Abomasal ulcers Flashcards
(37 cards)
1
Q
primary and secondary causes of abomasal ulcers?
A
Primary: Cause is unknown
Secondary:
* Lymphoma
* BVDV
* Rinderpest
* MCF
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
3
Q
pathogenesis of abomasal ulceration
A
- The exact cause of abomasal ulcers is still obscure and may be multifactorial.
4
Q
abomasal ulcer types
A
- nonperforating
- nonperforating with severe blood loss (bleeding)
- perforating with local peritonitis
- perforating with diffuse peritonitis
5
Q
issues associated with Type 1: non perforating ulcer
A
- Minimal: hemorrhage, focal abomasal
thickening, or serositis - Cause of chronic gastritis
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
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
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)
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
10
Q
what other diseases are abomasal ulcers assocaited with?
A
- Lymphosarcoma in older animals
- Concurrent diseases: metritis, mastitis, ketosis
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 (?)
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
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
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
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
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)
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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
acute diffuse peritonitis physical findings
- feces, abdomen
- how to examine abdomen?
* Feces: scant, constipation
* Abdomen:distended(ascites)
* Bilateral, pear-shaped abdomen
* Abdominal paracentesis
26
acute diffuse peritonitis physical findings
- general signs, vital parameters
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
peritonitis diagnostic plan? for Chronic localized peritonitis?
* History
* Physical findings
* Hematology
> plasma fibrinogen
> total serum protein
* Abdominal radiographs
* Abdominal ultrasound
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Chronic localized peritonitis
- abdominocentesis
> cytology, TP
28
pertionitis treatment
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
peritonitis prognosis
* Early and aggressive treatment increase survival rates
* Long-term sequelae (i.e. adhesions) may compromise a complete recovery
30
Traumatic Reticulo- peritonitis “Hardware disease”
- etiology
* 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
Traumatic Reticulo- peritonitis “Hardware disease”
- clinical signs
* 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
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* 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
Traumatic Reticulo- peritonitis “Hardware disease”
- clinical signs in chronic cases
* 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
Cows with pleuritis or pericarditis from hardare disease have what clinical signs?
* 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
Cows with pleuritis or pericarditis from hardare disease
- sequelae and prognosis?
Congestive heart failure
* marked submandibular edema
* brisket edema is a frequent sequela
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* prognosis is grave
* Penetration through the myocardium usually results in extensive hemorrhage into the pericardial sac and sudden death
35
hardware disease diagnostic plan
* History
* Clinical findings
* CBC-biochemistry profile
> Mild leukocytosis with neutrophilia
> Hyperfibrinogenemia
* Paracentesis
* Reticular radiography
* Ultrasound
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36
hardware disease low cost diagnostic idea?
* 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
hardware disease treatment?
* Antibiotics
* Magnet
* Confinement
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* Surgical treatment
> Rumenotomy to approach reticulum
