Forestomachs to rectum Flashcards
1
Q
What do you look at when doing a visual exam on a PE
A
Abdominal contours, stance of the animal
2
Q
What can you appreciate during asculation on a PE
A
Frequency of ruminal contractions
strength, duration, frequency, mixing verses eructation
3
Q
(1)what is noted on the palpation of the left paralumbar fossa and (2) deep palpation of the left abdominal wall
A
(1)Presence and strength of ruminal contractions
(2) Degree of rumen fill; consistency of ruminal contents
(normal = doughy; dehydration = hard, fist indent stays)
4
Q
How it the pain response test performed?
A
Withers depression test (“scootch test”; done where
scapulae come together); roll skin under your hand;
normal response is cow moving away from stimulus -
negative response means they are very painful
because they have pain deep in there abdomen that is
worse than you pulling on skin; negative scootch is
positive for pain in abdomen; they will also have
expiratory grunt
Deep palpation at the xiphoid process of the ventral
abdomen w/knee; can also use bar or board under that spot - if painful, makes an expiratory grunt = positive pain response
- Negative for pain = will kick you in the face
[“cast withers” = uterine prolapsed…not the same !]!
5
Q
What is noted during percussion and auscultation on a PE?
A
Pings, gas-distended viscera (LDA and RDA). Stethoscope on 10th-11th rib and percuss in the paralumbar fossa and down and forward to where the abomasum is. Gas in rumen=Hallow sound (pong), gas in abomasum is high pitched “ping”!
6
Q
What is noted when doing ballottement and auscultation on PE?
A
“Tinkling” of organs with a fluid-gas interface - checking rumen contents or fluid; can check for pregnancy advanced stages on R side, push fist into lower flank and see what material comes back and hits hand (fluid, fetus, rumen contents)
7
Q
Rectal examination can appreciate … on PE
A
Dimensions of abdominal organs; presence of abnormal gas or fluid within or outside viscera; position of palpable organs (aorta, left kidney, sublumbar lymph nodes, iliac artery bifurcation)
8
Q
What is examined when looking at the feces?
A
Quantity, consistency, color (indicative of what they have been eating), odor (pungent if in there for a long period of time), fiber length (large pieces = quick transit time, small pieces = slow transit time or not getting enough fiber)
9
Q
What is the reason behind these abnormalities of the feces?
- blood (red/black)
- Mucus
- Fibrin
- sand/stones
- Undigested feedstuffs
A
Blood (red = bleed in rectum, black = upper GI bleed)
Mucus = obstruction
Fibrin = inflammation/infection (salmonella, BVD)
Sand/Stones=dietary deficiency (fiber)
Undigested feedstuffs?
10
Q
How different is the PE of the right abdomen than the left?
A
It is not. Ballottement, auscultation, percussion, and palpation are used to assess the viscera on the right side as well.
11
Q
What are the two most common clinical signs associated with cattle diseases in general. How do they direct the diagnosis?
A
anorexia and rumenal stasis. diagnosis of digestive diseases must be based on negative findings in other systems.
12
Q
Primary vs. Secondary Indigestion (what causes each)???????
A
Primary: Bloat is the primary condition - Reticulum - Rumen – mixes, grinds to reduce fiber size - Omasum Secondary: Bloat is secondary to another condition - Abomasum - Liver - Pharynx - Severe systemic disease - High fever – mastitis, foot rot
13
Q
The normal physiology of forestomachs (in order)
A
Contraction starts in reticulum (dorsal sac
then ventral sac) –>Takes 1 min for contraction to go all
the way around –>Rumen is like a big fermentation vat
that works best w/small amount of food often –>Mixing of fluid and solid ingesta –>Maceration of fibrous feedstuffs –> Circulation of ruminal fluid – increased
surface contact, increased absorption of VFAs –> Filtering material for the reticulo-omasal orifice and lower GIT –> Removal of gas through eructation –> Regurgitation of fiber for chewing.
14
Q
What are the two cycles in rumination?
A
Primary cycle – mixing
Secondary cycle – eructation
15
Q
Definition and mechanism of bloat
A
Distention of the rumen with gas – esp. upper part of left flank
- *Failure of eructation**
- Normal bovine does not produce gas during fermentation more quickly than it can be eructated
16
Q
Microbial fermentation produces these two types of gas:
A
methane and carbon dioxide
17
Q
What 3 factors does the gas production (in bloat) depend on
A
- Ruminal microbial population
- Ruminal pH
- Substrate that cow eats –cow that eats grain vs. grass (clover/alfalfa produce more gas than
timothy/Bermuda)
18
Q
The role of eructation in bloat
A
Normally gas can be expelled quicker than it can be produced
Bloat is NOT due to excess gas production, bloat is due to failure of the eructation process
19
Q
What are the three causes of bloat?
A
- Failure of cardia to relax
- Obstruction of the esophagus or cardia
- Failure of reticulo-rumenal muscular contraction
20
Q
The normal function of the cardia.
A
When the animal gets ready to burb, the cardia relaxes and lets the gas out.
21
Q
Three ways the cardia can fail to relax
A
- reflex closure when the cardia isn’t cleared of ingesta
- Anatomic distortion – abscess, tumor (commonly lymphosarcoma), lymph node, mass or space
occupying lesion next to cardia changing position - Frothy bloat – gas trapped in foamy bubbles (not enough surfactant in rumen), not in free form,
can’t be eructated (froth physically blocks the cardia)
• Legume pasture bloat – clover, alfalfa, soybean
• Legume hay bloat - try to feed hay before putting out to pasture
• High concentrate bloat – grain and not enough fiber in diet
22
Q
What can cause failure of reticulo-rumenal muscular contractions and what are the symptoms?
A
hypocalcemia (milk fever)
Complete stasis
Abomasal distention*
23
Q
What are the 2 ways to help diagnose bloat?
A
- History – what has the animal been eating
- Physical examination
- General - auscult abdomen - from point of shoulder up to 13th rib and area of rumen
- Passage of stomach tube – determine if obstruction, free gas, frothy bloat
24
Q
True or False: Bloat is never life-threatening
A
False: During diagnosis we need to rule out acute life-threatening forms – cows can bloat quickly and severely
25
Treatment of bloat in an emergency situation
Trocharization
• Risk of peritonitis
• Before removing trochar – install some potassium penicillin, procaine penicillin
• Has to be emergency because you are creating a hole in the rumen and that will cause
some leakage upon removal, which can lead to peritonitis
• Can use trochars on horses - ie cecal trochar
o Can also inject Penicillin into cecum to try and kill off organism producing the gas
26
Treatment of acute bloat (non-emergency) -- 4 therapies
Remove esophageal obstruction
Administer foam destabilizers (for frothy bloat)
• Turpentine
• Gasoline
• Detergent (Tide)
• Therabloat (Poloxalene - DOC) – a surfactant
specifically designed for bloat – number one tx for
acute/frothy bloat!
Release gas via stomach tube
Administer calcium in cases of hypocalcemia
27
Treatment of chronic, free gas bloat
Release gas through stomach tube
| Surgical fistulation
28
Where is chronic free gas bloat usually seen?
common in feedlot cattle d/t pain from respiratory disease
To eructate the animal needs to inspire against a closed thorax…painful respiratory infections can prevent
animals from taking deep inspirations therefore causing them to bloat
29
What is the medullary center's neuronal control of rumen and reticulum contractions?
Motor impulses to the reticulum and rumen are generated when excitatory input exceeds inhibitory input
o Ratio of excitatory to inhibitory input determines:
- Rate / Magnitude / Duration of primary cycle of
contractions
30
What is the splanchnic nerve's imput to the rumen and reticulum contractions? Inhibit or excite?
Inhibitory
31
The Vagus nerve's imput to rumen and reticulum contrations? Inhibit or excite?
Excitatory
32
What nervous issues can cause rumen hypomotility or stasis?
Absence of vagal input from gastric centers,
| Ineffective motor response
33
4 things that can result in decreased motor response (in reference to rumen hypomotility or stasis)
Decreased excitatory input to gastric centers
Increased inhibitory input
Depression of gastric centers
Defective vagal innervation
34
What 2 things can cause depression of gastric centers?
Drugs that depress the CNS
| Endotoxemia
35
Describe the anatomy of the vagus nerves. What are the branches and what do those innervate?
Right and left vagus nerves
• Dorsal and ventral branches of vagus nerves
o Dorsal – to rumen, other stomachs
o Ventral – to reticulum, omasum, lesser curvature
of abomasum
36
Defective vagal innervation can cause what secondary forestomach disease?
Bloat
37
What 3 factors can increase ruminal motility?
Mild distention, tension generated during contraction
Eating, chewing
Increased acidity as abomasum empties
38
What 4 factors can decreased ruminal motility?
Severe ruminal distension
Pain (anywhere in body), but esp. abdominal pain
Abomasal distention (severe)
Increased concentration of undissociated VFAs
associated w/ ruminal acidosis, probably certain toxins
39
These receptors are stimulated by "Mild distension and tension generated during contraction" and are located at the Reticulum, reticuloruminal fold, and cranial ruminal wall
Low threshold tension receptors
40
Buccal receptors in the mouth are stimulated by what?
Eating and chewing
41
These "acid receptors" in the abomasum respond to what stimulus?
Increased acidity as abomasum empties
42
These receptors located in the Reticulum and cranial rumen and respond to severe ruminal distension
High threshold tension receptors
43
These chemical receptors respond to Increased concentration of undissociated VFAs associated w/
ruminal acidosis, probably certain toxins. Where are they located?
The mucosae of the reticulum and rumen
44
receptors in the abomasum that respond to abomasal distension are called...
Tension receptors
45
Two other names for traumatic reticuloperitonitis
traumatic gastritis and hardware disease
46
Etiology of hardware disease
**foreign object penetration of the reticulum resulting in localized or generalized peritonitis**
- Animal has eating nail/wire, fell into reticulum
- As reticulum contracts, nail/wire is pushed through peritoneal cavity leading to peritonitis - can also push into heart - if penetrates heart, animal will drop dead;
if just penetrates pericardium it inoculates that with bacteria --> pericarditis
47
The severity of hardware disease depends on these factors:
- Size, shape and nature of FB
- Location and degree of damage at the puncture site
- Degree of contamination at the time of puncture and subsequent to puncture
48
What are the common sequelae to traumatic reticuloperitonitis?
```
Perforation
Acute local peritonitis
• Recovery
• Chronic local peritonitis
o Vagus indigestion
o Diaphragmatic hernia
• Acute diffuse peritonitis
• Acute pericarditis
```
49
What are some uncommon sequelae to traumatic reticuloperitonitis?
Rupture of left gastroepiploic artery – death
due to internal hemorrhage.
Splenic, hepatic, diaphragmatic, pleural abscesses
Pneumonia
Endocarditis
Arthritis
Nephritis
Rupture of coronary artery or ventricular wall – cardiac tamponade
50
Fibrinous adhesions are an acute process in hardware disease. What do they turn into and how quickly does this occur?
They turn fibrous and this can happen in 10-14 days
51
What are some clinical signs in the acute phase of Hardware disease?
Acute phase – fever, anorexia, depressed, decreased or absent rumen contractions
52
What are some signs seen later in hardware disease?
Cranial abdominal pain (anterior part of abdomen) reluctance to move or lie down, trembling of triceps muscle
Expiratory grunt, arched back stance – stand w/neck stretched out
Often stand with front limbs higher than hind limbs to take weight off chest - elbows abducted from body – stand uphill
Vomiting sometimes observed
Other signs referable to penetration
• Muffled heart sounds
• Distended jugular veins associated with heart
failure
Neutrophilic leukocytosis with a left shift - above 12,000; btw 12,000and 20,000
• Immature WBCs seen in peripheral blood b/c mature WBCs are being used up quickly due to infection – can’t keep up with demands.
53
Other differentials for hardware disease:
- Other causes of peritonitis
- Other causes of heart failure – if distended jugular veins
- Systemic diseases accompanied by pain and/or sepsis
54
What are the conservative treatments suggested for cattle with hardware disease?
- Earliest method of treatment – put cow on inclined plane w/ front limbs higher to take weight off diaphragm, object may fall back into reticulum and heal.
- Conservative medical treatment
- Magnet – FB attracted to magnet, can give
prophylactically to heifers 1.5-2 years - heavy
magnet, drops into reticulum, attracts metal
objects and holds them in place until they erode
away
- Can use compass, stud finder, another magnet or
ULS to see if cow already has a magnet.
- Abx (Can also place cow on incline place to relieve pressure and give Abx to help recovery)
55
True or false: surgery is a treatment for hardware disease.
True
56
How can hardware disease be prevented?
Give magnet to heifers around 16 mo. of age - will attract any metals that animal eats
57
Vagal indigestion is characterized by what?
gross distention of the rumen and sometimes bloat -- food doesn't pass through the rumen into other stomachs
58
T/F: Vagal indigestion is presented acutely
False it is more of a chronic condition
59
What is an old term for vagus indigestion
"Hoflund’s syndrome"
60
By experimentally cutting the vagus nerve what 4 *experimental* conditions can occur?
1. Functional stenosis between the reticulum and the omasum with atony of the rumen and reticulum
2. Functional stenosis between the reticulum and omasum with normal or hyperactive ruminal and reticular motility
3. Permanent functional stenosis of the pylorus with atony or normal activity of the reticulum
4. Incomplete pyloric stenosis
61
What are the two natural conditions that occur with vagal indigestion?
1. Anterior functional stenosis -- omasal transport failure
| 2. Posterior functional stenosis -- failure of abomasum to empty into pylorus
62
Which is more common; anterior or posterior functional stenosis?
Anterior functional stenosis
63
Describe the pathophysiology of an Anterior functional stenosis? Where would associated pathology be found?
Ingesta fails to flow through into the abomasums – distention leads to lack of motility.
(Ruminal hypermotility is more common than hypomotility)
o Reticulo-omasal orifice is wide but food won’t flow through due to lack of motility.
**Associated with pathology of the posterior thorax or anterior abdomen.
64
Which two stomachs does posterior functional stenosis distend with ingesta?
The rumen and abomasum
65
What causes a posterior functional stenosis?
Caused by tumor, fat necrosis – something that obstructs pyloric outflow.
*May also be sequel to disease which affects the blood supply to the muscular wall of the abomasum*
66
Sequestration of what element is common with posterior functional stenosis? How can this be identified and why does it happen?
Sequestration of chloride is a common problem and can be identified by serum determination
o Cow regurges fluid from abomasum back into rumen
67
What are the clinical signs of vagal indigestion?
- Gradual onset, gradual abdominal distention, decreased fecal output
- Typical abdominal appearance – rumen greatly distended in ventral sac (so that rumen takes
entire left side and lower half of right - can feel this upon palpation)
- LN get enlarged due to inflammation of this part of abdomen
- Hypochloremia – *differentiate anterior from posterior* - nothing wrong on CBC; normal Cl in a cow 99-110; if Cl is sequestered in stomach/digestive tract, end up with failure of Cl absorption and a drop in Cl in blood, can get as low as 55-60 - lower it gets, the worse the prognosis
- <99 = alkalotic
o if can’t differ - will have to do surgery on L side to differ from rumen or reticulum
o Auscultation reveals bradycardia and A fib.
68
Which clinical signs are a good indications that a case of vagal indigestion might need surgery?
Enlarged ventral abdomen and enlarged LN are a good indication that surgery is needed
69
Differential diagnoses for Vagal indigestion
- True intraluminal intestinal obstruction: Plant material (Phyto-bezoar), Blood clot – BVD or clostridial disease, Twine
- Diaphragmatic herniation
- Advanced pregnancy or hydrops of the uterus – uterus fills up whole abdominal cavity and
blocks flow of ingesta out of the abomasum into the rest of the GIT
70
Therapy for vagal indigestion
Surgery –L side approach usually exploratory laparo-rumenotomy or other specific corrective procedure
o Overall recovery rate is about 30% for vagal indigestion type problems
71
T/F: Motor dysfunction can cause fermentation issue, but fermentation issues cannot cause motor dysfunction.
False: Fermentation disorders can cause motor dysfunction
72
What can motility disturbances be attributed to?
Motility disturbances may result in decreased microbial activity but are primarily attributable to
changes in ruminal fluid or from feed changes; they result from lesions that disrupt neuromuscular
impulses
73
How do primary fermentation issues occur?
Arise from food abnormalities – change of food in any kind of way
o Ration adjustments are part of the solution
74
What are the properties of normal rumen fluid?
Properties:
- Olive, brownish-green - varies slightly based on what animal is eating
- Slightly viscous – due to saliva
- Aromatic, strong odor
- pH - remember that it is usually slightly acidic (normal pH = 5.5-7)
- Roughage diet – 6.0 to 7.0
- Grain diet – 5.5 to 6.5 (more acidic)
- Multiple forms of protozoa, all of which are active
- Chloride concentration < 30 mEq/liter – tells you about obstruction
75
The animal control factors that influence normal rumen fluid
Salivation
Mixing and rumination
Ingesta outflow - blocked makes more alkaline (?)
Eructation
76
The diet control factors that influence normal rumen fluid
```
Quality
Quantity
Rate of delivery
Balance of elements
Solubility
Particle size
Toxic substances
```
77
The microbes that contribute to normal rumen fluid
Bacteria – mostly anaerobes
Protozoa
• Role unclear – fermentation can proceed without them
• Can reflect changes within the environment of the rumen
• Healthy animal = happy protozoa
78
Feed characteristics that influence fermentation
- Excess or deficiencies of feed substrates produce an imbalance in the composition of the microbial population
- Abnormalities in fermentation can ensue when potentially acceptable feeds are introduced too abruptly, or when cattle are fed feeds with excesses or deficiencies in specific nutrients for too long a period of time
- An overgrowth of ruminal microbes that degrade excessive amounts of some dietary constituents can lead to the production of fermentation end products that impair ruminal function
- An insufficient supply of nutrients reduces microbial activities, and in an extreme cases, reduces the digestibility of feedstuffs
79
The inactivity of rumen microbes results in...
Results in deficiency of nutrients required for active microbial growth
80
The most common cause of rumen microbe inactivity
Most common cause is anorexia – secondary to another problem
81
The best approach to treating rumen microbe inactivity
Responds well to treatment of primary disease – adjunctive therapy speeds recovery
82
Examples of rumen microbe inactivity
Examples of this type of problem include “hay belly” and rumen impaction
83
What is the most common type of indigestion in cattle
simple indigestion
84
Cause of simple indigestion
Sequel to an abrupt change in the animal’s diet - a different quantity or quality of grass
85
Simple indigestion: the extent of the disease
Usually mild and self-limiting - can deal with it; will not make them really sick
86
What is the strength of rumen motor activity in simple indigestion
Ruminal motor activity is reduced but not absent
87
Treatment for simple indigestion
Treat with mild laxative (like a Pepto bismol - has Mg hydroxide) and rumen stimulant – cow will get
better despite what you do
88
What is the most severe form of fermentative indigestion? - the one we have to worry about!
Acute ruminal acidosis
89
What is the pathophysiology causing acute ruminal acidosis?
rapid intra-luminal fermentation associated with excess amounts of carbohydrate, lack of acclimation to the substrate
90
When acute ruminal acidosis occurs in beef vs dairy cattle
Feeder cattle
- Starting cattle on feed
- Sudden change in ratio – usually roughage to grain
- Sudden increases in feed amounts
- Weather changes – snow precludes cow from eating
for a day or two, then cow gorges itself
Dairy cattle
- Sudden increase in grain feeding – lactating dairy cattle placed on higher nutrition plane
- Sudden alterations of the ratio
91
10 steps in the pathophysiology of acute rumen acidosis (memorize!!!!)
1. Rapid decrease in ruminal pH - maybe even below 5
2. Decline in rumen protozoa
3. Increase in gram positive organisms – strep and lactobacillus (They like acidic environments, grow more rapidly and produce more lactic acid)
4. pH decreases more and fluid is drawn from intravascular space into rumen
5. Increase rumen lactic acid
6. Rumen osmotic pressure increased leading to hypovolemia (lactic acid draws water into the rumen from vascular space; water comes from vascular space so animal gets dehydrated, maybe even hypovolemic – sludging of the blood)
7. As pH goes below 5, strep dies off and lactobacillus increases
8. Chemical irritation of the rumen occurs – rumenitis, possible fungal growth
9. Histamines increase, endotoxins increase
- Due to tissue damage
- Go to liver – liver tried to filter it out
- If liver gets overwhelmed by endotoxin –
endotoxemia (can’t filter out endotoxin)
10. Diarrhea develops, systemic effects are severe (development of laminitis, etc.) if they survive
92
What are the two organisms that proliferate in acute rumen acidosis?
Strep and Lactobacillus (gram positive organisms)
93
Which organism in acute rumen acidosis can survive pH below 5?
Lactobacillus
94
Clinical signs of acute rumen acidosis
```
o Complete anorexia
o Marked depression – sternal recumbency
o Rumen atony
o Dehydration
o Abdominal distention – rumen distention due to fluid being drawn in - can’t breathe because there is too much pressure on thorax
o Diarrhea
o Coma
```
95
What is the quick diagnosis of acute rumen acidosis based off?
The history of eating too much
96
If the animal survives the episode of acute rumen acidosis, what are the lasting consequences?
- Mycotic rumenitis – normal flora but will overgrow with acidic pH
- Liver abscessation
- Polioencephalomalacia – rumen microflora disturbed, don’t produce thiamine (bacteria that produce thiamine get killed off)
- Laminitis – right away or can take about 6 month
97
T/F: The animal will show signs of diarrhea before death
False: Death may be sudden with or with out the animal showing signs of diarrhea
98
T/F: Prevention is Key to controlling acute rumen acidosis
True!!!!!!!
99
How do you diagnose acute rumen acidosis?
o History – occurs 12-18 hours after diet change
o Physical findings
o Very low rumen pH
o Hemoconcentration, low blood pH
o Increased blood lactates and pyruvates – not done in field, only hospital setting (done more often with horses than cows)
100
The 3 general aspects of treating acute rumen acidosis
1. Control of the rumen acid
2. Control of dehydration
3. Symptomatic treatment
101
What are 4 methods of controlling the rumen acid as a treatment for acute rumen acidosis?
- Alkalinizing agents – oral bicarb, magnesium
carbonate (Na bicarb)
• Can be added to the rumen but if the rumen is
already very distended it will just make the
animal more uncomfortable (give it IV in those
situations)
- Abx – oral penicillin " kill of strep and lactobacillus
• Systemic Abx " to prevent abscesses in the liver
• Procaine Penicillin works well for this
- Rumen lavage (if acute) – pass large stomach tube
and pump water into rumen, risky
• Very stressful, don’t want to kill the animal with
the treatment!
- Rumenostomy - can remove food
102
When giving fluids for treatment of acute rumen acidosis what is the route and why, and what type of fluids should be given?
Give Fluids IV not oral! Oral will distend the rumen further and restrict breathing. LRS or Na bicarb
103
What symptomatic therapy can be given for the treatment of acute rumen acidosis?
- Antihistamines
- Abx – systemically to counteract liver abscessation
and infection - don’t have to be worried about creating
endotoxemia from killing off the bacteria
• Procaine pen
- Anti-inflammatory drugs – flunixin to counteract
endotoxin
- Thiamine for polioencephalomalacia or as preventative
• Give asap
- Rumen transfaunation
• As cow is getting better, collect normal rumen
flora from normal cow and give it to the sick
cow
• Inoculate rumen with normal, good microflora
104
How can acute rumen acidosis be prevented?
Especially important for feedlots
o Ration adaptation – gradual change!!!!!!!!!!!!
o More difficult in dairy cattle because must feed them
or will breakdown fat and muscle to make more milk
o Feed additives such as sodium bicarb, ionophores, probiotics
- For dairy cows, help control and regulate feed intake and digestive process - help control rumen acidosis problems
105
Chronic rumen acidosis is also called what?
sub-acute rumen acidosis (SARA)
106
How does SARA develop?
o Results from feeding high proportions of (finely ground) concentrates at the expense of appropriate quantities of long stemmed or adequate particle size roughages
o High concentrate and low fiber " atrophy of ruminal epithelium, gradual decrease in pH
107
How does SARA differ in time frame from Acute rumen acidosis?
The condition develops over a longer period of time
o Mainly dairy cows b/c occurs over a long period
of time and feeder cattle are usually slaughtered
before then
Insidious onset of symptoms - happens over a much longer period of time so don’t notice signs at first
108
What other (3) conditions are associated with SARA?
o Low milk butterfat test
o Chronic laminitis – SARA is basis of many hoof
diseases in dairy cows
o Chronic indigestion
109
How do you treat SARA (diet wise)?
Alter the ration to include more fiber and roughage with adequate particle size and buffer the ration with sodium bicarb
o Longer fiber length promotes chewing " saliva "
bicarb buffers the rumen
o Stimulates rumen papilla
110
Magnesium hydroxide and magnesium carbonate change the pH in what way?
They are alkalizing agents (oral)
111
vinegar and acetic acid change the pH how?
acidifying agents
112
For treatment of general fermentation indigestion what 2 elements are important to correct through parenteral supplementation?
abnormal calcium and potassium
113
How often should transfaunation be performed in the case of fermentive indigestion?
Perform transfaunation daily until the animal’s appetite, defecation and ruminal motility return to normal
114
How are inspissations/impactions of the ventral ruminal contents resolved when treating fermentive indigestion?
Resolve inspissations/impaction of ventral ruminal contents by administering mineral oil and kneading
the left flank
115
"Over eating disease" is the lay term for this disease. What does the disease do?
Enterotoxemia. Acute infectious but non-contagious disease characterized by sudden death in feedlot cattle
116
The disease causing agent for Enterotoxemia
Clostridum perfringens type A,C, or D
117
GI hemorrhage in adult cattle is associated with what type of Clostridium perfringens? This type is also not included in the typical clostridial vaccine.
Type A (Aspergillus????)
- Acute onset, painful abdomen with hemorrhage - may even see blood clots in the rectum
- Must get this vaccine seperately.
118
What are the risk factors for Clostridium perfringens type A
o High production – early lactation = DAIRY COWS
o < 100 days in milk
o Aggressive eating
o Second lactation or greater cows
o Recent feed changes
o Feeding TMR and selection for smaller particle size or decreased long stemmed fiber
o Rumen acidosis
o Excessive rumen fill with spillover into the intestines of contents with high soluble protein and carbohydrate levels
o Feeding corn silage ensiled < 1 week
o Decreased intestinal motility
119
The clinical signs for Clostridium perfringens type A
```
o Acute onset
o Anorexia
o No milk
o Painful and distended abdomen
o Intestinal hemorrhage
```
120
What is the prognosis for C. perfringens type A?
guarded to poor
121
What type of Clostridium perfringens is related to hemorrhagic enteritis in Calves?
Type C. Necrotic enteritis in newborn calves – can die very quickly (peracute) - right after born or within first few weeks of life
122
T/F: Diarrhea may not even develop in calves with Clostridium perfringes type C before they die.
True :( Die very quickly, even 10-20min; usually diagnosed at necropsy
123
What management practice does C. perfringens type C seem to be attributed to?
management of feeding animals
124
The risk factors involved with C. perfringens type C
o Ingestion of organism with colostrum
o Ingestion of protein rich diet in a protease-deficient intestinal tract may
allow rapid growth of the organism
o Inconsistent feeding practices
o Limited access to water after feed consumption
o Abnormal intestinal flora from abundant oral medication
o Stressful interventions that result in erratic intake
125
What type of Clostridium perfringens produces mucoid and catarrhal enteritis in FEEDLOT cattle?
Type D.
126
The clinical signs associated with C. perfringens type D
* mucoid and catarrhal enteritis
* Convulsions
* Paralysis of posterior limbs
* Colic signs
127
T/F: C. perfringens type D is in the clostridial vaccination as morbidity and mortality are low.
False: Type D is usually included in the vaccine. While Morbidity is around 5-10%, mortality is near 100%
128
What is the diagnosis of Clostridium perfringens (Enterotoxemia) based on?
o History
o Clinical signs
o Lesions
o Laboratory samples
129
What laboratory samples should be submitted to the lab if enterotoxemia is suspected?
- Intestinal contents
- Blood clots
- Intestinal lining placed in formalin
- Liver
- Blood or serum
- Feces
130
What methods can be used to prevent enterotoxemia?
- Management to gradually get cattle on feed
- Avoid overfilling on concentrates
- Rumen buffers
- Abx in feed
- Vaccination available for types A, C and D
131
What are some key factors for prevention of enterotoxemia?
Maintain healthy flora, Limit oral medication, Properly fermented feeds, Limit bacteria in colostrum, Feed one colostrum meal, Consistent feeding practices, Adaptation before change, Appropriate fiber length, storage and fermentation of TMR, Avoid rumen acidosis, Manage intensive MR feeding carefully, Water availability for calves, Vaccination, Control other GI infections
132
What 6 diseases can be passed through colostrum?
* Johne’s
* Salmonella
* BVD
* BLV
* Mycoplasma
* Infectious mastitis – strep agalactiae, staph aureus
133
Potential causes of peritonitis
DDx includes many common bovine diseases
o Foreign body penetration of stomach
o Perforations of the reproductive tract: Common due to bad AI technique or tearing during parturition
o Ulcers – abomasum, SI, occasionally colon
o Umbilical infections - can be associated with persistent urachus (Brahman cattle)
o Complications of surgery or other procedures such as intraperitoneal injections or trocharization of the rumen
- IP injections are used b/c they are less stressful for beef cows
- May accidentally hit duodenum if in right paralumbar fossa
- Don’t go on left due to rumen
134
Clinical signs associated with peritonitis
o Related to the extent of sepsis
o Arched back – pain; “roached back”
o Bruxism – also called odontopreces; “teeth grinding”
o Expiratory grunt
o Shock, fever, pain – very acute
o Bloated appearance and/or “pings” related to GI stasis
o Rectal examination may reveal adhesions or “stovepipe rectum”
135
What is stove-pipe rectum and what disease is it associated with?
Chronic peritonitis:
Chronic peritonitis may form adhesions, feel crepitation on palpation
• Fibrinous adhesions = new event, last up to 2 weeks
• Fibrous adhesions = older, firm and won’t break down with rectal exam
Rectum can be dilated and full of air – stovepipe rectum
Don’t know what caused it, but it’s chronic
136
3 ways to diagnose peritonitis
o Clinical signs
o Clinical pathology – elevated WBC Count - >12000
o Exploratory laparotomy – very think fluid
137
Treatment is:
symptomatic
138
What is the definition of Left displaced abomasum (LDA)?
• Definition – abomasums found in the left lateral aspect of the abdominal cavity trapped between the
rumen and the body wall in ventral aspect
139
LDA is a ____ disease. What does this mean?
• Considered a production disease. It is caused by pushing cows past their limits in production.
o Other production diseases---laminitis and chronic rumenitis
140
What are the 5 components of LDA's multifactoral etiology?
- Genetic factors
- Physical factors
- stress
- nutrition
- atony of the abomasum
141
What genetic factors contribute to LDA?
No breed predisposition – certain lines within a breed are at greater risk
Animals with larger, deeper, abdominal cavities are at greater risk
142
What physical factors contribute to LDA?
- Displacement of the stomachs during pregnancy by the gravid uterus – twins
- Lack of exercise may contribute to accumulation of gas
- Physical positioning – reclining on right side
143
How is atony of the abomasum an etiology for LDA?
- Secondary to another disease such as ketosis, milk fever, metritis, retained fetal membranes
- Secondary to diet containing or predisposing to large amounts of VFAs, too much concentrate, not enough effective fiber
- Increase concentration to forage ratio in the post-partum period.
144
T/F: increased particle size of the diet can contribute to LDA?
False: decrease particle size can cause LDA
145
What is the occurence/presentation of LDA?
| - production style, gender, point in production cycle, age, time of year
o Primarily in dairy cattle – females - very rare to see in beef, whether male or female
o May occur pre-partum – but usually diagnosed within 6 weeks post-partum; lactating cows
o Cows 4-6 years old most commonly affected - mature cow - not a lot of cows reach this age
anymore
o See more displacements in Feb-May - as cows fed throughout winter, they gradually become
more alkalotic, and this has something to do with increased risk of DA
146
What is an acceptable incidence of LDA in a herd?
Expect about 3-5% incidence per year in productive, well managed herds
147
T/F: LDA is often preceded by or found concurrently with another disease
True
148
Clinical signs associated with LDA
o No fever unless accompanied by a septic process
o !!!***Selective appetite for roughages instead of grain***!!!, otherwise off feed with decreased milk production - will not eat grain!
o Auscultation in the left flank area reveals typical tinkling sound of gas trapped within a hollow
viscus - characteristic ping - sounds like flicking a basketball
o Mild, hypochloremic metabolic alkalosis. This usually spontaneously corrects when you correct the LDA/RDA
149
Ddx for enlarged abomasum being prominant against the left flank
When pregnant, the uterus fills up the whole caudal part of the abdomen, lifting rumen up off body floor - grows in omental sac so it stretches the omentum and it pushes the abomasum out
of place
150
T/F: Cattle stop eating when they have LDA
False: They have a selective appetite for roughages instead of grain***!!!, otherwise off feed with decreased milk production - will not eat grain!
151
Diagnosis of LDA is based on these:
o History
o Clinical signs - swollen, distended abdomen; diarrhea
o Selective appetite - Will eat grass and hay but will NOT eat grain
o Physical exam findings - MOST cases can be diagnosed by auscultation
*BODY TEMPERATURE IS NORMAL
152
What are the conservative treatments for LDA?
o Rolling the cow: Put cow down on right side --> Roll cow into dorsal recumbency --> Continue to roll cow over onto the left side and let her stand when ready
• Theory: Gas rises and fluid and solid viscera falls
o Fill the rumen with warm water after intubation
o Give smooth muscle stimulants
o Conservative vs. surgery - has to do with cost
153
What is the surgical treatment for LDA?
Any of several surgical procedures - to fix the abomasum into position; all ways have about the same percentage of success
o Total cost (including lost milk): $300-500
154
What is the prognosis of a cow with LDA?
Usually very good unless it is complicated
155
What are some measures to prevent LDA
Cows that *eat more grass* are less likely to have DA because their diet has more fiber - so cows that get DA are usually production animals " “production disease”
• *Lots of fiber (coarse roughage)* - have to chew, swallow, regurg, chew again - stimulates saliva - saliva helps buffer rumen with the bicarb it contains - rougher chop is better for digestion; fine ground/fine chopped - done to enable more to be put together, it is palatable and high energy, but particles are so small that they don’t stimulate the rumen
• Obesity may be a contributing factor - *monitor BCS*
• Want most cows to calve August to November
o Higher demand for milk in fall b/c school
o Make milk base in December
156
Which has a better prognosis, LDA or RDA?
LDA. A right displacement or twist is considered an emergency because it involves occlusion of vessels that can lead to infarcts
157
What is the gender presentation for RDA?
It can happen to males and females
158
What organs are involved in a RDA and what is the position?
Usually involves a degree of volvulus of the abomasums – omasum and/or reticulum may also be
affected
159
How does a metabolic alkalosis during a RDA?
Chlorine can sequester in the abomasum leading to hypochloremia which leads to metabolic alkalosis
160
What might the presentation of a RDA be in contrast to a LDA?
Often characterized by a sudden onset of clinical signs – more severe effect upon the animal
Metabolic effects are more severe – no passage of feces, look obviously sicker than LDA
161
What in the diet can predispose to an RDA?
Affects all cattle, esp. those on high concentrate, low fiber rations
162
What two factors can indicate a poorer prognosis?
Prognosis deteriorates if more than one part of the stomach is affected
Anion gap greater than 30 mEq/L associated with a poor prognosis
163
RDA presents with what body temperature?
NORMAL
164
What nerve block would you do for an RDA? What does it block and how can you tell it's working?
Do a paravertebral nerve block
o Blocks paravertebral fossa
o Can tell where it’s blocked b/c will be warmer due to vasodilation
165
Treatment for an RDA?
• Treatment is usually surgical
o Centesis of gas from the abomasums may allow it to untwist – emergency therapy only, not a long-term fix
o Be careful not to rupture – very thin wall
166
Etiology of abomasal ulcers (possible factors)
Etiology:
o Hyperacidity and stress may be factors
o Physiologic factors that protest the mucosal epithelium may be damaged
o Diet may be a factor
o High rate of occurrence in veal calves but apparently without affecting growth or causing signs of disease
167
What are the two types of abomasal ulcers?
- large bleeding ulcers
| - small diffusely located in the abomasum
168
What clinical signs would be seen with Large bleeding abomasal ulcers? What GI disease may lead to this?
Large bleeding ulcers
- May be sequel to GI disease such as BVD or LSA
- Associated with the clinical sign of melena
- Occurs in Veal calves too
169
What clinical signs would be seen with small erosional abomasal ulcers? What can lead to these?
Often sequel to systemic disease or stress
| May not bleed, but are sometimes associated with perforation and resulting peritonitis
170
What are two sequelae of abomasal ulcers?
o Anemia and poor thrift result from bleeding ulcers
o Peritonitis results from perforating ulcers
- May result in diffuse peritonitis with rapid
deterioration of the situation
- May result in bursitis of the omental bursa
- May result in localized peritonitis and adhesions
between the abomasums and other structures and
a functional disturbance
171
How do you diagnose abomasal ulcers?
o Clinical signs - often not many clinical signs, unless associated with lymphosarcoma - therefore generally not seen because hard to diagnose
o Exploratory surgery
o Not easy to Dx!
172
Therapy for abomasal ulcers
Symptomatic treatment (same meds as people therefore it is expensive because the doses are so large)
o R/O neoplasia with bleeding ulcers
o Abx, protectants
o Do not use anti-prostaglandin drugs - NSAID
o Cimetidine and other drugs may be too expensive
and dosages aren’t established
173
What is the etiology of abomasal impactions in cattle (general)
sand or foreign bodies, such as twine (eat sand when craving fiber)
174
Etiology of abomasal impactions specific to calves
hair balls (from grooming), blockage of pylorus (hair acts like a valve at pylorus)
175
Etiology of abomasal impactions specific to beef cattle
ingestion of poor quality roughages in large amounts
176
Clinical signs of abomasal impactions
o Slowly developing rumen and abomasal enlargement; bilateral swelling
o Varying degrees of motility disturbances
o Decreased fecal output
177
Treatment for abomasal impaction
o Laxatives
o Surgery
o Results often disappointing, salvage may be best
option :(
178
What are some things that can cause intestinal obstructions?
o Many problems related to ileus
o Intussusception
o Developmental anomalies – atresia coli
o + others
179
Clinical signs associated with intestinal obstructions.
o Colic may be the earliest sign, but may be missed; related to pain -- Have to be there when it happens b/c go through this stage very quickly.
o Peculiar stretching stance often referred to as a trestle-table stance – take weight off abomasum
o Reduced fecal output; often only a mucus plug
o Motility and rumination suppressed or absent as a result of pain
o Heart rate may increase as the disease progresses with dehydration and shock
o Body temp may fall below normal –> hypothermia
o Progressive depression (then death)
o Disease may not be rapidly fatal as in horses but
rather will linger for days or weeks
o Hypochloremia may be severe – very poor prognosis
if the level falls below 60 - Cl gets sequestered and
does not get into the system
180
How is a diagnosis of intestinal obstruction made?
```
o Clinical signs
o Auscultation and percussion of the abdomen
o Appearance/shape of the abdomen
o Rectal exam findings -
o Exploratory surgery
```
181
Ddx for intestinal obstructions with colic
```
Photosensitivity
Acute enteritis
Pyelonephritis
Urethral calculus
Intestinal tympany
??Neoplasia, Hydrops of the uterus, Rectal perforation and peritonitis??
```
182
Ddx for intestinal obstructions with reduced fecal output
Rumen impaction
Abomasal volvulus
Vagus indigestion
Fat necrosis
183
Ddx for intestinal obstructions with postural abnormalities (stand with front feet forward and hind feet further behind - front feet far apart and hind feet close together)
Laminitis – can usually differentiate by
examining feet for heat and pain
Uterine torsion
Fracture of the phalanx
184
Treatment for intestinal obstructions
o Therapy for ileus
o Surgical correction
o Restoration of fluid, acid-base and electrolyte
balance
185
Common examples of intestinal illeus
o Cecal dilatation/volvulus - cecum usually not felt, unless distended with gas, fluid - if distended and
torsed, usually need sx - like lab, perform typhlotomy to reduce tension; if recurrent, can perform typhlectomy
o Fat necrosis - feel irregular shapes of solidified necrotic fat - can be confused with caruncles/cotyledons
in uterus
- Causes: Fescue and ???????
- No fever, anorexic, can’t do a rectal, no passage of
feces
- BAD prognosis
o Intestinal volvulus - distended loops of bowel and no feces
o FBs
o Intussusception - tx usually involves resection and anastomosis, especially if long standing with inflammation and/or necrosis
o Umbilicus – urachus (Brahma breads), umbilical vein, 2 umbilical arteries - if feel thickened cord in that area, think it would be persistent urachus, running from urinary bladder to umbilicus; this can warp around loops of bowel and cause pain and colic - seen more in Brahman, or Brahman cross (Beefmaster, Santa Gertrudis)
186
Etiologies of rectal prolapse
o *Iatrogenic* Seen in sheep when tail is docked too
close to anus
o Usually a sequela to tenesmus - it is an expression of
another problem
o May accompany a wide variety of problems (Diarrhea, constipation, rectal irritation from any cause, Dystocia, urethral obstruction, chronic coughing)
o Elevated intraabdominal pressure from a number of causes
o Toxicities (Lead, Zinc, Estrogen)
187
Which toxicities can cause rectal prolapse?
Lead, Zinc, Estrogen
188
What are 3 stages of rectal prolapse?
o1. Rectal mucosa and submucosa tissue protrude through the anus
o2. Complete prolapse with eversion of part or all of the ampulla recti through the anus
o3. Complete prolapse with intussusception of the rectum through the anus
189
Treatment of rectal prolapse
o Recognize cause
o Treat edema
- Sugar to draw out fluid/edema
- Purse string suture - to prevent recurrence
o In early cases with little damage, the prolapse can be replaced after cleansing
- May need retention suture
- Epidural analgesia may be required
o With cases of trauma, amputation may be necessary
