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Farm > Cattle non infectious GI basics > Flashcards

Cattle non infectious GI basics Flashcards

1
Q

What is cheilognathoschisis

A

Congenital cleft lip

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2
Q

What is palatoschisis

A

Congenital cleft palate

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3
Q

How does palate fusion work and what implication does this have if we see a hard palate defect

A

Closure if from rostral to caudal
So any animals with a hard palate defect also have a soft palate defect

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4
Q

Which breeds of cow might have inherited midline fusion defects

A

Hereford
Charolais

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5
Q

Treating oral lacerations

A

Should heal without surgery; do daily lavage, antibiotis and NSAIDs

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6
Q

WHat organisms is mostly responsible for tooth root abscesses

A

Trueperella pyogenes

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7
Q

Signs and treatment of choke in cows

A

Signs = neck extension, drooling, no eructation, bloat, dyspnoea
Treatment = don’t feed/water due to aspiration pneumonia risk, resolve bloat, remove blockage

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8
Q

Where is the most common place for blockage; causes choke

A

Thoracic inlet
- May be foregin bodes inside oes
Could be extra-oesophageal e.g haematoma, abscess, tumour

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9
Q

What signs would we see with oesophageal trauma

A

Subcutaneous emphyema, anorexa, depression, swelling at site
- Should heal with antibiotics if no food leakage; larger perforations need surgery

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10
Q

What is oesophageal diverticulum

A

Acquired condition of oesophagus
- May be true diverticula i.e due to scar tissue or false due to defect in oesophageal musculature

Acquired condition: causes regurgitation, dysphagia, may palpate swelling in neck

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11
Q

How can we treat oesophageal diverticulum

A

Mucosal inversion and reconstrction; gives less risk of leakage post-surgery

Diverticulectomy: more risk of leakage and infection (cut off diverticulum and sew back up )

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12
Q

Which animals do we tend to see simple ruminal indigestion in

A

Hand fed dairy cattle, beed cattle
Due to variability in feed quantities
> Usually associated with sudden change in ruminal pH or physical impairment due to accumulation of indigestible feed

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13
Q

Treating simple ruminal indigestion

A

Stop feeding feed
Oral laxative/antacid
If too much urea/protein can give 5% acetic acid to correct the pH
Calcium parenteral
Transfaunation

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14
Q

Which microbes can be supplemented to enhance lactate use in rumen

And what can be used to inhibit lactate producers

A

Yeast are good at using lactate
Monensin sodium ionophore can be used to inhibit lactate production

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15
Q

what is subacute ruminal acidosis and when would we consider a herd at high rrisk

A

= intermittent periods of low ruminal pH (5.2-5.6) due to feeding excess rapidly fermentable carbohydrates and too low fibre

See herd effects: decreased milk production, poor BCS, unexplained diarrhoea

Consider herd high risk if >25% of animals tested have a ruminal pH less than 5.5

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16
Q

What complications can arise as a result of subacute ruminal acidosis

A

Caudal vena cava syndrome
Laminitis
Unexplained diarrhoea

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17
Q

Management practices to avoid SARA

A
  • Higher fibre: do 60:40 fibre: carbohydrate
  • Gradual introduction of grain
  • Supplement diet with yeast to use up lactate
  • Add monensin sodium ionophores to inhibit lactate producing bacteria
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18
Q

Pathology of acute ruminal acidosis

A

Sudden drop in ruminal pH with acute clinical signs and risk of death
- introduction of rapidly fermentable carbs –> increase in gram +ves–> increase lactate production –> pH falls below 5 –> kills other organism, impairs motility of gut + increases osmotic pressure so causes fluid to move into the rumen

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19
Q

Dealing with severe acture ruminal acidosis (pH<5, HR >100, dehydration >8%)

A

RUmenotomy/rumen lavage immediately
IV fluids with sodium bicarbonate
Antimicrobials
NASIDS
Thiamine (to avoid CCN; polioencephalomalacia), calcium

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20
Q

What does a sluggish palpebral reflex indicate

A

High plasma D lactate concentrations

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21
Q

What are ruminal drinkers

A

Where calves on liquid diet get failure of reticular groove to work, so passage of milk into the rumen –> breakdown causes ruminal acidosis, hyper-D-lactaemia, metabolic acidosis

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22
Q

What does milky coloured, sour smelling rumen material suggest

A

Ruminal acidosis due to ruminal drinking (failure of reticular groove)

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23
Q

What is the cause of primary reticular groove dysfunction (ruminal drinkers)

A

Stress

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24
Q

WHich demographic do we see chronic ruminal bloat in

A

Calves <6 months
Probably a developmental defect

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25
Q

What is primary ruminal tympany/frothy bloat

A

= due to entrapment of normal gases from fermentation in stable foam

Get more stable foam with: soluble leaf proteins; or may get less salivary mucin (normally anti-foaming) on succulent forages
Also more gas on bloat producing pastures

Risk = high grain, legumine pastures/hay, young crops, veg crops

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26
Q

How to treat frothy bloat

A

Need anti-foaming agents; vegetable oil, polozalene, dimethicone, simethicone
MAy need to do emergency rumenotomy; or pass a rube

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27
Q

What is free gas bloat/secondary ruminal tympany

A

Due to physical obstruction of eructation
- Oesophageal obstruction, failure of eructation reflex (e.g in lat recumbency), tetanus, failure of oes groove

Will palpate gas on top of solid/fluid contents; high pitched pig

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28
Q

How to deal with free gas bloat

A

Remove obstruction
Pass stomach tube to immediately relieve bloat

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29
Q

Preventing pasture bloat

A

hArd; can drench with anti-foaming agents twice daily at milking, apply agents to field/water, do monensin slow release capsiles

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30
Q

What is ruminal parakeratosis

A

Where there is hardening and enlargement of ruminal papillae
Due to decreased ruminal pH and increase in VFAs in finishing cattle fed high concentrate diet
Or in calevs with prolonged ruminal acidosis

Causes reduced weight gain and ruminal tympany but usually identified post mortem

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31
Q

What neoplasias can affect the rumen/reticulum

A
  1. Fibropapillomas from bovine papillomaviruses 1,2,5
  2. Squamous cell carinoma; when bracken fern is ingested can get malignant transformation of fibropapillomas
  3. Lymphosarcoma from BLV or spontaneous

Can cause some interference with eructation depending on where mass is

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32
Q

What is traumatic reticuloperitonitis

A

Where sharp objects rae injected, penetrate reticulum wall and cause localised peritonitis

See anorexia, fever, milk drop, rumen hypomotility, +ve grunt test for abdominal pain

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33
Q

Treatment/prevention for traumatiic reticuloperitonitis

A

Treatment = administer oral magnet, antibiotics, NSAIDs; i this doesnt work go for surgery to look at peritonisit, lance abscesses, remove foreign body

TO prevent: give reticulo-ruminal magnet to all cows over 1 year and bulls, good disposal of waste, put electromagentic device in feed mixer

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34
Q

What are some complications of traumatic reticuloperitonitis

A

reticular abscesses
Traumatic reticulopericarditis
Traumatic reticlosplenitis (left) and hepatitis (right)

35
Q

Diagnosing omasal impactin

A

Due to feeding tough fibrous feed esp wheat straw
See recurrent bouts of indigestion, pain response and hard distended omasum when palpating right hand side 7th-9th intercostal space
Increase in serum gastrin and motilin

36
Q

Treating omasal impaction

A

Give mineral oil e.g liquid paraffin for a few days

If detected during rumenotomy, can pass tube into omasum and do a omasal flush to break up the impacted feed (knead through medial rumen wall)

37
Q

What is Hofland’s syndrome

A

Vagal indigestion

38
Q

Does vagal indigestion require damage to the vagal nerve

A

No

39
Q

Some causes of vagal indigestion (categoried)

A

Vagal damage: trauma, megoesopahus/oes abscess, reticuloperitonitis, RDA or AV

Vagal impairment: mediastinal LN enlargement, neoplasia

Non-vagus: impairment of reticular/ruminal motility due to adhesions/abscesses, uterus limiting intestines in late pregnants, obstruction of any orifices b/w compartments with rope/placenta/masses

40
Q

When would we do an atropine test (in relatino to vagal indigestion)

A

Where there is bradycardia and chronic indigestion
- TO differentiate whether bradycardia is vagal in origin or due to cardiac disease

If subcut atropine causes a significant increase in heart rate suggests some vagal nerve dysfunction

41
Q

How can we use rumen chloride concentrations to distinguish between proximal stenosis and distal stenosis

A

PRox: 20mmol/l Cl-
Distal: 57mmol/L Cl-

42
Q

When would we not bother surgery with vagal indigestion due to too poor prognosis

A

+ve atropine test
If it developed in days following RDA/AV surgery

43
Q

When would we attempt to deal with vagal indigestion with guarded prognosis

A

Mechanical obstruction of reticulo-omasal orifice, reticuloperitonitis, abscesses,, later pregnancy

44
Q

What are non-dietary cases/secondary impaction causes of abomasal impaction

A

Hypomotility in post parturient dairy cows
Mechanica interaction between pregnant uterus and abomasum
Vagal indigestion reducing motility.emptying
Traumatc reticuloperitonitis causing neurological or mechanics, obstruction of outflow from pylorus
Outflow disturbance due to abomasal volvulus, adhesions masses

45
Q

Signs of abomasal impaction

A

Detect large firm mass on right flank palpatino
BIochem changes relating to reduces emptying: metabolic alkalosis, hypochloraemia, hypokalaemia,

46
Q

Treating abomasal impaction

A

Minteral oil lubricant (could put this directly into abomasum via rumenotomy)
Laxative
Prokinetic
Induction of parturition

47
Q

Are abomasal intraluminal obstructions common

A

No because the reticulo-omasal orifice works as a filter to large opjectsq

48
Q

WHat is the basic principle of abomasal displacement syndromes

A

Reduction in abomasal emptying due to hypomotility or atony
–> Get gas accumulation causing abomasum to become buoyant and float dorsally

Key = reduction in motility + increase in gas

90% of time goes to left (LDA)
10% of time goes right (RDA or AV)

49
Q

How can high concentrate feeding predispose to abomasal displacement

A

Ruminal content osmolality increases, draws water in and causes more rapid passage into abomasum

Get undigested material in abomasum and digestion leads to gas production

50
Q

How does parturition predispose to abomasal displacement and at which stage do we see the different types

A
  • ABomasum has been distorted by uterus
    Post calving get freeing up of lots of space

Most RDAs/Avs seen post-parturitent; most LDAs seen in early lactation

51
Q

Signs with LDA

A

mild drop, inappetance, change in faeces, less ruminal contraction, distended abdomen may be visible

High pitched ping + fluid splash on left side
Transrectal may feel that rumen has been pushed medially away from left body walll

Biochem: metabolic alkalsis, hypochloraemia/kalaemia

52
Q

Is rolling a good treatment for LDA

A

No because recurrence very likely

53
Q

What signs do we see in abomasal volvulus and how is it different to LDA/RDA

A

More acute onset and more severe
Much more distended abomasum; can see sprung rib cage; hear ping even cranially to 10th rib (covers 8th to 13th)

Colic, weakness, signs of shock and endotoxaemia due to ischaemia of abomasum ( can get necrosis), tachtcardai etc

Also see high L lactate

54
Q

What would drainage of abomasal fluid/blood from an area of cellulitis suggest is going on

A

abomasal fistula has developed after ventral surgical or blind abomasopexy

55
Q

Where do we see abomasal ulcers in adult cattle vs milk fed calves

A

In adult cattle = fundus
In calves = pyloric antrum

56
Q

Grading abomasal ulcers basic

A

U1 = non-perforating with minimal haemorrhage (subdivided into a-d)
U2 = non-perforating with erosino of large blood vessel and massive intraluminal haemorrhage
U3 = perforating with local peritonitis
U4 = perforating with generalised peritonitis
U5 = oerforating into omental bursa, causing omental bursitis

57
Q

What type of ulcers are more common in calves; bleeding or perforating

A

Perforating

58
Q

Which microbes are important in abomasal tympany

A

Gas forming ones; esp clostridia
C perfringens A important

59
Q

How does abomasal tympany syndrome/abomasitis/abomasal bloat/brazy-like disease work

A

Mild fed calves 2-6 weeks old
Related to large milk quantities at infrequent intervals or high glucose/salt solutions which delay abomasal empying

Get sudden filling of abomasum and delayed emptying which allows gas producting microbes to proliferate e.g C perfringens A so get gas build up and tympany

60
Q

What is a good antibiotic with clostridial efficacy e.g for abomasal tympany syndrome in calves

A

Procaine penicillin

61
Q

Which demographic do we tend to see abomasal trichobezoars in

A

Milk fed calves (veal); lack fibre

62
Q

What is the difference between volvulus and torsion

A

Volvulus = rotation of viscera around its mesenteric attachment
TOrsion = rotation around own axis

63
Q

Volvulus/torsion of the mesenteric root effects

A

Involves most of the intestine; leads to rapid ischaemic necrosis, cardiovascular shoc
High mortality

64
Q

Volvulus of the jujunoileal flange

A

Dont commonly get arterial occlusions due to fat deposits; more so get venous occlusion; causes oedema, shunting of blood and then iscahemia

Signs relate to obstruction (c/f cardiovascular shock)
On rectal palpation feel distended intestine loops and excessive tesion on intestinal mesentery

65
Q

What demographic is most commonly affected by intussusception

A

Calves <2 months old

66
Q

Which area of the gut might we have to do manual reduction of intussusception due to difficulty of resection and anastomosis

A

Spiral colon

67
Q

Signs of intussusception

A

Slowly appears over days; mild colic, anorexia, then pain subsides and get progressive lethargy and depression

On rectal feel distended loops of intestine; may feel intuscuception as a hard sausage like structure

68
Q

How to treat an intussusception

A

Right flank laparotomy, exteriorise segment and do resection and anastomosis
Low survival

69
Q

Dealing with intestinal entrapment

A

Cut the tight band; then check intestine for signs of ischaemia; if ischaemic should do resection and anastomosis

70
Q

What is gut tie/pelvic hernia

A

Rare condition in castrated steeds/bulls where the cord forms obstructures that incarcerate the intestine; or traction can tear peritoneal fold of ductus deferens and allow loops of jejunum into pelvic cavity to get entrapped

71
Q

When are we likely to see obstruction of small intestine/spiral colon by trichobezoars

A

When infected with lice/mange, during coat shedding, in cattle on low fibre diet e.g veal calves

72
Q

What are classic biochem changes with any gut obstruction

A

Metabolic alkalsos, hypochloraemia, hypokalaemia

73
Q

What demographic is caecal dilation/dislocation seen in

A

Dairy cattle during lactaton; may be related to hypoclacaemia

74
Q

What is atresia colon and what signs do we get

A

= absence of a portion of the colon; usually ascending colon at midspiral loop
Likely due to vasculature compromise in early embryogenesis
[Seems to be inherited in holstein freisian studies]

In first few days of life see anorexia, abdominal distension, depression, absence of faecel, colic, tachycardia

Ultrasound shows intestinal ileu

75
Q

Treatment for atresia coli

A

Anastomosis of proximal spiral colon to descending colon to create bypass

Poor prognosis
IF FPT involved then give plasma before surgery

76
Q

When should we euthanise a cow with a rectal laceration

A

If there is a full thickness tear communicating with the periteonal cavity; will get septic peritonitis

77
Q

Which demographic do we typically see rectal prolapse in

A

Feed lot cattle between 6 months and 2 years old

78
Q

Classifying rectal prolapses

A

1 = just mucosa prolapses through anus
2 - complete prolapse of rectum layers
3 = complete prolapse of rectum layers + intussusecption of colon into the rectum
4 = Get some prolapse of intussuscepting descendign colon

79
Q

What surgery might we do for a type IV rectal prolapse

A

Laparotomy, resectino of affected tissue and end to end anastomoses

80
Q

What suture do we use to retain a rectal prolapse

A

Purse string; remove after a wekk
+ give topical lidocaine to stop straining

81
Q

What is atresia ani

A

Heritable condition where no anal opening; can’t defecate and get subcutaneous bulge forming where anus would be
Do reconstruction under caudal epidural

82
Q

What GI condition can fat necrosis lead to

A

Extraluminal obstructions

83
Q

What might be described as ‘floating corks’ on rectal palpation

A

Fat necorsis masses

84
Q

What are risk factors for fat necrosis

A

Overconditioning, lack of exercise, genetics (channel island cattle, japanese), fescue pastures (infected with endophyte neotyphodium coenophialum)

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