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3. Food Animal 2 > Abomasal ulcers > Flashcards

Abomasal ulcers Flashcards

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1
Q

primary and secondary causes of abomasal ulcers?

A

Primary: Cause is unknown
Secondary:
* Lymphoma
* BVDV
* Rinderpest
* MCF

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2
Q

what animals are susceptible to abomasal ulcers? when? depends on what?

A
  • Lactating cow, mature bulls, veal calves, beef calves

Lactating cows:
* Around parturition and between 3-6 months in lactation
* Summer months, grazing on pasture (what?)
* Amount of rainfall and fertilizer used
* Stocking rate and milk production

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3
Q

pathogenesis of abomasal ulceration

A
  • The exact cause of abomasal ulcers is still obscure and may be multifactorial.
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4
Q

abomasal ulcer types

A
  1. nonperforating
  2. nonperforating with severe blood loss (bleeding)
  3. perforating with local peritonitis
  4. perforating with diffuse peritonitis
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5
Q

issues associated with Type 1: non perforating ulcer

A
  • Minimal: hemorrhage, focal abomasal
    thickening, or serositis
  • Cause of chronic gastritis
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6
Q

issues associated with Type 2: ulcer causing severe blood loss

A
  • Severe intraluminal hemorrhage and anemia
  • Abomasal distention: metabolic alkalosis, hypochloremia, hypokalemia, and hemorrhagic anemia
  • Melena
  • Rumen chloride may be increase (40%) of cases
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7
Q

issues associated with Type 3: perforating ulcer with acute local peritonitis

A
  • Full thickness perforation with leakage of abomasal contents
  • Localized peritonitis, adhesions with adjacent viscera, omentum and peritoneal surface
  • Omental bursitis and empyema
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8
Q

issues associated with Type 4: perforating ulcer with diffuse peritonitis? where do they occur in nursing beef calves?

A
  • Full thickness perforation with leakage of abomasal contents
  • Nursing beef calves: 90% occur in the body of the abomasum (greater curvature)
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9
Q

what ages of cattle are affected by abomasal ulcers? associated with what lifestyle factors?

A
  • Occur in all ages of cattle
  • Associated with stress & high concentrate diets
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10
Q

what other diseases are abomasal ulcers assocaited with?

A
  • Lymphosarcoma in older animals
  • Concurrent diseases: metritis, mastitis, ketosis
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11
Q

calves with abomasal ulcers - what kind do we usually see? may be associated with?

A
  • Usually see perforation with peritonitis
  • May be associated with copper deficiency (?)
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12
Q

what proportion of adult cattle with abomasal ulcers have hemorrhafe, and local or diffuse peritonitis?

A
  • 1/3 significant hemorrhage
  • 1/3 perforating with localized peritonitis
  • 1/3 perforating with diffuse peritonitis
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13
Q

clinical findings for abomasal ulcers?

A
  • Abdomial pain, anorexia, decreased rumen motility and tympany
  • Anemia, and hemorrhagic shock in severe cases
  • Tarry, black feces and black blood clots
  • Pale MM, tachypnea, tachycardia
  • Fever
  • Teeth grinding (bruxism) and groaning
  • Dehydration
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14
Q

clin path for abomasal ulcers - what test to run? findings?

A
  • Fecal occult blood test
    > Sensitivity 0.77, specificity 0.97 (296 cattle)
  • Abdominocentesis
    > Peritonitis
  • CBC+Biochemistry profile
    > Leukocytosis/neutrophilia
    > Increased fibrinogen
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15
Q

abomasal ulcers treatment

A
  • Dietary changes
    > Hay, ryegrass, nograin
  • Rumen transfaunation
  • Decrease stress
  • Avoid steroid & NSAID use
  • Treat concurrent problems
  • Blood transfusions
  • Antibiotics
  • GI protectants
  • H2 antagonists
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16
Q

abomasal ulcer prevention

A
  • Dietary management
  • Avoid abrupt changes in rations
  • Adequate fiber source
  • Minimize stress
  • Avoid over crowding
17
Q

what is the peritoneum and what is included in it?

A
  • Serous membrane
  • Two layers:
    > subserosa: conective tissue (collagen, fat, reticulum cells, and macrophages)
    > Mesothelial squamous cells (serosa)
  • Lymphatics
  • Stomata (channels between mesothelial cells)
18
Q

function of peritoneal fluid? how much should there be? what is its normal SG, protein, and cell content?

A
  • Lubrication for viceral organs
  • Aprox 1 mL of peritoneal fluid/kg BW
  • Specific density: 1.016
  • Total protein: < 3 g/dL
  • Cells: (<10,000): macrophages, lymphocytes, eosinophils and mesothelial cells
19
Q

etiology of peritonitis

A
  • Visceral rupture
    > Uterine rupture
    > Rectal tear
    > Ruptured bladder
  • Omphalophlebitis
  • Fat necrosis
  • Hematogenous infections
20
Q

Chronic localized peritonitis
- sequel to:

A
  • acute localized peritonitis (TRP)
  • abomasal ulcer perforation
  • post-surgical
  • penetrating wound
21
Q

acute diffuse peritonitis
- sequelae to:
- is it serious?

A
  • Traumatic reticuloperitonitis
  • Abomasal ulceration > perforation
  • Metritis > ruptured uterus
  • Rumenitis > rumen perforation
  • Rectal perforation
  • Ruptured abdominal abscess
  • FATAL condition
22
Q

pathophysiology of peritonitis, systemic consequences

A
  • Contamination/injury > inflammatory cascade (mesothelial cells) > white cells recruitment and humoral factors (opsonins, antibodies, complement)
    <><>
    Systemic consequences:
  • Hypovolemia, hypoproteinemia,
    bacteremia/septisemia, toxemia
  • Fibrin deposition, lymphatic obstruction
23
Q

peritonitis clinical signs

A
  • Non-specific but suggestive of GI dysfunction
  • Severity: mild, recurrent, acute, sudden death
  • Abdominal rigidity, tenderness, distention,
  • Scleral injections, fever, anorexia
  • Rumen atony and intestinal ileus
24
Q

chronic localized peritonitis physical findings
- appetite, milk production, TPR, pain

A
  • Decreased appetite
  • Decreased milk production
  • TPR maybe normal
  • ± Abdominal pain
25
Q

acute diffuse peritonitis physical findings
- feces, abdomen
- how to examine abdomen?

A
  • Feces: scant, constipation
  • Abdomen:distended(ascites)
  • Bilateral, pear-shaped abdomen
  • Abdominal paracentesis
26
Q

acute diffuse peritonitis physical findings
- general signs, vital parameters

A

critically ill
toxemia (severe, profound)
stiff, reluctant to move
Sepsis/shock:
* Temperature: normal to subnormal
* Tachycardia : HR 120 bpm or >
* Pulse: weak, “thready”
* Cold extremities
* Dehydration

27
Q

peritonitis diagnostic plan? for Chronic localized peritonitis?

A
  • History
  • Physical findings
  • Hematology
    > plasma fibrinogen
    > total serum protein
  • Abdominal radiographs
  • Abdominal ultrasound
    <><>
    Chronic localized peritonitis
  • abdominocentesis
    > cytology, TP
28
Q

pertionitis treatment

A
  1. Stabilize the patient
    * IV fluids, correct electrolytes and
    acid-base disorders
    * Plasma or whole blood transfusions
  2. Identify and correct the primary causer
    * Exploratory laparatomy
  3. Treat infection by medical or surgical procedures
    * Antimicrobials, abdominal lavage
29
Q

peritonitis prognosis

A
  • Early and aggressive treatment increase survival rates
  • Long-term sequelae (i.e. adhesions) may compromise a complete recovery
30
Q

Traumatic Reticulo- peritonitis “Hardware disease”
- etiology

A
  • Common disease
  • Accidental swallowing of metal foreign
    objects
  • Penetrate the reticulum > localized or generalized peritonitis
  • Intramural inflammation of rumen- reticulum > interference with chemo- mechanoreceptors
  • Diaphragm, pericardium, heart and liver can be affected
31
Q

Traumatic Reticulo- peritonitis “Hardware disease”
- clinical signs

A
  • Sudden rumino-reticular atony and a sharp fall in milk production
  • Decreased fecal output
  • Rectal temperature is often mildly
    increased
  • Heart rate: normal or slightly increased
  • Respiration: shallow and rapid
    <><>
  • Anterior abdominal pain
  • Kyphosis
  • Reluctant to move downhill
  • Arched back; an anxious expression; a reluctance to move;
  • Uneasy and careful gait
  • Groaning when:
    > forced sudden movements, defecating, urinating, lying down, getting up, and stepping over barriers
32
Q

Traumatic Reticulo- peritonitis “Hardware disease”
- clinical signs in chronic cases

A
  • feed intake and fecal output are
    reduced
  • milk production remains low
  • Signs of cranial abdominal pain become less apparent
  • Some cattle develop chronic vagal indigestion (ventromedial reticulum adhesions)
33
Q

Cows with pleuritis or pericarditis from hardare disease have what clinical signs?

A
  • Depressed, tachycardic (>90bpm) and pyrexic (40°C)
  • Shallow respiration and muffled lung sounds and pleuritic friction rubs
  • Gas and fluid splashing sounds on auscultation > washing machine murmur
  • Jugular vein distention with a pronounced jugular pulse
34
Q

Cows with pleuritis or pericarditis from hardare disease
- sequelae and prognosis?

A

Congestive heart failure
* marked submandibular edema
* brisket edema is a frequent sequela
<><>
* prognosis is grave
* Penetration through the myocardium usually results in extensive hemorrhage into the pericardial sac and sudden death

35
Q

hardware disease diagnostic plan

A
  • History
  • Clinical findings
  • CBC-biochemistry profile
    > Mild leukocytosis with neutrophilia
    > Hyperfibrinogenemia
  • Paracentesis
  • Reticular radiography
  • Ultrasound
    <><>
36
Q

hardware disease low cost diagnostic idea?

A
  • A grunt may be elicited by applying pressure to the xiphoid or by elevating this area firmly and then pinching the withers
  • The grunt can be detected by placing a stethoscope over the trachea and applying pressure or pinching the withers at the end of an inspiration.
  • Tremor of the triceps and abduction of the elbow may be seen
37
Q

hardware disease treatment?

A
  • Antibiotics
  • Magnet
  • Confinement
    <><>
  • Surgical treatment
    > Rumenotomy to approach reticulum

3. Food Animal 2 (20 decks)

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