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916 Cards in this Set

  • Front
  • Back
Age range of a "neonate"
birth to 1 month of age
name for a male foal
name for a female foal
Age range of a "foal"
>1 month to weaning (still at mom's side)
at what age should a foal be weaned?
4-6 months (if less than 4 months, must prepare the GI tract)
Age range of a "weanling"

problem with weaning
>4-6 months (up to 12 months)

can be very traumatic --> respiratory infections (think of nursery school)
Age range of a "yearling"
12-18 months (hips may be higher than withers bc still growing)
Age range of a "long yearling"
18-24 months
Age that a horse is considered "adult"
2 years
Name for a castrated male horse
Most common reason to spay a female horse
granulosa cell tumor (not done routinely)
List of the some "Light horse" breeds
american quarterhorse
american painhorse
List of some "Draft horse" breeds
Light horse:
1. height
2. weight
3. temperament
4. what they're built for
1. >15 hands tall (4" to a hand)
2. < 1500lbs
3. hot-blooded/temperamental
4. fast/athletic
Problem with thoroughbred breeded
only natural breeding recognized (no AI)
what are thoroughbreds bred for?
endurance racing
Breed disease predispositions: Thoroughbreds

--which 2 are genetic
-Recurrent Exertional Rhabdomyolysis (Tying up) - genetic
-Exercise induced pulmonary hemorrhage ("bleeders") - genetic
-gastric ulcers
-osteochondrosis dessicans (when pushed to grow too fast)
Body characteristics of Arabians
dished head
large eyes
arches neck
Breed disease predispositions: Arabians
-SCID (severe combined immunodeficiency)
-Cerebellar abiotrophy (born normal)
-idiopathic epilepsy
What are American Quarterhorses bred for?
short races
Breed disease predispositions: American Quarterhorse
-HYPP (hyperkalemia periodic paralysis)
-PSSM (polysaccharide storeage myopathy)
-HERDA (Hereditary equine regional dermal asthenia - skin slips/falls off)
what are Standardbred horses primarily bred for?
harness racing
facial features of standardbred horses
Roman nose
longer head
Breed disease predispositions: Standardbred
-musculoskeletal racing injuries
-granulomatous enteritis
What is unique about the saddlebred horses?
Five-gaited (high stepping)
Breed disease predispositions: Saddlebred
inguinal hernia (Tennessee Walker)
What is "soring"?
painful stimulation (ex tacks, pins) on the feet of saddlebred horses to train the high-stepping gait for show - illegal!
Color patterns of the American Painthorse
-Overo - dark on front and over the top, color over at lest 2 or 3 limbs
-Tobiano - white on the back
Why so American Painthorses have a breed disease predisposition similar to american quarterhorses?
bc they are quarterhorses, they just happened to throw this paint color, so they can be reqistered as both
Breed disease predispositions: American painthorse
-Consistent with American quarterhorse:HYPP, PSSM, HERDA
-Ileocolic agangliosis: lethal white foal (no neurologic function to the GI - myenteric plexus missing)
Name the five distinctive characteristics of the appaloosa

-how many of these characteristics does each horse have?
coat pattern (spotted, though may be a solid color)
mottled skin
white sclera
striped hooves
thin mane/tail

-at least 3/5 of these characteristics
Breed disease predispositions: Appaloosa
-*Equine Recurrent Uveitis (moon blindness)
-SCC (along mottled areas - eyes, ear, nose)
Draft Breeds:
1. height
2. weight
3. temperament
4. what are they bred for?
1. >17 hands tall
2. >1500lbs
3. cold-blooded/docile/stoic (won't show colic signs until it's really bad)
4. military --> farming --> competitions (pulling/plowing competitions)
Which draft breed is the largest?
Belgian drafthorse
What does a belgian draft horse look like?
chestnut colors with white mane and variations of white face and leg markings
Breed disease predispositions: Belgian drafthorse
-JEB (Junctional epidermolysis bullosa ) aka foal disease (dz of mucocutaneous jncts - skin sloughing, no tx - euthanize)
What feature (besides height) is distinctive about the Clydesdale
"Feathers" - large amount of hair on the fetlock
what colors could a Percheron draft horse be?
grey or black
How do you measure American miniature Horses?

what is the average height?
in inches (NOT hands!!)

<34-38 inches
Breed disease predispositions: American Miniature horses
fecalith!! (will eat anything)
-dental problems
Friesans fall under which category of horse?
"other" - lighter than draft breeds, breeders don't like them know as "drafts"
Breed disease predispositions: Friesan
-esophageal disorders - megaesophagus, esophageal hypertrophy
-neonatal dysphagia
what are warmblooded horses bred for?
sport (dressing, show jumping)
Name some warmblooded horse breeds
At what age do warmblooded horses reach their peak competition age?
around 8-15 years old
Horse coloring: Palomino
cream colored w/white mane and vail
Horse coloring: Bay
brown with black mane and tail
may have some black points
Horse coloring: Chestnut
aka Sorrel
reddish brown with mane just slightly darker than body
Horse coloring: two variations of Chestnut/Sorrel
-Chestnut w/flaxen (blonde) mane and tail
-liver chestnut (a little less orangy)
Horse coloring: Dun
zebra striping along legs (w/dorsal stripe)
Horse coloring: Buckskin
similar to Palominos and Duns but always has a black mane and tail (unlike Palominos) w/NO dorsal stripe (unlike Duns)
Horse coloring: how do you differentiate between white and grey?
white: pink skin
grey: grey or black skin
Horse coloring: name the 5 head patterns and describe them
1. Star - white starshaped pattern between the eyes
2. Snip - short vertical white line between the nostrils
3. Blaze - vertical white line from between the eyes to between the nostrils
4. Bald face - a blaze extending out towards the eyes and nostrils
5. Star, Strip, and Snip - a star, a snip, and a line slightly longer than a snip between them
Horse coloring: name the 4 leg markings and what they look like
1. Coronet - white line directly above the hoof
2. Pasterns - white from hoof to directly under the fetlock
3. Socks - white from hoof to between the fetlock and hock
4. Stockings - white from hoof to directly under the hock
Core equine vaccines
EEE/WEE (equine encephalitis)
What is one very common reason for colic?
any recent change in diet (be it schedule, feed, etc)
Change in routine or intensity of exercise could cause what?
GI ulcers
What is "pulse pressure?"
the difference between systolic and diastolic pressure
What happens to the heart rhythm if there is a decr of oxygen to the tissues?
the beats are close together
When will you feel the retropharyngeal lymph nodes?
if they are enlarged (ex Strangles)
Where would you see a jugular vein pulsation normally?
possibly in the thoracic inlet (if it extends of the neck, it's ABNORMAL)
Primary sight for venipuncture of the jugular vein and why?
upper 1/3 of the neck bc that's where the jugular vein and carotid artery are furthest apart
Where is the primary site for IM injection? What are the borders?
muscles of the neck

base of the nuchal ligament, proximal portion of the cervical vertebral bodies, start of the shoulder musculature
Normal heart rate of the horse
What do each of the heart sounds (S1-S4) indicate?
S1- closure of the AV valves
S2- closure of the semi-lunar valves
S3- early diastole/rapid passive filling of the ventricles
S4- atrial contraction (right before closure of AV valves)
Heart sounds:
1. between S1 and S2 = ?
2. everything outside of S1 to S2 = ?
1. systole
2. diastole
Which arrhythmias are non-pathologic in a horse at rest?
sinus block
1st degree AV block
2nd degree AV block (horse has a strong vagal tone which keeps the HR low, so it can drop beats)
What does the P wave indicate?
atrial contraction (S4)
What is sinus arrhythmia?
normal irregularity heard in conjunction with the respiratory cycle
What is the most common pathologic arrhythmia?
atrial fibrillation
Normal respiratory rate of a horse
Is it normal or abnormal for the rebreathing exam (with the plastic bag) to invoke coughing?
What would you examine and what would you expect to see in a horse with laminitis?
-palpate digital pulses - will see "bounding"
-palpate coronary band - edema, cleft may drop (can push thumbnail in
-palpate hoof capsules - will feel heat
-see if horse willingly lifts each foot
-turn horse in small circles, both directions
Normal rectal temperature of a horse
99-101.5 degrees F
What CS indicate urinary tract dysfunction?
urine scalding, straining, polliakuria
Where do you measure a horse with a weight tape?
around the barrel/thorax at the level of the withers
What body condition score scale is used for a horse?
1 thru 9
What are the 6 points of BCS?
A "poor" BCS for a horse = what number(s)?
condition score 1-3
A "moderate" BCS for a horse = what number(s)?
condition score 4-6
A "fat" BCS for a horse = what number(s)?
condition score 7-9
How much should a horse weight (approx)
1. Foal
2. Weanling
3. Yearling
4. Adult (>2yrs)
5. Light horses (Arabs)
6. Draft breeds (ex Clydesdale)
1. 50kg
2. 100-200kg
3. 300-400kg
4. 500kg
5. 400-500kg
6. 1000kg
the digestive tract of a horse is best suited for what type of feed?
forage diet
What type of feed do we give horses more of in "captivity" than what they were used to in the wild?
concentrate feeds (grains(
what is part of the foregut in horses? (4)
small intestine
What is part of the hindgut in horses? )4_
large colon/ascending colon
small colon
What is the purpose of the foregut?
digestion and absorption of non-fibrous feed and ingredients
(protein, fat, sugar/starch, water, vitamins/minerals)
What is the purpose of the hindgut?
digestion and fermentaion of fibrous feed ingredients
(cellulose, hemicellulose)
Which (cellulose or hemicellulose) is digested in the cecum/large colon?
What is unique about horses that also occurs in rabbits? (yes i knot he word unique doesn't fit when there's another animals that has the same trait so :P )
they are hindgut fermenters
What are the lips used for?
Why is a deficit of cranial nerve VII so bad?
it controls the lips, which are needed for prehension
How do horses chew? What is different about the way their chewing habits?
lateral excursion

they chew continuously (up to 60,000xs) a day to increase surface area
What type of teeth do hroses have?
What are the incisors used for and how many do they have?

6 upper, 6 lower
What are the canines used for and how many do they have? What is unique about them?

2 upper, 2 lower

occur only in males
What are the premolars used for and how many do they have?

6 upper, 6 lower
What are the molars used for and how many do they have?
6 upper, 6 lower
Which teeth are considered the cheek teeth?
premolars and molars
T/F: the upper jaw of a horse is very narrow
false: the lower jaw is very narrow
What are the signs of poor dental health in the horse?
quidding (feed falls out of mouth)
abnormal head position during chewing
loww of condition
Which salivary glands does the horse have?
What, from the saliva, aids in digestion?
What, from saliva, buffers stomach acid?
How much saliva can be produced a day?
up to 40L
What makes up the upper esophageal sphincter?
cricopharyngeus muscle
What makes up the lower eso sphincter?
distal part of the musculature of the eso (important for prevention of vomiting)
What volume can the equine stomach hold?
how long does it take to empty? What is this ideal for?
2-12 hours (rapid)

ideal for forage diets
The small intestines is the primary site for what?
digestion and absorption of protein, fat, starches/sugar, and vitamins/minerals
large meals promote what?
rapid transit to cecum
T/F: digestive enzymes from the liver and pancreas are released every few hours from the common bile duct
false: the enzymes are released CONTINUOUSLY from the common bile duct bc the horse has no gallbladder
T/F: rate of passage through cecum is relatively rapid
false: it is relatively slow
Where does fermentation initiate?
in the cecum
What is necessary for good equine GI health?
microbial "happiness"
Explain microbial fermentation
fibrous and non-fibrous CHO (grasses) are takes up by the microbe and metabolized and released as:
1. VFAs used for energy
2. gas - wasted energy
3. Vit B and K
What is the problem with fasting a horse?
microbial numbers decr when feed is withheld for >8hrs it may take >1wk to repopulate
What's the problem with a heavy CHO diet?
incomplete prececal digestion leads to overpopulation of specialized bacteria (bacillus, lactobacillus, and streptococcus) --> reduces number of normal microbes --> mucosal damage + impaired cecal motility --> colic
T/f: bacillus, lactobacillus, and streptococcus (the 3 main microbes that overpopulate the GI with a heavy CHO diet) are normal cecal inhabitants
The large/ascending colon is the primary site for what? what else happens there?
primary site for water resorption

-additional site for microbial fermentation and microbial production of Vit B & K
-VFAs are absorbed
What happens in the transverse colon?
no real clue on my part, but it has no real digestive responsibilities
What happens in the small colon?
water is absorbed and fecal balls are created ('road apples")
What is the nutritional equation for energy?
Fiber + CHO + Fat
**Nutritional requirements of most horses may be met by feeling what?
good quality hay/pasture, water, and a trace mineral salt block
What is the daily requirement of water?
8-12 gallons/day
Excess energy may result in what problems? (6)
Developmental Orthopedic Dz
Equine Metabolic Syndrome
Reduced performance
What is a calorie (cal)?
the amount of heat required to heat 1g of water 1 degree celsius
What is a Megacalorie (Mcal)?
1,000Kcal = 1,000,000cal
Forage feeds = ?
structural CHOs = fiber
What are the most common forages? (2)
pasture forage and hay
legumes and grasses
What does forages provide?
maintenance digestible energy
for Gi health, what % of the diet should fiber be?

ideal: 1.5-2% bwt (lbs)/day
How is hay measured?
in "flakes"
What is the most important part of the diet?
When can something else take the palce of hay?
when it has >15% crude fiber (for older horses with bad/no teeth so they don't have to chew)
How does fiber lead to energy?
fiber digestion --> VFAs (produced by microbial ingestion of forage feeds)
What is the primary energy source of a horse?
VFAs (30-70% daily energy)
How are VFAs absorbed?

What is VFA absorption related to?
across LI wall (passive diffusion down pH gradient as free acids)
directly into portal blood (travel to liver/muscle tissue)

related to water/salt movement
the rate of absorption of VFAs (acetate, butyrate, proprionate) is related to what? which is the most absorbable (list in order from most to least)
molecular weight

acetate > proprionate > butyrate
What does VFA absorption do for the intestines?
maintains intestinal pH
What is the optimal intestinal pH?
6.5 for microbial health
What is one of the biggest sources of glucose in the horse? (hint: it's one of the primary VFAs)
What are the guidelines of digestibility for hay quality?
mature & stemmy = less digestible
immature, leafy (aka protein), & small stems = more digestible
T/F: you should avoid round bales of hay when feeding
true bc they could be moldy and have botulism or cause a respiratory allergy (RAO)
T/F: you should avoid straw when feeding
true bc straw is an agricultural biproduct with no nutrient quality that has no digestibility and increases a horses risk of colic
What is in straw in high concentration that should be avoided?
lignon bc it is unuseful
what is the most accurate assessment of hay and pasture quality?
Forage testing/Hay analysis
"complete feeds" are designed to be fed in place of what? What % of fiber is required

What % of the diet should coem from forage?
Beet pulp is what type of feed?
Beet pulp has what % of fiber in it? What is it low in? What is it high in?
</= 28%

low in protein, high in Ca
Why do you moisten beet pulp with water/
to prevent eso choke
Bran is what type of feed?
What is the % fiber content of Bran?
T/F: Bran is more suitable for fiber supplement than beet pulp?
false: beet pulp is more suitable than bran bc bran is a low density feed, meaning it requires a lot of bran to meet fiber needs
Bran is often used as what?
Fresh grasses contain what % water?
**What is the disadvantage of fresh grass?
high CHO content of spring grass can trigger colic and laminitis
How do you introduce a horse to grazing/fresh grasses?
SLOWLY (incr time spent in pasture each day)
When is the best time to graze and why?
early mornings because low non-structural carbohydrates in grasses
Pasture grass is contraindicated in which horses?
those predisposed to laminitis (chronic dz)
Equine metabolic syndrome
Equine cushing's syndrome
What are non-structural carbohydrates (NSC)?
simple sugars
Where are NSC digested and into what?
small intestine --> glucose
in the SI, what helps with starch digestion?
amylase (non-digested starch passes into the hindgut)
Why would the cecum receive non-digested starch?
bc horses have a limited prod'n of amylase
What are some examples of NSC?
oats, corn, molasses, concentrates/grain
What % of NSC should be digested in the SI? too much at one time is a well-known cause of what?

What are specialized microbes in the cecum for starch fermentation (if the starch isn't digested in the SI)? What is the problem with them?
bacillus, lactobacillus, streptococcus

produce lactic acid as a byproduct, which alters cecal pH, injures mucosa --> dysmotility
How does the starch reaching the cecum lead to colic? what else can happen?
dysmotility --> gas distention in the cecum/colon --> colic

when the normal microbe populations begin to die --> gas prod'n, endotoxic shock --> laminitis
How can you improve pre-cecal digestion of starch so none of this nonsense happens?
-feed NSC separately from forage (save amylase)
-decr amt of starch intake/meal/day
-consider source: oats are highly digestible, corn requires processing to incr digestion, grinding/popping/heat tx
NSC provides what type of energy? What animals is it good for?
rapidly available energy

race horses, high performance, lactating mares, underweight/thin
Avoid NSC if the horse has what? (4)
cushing's syndrome
Equine metabolic syndrome
How much starch is too much?
2g starch/kg bwt leads to digestive upset

split starch into 2-4 small meals/day
What is the glycemic index used for?
developed in human med to determine which foods are best suited for diabetic patients
What types of feed give a horse instant energy?
high glycemic feeds - CHO break down quickly during digestion, releasing glucose rapidly into circulation
What types of feed allow for a more balanced energy release?
low glycemic feeds - CHO break down more slowly, releasing glucose more gradually into the bloodstream
What happens with high glycemic index feeds/
get a "bottomed-out" feel after an energy high
Fluid Therapy!!
What are the c/s of hypovolemia?
decr pulse pressure
reduced jugular fill
cold extremities
decr urine output
depressed mentation
What are the c/s of dehydration?
tacky mucous membranes
prolonged skin tent
sunken eyes
incr urine specific gravity
irritable behavior
muscle cramping
You will be unable to detect dehydration less than what percent?
What % is mild dehydration and what are the c/s?

decr skin turgor
very slightly tacky mucous membranes
What % is moderate dehydration and what are the c/s?

depressed mentation
tacky mm
CRT >2-3sec
correlated with hypovolemia
What % is severe dehydration and what are the c/s?

cool extremities
poor perfusion
CRT > 4sec
not sure will survive
What are the parameters used to assess volume status? (3)
pulse pressure (the difference between systolic and diastolic pressure)
jugular vein fill
temp of distal extremities
What is the one fluid where you must measure colloid oncotis pressure because the refractometer won't work to get a total solids?
With volume depletion, what should these parameters look like:
1. urine specific gravity
2. serum creatinine
3. PCV
1. concentrated (>1.025)
2. pre-renal azotemia (BUN + CREA), CREA >1.5mg/dl
3. hemoconcentrations
Why would lactate be produced with volume depletion?
anaerobic metabolism due to poor tissue oxygenation
What does central venous pressure (CVP) measure?
What are the four parameters that will incr as dehydration % incr?
heart rate
What is the most important reason to measure CVP in a horse?
we may give it fluids but that's a problem if it has renal disease
what does a decreased CVP indicate?
what does an increased CVP indicate?
fluid overload
What are the 4 phases of fluid therapy and do they overlap?
Ongoing losses

what is the most important part?
reversal of hypovolemia (imperative and must be immediate!!)
What is a shock dose of fluids?
one blood volume
What is one blood volume?
8% of body weight (kg)
Why would you not give oral fluids with a hypovolemic patient?
the GI is not getting any blood so it won't absorb
Where can you place an IV catheter? (3) Which is the primary site in horses?
**jugular vein - primary site
cephalic vein

lateral thoracic vein
What are the two types of catheters (materials) used?
Teflon catheter:
1. rigid of supple
2. least or most thrombogenic
3. long or short term
1. rigid
2. most thrombogenic
**3. short term use (>72 hours)
Polyurethane catheter:
1. rigid or supple
2. least or most thrombogenic
3. long or short term use
1. supple (making it more difficult to place)
2. least thrombogenic
**3. long term use
Over-the-needle catheters are used for long or short term?
short term
Over-the-wire catheters are used for long or short term?
long term (very supple, non-thrombogenic)
Which type of fluids are most used for hypoproteinemic patients?
What are the primary electrolytes in crystalloid fluids?
Na and Cl
How much crystalloids should you administers?
304xs the amount required bc designed to leak from the intravascular space
What is isotonic fluid?
a crystalloid fluid with a tonicity equal to that of plasma

What is the point of isotonic fluid?
allows brief volume expansion without cause e-lyte balances
Why would you not give 0.9% NaCl to rescusitate?
want to give something a little more balanced to resuscitate
What is hypertonic saline?
7% NaCl (equal parts Na and Cl)
What does hypertonic saline do?
provides immediate expansion of vasculature volume
--creates a hypertonicity of the ECF
--redistribution of fluid from ICF

vol expansion 2-3xs vol infused
What should be done after giving hypertonic saline? What is the Rule of Thumb?
give crystalloids

for every 1L hypertonic saline, replace with 10L crystalloid
What is hypertonic saline used for?
resuscitation (NOT a maintenance fluid)
What are the added benefits of hypertonic saline?
improves CO by increasing SV (affects preload)
reduces capillary endothelial swelling
suppresses degranulation of PMNs
prevents PMN-endothelial adhesion
blocks nuclear transcription of inflammatory cytokines
What do colloids do?
plug capillary endothelium (leaky vessels from endotoxin-mediated damage)
draw fluid into vessel from interstitium by incr colloid oncotic pressure

useful for hypoproteinemic patients
List some colloids (2 specifically)
frozen plasma
What are the advantages of frozen plasma?
excellent source of albumin, anti-endotoxemic factors, clotting factors
easily read on refractometer
What are the disadvantages of frozen plasma?
slow administration
transfusion rxn
requires time to thaw
blood administration set
What are the two most common signs seen with transfusion reaction?
incr TPR and utricaria (hives)
What are the advantages of hetastarch?
it's a synthetic product
bolus administration
no thawing
does not require transfusion set
less costly
What are the disadvantages of hetastarch?
cannot measure on refractometer --> COP
has been associated with prolonged bleeding times at higher doses
she put that in, I had it starred, so there it is! Hope you feel wise after that.
What is the equation for rehydration?
dehydrate % X body weight (kg)
What are the guidelines of rehydration?
slow replacement of fluid
--as compared to patients w/volume depletion
--rehydration over 12-24 hours
--crystalloid (isotonic) fluid
deficit replacement does nto alway require IV administration
dehydrated patients may require 2-3x maintenance requirements
What is the formula for maintenance fluid tx?
50mL/kg/day or 1mL/lb/hour
T/F: frozen plasma has a higher colloid oncotic pressure (COP) than hetastarch
false: hetastarch has a higher oncotic pressure
What fluid should be used for maintenance?
crystalloid fluid/isotonic

possible electrolyte supplementation
nearly every IV fluid plan includes what?
Calcium supplementation
When should potassium be supplemented?
for hypokalemic or horses on IV fluids >24 hours
**What should you be very careful about with potassium?
K must be <0.5 mEq/kg/hr
When should magnesium be supplemented?
critically ill patients of patients with hypomagnesmia
how are ongoing losses typically replaced?
by increasing maintenance requirements (2xs maintenance, 3xs maintenance, etc)
Classic diarrhea in horses is just like what?
losing blood- lose massive amounts of electrolytes and water
What is the problem with hypertonic saline in hyponatremic patients?
it can cause osmotic demyelination and cell shrinkage
how does chronic hyponatremia develop?
7% NaCl --> osmolality changes --> fluid pulled from calls --> osmotic demyelination syndrome --> cells shrink

YOU'RE DONE FLUIDS!! Now give yourself a pat on the back bc I thought I was done the nutrition packet but apparently I wasn't so back to that...
Why are many feeds supplemented with fat?
bc it is an important source of energy without CHO overload (more calories in less volume)
horses typically consume what % of fat/day?
Fat is required for the absorption of what?
Fat soluble vitamins: A, D, E, K
What are essential fatty acids?
fatty acids that must come from the diet
What are essential fatty acids for?
necessary for hormone and cell membranes: linoleic acid (omega 3 and omega 6)
fat is high in what?
energy density
What do unsaturated fats do?
improve skin and coat condition
How much fat should be consumed by:
1. pasture pet
2. please horse
3. performance horse
4. growing/lactating horse
1. 3%
2. 3-6%
3. 6-12%
4. 14-16%
What can be used for fat supplementation and how much should be fed?
corn oil, vegetable oil, safflower oil
...i think the mosquitoes are plotting against me
T/F: dietary intake is required for very for amino acids
Where is protein absorbed and excreted?

Where is it metabolized?
digested and absorbed in the SI
excreted in the kidneys

metabolized by the liver
What is protein?
the precursors for energy (it can turn into heat and energy that needs to be burned off)
Which protein is the rate-limiting step for growth?
Lysine (this si critical for growth)
Which feeds have high protein content?
legumes (alfalfa, soybeans)
seeds (esp oil seeds)
Protein should be what % of the diet?
Name a non-protein nitrogen source that you can feed to cows for protein
...ok I've got nothing. brain = fried
What form is used for a construction quote?
(SAP, 12-4)
Where does a horse get water-soluble vitamins? Which vitamins are water-soluble?
produced by the body

Vitamins B & C
Where does a horse get fat-soluble vitamins? Which vitamins are fat-soluble?
dietary intake

Vitamins A, D, E, K
Vitamin A
1. what is it turned into in the body?
2. what function is it needed for?
3. where is it found?
1. beta-carotene --> retinol
2. essential for vision
3. high-quality leafy forages/pasture grazing
Vitamin D
1. what is it needed for?
2. where is it found?
1. essential for calcium:phosphorous balance
2. obtained through UV light exposure and feed
Vitamin E
1. What is it turned into in the body?
2. what is it needed for?
3. Where is it found?
1. alpha-tocopherol
2. essential antioxidant
3. high quality hay and grains
Vitamin K
1. What is it needed for?
2. Where is it found/produced?
1. blood coagulation (factors II, VI, IX, X)
2. produced by intestinal microbes, forage
Vitamin B
1. What are the two subsets?
2. what are these needed for?
3. Where are they found/produced?
1. Thiamin (B1) & Riboflavin (B2)
2. neuronal health and RBC production
3. intestinal microbes
Vitamin C
1. What does it become?
2. Who may require supplementation?
1. ascorbic acid (antioxidant)
2. performance horses/foals
Which vitamins are now essential animo acids?
vitamin B, C, and mostly K
What are PIVKAs?
proteins induced by Vitamin K antagonism
Where does a horse get water-soluble vitamins? Which vitamins are water-soluble?
produced by the body

Vitamins B & C
Where does a horse get fat-soluble vitamins? Which vitamins are fat-soluble?
dietary intake

Vitamins A, D, E, K
Vitamin A
1. what is it turned into in the body?
2. what function is it needed for?
3. where is it found?
1. beta-carotene --> retinol
2. essential for vision
3. high-quality leafy forages/pasture grazing
Vitamin D
1. what is it needed for?
2. where is it found?
1. essential for calcium:phosphorous balance
2. obtained through UV light exposure and feed
Vitamin E
1. What is it turned into in the body?
2. what is it needed for?
3. Where is it found?
1. alpha-tocopherol
2. essential antioxidant
3. high quality hay and grains
Vitamin K
1. What is it needed for?
2. Where is it found/produced?
1. blood coagulation (factors II, VI, IX, X)
2. produced by intestinal microbes, forage
Vitamin B
1. What are the two subsets?
2. what are these needed for?
3. Where are they found/produced?
1. Thiamin (B1) & Riboflavin (B2)
2. neuronal health and RBC production
3. intestinal microbes
Vitamin C
1. What does it become?
2. Who may require supplementation?
1. ascorbic acid (antioxidant)
2. performance horses/foals
Which vitamins are now essential animo acids?
vitamin B, C, and mostly K
What are PIVKAs?
proteins induced by Vitamin K antagonism
umm, my caps lock key just broke bc the little light next to it is on which means is should be typing in capital letters, but clearly, it's not. something to think about...
What are macrominerals? List them
minerals required in greater amounts

What are microminerals? List them
minerals required in lesser amount

What should the Ca:K ratio be in young horses? Why?
Ca > P (1.5-3:1) --> growth (too much K and won't grow/ossify properly)

Adults can go up to 6:1 w/o problem bc not growing
Selenium depends on what?
it's a soil-dependent mineral
how does selenium deficiency present?
white muscle dz aka nutrional myodegeneration
Again, nutritional requirements of most horses can be met by what?
feeding good quality hay/pasture
trace mineral salt block
T/F: from birth to 1 month of age (neonate), the foal's only needs mare's milk and water is not needed
true: mare's milk is the sole source of nutrition in a neonate
What is the digestible energy requirement in a neonate?
What is the digestible energy requirement in an adult?
32kcal/kg/day (= 16mcals/day)
how many kcal/L are in mare's milk?
500-600 = great energy source
What is not found in mare's milk that is usually needed for a balanced diet?
CHO or fiber
Foal's consume how much milk each day?
20-25% of body weight
What should be a foal's daily weight gain?
When is a mare's peak milk prod'n?
~45 days
How often do foal's nurse?
When do foals actually start ingesting something other than mare's milk?
~10-14 days old
A foal consumed a significant amount of fiber/grain by what age?
4-6 weeks
T/F: copraphagia is normal and a horse does it 1-2xs a week
false: 1-2xs/day
T/F: can use calf milk replaces for an orphan foal
What is most similar to mare's milk?
goat's milk
What do you have to be cautious of when bottle feeding a foal?
aspiration pneumonia (foal's neck must be extended horizontally for correct bottle feeding)
What should mare's milk replaced provide?
>20% protein
>20% fat
<0.5% fiber (milk-based proteins)
acidified product (enhances nutrient digestibility and maintains quality during reconstitution)
which is better? list in order

goat's milk, nurse mare, commercial product
nurse mare > goat's milk > commercial product
What is "creep" feeding?
prepares foal nutritionally for the weaning process

allows foal to ingest additional calories w/o interference from mare
When does creep feeding begin?
~2mos until weaning
When are foals weaned?
Why are foals weaned in groups?
to limit stress
What does successful weaning depend on?
dry matter intake prior to weaning

creep feading is important to avoid "post-weaning slump"
T/F: too many nutrients can be just as bad as soo little
The daily requirement of 32kcal/kg/day is standard for what type of horses?
pasture pets
At what age are horses orthopedically mature?
>2yrs old
How do you feed a mature horse?
1-2% body weight in lbs per day
T/F: Ca:P ratio is not a concern for mature or nonpregnant horses
# of calories is measure in...?
calories/day is measure in...?
When I was your age...
When is a horse considered senior?
>/= 20 years
What is the goal when feeding a senior horse?
maintain BCS of 4.5-6
How much should a senior be fed?
1.5-2% body weight/day
T/F: unlike humans, horses do not have decreased metabolic activity with age
What should be done with fee in winter/cold climates?
incr intake
Sign of aging in horses
graying muzzle and/or coat
decr mobility due to osteoarthritis
halitosis due to poor teeth and gingivitis
Why are teeth likely to be an issue in senior horses?
hypsodont- wear out with time, present but possibly not functional
dental health is vital for longevity maintain BCS)
dentist important (annual/biannual basis)
What can you feed a geriatric horse that's easy to chew and swallow? (sounds dirty, right? RIIIIGHT!?!!)
cubed forage/pelleted diets
beet pulp
What needs to be kept in mind when feeding a geriatric horse
easy to chew/swallow
highly palatable
dust free (heaves)
protein ~12-16%
provide essential vitamins/minerals
aid digestion (high quality fiber)
incr fat if weight gain necessary
When are complete feeds used?
meant to be fed in place of hay
What do you need to consider for energy requirements for specific horses
level of activity
production status
I have no clue how to ask the next two slides in question form, but it's important so it's going in
ready? here it comes...
Aerobic exercise and nutrition
-HR </= 150bpm
-O2 requried for energy prod'n
rate of energy required is slow- heart/lungs supply O2, aerobic pathways cannot support prolonged of intense training
-glucose/glycogen: from NSC
-fatty acids (O2 required)
Anaerobic exercise and nutrition
-HR >/= 150bpm
-few substances capable of providing energy for anaerobic exercise
-efficiency of energy prod'n is less at higher rates of exercise
-glucose/glycogen: from NSC
-protein: breakdown products - glucose
What is considered light exercise?
aerobic exercise (~20mcal/day)

extra calories/energy from gains
What is considered moderate exercise?
remains aerobic exercise (~24mcal/day)
incr frequency, intensity, length of workout

grain/fat supplement
trace mineral salt block
What is considered heavy exercise?
aerobic + anaerobic exercise (>32mcal/day)
one hour speed work w/6-12 hours slow work
Which horses are considered high performance horses?
those w/high energy jobs

show horses
race horses
working horses
What is the feed requirement for working horses?
-at least 50% of total ration as forage
-high quality grass hay or alfalfa/grass mix
-high quality protein
-fed to meet IMMEDIATE needs (ex restrict grain on rest day)
-water/salt consumption is CRITICAL
If NSC is at the upper limit, yet the horse requires more supplementation, what should be added to the diet?
What is the primary concern when feeding a breeding stallion (Barney Stinson...I hope you watch "How I Met Your Mother")?
maintenance of body condition
How do you feed a nonbreeding stallion?
forage and vitamin/mineral supplement (just like everyone else)
What % of hay and concentrate should be fed when a breeding stallion is breeding?
concentrate: 0.5%
Hay: 1.75-2% (incr forage)
What happens if the BCS of a breeding stallion decreases?
can see loss of libido
What is the gestation length of a mare?
11 months (340 days)
What happens to the mare in the last trimester?
-gains 15% of body weight with growth of fetus
-significant incr in nutritional requirements
When should feed intake increase for a pregnant mare?
in last trimester and after she foals (increases A LOT after she foals)
T/F: feed should be slightly increased in a pregnant mare as soon as she conceives
false: ZERO increase in nutritional requirements in the first 8 months of pregnancy
What feed requirements incr in the last 3 months of pregnancy and how should the horse be fed?
incr in:
--minerals/electrolytes (esp Ca & Phos)

feed as a "light working" horse (>20mcal/day)
T/F: It is difficult to overfeed a lactating mare
What BCS should be maintained?
>/= 6/9
List the ideals for feeding management of horses
-assess/assign BCS
-feed at the same time each day
-feed on an individual basis
-feed at least 2xs daily )if confined, allow access to hay throughout the day)
-minimum 1% BW/day in hay/forage (>50% diet = fiber)
-feed concentrates ONLY IF NEEDED (growing, hardworking, lactating mares
List the feeding guidelines
-feed by weight, not volume
-reduce rate of intake (slow down chow hounds)
-consider dynamics (individual competition/pecking order)
-make ANY change GRADUALLY (>/-10-14 days)
-use BCS guidelines
What is the leading cause of death in equine? What can it be caused by?
endotoxemia (big surprise, right?)

colic, colitis, septic foals
What is a major complication of endotoxemia?
T/F: endotoxemia increases the risk of SIRS
true: or SIRS can lead to entotoxemic shock
What is SIRS?
systemic inflammatory response syndrome
What does the endotoxin come from?
LPS (lipopolysaccharide)
What is the LPS?
the structural cell wall component of all gram negative bacteria
What anchors LPS in outer cell wall?
Lipid A (this is the toxic principle of LPS and is similar in all bacteria spp)
What is the defining characteristic of each LPS, and also the virulence factor?
O-chains (they're antigenic) (high structural variability, unlike Lipid A)
Which part of the LPS interacts with the host immune system?
Why is endotoxin so bad?
if it gains access to the bloodstream, it may overwhelm normal host defense mechanisms, causing a cascade of inflammatory responses which are ultimately responsible for the clinical signs associated w/endotoxemia
What are the c/s assoc w/endotoxemia?
leukopenia or leukocytosis
What diseases in equine are commonly assoc w/endotoxemia? (6) What is the most common?
**Enterocolitis (most common)
Wound infection
neonatal septicemia
What are the normal daily defenses against LPS?
enterocyte endothelium
mucus layer (produced by prostaglandins)
tissue macrophages (MO)
Kupffer cells
What are 3 ways for endotoxin to enter the bloodstream?
-Damage to GI mucosa or uterine inflammation allows translocation of endotoxin into the bloodstream
-Endotoxin may be inhaled
-Iatrogenic administration (colonic ulceration/NSAIDS, IV catheters)
**Explain how endotoxin in the bloodstream works
LPS targeted by LPS-binding protein (LBP) --> this complex joins CD14+toll-like receptor (TLR4) on phagocyte surface --> MD2 stim allows translocation of LPS signal to cytoplasm (allows endotoxin into cell) --> IC signaling pathways lead to upregulation of nuclear transcriptiong factors (NF-K-beta)
What happens after the upregulation of nuclear transcription factors (and yes, this is bc there's not enough room to cram all of this onto one card)
--> produce inflammatory cytokines (IL-1 and TNF) --> responsible for c/s of --> endotoxemia
How are inflammatory cytokines responsible for the c/s of endotoxemia?
cytokines regulate inflammatory and immune responses by signaling between cells
T/F: decreased plasma TNF is associated with increased mortality rates w/acute GI dz and in septic foals
false: INCREASED plasma TNF is associated w/increased mortality rates
T/F: TNF is considered one of the initial and primary responders to endotoxin and is central in the pathogenesis of endotoxic shock
The c/s of endotoxemia are mediated by what 3 things?
1. release of inflamm cytokines
2. activation of the intravascular coagulation pathways (exposure of endothelial tissue factor)
3. complement protein activation.
What happens when LPS cleaves the phospholipid cell membrane on every cell in the body?

(it may be easier to look at slide 1 on page 3 of endotoxemia packet for a flow chart)
arachadonic acid cascade is initiated, leading to 2 pathways:
--cyclooxygenase pathway = prostanoids/PGH2) --> prostaglandin prod'n (PGI2, PGE2, PGF2) and thromboxane A2
--lipooxygenase pathway (leukotrienes) --> vasoconstriction, bronchospasm, incr vascular permeability
The short, sweet version of endotoxemia

(a little too simplistic, but whatever)
endoxotin --> destroys endothelium --> tissue damage --> endothelium can no longer protect i=tissue from further damage)
What 6 things are released/produced/etc with endotoxemia?
Nitric Oxide is produced
Histamine is realsed
Reactive Oxygen species (respiratory burst of neutrophils)
TF stimulation (endotoxin works on endothelium)
Neutophil activation (selectins, integrins)
What happens with neutrophil activation?
they are released from the endothelium --> neutrophils stick --> respiratory burst --> endothelial damage/permeability
ALL of the mechanisms of endotoxemia lead to what?
altered vascular permeability (vessels saggy/permeable/loss of tone --> blood pools --> systemic hypotension --> inadequate perfusion of tissues --> distributive shock
What is the hallmark of endotoxemia and endotoxemic shock?
altered vascular permeability
C/s of EARLY HYPERdynamic shock (15-45min following injury)
anorexia, yawning, sweating, depression, fever, recumbency
colic (PGs stim pain/affect horse's pain sensation)
altered vasc permeability (bright red mucous membranes), incr CRT
muscle fasciculations
C/s of LATE HYPOdynamic shock (>90min after injury)
diarrhea, obtunded mentation, hypothermia, circulatory failure
prolonged CRT (can leave thumb print)
dark red/purple mm (blood pooling outside vasculature walls)
3rd space fluid retention (another reason for colic)
coagulopathy (hypercoagulable)
multiple organ failure (laminitis)
what will you see on bloodwork?
neutropenia, lymphopenia, thrombocytopenia (plts <100,000)
prolonged APTT & PT
incr FDP (D-dimer)
reduced fibrinogen concentration (not as high as expected for level of illness)
What is FDP? Why are they increased?
fibrinogen degredation product

show inflammation
Why is there a neutropenia?
neutrophils are stuck on sides of endothelium

this is UNIQUE to horses (small animals get neutrophilia)
Why is there a hyperlactatemia?
bc there is not enough tone in the vessels to use O2 so anaerobic metabolism takes place
T/F: there is a very specific, outlined plan of treatment for endotoxemia
false: there is no one specific therapy
What is the one bright hope for tx of endotoxemia since all other txs have failed miserably? What is the problem with it?
Activated protein C (anticoagulant)

side effects = fatal hemorrhage
it's also very expensive
What is the best chance of survival for a horse with endotoxemia?
early, aggressive cardiovascular resuscitation (w/in the first 6 hours)

use of O2, Iv fluids, pressor therapy (improves contractility and supports BP), packed RBCs
**What does early goal-directed therapy include?
1. CV resuscitation
2. laminitis prevention
3. removal of the cause(s) of endotoxemia
4. neutralization of free-circulating LPS
5. inhibition of LPS-mediated inflammation
what can be used?
hypertonic saline
colloid therapy (hetastarch, frozen plasma)
isotonic crystalloid therapy
What is the first line of defense? why?
hypertonic saline bc it:
--transiently increases vascular volume
--suppresses degranulation of PMNS (which decr formation of ROS/reactive oxygen species and prevents respiratory burst)
--blocks nuclear transcription of inflamm cytokines
what is the maximum amount of hypertonic saline that can be given to an average size horse?
2L (must follow w/crystalloids for several hours)
Why would you give Hetastarch?

What do you need to be careful of?
higher COp than plasma
incr vascular volume (~24hrs)
plugs holes created along endothelium lining --> keeps fluid from leaking out

prolonged aPPT (incr bleeding tendencies)
Why would you give frozen equine plasma?
excellent source of:
--oncotic pressure
--anti-endotoxemic and clotting factors

(oh please please please prevent this bc if you don't we'll all have to hear about how bad laminitis is AGAIN and I don't think I could stand it)
Most successful if initiated when?
PRIOR to development of c/s (any horse at risk should receive prophylactic care)
What are the two types of prophylactic care for laminitis?
cryotherapy and NSAIDS
What are you trying to achieve with cryotherapy?
50% reduction in metabolic rate w/10 degrees Celsius decrease in hoof temperature

timing of initiation and duration is CRITICAL for success
T/F: crytherapy can be used before c/s of laminitis and once c/s begin
false: it is NOT useful once signs appear
How far up do you ice the foot?
up to (and including?) the pastern
What NSAID is usually used and what does it do?
flunixin meglumine (Banamine)
-At low dose: prevents LPS-associated prostanoid prod'n, minimizes early response to endotoxin
-At higher dose: COX inhibitor, consistently provides excellent visceral analgesia
What are the side effects of Banamine?
deleterious effect: delays mucosal healing, renal and GI toxicity

(remove ischemic bowel or drain septic fluid from cavities)
Broad spectrum ABx is warranted but must be used with caution in animals with what/
When do you use ABx?
-horse is <3mos old (materal Ab prod'n waning)
-suspicion of Clostridial or antimicrobial-associated enteritis
-there is a degenerative left shift or PMN or lymphocyte count <1000
-there is clnical evidence of dyshemostasis (jug thrombosis or abnormal coagulogram)
What combination therapy can be used to neutralize endotoxin?
plasma therapy
Polymyxin B
At what point in the process do you want to catch the endotoxin?
the first thing the endotoxin sees is the LBP so you want to get a hold of the endotoxin before LBP sees it and drags it into a cell
What is Polymyxin B and what does it do?
it is a cationic cyclic polypeptide antimicrobial drug

scavenges free endotoxin (inhibitory effects)
--suppress NF-K-beta activity
--decr prod'n of pro-inflammatory cytokines
What do you need to make sure of when using Polymyxin B?

Possible side effects?
make sure the horse is well hydrated (dilute in 1-5L of crystalloid)

renal toxicity
What can be used to inhibit inflamm?
2% lidocaine
Ethyl pyruvate
Polymyxin B2
What does lidocaine do?

how can it be given?
helps w/reperfusion injury

What happens when you combine lidocaine with Banamine?
prevents retardation of mucosal healing (which is a bad effect of Banamine itself)
name a methylxanthine derivative that can be used to inhibit inflamm
What does pentoxifylline do?
-dose-dependent suppression of inflammatory cytokines
-Rheologic agent (deformation/bending of RBCs so they can reach smaller spaces and be of more use - aka foot/laminitis)
-inhibits TNF, promotes PGI2
-in vitro: stimulates IL-10, suppresses PMNs, inhibits NF-K-beta
What does DMSO stand for?
dimethyl sulfoxide
what does DMSO do?
free radical scavenger
laminitis prophylaxis/tx (not proven)
problem with DMSO
can cause hemolysis
causes animals to stink

(relatively harmless as long as its diluted)
What does Ethyl pyruvate do?
prevents pro-inflammatory cytokine effects

still being researched
What is the bottom line of endotoxemia treatment? (4)
Recognize patients at risk of endotoxemia
Restore perfusion/oxygenation
Ameliorate clinical signs
Prevent laminitis
I'm really starting to hate this. Just shoot the horse and move on. NEXT!
What is laminitis?
the dz which causes degeneration, necrosis, and inflammatin of the dermal and epidermal laminae of the hoof wall in horses (simply put: inflamm of the lamina)
What % of horses are likely to get laminitis?
What is digital lamina and what does it do?
interdigitations of sensitive and insensitive lamellae

holds P3 in close proximity to the hoof
acts as suspension mechanism
Laminitis is more commonly in which foot?
The laminar suspension mechanism depends on what?
the maintenance of the cytoskeleton and integrity of the basement membrane
How can laminitis be caused by endotoxemia/
the lamina is considered a "vital organ" which is affected by the inflammatory mediators of endotoxemia

laminar inflammation is potentiated by SIRS (systemic inflammatory response syndrome)
Laminar degeneration is initiated by what?

What is the pathogenesis?
diseases that elaborate inflammatory mediators

mediators are cytotoxic to epidermal laminae --> activate MMPs --> lead to dissolution of sensitive/insensitive attachments --> laminar support system fails --> clinical laminitis
Which is the sensitive laminae: dermal or epidermal tissue?

Which is the insensitive laminae?
sensitive- dermal
insensitive- epidermal
T/F: Disorders that decrease laminar energy delivery or protein synthesis have the potential to initiate laminar degeneration.

Why/why not?

bc maintenance of the cytoskeleton is an energy dependent process
What provides laminar energy?
Why are both Cushing's and Equine metabolic syndrome causes of laminitis?
bc they cause insulin resistance, therefore glucose stays in the bloodstream and doesn't get into the tissues
Swelling of the lamina can lead to what? Why?
compartmental syndrome (squeezing) --> pressure necrosis (abscessation)

bc the lamina resides inside the rigid hoof wall
When do the sensitive and insensitive laminae separate?
hours before the onset of clinical signs
What are the common risk factors of laminitis?
Septic metritis
Contralateral limb laminitis
Dietary changes
Endocrinopathic laminitis
Black walnut toxicity
Which is the primary risk factor for laminitis in the ICU?
T/F: endotoxin alone does not cause laminitis
true: the inflammatory cytokines produced in response to endotoxemia cause laminitis
What causes septic metritis in the mare which can cause laminitis?
retained placenta
Contralateral limb laminitis is aka?
Support limb laminitis - caused by bearing excess weight on a limb due to injury on the opposite limb
What in the diet can cause laminitis?
increased readily digestible CHO
grain overload (incomplete pre-cecal digestion, acid burn in the colon)
grazing lush spring grass (ponies, horses with EMS)
What endocrinopathies can cause lamintis?

Equine Cushing's dz (aka Pars Pituitary Intermedia Dysfunction)
Equine Metabolic Syndrome
Insulin resistance (impaired glucose utilization, glucocorticoid excess)
Inflammatory upregulation

cannot take up insulin
What are the main c/s of acute laminitis?
bounding digital pulses
heat in hoof capsules (cool the feet, want them body temperature not hot)
coronary band edema/cleft ("sinking" bc laminitis has fully detached)
Shifting weight
Other random c/s of acute laminitis
refusal to pick up feet
reluctant to walk/turn small circles
PAIN (tachycardia/pnea, anorexia, depression)
lameness score = Obel grade 3
What does a lameness score of Obel grade 3 mean?
the horse moves very reluctantly and vigorously resists attempts to have a foot lifted
When do structural changes associated w/laminar destruction begin?
hours before signs apparent
T/F: the death of cells/separation of sensitive and insensitive laminae can be seen right away on a radiograph
false: cannot be visualized initially
What should acute radiographs be used for?
a baseline for what the hoof should look like
**What may be the only indicator of laminar inflammation on a radiograph?
thickening of the dorsal hoof wall
What can be seen on radiographs of P3? Where should the coffin joint be?
rotation, sinking

coffin joint should be even with the coronary band - if it's not = sinking
How should laminitis radiographs be taken?
later films with hoof on a block (want to know the depth of the sole
What % can the coffin bone be rotated, yet it still be considered normal?
0-5% (any more = rotation)
Where will the foot be sensitive with hoof testers?
T/F: a digital nerve block can dx chronic laminitis
unsure (ha!) - it can be used to help diagnose, but it will only block the heel of the hoof
Which nerve block is better?
abaxial nerve block (75-80% improvement bc it blocks the toe)
What is the key to tx of laminitis?
prophylactic therapy!!
the acute phase of laminitis is considered what?
a medical emergency!
What 3 things can be done for prophylactic therapy for laminitis?
anti-inflammatory therapy
sole support
Which 2 NSAIDS are used for prophylactic therapy? What do you need to make sure of?
Banamine and Phenylbutazone

avoid IM injection bc it causes inflammation, abscess, and clostridium infections
How would shoe removal help prophylactically with laminitis?
promotes digital circulation and allow horse to stand as it wants
reduces tension on the laminae

(deep bedding in stall also helps)
If c/s of laminitis appears, then what?
multimodal therapy!!
What can be used for pain management? (8 possibilities)
Opioids (butorphanol CRI, morphine, fentanyl patch)
Alpha2-agonists (detomidine CRI)
2% lidocaine
Gabapentin (chronic)
Regional anesthesia
what can be used for sole support?
stryofoam cushion
commercially available products (reprosil, advance cushion support)
What type of bedding should be used?
deep- deep sand, peat moss
What other therapies can be used?
DMSO- osmotic, free radical scavenger
Pentoxifylline- reduces prod'n of cytokines, thromboxanes, and expression of TNF
How about exercise?
strict stall rest - no forced exercise for at least 1 month once NSAIDS are discontinued (not even walked around the stall)
What causes the chronic lameness from chronic laminitis?
abnormal hoof conformation
What does the hoof look like w/chronic laminitis?
growth at toe (ski/slipper shoes)
lack of growth at heel
growth rings prominent and not parallel
sole flattened
What do you see on rads with chronic laminitis?
deformation of P3

(remember: acute laminitis = normal radiographs)
With chronic laminitis, why is there chronic pain?
recurring abscessation
hoof cracks and chips
tendency toward sole bruising --> abscesses
What is the classic sign of chronic laminitis?
pedal osteitis
When is a venogram useful?
when rads are normal but horse remains sore (evaluates sinking/loss of blood supply)

(inject contrast into foot to see what's going on with blood supply)
How would you decr stress on the DDF?
easy breakover- decr toe length (cut off the fulcrum), wedge heel up --> makes it easier to walk bc don't have to lift foot as high
What are two other therapies you can use?
groove coronary band to stimulate growth (promote normal growth rings
maggot debridement therapy
What is the most you are hoping for with derotation of the coffin bone?

How do you do this?
pasture soundness

shape the foot around the coffin bone (chop off the heel)
What is the prognosis if rotation occurs?
guarded for return to previous level of exercise
What is the prognosis for sinkers?
very poor
T/F: without rotation and sinking, horses may still experience prolonged alteration of hoof growth w/a tendency toward cracking, sole bruising, etc that can lead to recurrent lameness
You can't get rid of it. Ever. It's like a bloodsucking leech.
T/F: the duodenum is short, a little > 1meter
false: it's a little < 1meter
T/F: pancreatitis is rare in a horse
true (amylase and lipase are rarely measured)
What is the surgical landmark that runs along the whole small intestines?
the duodenal-colic ligament
How long is the jejunum? Is it thick or thin walled?
long - 25 meters
thin walled
How long is the ileum? What dose it have that makes it distinguishable among the intestines?
1-3 meters

antimesenteric band
T/F: the ileum is more muscular than the rest of the SI
T/F: there is a dual blood supply to the ileum and the cecum
false: there is a single blood supply
What is the first structure visualized w/a ventral midline incision?
the cecum
What part?
the body
What is the lateral band of the cecum called? What does it attach?
the cecocolic fold

attached the cecum to the lateral free band of right ventral colon
How many bands does the cecum have?
Which band(s) hold the blood supply
the lateral and medial bands
What is the lateral band continuous with?
the cecocolic fold
Which band is continuous with the ileocecal fold?
the dorsal band
How far do the bands go?
only halfway to the apex
T/F: the sternal flexure is not fixed to the abdomen unlike the right dorsal and ventral colons
false: the PELVIC flexure is not fixed to the abdomen
How many bands does the pelvic flexure have?
how many bands does the dorsal colon have?
Where can the colon get hung up and may need to be rolled?
nephrosplenic ligament
T/F: sacculations are everywhere in the colon, except for the ventral colon
false: sacculations are everything except for the DORSAL colon (smooth)
Where are fecal balls made?
which part of the intestine has more mesenteric fat?
T/F: the stomach is relatively large for the size of a horse
false: it's relatively small
T/F: not all colic is GI
List some c/s of colic (10)
kicking at belly
laying down
looking at sides
curling lip
playing in water
grinding teeth
refusing feed
change in attitude
decr fecal output
What will you see in a severe, acute case of colic?
down and rolling or evidence horse has rolled
breathing ahrd
abdominal distention (bloat)
Why could you see dysphagia w/GI dz?
CrNN IX and X run through the guttural pouch
rectal tears will most likely be in which part: dorsal or ventral?
What alpha2s should most likely be used for chemical restraint?
Why are parasympatholytics good for chemical restraint for rectal palpation?
they decr GI motility and rectal pressure
T/F: you can commonly palpate the duodenum on rectal palpation
false: can rarely be palpated
What portion of the LI is your arm in during rectal palpation? What can you palpate rectally?
arm is in the small colon (lg antimesenteric band)
aorta, left kidney, and caudal border of the spleen
dorsal colon and pelvic flexure
cecum on right
ventral cecal band (strumming thick cord; dilated = huge structure on right)
T/F: you, as the vet, are liable for all damages incurred during rectal palpation (tearing)
false: if proper protocol and proper education to the client are done, you are not liable for rectal tearing
How is rectal tearing classified?
grades I-IV
Which horses are predisposed to rectal tears?
old horses, minihorses, arabians (stupid arabians, always messing shit up...tee hee)
What do you avoid when sedating a horse? Why?

decr BP
how do you knwo if a caudal epidural worked?
tail tone is gone
how do you prevent rectal tearing from progressing?
rectal tampon
purse-string suture the anus
Where do you apply the rectal tampon?
10cm cranial to the tail
What is a grade I rectal tear?
mucosa and submucosa tear

simple, almost all survive

most exam tears are grade I
What is a grade II rectal tear?
muscularis tear only

no blood
incr level of survival
What do you tx a grade I tear with?
medical management = success
Abx (TMS)
NSAIDS (Banamine)
daily laxatives
pelleted diet - softenef
monitor for fever, LPS, dyschezia
How do you manage a grade II tear?
no tx necessary - can be incidental finding
can predispose to rectal impactions
can progress to grade IV
What is a grade III rectal tear?

What is a grade IIIa tear? IIIb?
all layers except serosa tear

IIIa- torn outside of mesocolon/mesorectum

IIIb- ruptures into retroperitoneal space - can easily become grade IV tear
What is a grade IV rectal tear?
full thickness tear

feces in abdomen
Which tear(s) is/are life threatening?
grades III & IV
What do you do for a grade III tear?
tx as for grade I
incl IV antomicrobials (penicillin, metronidazole)
anti-endotoxemic tx
tetanus prophylaxis
rectal packing
**peritoneal paracentesis (RBC count, TP, fluid visualization)
What do you do for a grade IV tear?
usual fatal bc of overwhelming fecal contamination of the abdomen
few reports of survival
Medical vs surgical management of rectal tears: what are the 3 options?
abdominal lavage
rectal lines
loop colostomy
What do you need to be careful of when doing a peritoneal paracentesis?
What does normal peritoneal fluid look like?
clear transudate
straw to yellow color
TP < 2g/dl
WBC < 5000
What does abnormal abdominal fluid look like and what does it mean?
serosanguinous- bowel devitalization, splenic puncture, SQ blood vessel
green fluid- entercentesis, bowel rupture
thick orange fluid- peritonitis
What does septic peritoneal fluid look like/have? why?
glucose < 50 points lower than that of serum blood glucose
elevated lactate
very low pH

when bacteria are present they metabolize glucose and produce lactate as a metabolic by-product, thereby lowering the pH of peritoneal fluid
What is the normal glucose in serum blood gas?

normal lactate?

normal pH?
glucose: 80-100 mg/dl

lactate < 1mmol/L

pH = physiologic 7.4
What can occur during laproscopy
acid/base abnormalities (pump CO2 into abdomen and put pressure on the diaphragm??)
What can you CT/MRI in a horse?
limbs and head only
T/F: abdominal U/S is an invasive but routine part of GI evaluation that requires an alcohol interface
false: is it a routine part of GI evaluation that requires an alcohol interface, but it's NONinvasive
On U/S, what does fluid look like? bone?
fluid = black (anechoic)
bone = white (hyperechoic)
Where will you find the stomach?
left side
Where will you find the duodenum?
right side of abdomen
ventral to caudal pole of the right kidney
caudal to liver
T/F: when looking at an U/S of the SI, lollipop formation ("bubbles") is a normal finding
false: it's BAAAADD - means the SI is dilated
From which side do you visualize the LI and cecum with an U/S?
right and left body wall, ventrum
What will you see?
very large diameter
obscures visceral organs (U/S bea,s cannot penetrate gas or bones)
T/F: scintigraphy is a good diagnostic tool for the SI
false: not very good for GI but great for orthopedics
When can you do a full-thickness biopsy?
ventral midline celiotomy
when can you do a mucosal biopsy?
endoscopy (upper GI only)
rectal mucosal biopsy
If you get a fecal float that is negative for sand, can you rule out a sand impaction?
When are absorption tests used? how do they work?
use in chronic weight loss

18-24hr fast --> administer 10% soln D-xylose or D-glucose --> take blood samples --> plot curve
What should a normal result be? What does it mean is the results are abnormal?
peak "inverted V" between 60-120 minutes

almost straight line = not absorbing glucose
Is gastric reflux normal on a horse?
When passing a stomach tube, how can you be sure the tube is in the esophagus and not the trachea?
visually observe tube passing down esophagus (left neck)
negative pressure when inhale back on tube
auscult gas bubbles in stomach when air is forced into tube
palpation only works on foals (not adults)
...yeah, i've got nothing.
what is the most common c/s for esophageal dz?
What cranial nerves control mastication?
Which cranial nerves control swallowing?
V, IX, X
T/F: dysphagia could be caused by guttural pouch dz
true (some of the cranial nerves run through there)
what is dysphagia>
difficulty swallowing
Ptyalism can be caused by what?
oral davity pain
poor dental health
how does a horse get "slobbers?" What does it cause?
eating clover

causes salivation (but it's not pathogenic)
When should you consider the esophagus for dz?
when you can:
--confirm good oral health
--confirm guttural pouch health
--confirm integrity of Cn function
Choke aka...
esophageal obstruction
What are the most common sites for eso obstruction?
caudal 3rd of the eso
apex of the heart
eso hiatus
what are the acute symptoms/c/s of choke?
frothy nasal discharge
feed from nostrils
With choke, how should the horse be positioned when sedating and why?
head lower than point of the shoulder to prevent aspiration
What can be used to sedation/relax the eso for choke?
Bucospan (N-butylscopolammonium bromide) - parasympatholytic
oxytocin (promotes eso relaxation)
What do you do after choke is confirmed?
pass an NG tube --. pump water while gently applying pressure to obstruction --> keep horse's head low as long of fluid will come out the nose (prevent aspiration) --> repeat
What do you do if that is unsuccessful?
place horse in stall, NPO, IV fluids, and give it TIME (it will likely resolve on its own) (replace bicarb and e-lytes bc losing saliva)
You can use NSAIDS for prolonged choke, but what is the problem with using Banamine?
it can disrupt mucosal healing, though it is helpful initially
What would sulcralfate do?
promote healing of eso
What is a complication of choke?
What is the first c/s of aspiration pneumonia?
how do you tx aspiration pneumonia?
broad spectrum ABx
IV therapy (esp if still obstructed)
Oral TMS when choke is over
T/F: circumferential lesions heal better than linear?
false: linear heal better than circumferential
The stricture is the smallest at what point?
between 21 & 28 days
Eso rupture is also a complication is choke. What breed does this occur in mostly? Where does it usually tear? What will you find

intrathoracic tear

pleural fluid accumulation
What do you need to consider nutritionally with choke?
refeeding (eso inflamed, motility may be abnormal, reobstruction is LIKELY)
modify diet (feed mash, soft hays)
What is diet change isn't enough?
esophagotomy (done easily in horses when standing)
--done on the LEFT side
What can cause a motility dysfunction of the esophagus?
What should be considered with megaesophagus?
acquired vs congenital
functional obstruction (c/s of choke)
R/O underlying myopathy
tx underlying dx, dietary modifications
what is the prognosis for megaeso?
poor if it is congenital
Rollin', rollin', rollin', Keep that ingesta rollin'.. Get 'em up, move 'em out!
T/F: glandular mucosa has limited defenses against gastric acid
false: SQUAMOUS mucosa has limited defenses against gastric acid
Where is the forage ball and what does it do?
in the lower half of the stomach and it protects the squamous epithelium from exposure to HCL and bil acids
Which parts of the stomach has the squamous mucosa?
upper half
Lesions in the squamous mucosa are most common with what?
decr feed intake or limited forage
What defenses does the glandular mucosa of the lower stomach have against gastric acid?
mucus barriers and bicarb secretion
rapid regeneration and repair (higher rate than sq cells)
What neutralizes HCL?
reflux of duodenal secretions (pancreas/hepatocytes)
...sounds like the name of a retarded gremlin

but it really stands for Equine Gastric Ulcer Syndrome
What is the term EGUS used for?
term for clinical finding of ulcers in the equine stomach
Where in the stomach are the ulcers found?
erosions/ulcers of sq epithelium along the margoplicatus
lesions in glandular mucosa and pylorus +/- duodenitis
Which breeds have a high prevalence for gfastric ulcers?
performance breeds (ex thoroughbreds)
Name the risk factors for EGUS
housing in stalls vs pasture
high CHO diets
incr intensity exercise
helicobacter pylori
c/s of EGUS in adults
mild intermittent colic (coincides with meals)
dexr appetite
failure to finish grain
loss of body condition
poor hair coat
alterations in attitude
Where do foals get EGUS?
glandular portion of the stomach
What are the risk factors for foals?
NSAID administration
c/s of EGUS in foals
mild --> severe pain
bruxism (teeth grinding)/ptyalism
What can be used to help dx EGUS?
What can prostaglandins do to help?
good for mucosa blood flow and cytoprotective barrier
**T/F: there is no correlation between the presence of squamous and glandular lesions
D/Dx for EGUS
gastric impaction
gastric neoplasia

**Remember your signalment!
if endoscopy is not available, what else can be diagnostic?
response to therapy
--improvement in attitude
--weight gain
--resolution of colic
--improved coat condition
How do you tx EGUS in adults?
decr concentrate, incr roughage
H2 receptor antagonists (Cimetidine, Ranitidine)
H+ pump inhibitors (omeprazole)
T/F: Regardless of previous risk factors, ulcer dz may develop w.i 24 hours of inappetance/stall rest
How do you treat pyloric dz?
may require prolonged therapy
dietary modifications
prophylactic anti-ulcer therapy
T/F: squamous ulcer dz is more difficult than pyloric dz
false; pyloric dz is more difficult
...yup, still fried
What does the Si do?
absorption of nutrients
absorption of CHO, fat, proteins
What does the Si have that allows for all the absorption? what happens if it fails?
brush border created by SI villi

failure of absorption by the villous tip leads to malabsorption syndrome
**What is the hallmark of malabsorption?
weight loss
What are the c/s of acute enteritis?
COLIC!! - #1 sign
functional obstruction (tract is patent but things are keeping it from moving)
*dilated loops of SI on U/S
copious gastric reflux (in stomach, not thru nose)
*rectal palpation many loops of SI
incr Tp in peritoneal fluid
What are the c/s of chronic enteritis?
WEIGHT LOSS - #1 sign
+/- colic
*thickened SI walls on U/S (compare to acute)
T/F: It is uncommon for IBD to cause diarrhea
what are the 5 types of IBD?
Granulomatous enteritis
Multisystemic eosinophilic epitheliotropic enterocolitis
Lymphocytic-plasmacytic enteritis
Eosinophilic enterocolitis
Idiopathic Focal Eosinophilic enteritis
In horses, IBd is typically defined by what?
granulocytic cells (other than PMNs)
How do you dx IBD?
biopsy is the gold standard

histopath needed to differentiate types
c/s of IBD
progressive weight loss despite good appetite
protein-losing enteropathy (hypoalbuminemia in absence of proteinuria or liver dz)
intermittent colic
NOT diarrhea (SI dz)
What will you see on U/S with IBD?
incr SI wall thickness
what is used to perform an absorption test and why?
xylose bc it is one of the only things that cannot be elevated due to anything other than absorption

absorption test should have an inverted V shape - straight ling across means no absorption (I THINK!!)
How do you tx IBD?
immunosuppressive doses of corticosteroids but it's largely unsuccessful
Signalment for granulomatous enteritis (GE)
toung horses
standardbreds are genetically predisposed
What do you see on histopath for GE?
Macrophages (MOs) bc "granulomatous"
What are the possible causes of GE?
several infectious agents have been implicated incl M avium
possibly immune-mediated response to dietary, parasitic, or bacterial antigens
Where do you see multisystemic eosinophilic epitheliotropic enterocolitis (MEED)?
young horses
What do you see with MEED?
tissue eosinophilia
(some lymphs and MOs)
MEED is one of the only dzs where you'll see what?
eosinophils in the periphery
Lymphocytic-plasmacytic enterocolitis (LPE) is what?
What will you see on histo with LPE?
lymphocytes and plasma cells present in the lamina propria w/villous atrophy
C/S of LPE

how do you dx?

rectal biopsy
T/F: horses w/idiopathic focal eosinophilic enteritis (IFEE) vary from typical IBD cases bc they present with signs of acute colic and no evidence PLE
What is therapeutic for IFEE?
surgical decompression
What causes proliferative enteropathy?
Lawsonia intracellularis (infectious)
T/F: L intracellularis usually present as a herd problem
false: usually individual cases
What cells does L intracellularis affect?
What is L intracellularis?

How do you get it?

What age is affected?
obligate intracellular bacterium


weanling foals (4-6mos)
What are the risk factors for L intracellularis?
dietary changes
**Hallmark of L intracellularis
chronic wasting
what else do you see with L intracellularis?
severe hypoproteinemia
grossly thickened SI w/mucosal ulceration (corrugate appearance)
It's affinity for crypt cells has what effect?
leads to decr brush border enzyme activity --> decr absorptive capacity
weight loss
malabsorptive diarrhea
c/s of L intracellularis
ill thrift (growth retardation, poor hair coat, pot bellied, muclsa thickening/villous atrophy)
peripheral edema (hypoproteinemic)
diarrhea (inappropriate absorption of nutrients, soft formed, black and tarry feces)
What will bloodwork show?
moderate --> severe hypoproteinemia
mild anemia
neutrophilic leukocytosis
prerenal azotemia/e-lyte imbalances may be assoc w/diarrhea
How do you dx L intracellularis?
gold standard: isolation/culture from tissue (VERY DIFFICULT)
--warthin starry silver stain

biopsy required antemortem
How do you tx L intracellularis?
supportive care
antimicrobials (tetracyclines, macrolides (esp erythromycin or azithromycin combined w/rifampin)
prognosis for L intracellularis
good ~93%

foals w/clinical dz suffer poor growth and small stature
What is Duodenitis-proximal jejunitis (DPJ)?
an anterior enteritis of potentially infectious etiology

a syndrome of inflamm and edema of the duodenum and prox jejunum, excessive fluid and e-lyte secretion into the SI and consequently, high volumes of enterogastric reflux
What can you see with DPJ?
SI distention
copious reflux
abdominal pain

functional gastric ileus (no mechanical/physical obstruction to flow of ingesta)
Where does the reflux come from?
SI distention
Where does the accumulated fluid come from?
-augmented pancreatic and biliary secretions
-bacterial/inflammatory/toxin-mediated secretion
-progressively incr intraluminal pressure (reduced fluid absorption, incr secretion) --> results in abnormal peritoneal fluid TP
-parotid saliva
What is the cause of DPJ?

true cause remains unknown but suspected inflamm syndrome (salmonella, clostridium, neorickettsia risticii)
Where are the gross lesions primarily found?
T/F: Serositis is a common finding in DPJ
true: bright red to dark red petechial and ecchymotic hemorrhages on the serosal surface of the proximal SI
What will you find on histpath?
hyperemia, edema, hemorrhage, fibrinopurulent serosal exudation (fibrin being laid down in sedentary bowel)D
How do you definitely dx?
surgery or nrcropsy
D/dx of DPJ
all SI obstructions (simple or strangulating)
When would DPJ NOT require medical therapy?
clinical deterioration/failure to improve
What will you find on rectal exam of DPJ?

on U/S?
dilated loops of SI (many loops, fluid filled and palpable)

U/S: large dilated SI loops, fluid-filled, poor motility, incr wall thickness
What would make it a surgical lesion?
tight, turgid, distended
what would you find on abdominocentesis?
dark yellow/orange
incr protein (>2.5g/dl)
normal to elevated WBC
What is the primary therapy for DPJ?
gastric decompression (indwelling stomach tube)

monitor ins and outs
T/F: fluid replacement is critical with DPJ
true: IV required, monitor e-lyte status, hydration, and body weight
Tx for DPJ
anti-inflamms (NSAIDS or lidocaine)
prokinetic therapy (metoclopramide, bethanecol, erythromycin)
nutritional support (NPO >72 hours)
laminitis prophylaxis (endotoxemia!!)
What are some possible complications of DPJ?
adhesion formation
pharyngitis/esophagitis (can lead to eso rupture)
cardiac arrhythmias

(duh duh DUUUUUHHHHH!!)
What is obstruction?
something that's in the lumen that plugs it

mechanical obstruction
luminal obstruction impeded flow of ingesta but NO interruption of blood flow
What is strangulation?
something from outside the lumen that also cuts off blood supply

mechanical obstruction
occlusion from serosal surface
both lumen and blood supply interrupted
could result in devitalized bowel --> endotoxemia, hemoconcentration, dehydration
c/s of obstruction
mild --> moderate pain
good response to analgesia
minimal CV compromise
peritoneal fluid WNL
+/- gastric reflux
+/- need to surgery
c/s of strangulation
mild, moderate, or severe pain
only brief response to analgesia
CV deterioration (endotoxemia, hemoconcentration, dehydration)
peritoneal fluid abnormal
+/- gastric reflux
what can cause obstruction in the SI of a horse?
ascarid impaction (roundworm)
ileal impaction
almost done almost done almost done...shit, there's another packet.
what is the name of the equine roundworm?
Parascaris equorum
What is the signalment for horses with roundworm?
typically <1yr bc resistance at ~18-24 mos
affects foals w/poor deworming hx
How do the worms cause colic?
adult worms live in lumen of SI tract

if there is a heavy burden, deworming can cause all the worms to die and obstruct the lumen
C/S of roundworm impaction
gastric reflux (worms!!)
How do you dx roundworm impaction?
abdominal U/S
nasogastric fluid
peritoneal fluid
how do you tx roundworm impactions?
gastric decompression/lavage
anti-inflamm therapy
surgery- worms are toxic and damage wall of SI so necrosis/bowel rupture is not uncommone
Prognosis for roundworm impaction
guarded due to severe inflamm resposne triggered by the death of the adult worms
medical resolution for impaction has a more favorable prognosis than surgical
When should you first deworm a horse?
~60 days (repeat 2-4 months after)
What are the roundworms resistant to?
What is the best choice for prevention of roundworms?
Best antihelmintic depends on what?
farm sensitivities and FEC
How would you treat a foal who is suspected to have a very large worm burden?
use a less effective antihelmintic to reduce mass killing and possibly avoiding the risk of obstruction
What is this caused by/
coastal bermuda grass
When can you feel the ileus on rectal palpation
early in dz
T/F: peritoneal fluid will be normal
true bc it's nonstrangulating
can the impaction resolve w/o tx?
possible - natural motility may resolve it (myenteric plexus)
Early tx
analgesia, IV fluids, mineral oil ?

monitor vitals closely
monitor for escalation of pain
Late tx
gastric decompression

+/- surgery
deterioration in peritoneal fluid
prognosis for ileal impaction
good, though postoperative ileus is a risk (distention of bowel, inflammation)
How do you prevent ileal impaction?
avoid coastal bermuda grass
course fibrous feeds
proper deworming (tapeworms sometimes perturb ileal motility)
And the question is "things we're like to do to most of the people on this island..."
What can cause strangulation of the SI?
Si volvulus
abdominal incarceration (epiploic foramen entrapment, mesenteric rent, gastrosplenic ligament, inguinal ring hernia)
pedunculated lipoma
What are the types of intussusception? (3) Which is most common?
*ileo-cecal - most common
How does an intussusception work?
oral segment (intussusceptum) invaginated into aboral segment (intussusceptiens) towards the rectum --> telescoping bowel obstructs the flow of ingesta --> oral segment becomes distended
T/F: intussusception may involve any portion of the GI tract
intussusceptions are most common in what age/
young (<3yrs)
foals and weanlings
What can cause intussusception/
deworming, abrupt dietary changes, GI parasitism
What type of intussusception do ascarids like to cause?
jejuno-jejuno intussusception
What type of intussusception do tapeworms like the cause?
ileocecal and ileocolic intussusceptions
intussusception are usually acute or chronic?
acute (chronic in rare cases)
What will you find on rectal exam?
dilated SI
What will you see on U/S?
target lesion/bulls-eye
T/F: peritoneal fluid will be normal
false: it will be abnormal bc blood supple is strangulated by the intussusception itself
Tx of intussusception
resection and anastomosis
T/F: You can pull an intussusception apart in sx and it be fine
FALSE!!!! bc it WILL happen again
Prognosis of a simple intussusception
prognosis of ileocecal intussusception
guarded bc the devitalized ileum must be resected and a jejunocecostomy is required

will get necrosis of ileal stump
What type of worm can cause intussusception?
tapeworm (Anoplocephala perfoliata)
Where dose this worm like to be?
affinity for ileum/cecum

ileocecal intussusception
cecocolic intussusception

You will see NO proglottids in the feces
How do you dx tapeworm intussusception?
U/S, poor deworming hx
How do you prevent tapeworm intussusception?
T/F: horses can live w/o the cecum bc the colon can pick up enough slack
Where does the Si twist?
root of the mesentery (complete interruption of intestinal blood supply)
This is a common cause of colic in what age?
young foals
T/F: SIV can be caused by GI parasitism
It is really really bad if which artery twists?
cranial mesenteric artery bc all of the SI is supplied by it
c/s of SIV
gastric reflux
poor tissue perfusion
absent borborygmi
distended SI onr ectal
serisanguinous peritoneal fluid (incr WBC, incr TP, metabolic acidosis --> prod'n of lactate)
Tx of SIV
surgical intervention
How much of the Si can be resected?
</= 50%
Why can't you resect > 50%?
short bowel syndrome
Bowel may pass through a mesenteric rent,m inguinal ring, the gastrosplenic ligament, or the epiploic foramen
T/F: mesenteric rents are often iatrogenic
false: they're often idiopathic (blunt abdominal trauma or accident)
Inguinal hernias occur in whom?
stallions (must always palpate scrotum!!!)
The gastroplenic ligament is what?
the lesser omentum (connect stomach to spleen)
Where is the epiploic foramen?
right craniodorsal abdomen

landmarks: caudate lobe of the liver, caudal vena cava, portal vein, pancreas
SI incarceration most commonly involves what?
the ileum (required jejunocecostomy for repair)
How do you definitely dx this? Why?
must take to sx to definitely diagnose SI incarceration bc all you can see on exam is gas/fluid distention and gastric reflux building
in SI incarceration, bowel lumen occlusion is from where?
serosal surface, not luminal space
prognosis for SI incarceration
fair for most conditions (higher survival rates coincide with early prompt surgical intervention)
What are the potential post-op complications?
adhesion formation
sound funny...
what is a lipoma and how does it cause strangulation?
fatty "tumor" w/pendulous stalk, surrounds loop of bowel, causes strangulation
What is the usual signalment for this?
arabians (overrepresented)
older horses (8-20 years)
fat geldings
What c/s will you see?
acute colic
tx for pedunculated lipoma?
sx to remove lipoma
good (though same complications: POI, adhesions)
Why would you think this is a luminal obstruction?
dessicated feed may be palpated in the large colon w/a strangulating lipoma, but this is not a "typical" feed impaction
--> take a look at the patient!! CV deterioration is NOT a c/s of luminal obstruction (incr HR, poor CRT, cold distal extremities --> NOT IMPACTION!!)
LAST PACKET PAST PACKET PAST PACKET (this is gonna take forever)
Diarrhea is the primary sign of what
LI dz (colon)
In adult horses, what is diarrhea considered?
What is colitis?
ACTIVE inflammation of the colon
cardinal sign of colitis
diarrhea (though not all patients with colitis have diarrhea
What is the acute colitis affector cell?
c/s of colitis
peripheral edema (hypoproteinemia)
colic pain (may be so intense it mimics sx lesion) - appears to escalate before onset of diarrhea (cramping)
+/- gastric reflux
Why do a rectal exam?
some horses with Si impaction may have diarrhea
what will you see on bloodwork with colitis?
PLE (inflamed colon wall)
**neutropenia w/left shift (toxic neutrophils) (cells marginated)
metabolic acidosis
**hyponatremia (Na dumped into GI)
What are the 4 things in bloodwork that should be the Big TipOFF
neutropenia w/left shift
metabolic acidosis
What will you see on abdominal U/S?
swirling fluid in colon/cecum
may see dilated SI
may see excess peritoneal fluid, possibly peritonitis (thickened colon wall)
d/dx for colitis
potomac horse fever
grain overload
cantharidin toxicity
r/o causes of chronic diarrhea (right dorsal colitis, sand enteropathy, cysthostomiasis)
definite diagnosis of colitis
May be difficult to achieve
use of signalment, hx, and season/time of year

fecal bacterial cultures
bacterial toxins in feces
What is the bright side about the tx of colitis?
no matter what the cause is, they're treated the same: supportive care

aggressive fluid therapy (colloid and crystalloid)
anti-endotoxemic therapy (NSAIDS, equine plasma, polymixin B, crytherapy)
antidiarrheals, antimicrobials
Why is hypertonic saline dangerous in this patient?
idiogenic osmoles --> can swell brain (answer in fluid therapy section)
What oral antidiarrheals can be used?
bismuth subsalicylate (pepto)
which antimicrobials?
penicillin + gentacin
oxytetracycline good for potomac fever (summer)
What are some complications of colitis?
prolapsed rectum
infarcted bowel
Since salmonella, clostridium, potomac horse fever (PHF), grain overload, and cantharidin toxicity all cause acute fever and have common c/s, we'll be look at the differences today
Most common serotype of salmonella in horses
S. typhimurium
T/F: there is no enteric host-adapted spp of salmonella in horses
Where is salmonella a big problem?
nosocomial infections in hospitlas
salmonella: transmission
T/F: zoonotic potential
risk factors
diet change
general anesthesia
small colon impaction
younger, older, sick more susceptible
pathophys of salmonella
bacT invades mucosa --> ungulfed by MO --> endotoxin produced --> Na/Cl/H2O into GI lumen --> impair mucosa barrier --> inflamm response --> PMNs attracted --> local tissue damage --> endotoxin
What will you see in the bowel lumen?
hypersecretion, ulceration, and protein/e-lyte loss
What cause the virulence of salmonella?
it's ability to survive in the MO
How do dx
c/s, bloodwork (neutropenia, hypoproteinemia)
fecal bact culture (at least 5 take 2 day apart)
PCR of feces/tissue/blood (at least 3 negative)
rectal mucosal biopsy
T/F: It's likely the horse is shedding salmonella
false: unlikely
mortality rate is variable (prolonged diarrhea/sepsis decr prognosis)
What is a reall poor prognostic indicator?
Why is biosecurity so important?
positive horses scan shed for days to months
Salmonella at a glance
decr appetite
+/- mild colic signs
C. perfringens (most common)
C. difficile
What is clostridium?
G(+) spore forming anaerobic rod (normal intestinal flora)
how can is overgrow and colonize the colonic mucosa?
antimicrobial therapy alters microflora
What is antibiotic associate diarrhea
antimicrobials interrupt intestinal microflora and cause this
most common ABx that cause antibiotic assoc diarrhea
erythromycin PO
ampicillin PO
lincomycin PO
Which clostridium is most common after ABx?
C. difficile
T/F: use of probiotics has been shown to prevent antimicrobial assoc diarrhea
What is the most pathogenic type of clostridium?
C perfringens type C
How does clostridium cause diarrhea?
elaboration of exotoxins cause enterocyte damage and incr intestinal permeability
T/F: Hemorrhage diarrhea is uncommon
false: it's common
why is definitive dx hard?
bc it is part of the normal flora
best techniques for dx
ELISA identification of toxins (A/B)

suspect is hx of Abx tx
site and smell
Which clostridium produced toxins A & B>
C difficile
How do you tx clostridium?
supportive care and laminitis prophylaxis

mortality rate is high
aka Shasta River Crud
Equine Monocytic Erhlichiosis
Potomac horse fever is a ...?
water based dz
caused by

this is carried by ?
neorickettsia risticii

flukes that infect aquatic insects/snails (horse grazing in pastures near fresh water)

ingestion of vector

late summer, early fall (warmth)
How does Potomac horse fever work?
N. risticii infects monocytes w/affinity for GI mucosa (blocks phago-lysosome fusion --> proliferation)

Early dz: infiltration of MO, mucosal damage
late dz: fibrinous, necrotizing typhlocolitis (cecum & colon)
c/s of Potomac horse fever
direct mucosal damage by N. risticii
upregulation of inflammatory mediators
60% have diarrhea
30% have laminitis
abortion syndrome

may be subclinical
**if ANY horse has decr appetite, chance in attitude, and fever, what do you do?
How do you dx?
serology- paired titers 9acute, convalescent samples
PCR detects antigen in blood or feces
tx for Potomac horse fever
**Oxytetracycline (dilution required bc Ca binding/"stone heart" --> will stop the heart)

if you don't see a difference in 24-48 hrs, it's something else
Prognosis of Potomac horse fever
5-30% fatal

several vaccines available (poor efficacy)
what are the most frequent complications?
laminitis and abortion
aka Blister Beetle Toxicity

swarm pastures in the southeasst
Where is cantharidin found?
it is a mucosal irritant found in blister beetles

ingestion of just 4 or 5 beetles can do the tricdk (c/s w/i hours)
how do horses get it?
**accidental ingestion most common when horses eating alfalfa hay
How does it work?
absorbed from GI, eliminated in kidneys

toxin acts as a mucosal vesicant: interrupts mitotic activity, altered cell permeability --> cellular lysis

cardiac muscle necrosis (not fully understood why)
reflect mucosal irritation
oral (salivation)
GI (colid and diarrhea)
urinary tract (hematuria, stranguria) ulceration

myocarditis (incr CK, cardiac troponin I) - can suffer fatal arrhythmias
What is the most distinguishing feature(s) of bloodwork with cantharidin toxicity?
What else (cardiac) may occur?
synchronous diaphragmatic flutter ("Thumps")
How do you dx cantharidin toxicity?
suspect in patients with hypocalcemia and concurrent GI/urinary signs
hx confirmation of eating alfalfa
observation of beetles
detect in gastric contents and urine
prognosis of cantharidin toxicity
>/= 50% fatality rate
if patient survives several days, recovery is possible
high CHO content
what can cause grain overload?
ingestion of heavy concentrate feeds
high starch/NSC content
how does this cause colic?
inappropriate ore-cecal digestion: insufficient amylase, too much CHO to cecum --> prolif of certain flora (lacto, bac, strep) --> incr lactate/proprionate --> decr cecal pH to 6 --> impairs normal flora --> decr fermentation, cecal/colonic dysmotility, subsequent gas distention, colic pain and laminitis
c/s of grain overload
colic (may be severe)
severe gas distention/bloat
GI ileus
tx of grain overload
gastric lavage (early)
mineral oil/charcoal
anti-endotoxemic therapy
laminitis prophylaxis
*severe gas distention may lead to abd compartment syndrome --> cecal trocharization
How much is too much grains?
feeding > 2.7 kg of oats/day incr risk of colic by 6xs

2g/kg/Bwt of starch/meal
sand colic
Whereis there a high prevalence of sand enteropathy?
S. Carolina
Coastal regions
c/s of sand enteropathy
-mild abdominal pain to severe acute pain (complete obstruction)
-diarrhea is common (small volume, evidence/fecal staining on tail)
-if acute obstruction --> endotoxemia signs
What will bloodwork look like?
ACUTE: neutropenia and left shift, colitis, endotoxemia, +/- hypoproteinemia, bright red mm

CHRONIC: +/- neutropenia, incr fibrinogen, PLE/hypoproteinemia
how do you dx sand colic?
may be palpable in feces (do fecal float)
peritoneal fluid = normal
U/S: haustra disappear
how do you tx sand colic?
mild colic: oral & IV fluids, analgesics for pain, anti-inflamms, therapy directed at removing sand over time (psyllium/metamucil)

possible pelvic flexure enterotomy to remove sand
how do you prevent sand colic?
management changes are VITAL
--provide hay in racks
--avoid overgrazing pastures
--prophylactic administration of psyllium to horses at risk
aka NSAID toxicity
What do NSAIDS do?
cause inhibition of COX pathway
when does colonic damage occur?
with overdose or at recommended doses to horses w/incr sensitivity
c/s of acute right dorsal colitis
similar to salmonella & sand colis

colic pain
depends on size of inflamm lesion
c/s of chronic right dorsal colitis
**edema <-- hallmark c/s
T/F: the right dorsal colon is most sensitive to NSAIDS
true (duh) thought mechanisms remain unclear
how do you dx right dorsal colitis?
c/s and hx
bloodwork (loss of albumin, neutropenia, incr fibrinogen)
may be dx of exclusion
U/S evidence (thickened wall)
What may accompany right dorsal colitis?
GI ulceration and renal papillary necrosis
How do you tx right dorsal colitis?
supportive care (may require COP support)
discontinue NSAIDs
dietary modification (feed complete pelleted rations may reduce mechanical load on colon)
corn oil (helps mucosal barrier)
synthetic PGs
Best pain management
lidocaine CRI (opioids decr intestinal motility and NSAIDs caused the problem in the first place)
prognosis for right dorsal colitis

complications: laminitis, colon rupture, colonic infarction, colonic stricture
small strongyles

(why do these keep coming back??)
What are the two life cycles?
1: L3 ingested --> cecal/colonic mucosa --> mature to L4 --> GI lumen --> complete life cycle in 5-6 weeks --> diarrhea

2: L3 ingested --> cecal/colonic mucosa and remain there --> encysted/hypobiotic for months to years --> very sick horses
Why does diarrhea occur?
occurs as a massive excystation (may present as acute colitis)
if chronic diarrhea develops, what is a significant c/s?
weight loss
When does this occur?
seasonal: end of winter, early spring
How do you tx cyathostomiasis?
many strains resistant to benzimidazole (fenbendazole)

moxidectin (>90% resolution in 1 week)

severe infestations: may be seen in feces or rectal sleeve
I may kill someone when i'm done
risk factors
ingestion of coarse feeds
meal feeding concentrates (water sucked out of ingesta)
inadequate mastication
poor dental health
insufficient water supply
*reduced water intake (one of the most common causes of constipation)
What are the most common sites of impaction? (2)
areas of luminal narrowing

pelvic flexure (left ventral colon region)
right dorsal colon (transverse colon junction)
feed impaction = ?
c/s of LI impaction
mild intermittent colic
decr appetite
signs of mild dehydration
mild tachycardia
borborygmi present
reduced fecal output
What will you find on rectal exam?
an unmistakable lesion!

large, firm mass in pelvic flexure (typically sits in pelvic inlet)
Is anything else abnormal?
NG tbe; no reflux
peritoneal fluid normal
What do you use as a marker for intestinal motility?
mineral oil (see if it's coming out the other end
how do you tx LI impaction?
**enteral fluid therapy (isotonic)
--goal is to overhydrate the colon and soften the feed
--also stims gastrocolic reflex
magnesium therapy: creates osmotic gradient into lumen
if more serious: cecal trocharization
What is a BIG NO-NO??
no food by mouth!

NPO until impaction is resolved with NO exceptions
T/F: horses will pass many piles of manure as an impaction is resolving
true (do serial rectal exams)

risk of reimpaction so go slowly when refeeding and monitor water consumption and fecal output
nephrosplenic ligament

(roll that horse, baby!!)
Where does the left dorsal colon become entrapped?
nephrosplenic ligament (no, really?)
c/s of nephrosplenic entrapment
-mild to severe colic
-perfusion parameters are normal
-rectal exam: taenia of LVC palpable coursing dorsocranially to L kidney, spleen enlarge and displaced cranioventrally
-peritoneal paracentesis: normal
-possible reflux
What will a normal U/S look like? What will a U/S look like with this?
normal: spleen, kidney, colon

nephrosplenic entrapment: can't see kidney
How many tx options are there?
What is option 1?
IV fluids
allow time for colon to empty
entrapment MAY resolve
What is Option 2?
alpha1 administration --> constricts spleen --> jog horse --> may bounce colon out of that spot

may combine with option 1
What is option 3?
roll the horse (requires short time general anesthesia): dropped to R lateral --> rolled thru dorsal to L later --> make complete 360 rotation

may combine with option 2
What is Option 4?
surgery (necessary when 1, 2, and 3 don't work)

reserves for those w/severe gas distention and pain
How do you prevent this?
chronic offenders: ablation of nephrosplenic ligament, colopexy, colonic resection