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LAM II - Test 1 > L2/L3 - Reticuloruminal Disorders (Parts I & II) > Flashcards

L2/L3 - Reticuloruminal Disorders (Parts I & II) Flashcards

1
Q

What are the 2 types of bloat?

A
  • Free gas bloat

- Frothy Bloat

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2
Q

_____ is usually a manifestation of an underlying primary disorder and occurs sporadically (usually one animal)

A

Free gas bloat

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3
Q

What is frothy bloat?

A

A primary disease where luminal gases are trapped in small bubbles within abnormally viscous digest.

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4
Q

TRUE/FALSE

Free gas bloat is usually dependent on feedstuffs.

A

FALSE
Frothy bloat is usually dependent on feedstuffs. It is a primary disease.
Free gas bloat is 2˚ and so not dependent on diet.

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5
Q

What are the conditions leading to free gas bloat?

A
  • Esophageal Dysfunction

- Ruminal motility Dysfunction

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6
Q

What are causes of esophageal dysfunction?

A
  • Intraluminal: foreign body (choke)**
  • Intramural: papilloma, granuloma, tetanus
  • Extramural: mediastinal lymphadenopathy
  • Positional: lateral recumbency hypocalcemia, surgery
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7
Q

What are causes of ruminal motility dysfunction?

A
  • Muscular inactivity: hypocalcemia, xlazine, atropine
  • Reticular adhesions: hardware, abomasal ulcers
  • Vagal nerve injury**
  • Abnormal rumen environment
  • Severe Abomasal distension (ie left displaced abomasum, milk engorgement)
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8
Q

What are high risk forages for frothy bloat?

A

Alfalfa
Sweet clover
Red Clover
Winter wheat

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9
Q

What are the CS of bloat?

A
  • Asymmetric abdominal distension (L paralumbar fossa)
  • Abdominal discomfort
  • ↑ HR, RR
  • Acute: death within 30min - 4 h
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10
Q

Restlessness, kicking at abdomen, rolling are signs of _____.

A

Abdominal discomfort

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11
Q

TRUE/FALSE

Animals can die of asphyxia d/t bloat.

A

TRUE

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12
Q

A cow is showing clinical signs consistent with bloat. What is the next diagnostic step?

A

Pass an orogastric tube

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13
Q

You pass an orogastric tube in a cow showing signs of bloat but there is resistance when passing it into the rumen. What are your Ddx?

A

If it enters the rumen → Esophageal disorder

If it does not enter the rumen → Choke

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14
Q

You pass an orogastric tube in a cow showing signs of bloat into the rumen with no resistance. What are your Ddx?

A
  • If free gas is released → Free gas bloat
  • No gas released & Multiple animals + bloat provoking diet → Primary bloat
  • No gas released & single animals + bloat provoking diet → omasal transport failure
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15
Q

What are you Ddx for Bloat?

A
  • Ruptured bladder
  • Hydroallantois
  • LDA
  • Abomasal volvulus
  • Mesenteric volvulus
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16
Q

What is the treatment for an animal with bloat that is in distress?

A

EMERGENCY!

Trocarization or Rumenotomy

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17
Q

What are the treatments for less severe bloat?

A

Stomach tube relief

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18
Q

What are the treatments for less severe frothy bloat?

A
  • Polaxalene (little bubbles converted to big bubbles)
  • Vegetable oils
  • Dactyl sodium sulfosuccinate
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19
Q

What are methods of controlling/preventing free gas bloat?

A
  • Chronic: temporary rumenotomy

- Find underlying problem (e.g. esophageal obstruction)

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20
Q

You are trying to find the underlying problem of free gas bloat. What kind of tests can you perform?

A
  • Rumen fluid evaluation
  • Esophageal endoscopy
  • Reticular U/S
  • Exploratory laparatomy/rumenotomy
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21
Q

What are preventative/control methods for frothy bloat?

A
  • Grazing management/adaption diets
  • Poloxalene (top dressing, mineral block, liquid supplementation)
  • Ionophores (monensin & Laslocid)
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22
Q

What are the kinds of rumen indigestion?

A
  • Simple (primary)

- Secondary

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23
Q

____ rumen indigestion has an acute onset, while _____ rumen indigestion is chronic.

A

Primary /Simple = Acute

Secondary = Chronic

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24
Q

What causes Primary/simple rumen indigestion?

A

Abrupt dietary change that results in self-limiting but rapid decline in rumen fermentation

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25
Q

What are some causes of secondary rumen indigestion?

A
  • Endotoxemic infection
  • Abomasum Disease
  • Metabolic disease
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26
Q

What are CS of primary rumen indigestion?

A
  • Acute Anorexia → Rumen motility is reduced to absent

- Diarrhea commonly observed within 24 hrs

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27
Q

What are CS of 2˚ rumen indigestion?

A
  • Rumination absent
  • Rumen underfilled
  • Fecal production depressed
  • +/- diarrhea
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28
Q

Match the following CS to 1˚ or 2˚ Rumen indigestion:

  1. Depressed fecal production
  2. Diarrhea
  3. Absent rumination
  4. Acute Anorexia
  5. Rumen Underfilled
A
  1. 2˚
  2. 1˚ (may be seen in 2˚)
  3. 2˚
  4. 1˚
  5. 2˚
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29
Q

TRUE/FALSE

Mild cases of rumen indigestion require rumen fistula for transfaunation.

A

FALSE

They are self-correcting

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30
Q

What are the treatment options for Rumen indigestion?

A
  • Rumen Transfaunation
  • Increase Rumen fill with 20-30L of fluid +/- : Na/K salts, propylene glycol, Niacin (ketosis), alfalfa pellets (prolonged anorexia)
31
Q

When inserting a rumen fistula, what is applied around the surgical area?

A

007 (oxytetracycline)

32
Q

What is the pathogenesis of rumen acidosis?

A
  • Lactic acid accumulation in the rumen raises osmolarity and fluid sequestration in rumen
  • Abnormal GI contents and distention inhibiting motility
33
Q

Rumen acidosis results from increased production of ______.

A

Lactic acid

34
Q

TRUE/FALSE

Lactic acid is poorly absorbed from the rumen compared to other VFAs.

35
Q

What lactic acid isomers are produced during rumen acidosis? Which is poorly metabolized in the body?

A

D & L Isomers

D is poorly absorbed

36
Q

What are the CS of rumen acidosis?

A
  • Incoordination and ataxia
  • Profound weakness and depression
  • Anorexia apparent (rumen stasis, abdominal pain, occasional grunting / grinding of teeth, severe dehydration)
  • Laminitis
  • Sudden death syndrome
37
Q

Describe the CNS pathogenesis of rumen acidosis.

A

-CNS depression from metabolic acidosis, ethanol, methanol, termini, tryptamine production.
Thiamin production → polioencephalomalacia
-Death of gram negatives and endotoxemia
-histamine release

38
Q

What is the general pathogenesis of rumen acidosis?

A
  1. Loss of body water → dehydration
    • contributes to acidosis
  2. Lactic acid is absorbed from rumen, small intestine → profound lactic acidosis develops
39
Q

What damage is caused by the acidic rumen pH?

A
  • Mucosal surfaces in the fore stomachs and intestines are damaged
  • Blood vessels thrombose and sections of rumen mucosa and submucosa slough allowing bacteria to invade
  • Liver abscessation via portal circulation
  • Mycotic rumenitis
40
Q

What kind of cattle does SARA affect?

A

Common problem in intensively managed dairy cows

41
Q

What are clinical signs of SARA?

A
  • ↓ DMI
  • Diarrhea
  • Lameness
  • Low milk fat test
  • Rumen stasis
42
Q

What are the two groups of cows at special risk for SARA?

A
  • Fresh cows

- High intake cows

43
Q

What factors can be evaluated to track SARA?

A
  • Source of and particle size of grain
  • Milk fat %, fat to protein ratio
  • Assessment of manure
44
Q

How is rumen acidosis diagnosed?

A
  • pH of rumen fluid <4 (SARA <5.5) collected via rumenocentesis
  • Metabolic Acidosis
45
Q

TRUE/FALSE

Mild cases of rumen acidosis will recover without treatment while severe cases should be treated.

46
Q

What are treatment options for severe rumen acidosis?

A
  • Emptying of rumen by oral lavage/rumenotomy (preferred)
  • Oral administration of rumen buffers (mg carbonate or Mg hydroxide)
  • Fluids to correct dehydration & acidosis
47
Q

What changes does grain cause to pH?

A

Acidifying

48
Q

How can rumen acidosis be managed?

A
  1. Allow time for adjustment to diets with grain
    a. Gradually ↑ grain in diet
    b. Program “step up” rations
    c. Limit intake until adjusted
  2. Feed adequate roughage - effective fiber (eNDF)
  3. Manage feed consumption
  4. Feed ionophores
49
Q

_____ is caused by inflammatory changes that develop in the rumen mucosa and underlying tissues in cattle fed high energy rations with inadequate roughage.

50
Q

What pathology is ruminates associated with?

A

Liver abscess

Laminitis

51
Q

TRUE/FALSE

Rumenitis is a sporadic disease.

A

FALSE

It can affect 100% of herd if not adapted

52
Q

What etiological agent is responsible for the liver abscess that occur d/t rumenitis?

A

Fusobacterium necrophorum

53
Q

What are the clinical signs associated with rumenitis?

A
  • Generally none
  • Chronic laminitis (big CS)
  • Decreased feed consumption/weight gain
54
Q

How is rumenitis diagnosed?

A

-Rumen fluid pH

55
Q

What are treatment options for ruminates?

A
  • Modify the roughage portion of feed
  • Adjust feeding intervals (↓ in pH fluctuations)
  • Antibiotics to reduce liver abscess?
56
Q

What are methods to detect whether a cow is sorting her feed?

A
  • Variation in manure consistency between individuals of cows receiving the same ration
  • Penn State Shaker box
57
Q

What are CS of Traumatic Reticulopericarditis?

A
  • Abducted elbows
  • Edema and jugular pulses
  • Washing machine murmur
58
Q

How would you diagnose traumatic reticulopericarditis?

A
  • Grunt Test
  • Abdominocentesis
  • Reticulography
  • U/S
  • Exploratory Laparotomy
59
Q

What clinicopathological findings might you see in a cow with traumatic reticulopericarditis?

A
  • ↑ Fibrinogen (acute)
  • ↑ Globulin (chronic)
  • +/- neutrophilic
  • Mild metabolic alkalosis
  • Cl in the rumen
60
Q

What will your abdominocentesis yield in a cow with traumatic reticulopericarditis?

A
  • ↑ WBC (PMN >6,000 nucleated cells /uL)
  • ↑ concentrations (>3g/dl)
  • Dry or normal tap- inconclusive
61
Q

What findings will you see on a reticulography?

A
  • Foreign body not attached to magnet

- Perireticular abscess, abnormal reticular size/shape

62
Q

What findings will you see when ultra sounding a cow with traumatic reticulopericarditis?

A
  • ↓ reticular motility
  • Fibrin deposition
  • Perireticular abscesses
63
Q

What are the surgical treatment options for traumatic reticulopericarditis?

A
  • Retrive penetrating object

- Drain perireticular abscess

64
Q

What are the medical treatment options for traumatic reticulopericarditis?

A
  • Administer magnet
  • PPG 5+ days
  • NSAIDs
  • Oral/IV luids
  • Stall rest
65
Q

What are the types of vagus indigestion?

A
  • Type I: uncomplicated TRP
  • Type II: Omasal transport failure
  • Type III: Abomasal obstruction
  • Type IV: late gestation indigestion
66
Q

What is type I vagus indigestion?

A
  • Uncomplicated TRP
  • Failure of eructation that results in free gas bloat and luminal distention
  • Usually d/t vagus nerve damage d/t TRP
67
Q

What is the pathogenesis of type II vagus indigestion?

A
  • Omasal transport failure
  • Failure of omasal transport preventing aboral movement of ingesta from reticulum to abomasum
  • May result from functional or mechanical outflow disturbances
  • Functional: vagus damage from mycoticomastitis, reticular abscesses, localized adhesions
68
Q

What is the pathogenesis of type III vagus indigestion?

A
  • Abomasal obstruction
  • Primary impaction d/t dry feed with limited water.
  • Secondary impaction d/t disturbances in motility or pyloric outflow failure
    • Following TRP, right displaced abomasum
69
Q

What is the pathogenesis of type IV vagus indigestion?

A
  • Late gestation indigestion

- During advanced pregnancy the enlarged uterus displaces abomasum which interferes with normal motility

70
Q

What are the CS of vagus indigestion?

A
  • Chronic progressive weight loss with abdominal distention

- Papple

71
Q

How is vagus indigestion diagnosed?

A

Usually rule out

72
Q

What are the treatment options for vagus indigestion?

A

Usually supportive only.

73
Q

What are the motility disorders?

A

TRP
Omasal
Abomasal

74
Q

What motility results in > 30 rumen chloride?

LAM II - Test 1 (6 decks)

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