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Sys Path II > Rumen, reticulum, & omasum > Flashcards

Rumen, reticulum, & omasum Flashcards

1
Q

What are the forestomachs lined by?

A

non-glandular stratified squamous mucosa

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2
Q

What are the resident flora & fauna of the forestomachs responsible for?

A
  • digestion & fermentation of cellulose generating short-chain fatty acids, which are directly absorbed across the epithelial lining into the blood
  • these fatty acids supply more than half of the energy from nutrients absorbed by the alimentary tract
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3
Q

What information does the postmortem exam of ruminal contents provide?

A

information about general metabolic states:
- dehydration (overly dry contents)
- primary bloat (voluminous frothy contents (may disappear after certain time)
- urea toxicity (ammoniacal odour & alkaline pH)
- organophosphate toxicity (odour of cooked turnips or a pungent insecticidal smell)
- grain overload (fermentative acidic odour & pH less than 5.0 (w/ putrefaction & autolysis ruminal pH returns to near-normal levels in cases of acidosis))
- lead toxicity (metallic lead (nonmagnetic pliable), paint flakes, or motor oil in rumen)

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4
Q

What information does the postmortem exam of ruminal mucosa provide?

A
  • the ruminal mucosal epithelium usually sloughs w/in a few hours after death
  • it separates from the lamina propria in large grey patches, which cover the ingest when the rumen is opened
  • persistent firm attachment of the ruminal epithelium is abnormal
  • this undue adhesion occurs in acute rumenitis (ex: grain overload or fungal infection) & over the healed lesions/ulcers (ex: ruminal necrobacillosis)
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5
Q

What is bloat?

A

(ruminal tympany)
- overdistension of the rumen & reticulum by fermentation gases
- bloat can be divided into primary & secondary tympany

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6
Q

What is primary tympany?

A

(legume bloat, dietary bloat, or frothy bloat)
- occurs up to 3 days after the animals begin a new diet
- certain legumes (alfalfa, clover) & grain concentrates promote formation of stable foam
- foam mixed w/ ruminal contents prevent eructation resulting in ruminal distension

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7
Q

What is secondary tympany?

A
  • (free gas bloat)
  • caused by a physical or functional defect in eructation of gas produced by normal ruminal fermentation
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8
Q

What are causes of secondary tympany?

A
  • esophageal obstruction (Ex: papilloma, lymphoma, esophageal foreign body or stenosis, enlarged mesenteric or tracheobronchial lymph nodes, etc.)
  • vagus indigestion results in a functional outflow problem from the forestomach & atony due to damage to the vagus nerve (associated w/ traumatic reticuloperitonitis, liver abscesses w/ secondary peritonitis, volvulus of the abomasum)
  • in bucket-fed calves, secondary bloat can occur, when large amounts of milk is ingested which escapes the reticular groove & flows into the rumen (ruminal drinkers), where putrefaction occurs resulting in abdominal distension
  • some of the recumbent Ru have difficulties to eruct ruminal gas; accordingly they may also be presented as “secondary bloat cases”. (it’s important to perform thorough necropsy in such cases to determine the primary cause of recumbency)
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9
Q

What are the clinical signs of bloat?

A

signs of primary & secondary bloat are the same
- distended left paralumbar fossa and abdomen
- increased respiratory & HRs
- decreased ruminal movements in late stages of disease

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10
Q

What is the cause of death with ruminal bloat?

A

compromised respiration due to pressure on the diaphragm & thoracic cavity

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11
Q

Why is the necropsy for primary bloat ideally performed less than 12 hours after death?

A

frothy ruminal content gradually disappears after death

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12
Q

Why is it important not to assume bloat if cow is found dead w/ an extremely distended abdomen & w/ dark (poorly oxygenated) blood oozing from its nose, mouth, & rectum

A
  • Ddx: ANTHRAX
  • all of these signs may be present in animals that died from any other ‘sudden-death’ causes, especially during the summer, b/c GIT fermentation can occur after death in a non-bloated animal, resulting in the production of abundant gas & postmortem abdominal distension
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13
Q

What are the most reliable postmortem indicators of antemortem bloat?

A
  • esophageal bloat line
  • cranial congestion (head & neck) & caudal normal colour of mucosae, subcutaneous tissues, & muscles
  • hemorrhage (blood clots) in bronchi & cranial sinuses
  • lymph edema in the caudal portion
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14
Q

What is an esophageal bloat line?

A
  • sharp line of demarcation in the esophageal mucosa btwn the congested esophagus cranial to the thoracic inlet & pale, bloodless (blanched) esophagus caudal to the thoracic inlet
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15
Q

What is the postmortem “pseudo bloat line”?

A
  • during the summer months, may sometimes form due to rapid postmortem bacterial generation of ruminal gases resulting in increased postmortem thoracic pressure before the blood forms clots
  • distinguishing postmortem bloat line from the real antemortem bloat line caused by ruminal tympany is sometimes v difficult
  • hence additional changes must also be present & OTHER DISEASES HAVE TO OFTEN BE RULED OUT before final diagnosis of bloat is made during the summer
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16
Q

Why does bloat cause cranial congestions (head & neck) & caudal normal colour of mucosae, subcutaneous tissues, & muscles?

A
  • blood cannot return from head & neck due to compressed vena cava cranialis at the thoracic inlet, while blood from the caudal portions can apparently return via paravertebral veins & subcutaneous milk veins, despite impaired venous return due to compression of abdominal portion of the vena cava caudalis by the rumen
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17
Q

Why does bloat cause lymph edema in the caudal portion?

A
  • most evident in the subcutis of stifle joint (personal observation) due to impaired return of lymph through compressed thoracic duct
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18
Q

What kind of foreign bodies can occur in Ru forestomachs?

A
  • trichobezoars (hair balls) & phytobezoars (plant balls)
  • ingestion of nails & wire can result in perforation of the wall of the reticulum w/ resultant reticulitis, peritonitis, or eventually possible pericarditis (hardware disease) -> if high risk of hardware disease exists, magnets can be placed in rumen to prevent the ingested wires & nails from penetrating the reticular mucosa
  • ingestion of lead plates from broken batteries may result in LEAD POISIONING manifested as polioencephalomalacia in cattle
19
Q

What kind of inflammatory diseases can occur in Ru forestomachs?

A
  • rumenitis due to lactic acidosis
  • bacterial rumenitis
  • mycotic rumenitis
20
Q

What are other names for rumenitis due to lactic acidosis?

A
  • ruminal acidosis, grain overload, rumen overload, carbohydrates engorgement, & chemical rumenitis
21
Q

What is the pathogenesis of rumenitis due to lactic acidosis?

A
  • sudden dietary change to an easily fermentable feed -> increase in dissociated volatile fatty acids -> ruminal stasis
  • change in ruminal microflora from cellulolytic gram (-) bacteria to gram (+) bacteria (Steptococcus spp., Lactobacillus spp.) involved in fermentation of carbohydrate-rich feed which results in a high concentration of lactic acid & decreased ruminal pH below 5 (normal = 5.5 - 7.5)
  • acidic pH eliminates normal ruminal flora & fauna & damages ruminal mucosal epithelium resulting in superficial rumenitis
  • death is caused by dehydration, acidosis, & eventual circulatory collapse (dehydration is secondary to the increased osmotic effect of ruminal solutes (organic acids), causing movement of fluids across the damaged ruminal mucosa into the rumen; acidosis is secondary to absorption of lactate from the rumen; mortality ranges from 25% to 90% & usually occurs w/in 24hrs
22
Q

What do you see on necropsy w/ rumenitis due to lactic acidosis?

A
  • severely dehydrated carcass
  • abundant grain, or porridge-like & acidic watery content is found in the rumen
  • the low ruminal pH disappears several hours after death (12-24hr) - IMPORTANT FOR DIAGNOSTIC PURPOSES. (w/ putrefaction & autolysis ruminal pH returns to near-normal levels in cases of acidosis -> post-mortem change)
  • intestinal contents are watery
  • ruminal mucosa is firmly attached (presumably due to pickling effect preventing post mortem degradation).
  • microscopic confirmation of ‘chemical rumenitis’ (based on intra-epithelial neutrophilic infiltration) may be necessary in animals necropsied more than 12 hours after death b/c low ruminal pH will disappear due to autolysis
  • animals that survive lactic acidosis may develop ruminal necrobacillosis & if they survive this, stellate scars (healed ruminal ulcers) may be seen in slaughterhouse or in animals that due consequently due to other causes
23
Q

What is bacterial rumenitis?

A
  • generally occurs secondary to ruminal acidosis
  • bacteria that colonize the damaged ruminal wall induce necrosis &/or suppurative inflammation & can be transported into the portal circulation & to the liver
24
Q

What bacteria are seen in bacterial rumenitis?

A
  • Trueperella (Arcanobacterium) pyogenes is a common cause of bacterial abscesses in the liver which can progress to CAUDAL VENA CAVA SYNDROME
  • Fusobacterium necrophorum results in hepatic necrobacillosis (hepatic coagulation necrosis)
25
Q

What is mycotic rumentitis?

A
  • occurs secondary to the damage to the ruminal mucosa caused by lactic acidosis or secondary to administration of antibiotics, which disturb the normal flora & allow fungi (Aspergillus, Mucor, etc.) to proliferate
  • ruminal lesions are generally red circular & well delineated because they are caused by infarction from thrombosis secondary to fungal vasculitis
  • fungi can spread to the placenta hematogenously & cause mycotic placentitis, which leads to abortions
  • RUMINAL CANDIDIASIS occurs in animals affected by debilitating conditions, treated w/ glucose &/or antibiotic therapy, or overfed milk-replacer (sour rumen) -> it could be accompanied by LINGUAL (thrush) &/or esophageal candidiasis
26
Q

What neoplasia can occur in the Ru forestomachs?

A
  • ruminal papillomas & fibropapillomas are induced by papilloma virus
27
Q
A

Frothy bloat -> primary bloat

28
Q
A

esophageal ‘bloat line’
- dark cranially & pale caudally

29
Q
A

congestion of cervical lymph node, normal caudal lymph node

30
Q
A

cranial congestion & hemorrhage in sinuses

31
Q
A

location is the thoracic inlet (first rib)

32
Q
A

traumatic reticulitis

33
Q
A

traumatic reticulitis -> fibrinopurulent pericarditis

34
Q
A

traumatic reticulitis -> constrictive fibrotic pericarditis

35
Q

What other organs than the heart can traumatic reticulitis affect?

A

lungs (pneumothorax) or liver

36
Q
A

grain overload (ruminal acidosis)

37
Q
A

ruminal necrobacillosis

38
Q
A

Multifocal hepatic necrosis of Bo liver (hepatic necrobacillosis)

39
Q
A

mycotic rumenitis

40
Q
A

mycotic ruminitis
- remember this circular pattern is particular to fungi & infarction

41
Q
A

mycotic omasitis
- distinct half circles here due to location

42
Q
A

healed ruminal ulcer -> stellate scar
- fibrosis that contracts to form this scar appearance

43
Q
A

healed ruminal ulcer -> stellate scar

44
Q
A

ruminal fibropapillomas

Sys Path II (11 decks)

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