;

138
Q

Treatment of volvulus of the jejunoileal flange

A

Immediate surgical correction.

139
Q

Volvulus of the duodenal sigmoid flexure

A

Volvulus of the duodenal sigmoid flexure results from a dorsal displacement followed by a counterclockwise volvulus (as view from the top of the cow) of the duodenal sigmoid flexure.

140
Q

Clinical signs of volvulus of the duodenal sigmoid flexure

A

similar to abomasal volvulus signs, however the ping location and diameter of the area is different;

141
Q

Treatment of volvulus of duodenal sigmoid flexure

A

Surgery is required.

142
Q

Post operative care for intestinal volvulus

A

· Maintain optimal hydration, electrolyte, and acid-base status;
· Continue antibiotic and NSAID;
· In cases where intestinal anastomosis was performed and the animals present, the use of prokinetic drugs to treat postsurgical ileus should be weighed against the risk of leakage at the intestinal anastomosis site (postsurgical ileus usually lasts 48 hours);

143
Q

Clinical signs of intussusception

A

Clinical signs appear slowly (compared to other intestinal obstructions) and evolve over several days;

Initial signs: mild colic (restlessness, kicking at the abdomen, lying down and getting up frequently, abnormal posture; present only up to the first 24 hours after onset); anorexia; lethargy; reluctance to walk;

After 24 hours: Pain signs subside; progressive lethargy; recumbency; depression; abdominal distension (within 24-48 hours after onset); progressive dehydration;

Heart rate variable and proportional to abdominal pain, intestinal necrosis, and dehydration;

Faecal output normal in the first 12 hours; minimal faecal output after 24 hours of the onset of disease. Dark scant faeces or only fibrin and mucus are common;

144
Q

Aetiology of intussusception

A

refers to the invagination of one segment of the intestine (intussusceptum) into an adjacent segment of intestine (intussuscipiens)

Initiating cause is rarely identified

145
Q

Treatment of intussusception

A

Surgical treatment is the only choice.

146
Q

Intestinal incarceration, entrapment, internal herniation

A

Sporadically small intestine can become entrapped in adhesions, embryonic remnants, or mesenteric rents.

The intestine becomes obstructed, and the blood supply can be compromised at the site of incarceration.

147
Q

Treatment of Intestinal incarceration, entrapment, internal herniation

A

Standing right flank laparotomy

In cases of entrapment in the mesenteric rent, the mesenteric defect may need to be enlarged before replacing the intestine

148
Q

Aetiology of gut tie

A

also called pelvic hernia

follows castration by manual traction of the spermatic cord in growing cattle.

149
Q

Treatment of gut tie

A

· Right flank laparotomy and transection of the fibrous band;
· Manual rupture of the fibrinous band transrectally (risk of rupturing the rectum!)

150
Q

Aetiology of obstruction of the small intestine or spiral colon due to trichobezoar

A

Trichobezoars (hairballs) generally form in the rumen or abomasum and pass into the intestinal tract where can become lodge within the small intestine or spiral colon.

151
Q

Clinical signs of Obstruction of the small intestine or spiral colon due to trichobezoar

A

initial signs of abdominal pain (restlessness, kicking at the abdomen, lying down and getting up frequently, arching the back, stretching out the legs while standing); progresses to recumbency and depression; Progressive bloat or abdominal distention and lack of faecal output;

152
Q

Treatment of Obstruction of the small intestine or spiral colon due to trichobezoar

A

Surgical approach to remove obstructive trichobezoar.

153
Q

Intestinal neoplasia

A

Partial to complete intestinal obstruction can occur with adenocarcinoma, lymphosarcoma and rarely other tumours.

Clinical signs: are vague; if complete obstruction abdominal distension and colic may occur; lymphadenopathy in lymphosarcoma;

Treatment:
Generally, not attempted unless all involved intestine can be resected along with the mass, e.g., adenocarcinoma or another tumour.

Prognosis: hopeless for lymphosarcoma; poor for adenocarcinoma.

154
Q

Caecal dilation and/or dislocation

A

Aetiology is still uncertain. Usually occur in dairy cattle during lactation. It may also occur in calves and bulls.

Caecal dilation: distension of the caecum without a twist; the caecum apex is directed caudal and positioned in front of or within the pelvic cavity.

Caecal torsion: rotation of the caecum along its longitudinal axis.

Caecal retroflexion: dorsal retroflexion (also called clockwise volvulus) and ventral retroflexion (also called counterclockwise volvulus), both occur from rotation of the ileocecocolic (ICC) junction or the proximal loop of the ascending colon (PLAC); the degree of rotation can vary from 90° to more than 360°.

155
Q

Caecal dilation

A

Clinical signs:
o Not specific;
o Reduction in milk production; reduced appetite; reduced faecal output; occasionally discrete signs of colic; ruminal and intestinal hypomotility; distension of right paralumbar fossa;

Treatment:
Medical treatment is indicated if general condition of the animal is normal or only slightly disturbed, and faeces are still present

156
Q

Caecal retroflexion

A

Clinical signs:
o More severe signs than in caecum dilation;
o Anorexia; obvious signs of colic; pronounced drop in milk production; tachycardia; rumen atony; absent or very sparse faeces with dry consistency and covered with mucus;

Only surgical treatment. Typhlotomy to facilitate caecal and PLAC emptying;

157
Q

Caecal torsion

A

Clinical signs: similar signs to caecal retroflexion

    Only surgical treatment. Typhlotomy or typhlectomy (caecum amputation) – in cases of recurrence or devitalization of the caecal wall;
158
Q

Atresia coli

A

It is the complete absence of a portion of the colon

Aetiology is unknown, but iatrogenic and genetic causes have been proposed.

Clinical signs:
o Usually appear by 1 to 3 days of age: anorexia, rapid development of abdominal distension and depression, dehydration, tachycardia, absence of faeces (early passage of mucus after birth may be reported by the farmer), weakness; may present signs of colic (restlessness, saw-block stance, kicking towards the abdomen); normal rectal temperature is common; anal sphincter and rectum appear normal; born normal with normal appetite, but showing decreased appetite;
o Can be detected in calves older, but usually under 11 days-old; severity of signs tends to increase with age;

Surgery is the only treatment for this condition

159
Q

Rectal laceration

A

Most commonly, rectal laceration result from accidental trauma during inappropriate rectal palpation technique on poorly restrained animals.

Clinical signs:
o At the time of the injury: fresh blood in the sleeve; tenesmus;
o After injury:
§ Injuries less than full thickness: tenesmus, inappetence, blood stained on the faeces; bellowing at attempts to perform rectal examination; pneumorectum;
§ Full thickness injuries: fever; GI ileus; tachycardia; arched stance; septic peritonitis signs may occur if rectal tear communicates with peritoneal cavity;

Treatment depends on severity, rest from rectal palpation and laxative diet

160
Q

Rectal prolapse types

A

· Type I – only rectal mucosa projects through the anus;

· Type II – complete prolapse of all layers of the rectum;

· Type III – variable amount of descending colon intussuscepts into the rectum and there is a complete prolapse of all layers of the rectum through the anus;

· Type IV – variable lengths of the peritoneal rectum and/or descending colon form an intussusception through the anus.

161
Q

Rectal prolapse

A

increase of the pressure gradient between the abdominal/pelvic cavity and the anus.

· Clinical signs: mucosal mass protruding beyond the anus with variable degree of oedema, inflammation, and necrosis;

· Treatment options:
o Replacement of rectal prolapse + purse-string suture;
o Surgical methods:
§ Submucosal resection + purse-string suture;
§ Stairstep amputation + purse-string suture ;
§ Laparotomy + resection of the affected tissue + end-to-end anastomosis (just for type IV prolapses);

162
Q

Atresia ani

A

Hereditable condition.

· Clinical signs:
o Signs appear shortly after birth: unable to defecate, absence of anal opening, rectal lumen bulges subcutaneously in the normal region of the anus during abdominal compressions;
o If undiagnosed until 24 hours of life: abdominal distension, depression, colic, tenesmus, and weakness;

Treatment:
Anal reconstruction performed under epidural anaesthesia, with or without sedation; in case of suspicion of multiple defects, an exploratory laparotomy must be performed previously to anal reconstruction.

Cattle II (11 decks)

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