Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
794 Cards in this Set
- Front
- Back
|
What is a neonate?
|
under 1 month
|
|
|
How old is a yearling?
Long-yearling? Adult? |
12-18 mo
18-24 mo >2 years |
|
|
Name "size" characteristics of a "light" horse?
|
>15 hands tall
<1500 lbs ("hot blooded" temperament) |
|
|
What are 4 diseases Thoroughbreds are predisposed to?
|
Recurrent Exertional Rhabdomyolysis
Exercise Induced Pulmonary Hemorrhage Gastric ulcers OCD |
|
|
What 3 diseases are Arabians predisposed to?
|
SCID
Cerebellar abiotrophy Idiopathic epilepsy |
|
|
What 3 diseases are Quarter Horses predisposed to?
|
Hyperkalemic Periodic Paralysis
Polysaccharide Storage Myopathy HERDA |
|
|
What 2 diseases are Standardbreds predisposed to?
|
Musculoskeletal racing injuries
Granulomatous Enteritis |
|
|
How do you impress a Standardbred owner?
|
by knowing it's a pacer if he's got hair loss from the hobbles (or a trotter if he doesn't)
|
|
|
What are Tennesseee Walkers predisposed to?
|
inguinal hernias
|
|
|
What 2 diseases are Belgians predisposed to?
|
Junctional Epidermolysis Bullosa (foals)
PSSM |
|
|
What organ do Fresians have a lot of problems with?
|
esophagus
|
|
|
What 3 diseases are Fresians predisposed to?
|
Megaesophagus
Esophageal Hypertrophy Neonatal dysphagia |
|
|
What dise are Minis predisposed to?
|
fecaliths!
|
|
|
What is the key difference between an equine owner & a dog owner?
|
the equine owner does a lot of research & self-medicates her horse w/ everything from dewormers to NSAID injections to supplements.
You MUST ask specific questions to find out what meds your patient has received |
|
|
What are the core vx?
|
EEE
WEE WNV Tetanus Rabies |
|
|
Most horses that colic have had what change in the previous couple weeks?
|
feed change (schedule, actual food, etc)
|
|
|
What is the link between lameness & colic?
|
Many (most?) owners will self-medicate w/ NSAIDs when their horse is lame--these meds predispose to colic
|
|
|
PEing the cow, we start w/ its rear. Where do we start on the horse?
|
w/ the face
|
|
|
What is the #1 cause of icterus in horses?
|
fasting hyperbilirubinemia
|
|
|
What 3 arteries do we use for pulse pressures?
|
facial
transverse facial great metatarsal |
|
|
Why do some practitioners palpate the larynx?
|
cause some of them can feel if a CAD muscle is atrophied--ie w/ laryngeal hemiplagia
|
|
|
What is the primary IM injection site in the horse?
|
neck (middle bottom part....E in the pic)
|
|
|
What are the other major IM injection sites in the horse (besides the neck)?
|
bw the semimembranosus & semitendinosus
pectorals gluteals (not great opportunity for drainage tho) |
|
|
What is the primary site for venapuncture?
|
jugular (upper 1/3)
|
|
|
What are other sites of venipuncture?
|
facial sinus & cephalic vein
|
|
|
What is the normal HR of a horse?
|
24-44
|
|
|
Which muscle are the valves deep to?
|
triceps
|
|
|
How do you know when systole is occurring in a horse?
|
it's from S1-->S2 (so anything from S2-->S1 = diastole)
|
|
|
What does S1, S2, S3, S4 represent?
|
1--closure of AV valves
2--closure of SL valves 3--early diastole/rapid filling of ventricles 4--atrial contraction |
|
|
What is sinus arrhythmia?
|
normal irregularity heard in conjunction w/ the respiratory cycle
|
|
|
T/F A 2nd degree AV block can be pathologic or non-pathologic.
|
True
|
|
|
How do you STOP a non-pathologic 2nd degree AV block?
|
by briefly exercising the horse (to inhibit the high vagal tone that is making the block occur)
|
|
|
Describe the audible intensity of Grades I-VI murmurs.
|
I--barely
II--very soft III--low-moderate IV--loud V--loud w/ thrill VI--don't need stethoscope to hear it |
|
|
What shape is the lung field?
|
triangular =)
|
|
|
What do you always have to auscult when listening to respiratory sounds?
|
the trachea!
(this is also an easy spot to get RR) |
|
|
T/F Normal equine respirations involve abdominal effort.
|
false
|
|
|
What is the normal RR?
|
8-15
|
|
|
Which sound is louder--inspiration or expiration. Why?
|
Inspiration because it is an active process (vs expiration which is passive)
|
|
|
Describe crackles, wheezes, pleural friction rubs.
|
crackles = fine popping or bubbling sounds
wheezes = musical notes pleural friction rub = fine grating sound from pleuritis |
|
|
What might you palpate on the distal limbs that signal laminitis?
|
bounding digital pulses
|
|
|
Hot hoof capsule =
|
laminitis
|
|
|
Why do we turn horses in small circles?
|
to detect lameness
|
|
|
What normal temp in horse?
|
99-101.5
|
|
|
Equine TPR =
|
T = 99-101.5
P = 24-44 R = 8-15 |
|
|
What are the daily requirements of water & digestible hay?
|
50 ml/kg/day
16-30 mcal/day |
|
|
How much hay should you feed a horse a day?
|
1.5-2% BW (in POUNDS)/day
|
|
|
What is a cause of colic signs specific to stallions?
|
scrotial hernia
|
|
|
T/F Weaning fucks w/ their mental & GI health.
|
true
|
|
|
What hormone do we use for estrus control in mares?
|
progesterone
|
|
|
What are some reasons for ovariohysterectomy of mare?
|
it's never done
Ovariectomy is done for GCTs |
|
|
What is a very common cause of poor performance in racehorses?
|
EIPH
|
|
|
What is a young racehorse filly prone to?
|
Tying Up aka RER
|
|
|
What predisposes racehorses to gastric ulcers?
|
high stress, high calorie diet, use of NSAIDs
|
|
|
What is the job of the cerebellum? (3)
|
rate, range, force
|
|
|
T/F Arabian foals are born w/ an abiotrophied cerebellum.
|
false--it withers up AFTER birth
|
|
|
What is SCID?
|
lack of T-cells, which causes infections showing up at 2-3 mos of age due to mothers Ab wearing off
|
|
|
Describe idiopathic epilepsy in Arabian foals.
|
transient, treat w/ phenobarb & gradually wean them off
|
|
|
What causes HYPP in Quarter Horses?
|
ATPase pump mutation--K+ is pumped out of cells
Can be bad enough to cause recumbency then death |
|
|
What is HERDA & who gets it?
|
Hereditary Equine Regional Dermal Asthenia
collagen dysfunction, which causes skin to be separated from the underlying collagen--this is usually seen when the horse is put under the saddle for the 1st time. irreversible, incurable, excruciatingly painful, euthanize. |
|
|
How long are harness races, and what is a horse's ''mark?"
|
exactly 1 mile
All the SBs take over a minute to finish, so if they say the horse's mark is 50 that means he runs it in 1:50 |
|
|
What form of IBD is "very very very common" in standardbreds?
|
granulomatous enteritis
|
|
|
Which breed is EVA very common in?
|
standardbreds
(she said it in class) |
|
|
What is soring?
|
making the bottom of the foot hurt so when the horse puts it on the ground it quickly snaps it back up = for racking
|
|
|
Describe what's wrong with a Lethal White foal.
|
No motility neurons of the GIT formed during gestation.
The GIT is patent, but can't pass meconium or move milk thru. The baby is colicky the 1st day of life. They are white with blue eyes (but not all white/blues are Lethal Whites) aka Ileocolonic agangliosis |
|
|
What is Moon Blindness?
|
equine recurrent uveitis
It is common in Appaloosas, & if Moon Blindness is going to progress to actual blindness, it's likely going to happen in Apps |
|
|
Where do Appaloosas get SCC?
|
pale, unpigmented skin like the eye, muzzle, .... perineum?? might have typed that wrong tho
|
|
|
Draft horses usually weigh...
|
1 ton (2000lb)
|
|
|
What do we have to remember about Draft horses if we get a call that one is down & colicking?
|
Drafts are very stoic. If they show pain chances are the disease process is advanced & you need to get there ASAP
|
|
|
What dz is common in, & restricted to Belgians?
|
Junctional Epidermolysis Bullosa
|
|
|
What is a JEB foal's problem?
|
deterioration of the mucocutaneous junctions... hooves slough, oral mucosal lesions
Euthanize |
|
|
What color are Clydesdales?
Belgians? Percherons? |
Clydesdales are all bay
Belgians are chestnut or sorrel w/ a white (aka flaxen) mane & tail Percherons are gray or black |
|
|
What would make you suspect Neonatal Dysphagia in a Fresian foal?
|
milk at the nostrils
|
|
|
What are some problems Minis have?
|
lots of dental problems
they're usually overfed therefore fat fecaliths often born w/ narcolepsy, which luckily they outgrow |
|
|
How short does a Mini have to be?
|
under 34-38 inches....soo under 34 inches? haha
|
|
|
What are fecaliths & where do they occur?
|
fecal impactions in the small colon (aka descending colon)
|
|
|
Who starts performing earlier in life--Thoroughbred racehorses or Olympic warmbloods?
|
thoroughbreds.... the warmbloods mature later in life & don't start performing til they're 6-8 yrs old!
|
|
|
How do you describe an insidious onset of colic?
|
horse kinda went off feed over the past few days, maybe kicked at his stomach every now & then, and then he's down
(vs acute in which he's fine one minute & down the next) |
|
|
What do Weanlings almost always get?
|
Snots
|
|
|
Name 2 respiratory agents in horse.
|
herpes-1 & equine influenza
|
|
|
EHV-1 --> ______ disease in older horses if it mutates
|
neuro
|
|
|
What's the problem with EHV-1 vx??
Who should you vx for EHV-1? |
it doesn't protect against the neuro aspect of the disease, & in fact vaccinated horses are more likely to get the neuro form??
you should vaccinate large groups of pregnant broodmares when they're pregnant (vs 3-4 horse facilities) |
|
|
How do horses get Tetanus?
|
cuts & wounds usually (always?)
|
|
|
Why not vx @ EVA?
|
Very strict regulations--they can't tell whether the Ab detected on titers is from the vx or is the wild-type so it makes export?/import? a nightmare
|
|
|
Why not vx @ Strep equi equi (which causes Strangles)?
|
not very efficacious
|
|
|
80% of colics have had a feeding change within the past ____
|
2 weeks
|
|
|
What zoonotic bacteria is shed in feces of stressed horses?
|
Salmonella
|
|
|
Why are trailered horses at risk for pneumonia?
|
they cough w/ their head down, but when they're being trailered there head is tied up, so their mucociliary escalator can't do its job.
Strep (natural inhabitant of the pharynx) is one of the agents that cause lower respiratory disease in these cases |
|
|
Do horses get Shipping Fever?
|
yes but I don't know that Mannheimia hemolytica is the cause (like in cattle).
|
|
|
How will a horse w/ hyperammonemia from liver disease present mentally?
|
he'll be obtunded
|
|
|
What is Cushings called in horses & why?
|
pars intermedia dysfunction because it rarely involves the adrenal gland
|
|
|
The Suspensory Apparatus is for...
What is a very painful disease of the suspensory apparatus? |
stability of the fetlock
suspensory laxity --> overextension of the fetlock |
|
|
Where do cranial nerves come from?
|
the base of the brain...
|
|
|
What muscle do you have to fight to open a horse's eye?
|
orbicularis oculi, it's a strong one
|
|
|
What might you suspect if a horse has tortuous sceral vessels?
|
endotoxemia
|
|
|
Fasting hyperbilirubinemia occurs after only a short period of fasting in the horse because of the short half-life of...
|
ligandin
|
|
|
What's one of your rule/outs if a horse has bright hyperemic mucous membranes?
pale? |
bright = endotoxemia
pale = hemorrhage or anemia |
|
|
What is Pulse Pressure?
|
the difference between systolic & diastolic blood pressures
|
|
|
What does a strong pulse pressure indicate?
|
good blood volume
|
|
|
Where is the:
Facial a Transverse facial a Great Metatarsal a |
facial is under the mandible
transverse facial is just behind the lateral canthus of the eye great metatarsal a is .... on the leg... |
|
|
Besides taking pulse pressure, what is the Great Metatarsal artery good for in foals?
|
good site for arterial blood gas sample in a FOAL
|
|
|
Where do you evaluate skin tenting in a horse?
|
neck or shoulder
|
|
|
What causes Strangles & where do the retropharyngeal LN live?
|
RPs live up underneath the guttural pouch
Strep equi equi --> Strangles (which causes swelling of the RP & submandibular? LN) |
|
|
What should the normal guttural pouch feel like?
|
sunken area behind the ramus of the mandible
|
|
|
What are the 3 borders of where you should give the neck IM injection?
|
nuchal lg
top of cervical vert shoulder musculature |
|
|
Why don't you want to give an IM injection in the gluteals?
|
poor drainage opportunities
|
|
|
What does jugular vein "fill" tell you about a patient?
|
hydration status
|
|
|
Why don't you IM inject a foal''s neck?
|
if it gets sore he wont extend his neck to nurse
|
|
|
Why won't you IM inject the triceps muscle?
|
if they get sore they won't walk
|
|
|
Why don't you inject meds into the carotid artery?
|
cause the brain wants everything to be detoxified thru the liver before it reaches it. if you inject into the carotid artery it'll go straight to the brain unchanged
|
|
|
Where on the neck are you going to stick to get your jugular blood sample?
|
upper third, just below the jugular bifurcation (which occurs at the ramus)
|
|
|
Where is the facial sinus located?
|
just under the facial crest
|
|
|
Where is the cephalic vein located?
|
medially, just above the carpus
great for a.m. low volume draws, ie PCV/TS |
|
|
A horse's resting HR is 24-44 bpm. Why is it so low?
|
because of high vagal tone
|
|
|
Instead of panicking because you're so dumb you can't find the horse's heart (me in 2 weeks), what are you going to do w/ your stethoscope?
|
go high! their hearts are huge & much more dorsal than a dog's!
|
|
|
bah Lub Dub click bah Lub Dub click bah Lub Dub click
|
4 1 2 3 4 1 2 3 4 1 2 3
That's a horse's heart rhythm |
|
|
What does any sound between S1 & S2 mean?
|
that it's happening during systole
|
|
|
What does any sound between S2 & S1 mean?
|
that it's happening during diastole
|
|
|
What is occurring to cause the 3rd heart sound?
|
the ventricles fill (sounds like a click as they suck the blood in...idk, make the sound w/ your mouth it kinda makes sense i guess)
|
|
|
What produces the 4th heart sound?
|
atrial contraction
|
|
|
Do horses have sinus arrhythmia?
|
not really
|
|
|
What does 2nd degree AV block look like on ECG?
|
skipped QRS complex (just a P wave representing atrial contraction)
|
|
|
Why does non-pathological 2nd degree AV block occur in horses?
|
because the vagal tone is so high
|
|
|
What 3 questions do you ask yourself to describe a murmur?
|
PMI?
Occurring during systole or diastole? Which valve? |
|
|
Don't forget to auscult the trachea
|
Don't forget to auscult the trachea
|
|
|
Normal # of respirations per minute?
|
8-15
|
|
|
What are flared nostrils a sign of?
|
not good--difficulty breathing
|
|
|
You are examining a horse that was in a trailering accident. He is having difficulty breathing.
Dorsally there are no lung sounds, tho ventrally there are. What do you suspect? |
pneumothorax (air rises)
|
|
|
A horse is dyspneic & febrile. Ventrally there are no airway sounds. What do you suspect?
|
pleural effusion (water sinks)
Do an U/S to ocnfirm diagnosis |
|
|
Colic w/ no gut sounds =
|
BAD
|
|
|
You want to be sure to auscult where on the horse's abdomen?
|
just cranial to the paralumbar fossa, & ventral
|
|
|
Why do we have to palpate each limb no matter what the chief complaint?
|
because lameness is so common in horses, no PE is complete without checking out the legs
|
|
|
Distal limb edema =
|
hypoproteinemia or diarrhea
|
|
|
Edema & swelling of the coronary band =
|
acute laminitis
|
|
|
Hot hoof =
|
laminitis
|
|
|
What do you always have to palpate in horse limb?
|
digital pulses
|
|
|
What do you have to remember about taking a horse's rectal temperature?
|
wear gloves
stand to the side of him do it at the very end of the exam |
|
|
When is a rectal exam warranted in a horse?
|
if he has colic or weight loss
|
|
|
EQUINE CLINICAL NUTRITION PACKET
|
EQUINE CLINICAL NUTRITION PACKET
|
|
|
What two diseases are a result of domesticating the horse & feeding a large amount of concentrate feeds?
|
colic & muscle-associated dz
|
|
|
What 5 structures make up the hindgut aka Lg Intestine? That's right, 5.
|
cecum
large ascending colon transverse colon small descending colon rectum |
|
|
Is the small intestine part of the foregut or hindgut?
|
foregut. the hindgut starts w/ the cecum
|
|
|
The foregut is responsible for digestion & absorption of which 6 things?
|
protein
fat sugar starch water vitamins minerals |
|
|
The hindgut is responsible for digestion of what?
|
grasses/grains (cellulose, hemicellulose)
|
|
|
Is lignin digestible?
|
nope
|
|
|
What nerve is responsible for a food bolus reaching the back of the throat so the horse can swallow?
|
hypoglossal, CN XII
|
|
|
T/F Horses don't get foreign bodies in their tongues.
|
False. It's not uncommon, so always check for it
|
|
|
Horses have a particular way of chewing called:
|
lateral excursion
|
|
|
Hypsodont teeth continually
|
ERUPT, NOT grow
|
|
|
Which is wider, the mandible or maxilla?
|
maxilla
|
|
|
Who has canine teeth?
|
males only
|
|
|
4 signs of poor dental health =
|
quidding (dropping feed)
weird head position while chewing weight loss colic |
|
|
What is a risk of dental work?
|
pneumonia
|
|
|
What are the 3 equine salivary glands?
|
Parotid, Submaxillary, Sublingual salivary gland
|
|
|
Submaxillary LN according to google are more commonly known as...
|
submandibular
|
|
|
Amylase comes from what two sources?
|
saliva & pancreas (a lot more from the pancreas)
|
|
|
When do horse's stop salivating?
|
when their parasympathetic system is interrupted--they do NOT stop salivating when they're fasting, which leads to dehyration & possible hypovolemia
|
|
|
Loss of water & bicarb (via saliva) can lead to
|
dehydration
|
|
|
What's the stomach's holding capacity?
|
8-12 L
|
|
|
How much water per day are horses supposed to drink?
|
8-12 gallons a day
|
|
|
What's the stomach's capacity?
How much water per day are horses supposed to drink? |
8-12 LITERS stomach capacity
8-12 GALLONS/day don't mess it up |
|
|
What is probably the main reason horses can't vomit?
|
there is very very very high pressure in the lower esophagus
|
|
|
What two types of mucosa are in the equine stomach?
|
squamous & glandular
|
|
|
What 3 enzymes are secreted by the equine stomach?
|
pepsin, gastrin, HCl
|
|
|
Which 2 mechanisms does the horse have to maintain gastric pH?
|
food bolus (which is a problem w/ meal feeding because there isn't always one in the stomach)
pancreatic & hepatic enzyme backflow into the stomach |
|
|
Because the stomach has such a small capacity, it makes what necessary?
|
rapid gastric emptying
|
|
|
What kind of muscle makes up the equine esophagus?
|
skeletal & smooth muscle
|
|
|
What makes up the lower esophageal sphincter?
|
cardia?
|
|
|
When might it be impossible to pass a stomach tube in a horse?
|
if the stomach is too distended, the angle at which the esophagus enters it gets too oblique & passing a tube thru it is impossible...that's NOT good
|
|
|
Where does fermentation begin?
|
Cecum
|
|
|
What is the volume of the cecum, and how does that compare to the stomach?
|
30 L which is more than twice the stomachs capacity.
(with cecal dysfunction, the volume held in the cecum can douvle) |
|
|
T/F. Happy microbial enzymes = happy horse.
|
True
|
|
|
Why does it take 9 whole hours for feed to leave the cecum?
|
Cause you want it in there long enough for everything to begin fermenting
|
|
|
Carbs are broken down by microbes into what three prosucts?
|
VFAs, gas, Cit K & B
|
|
|
What happens when a horse is fasted for more than 8 hours?
|
The microbes start dying off & it can take a week for them to repopulate!
|
|
|
Name three bacteria overpopulate the cecum when an overload of starch reaches the hindgut.
|
Bacillus
Lactobacillus Streptococcus (2 bacilli & a strep) |
|
|
Diet changes that are bad: (name 2)
|
Fasting >8 hours
Hi starch diet --> lactic acid overload& colic |
|
|
The large colon consists of the asc colon (&transverse). What are the 3 functions of the asc colon?
|
Some microbial fermentation
Primary site of water abs Microbes produce vit B & K |
|
|
What is the small colon's job?
|
Absorb some water
Create road apples (fecal balls) |
|
|
Nutritional requirements of most horses may be met by ingestion of what 3 things?
|
Good quality hay/pasture
Water Trace mineral salt block |
|
|
The equine stomach holds 8-12 liters at a time.
Hiw much water does an adult horse consume in a day? |
8-12 GALLONS
(50 ml/kg/day) |
|
|
Dehydration puts a horse at risk for what kind of colic?
|
Impaction
|
|
|
What is Equine Metabolic Syndrome?
|
Type II DM
|
|
|
Excess energy may result in what diseases (6)
|
Developmental Orthopedic Dz (OCD)
Equine Metabolic Syndrome Laminitis Obesity Reduced performance Colic |
|
|
Horses are huge so we measure their energy units in megacalories.
How many calories are in a megacalorie? |
A million!
(1,000 kcal) |
|
|
How many mcal/day should the following horses receive?
Pleasure/light work/moderate work/heavy intense work |
16/20/25/30+
|
|
|
How much crude fiber must a feed contain to be considered forage?
|
28-38%
|
|
|
For proper GI health, fiber must be ______ of the diet
|
>50%
|
|
|
A horse should eat what % of his body weight (IN POUNDS) of forage a day?
|
1.5-2%
|
|
|
A 1000 lb horse should eat how many pounds of hay a day?
|
15-20. Good # to keep in mind
|
|
|
Hpw does fiber = energy??
|
Fiber is digested into VFAs
|
|
|
VFAs provide what % of daily energy source?
|
30-70%
|
|
|
What is the optimal pH of the colon?
|
6.5
|
|
|
What does VFA absorption deoend on?
|
pH gradient between xolon &0 portal blood
|
|
|
Which VFA absorbs the fastest?
|
Acetate then propionate then butyrate
|
|
|
VFA absorption is related to the movement of:
|
Water and salt
|
|
|
Most VFAs have to undergo glycolysis in the liver. Which can be used directly by muscle tissue?
|
Acetate
|
|
|
High starch diets result in....
|
Lactic acid production --> lowered pH --> destruction of VFA diffusion across the membrane --> colic
|
|
|
Describe high quality hay
|
Immature leafy small stems
(cut right before it blooms) |
|
|
Blister Beetles love what kind of forage?
|
Alfafa
|
|
|
Why do you want to avoid round bales of hay?
|
Botulism
COPD |
|
|
Straw is NOT food. It is made of
|
Lignin, which is indigestible
|
|
|
What is necessary to determine the true nutrient content of hay?
|
Hay analysis
|
|
|
Complete feeds are designed to be fed in place of hay. How much fiber is required for this to be acceptable?
|
>15%
|
|
|
Beet pulp is a highly digestible fiber that is easy to chew and therefore a great choice of fiber for...
|
Older horses.
(soaked alfalfa cubes are another good source of fiber in geriatrics) |
|
|
Bran is a low-density feed. What does this mean in terms of volume?
|
That it would require a shit-ton of bran to meet fiber needs.
This is good to mix with warm water to encourage water consumption (bran mash) |
|
|
Fresh grasses = _____% water
|
90
|
|
|
What is a major risk associated with grazing on fresh spring grass (esp in the afternoon)?
|
High CHO content --> colic & laminitis
Best time to graze is early morning, apparently thr CHO content is lower then. |
|
|
Pasture grass is CONTRAINDICATED in which horses. Give examplwa.
(what the heck?!) |
Obese
Predisposed to laminitis Equine Metabolix Syndrome Cushings |
|
|
Tell me 4 NSC
|
Oats
Molasses Grain Concentrate (corn but were not supposed to feed this to horses) |
|
|
Whats the problem with digestion of NSCs?
|
The polysacchs have to be broken down into simple sugars before being digested & absorbed--his should be done by amylase in the SI but horses have limited production of amylase
|
|
|
How do concentrates lead to colic?
|
Incomplete pre-cecal digestion!
|
|
|
When NSC are fed in excess, undigested starch goes...
|
From the SI into the cecum, where it is FERMENTED instead of digested into simple sugars
|
|
|
What are the three specialized microbes for starch fermentation?
|
Bacillus
Lactobacillus Streprococcus |
|
|
What is the endproduct of starch fermentation in the hindgut?
|
Lactic acid, which causes colic, endotoxemia, and laminitis. No biggie
|
|
|
1.5-2% of body weight (in pounds) of _______ should be fed per day in adult horses.
|
Forage
|
|
|
Whats the maximum amount of starch that should be consumed per kg BW per day?
|
2grams starch
|
|
|
Why does she tell us to feed forage and NSC separately?
|
So no amylase is wasted on forage (it needs to be saved for the starch thats coming with the NSC)
So feed them a few hours apart |
|
|
A normal adult horse should get less than 2 grams/kg/day of starch and less than ______ of concentrates per meal.
|
2 pounds
|
|
|
Who needs a high glycemic feed?
|
Racehorses, etc. They need this for quick bursts of high intensity energy (or for extended periods of work) when their body undergoes anaerobic metab
|
|
|
What is an important source of energy without the
CHO overload? |
Fat! Like corn oil poured on feed
|
|
|
What are the two essential FAs?
|
Linolenic acid (omega 3 FA)
Linoleic acid (omega 6 FA) |
|
|
Fats are actually a better source of energy for a racehorse because it has calming effects (vs how they act all jacked up on caffeine with concentrates being source of energy)
|
True
|
|
|
% fat in diet for a pasture pet vs growing/lactating?
|
3-16%
|
|
|
What are the two sources of energy from fat?
|
Complete feed with high fat content or corn oil
|
|
|
Protein is not really an energy source. It is required for what processes?
|
Growth
Maintenance Repair |
|
|
How many essential amino acids are there?
|
10
|
|
|
What three organs need to be healthy in order to metabolize proteins properly?
|
SI (digestion & absorption)
Liver (metabolism & builds proteins from amino acids) Kidney (to excrete the urea) |
|
|
**Lysine is essential for growth. How much Lysine do youngsters require??**
|
0.6%
|
|
|
Ew vitamins.
|
SKIP!
|
|
|
ENDOTOXEMIA PACKET
|
ENDOTOXEMIA PACKET
|
|
|
What is THE leading cause of death in equine patients?
|
Endotoxemia
|
|
|
What does Potomac Horse Fever result in?
|
Colitis (and eventually endotoxemia)
|
|
|
What antibiotic do you treat Potomac Horse Fever with?
|
Oxytet. Hey, were gonna have to know it at some point this term
|
|
|
What is a devastating complication of endotoxemia?
|
Laminitis
|
|
|
What is a synonym for endotoxin?
|
Lipopolysaccharide
|
|
|
What makes endotoxin....toxic?
|
Lipid A
|
|
|
What is Lipid A's job?
|
To anchor the endotoxin to the cell wall
|
|
|
Which part of the endotoxin confers virulence?
|
O antigen
|
|
|
Does endotoxemia result in leukocytosis or leukppenia?
|
Leukopenia in horses (eg neutropenia and lymphopenia)
|
|
|
Name the 6 inflammatory processes responsible for the CS assoxiated wi endotoxemia.
|
Fever
Leukopenia Coagulopathy Hypotension Shock Death |
|
|
T/F. It is normal for horses to have gram negs living in their gut. It is not normal for them to escape into the bloodstream tho.
|
True
|
|
|
Horses in endotoxemic shock have hypotension despite...
|
Nomal blood volume (its just not where its supposed to be...its hanging out in saggy peripheral vessels instead of xontributing to central circulation & BP)
|
|
|
Name 6 diseases commonly associated with endotoxemia
|
Enterocolitis
Metritis Pleuropneumonia Peritonitis Wound infection Neonatal septicemia |
|
|
What are 4 normal defenses to endotoxemia (endotoxin in the blood)?
|
Enterocyte endothelium
Mucus layer Tissue macrophages Kupffer cells |
|
|
What are Kupffer cells?
|
I thought they were liver macrophages?
|
|
|
What are three ways endotoxins can make it to the blood?
|
Translocation from the GIT
Inhalation (round bales of hay) Iatrogenic admin (dirty IV line) |
|
|
What must we remember when administering parenteral nutrition (ie IV nutrition)?
|
To change the line once a day because bacteria love to grow in that stuff
|
|
|
Name two diseases we have discussed that damage gut mucosa.
|
Potomac Horse Fever --> colitis
Grain Overload --> lactic acid burn |
|
|
What is the acute phase protein that binds endotoxin?
|
Lipopolysaccharide binding protein (LBP)
|
|
|
What is LBP's job?
|
It shuttles the LPS to our immune cells so it can attack (gee thanks)
|
|
|
What are the two things that the LBP-LPS complex joins to on the phagocytic cell surface?
|
TLR4 and CD14
|
|
|
T/F. When endotoxin is present, LBP is upregulated.
|
True. Supply & demand.
|
|
|
T/F. MD-2 is required for LPS to get inside our cells.
|
True. Damn thing drags the LPS right into the cell
|
|
|
What is responsible for the production of inflammatory cytokines?
|
Nuclear transcription factors, esp NF kb?
|
|
|
What are your 2 major inflammatory cytokines in endotoxemia that a responsible for the CS?
|
IL-1 and TNF
|
|
|
Increaeed plasma concentration of ________ is associated with increased mortality rates witth GI dz & in septic foals.
|
TNF
(if theyre given antibodies against TNF they dont get as sick) |
|
|
LPS cleaves phospholipid membranes leading to....
|
Arachidonic acid cascade = COX & LOX pathways --> prostaglandin, thromboxane, leukotrienes
|
|
|
What are the 3 effects of leukotrienes?
|
Vasoconstriction
Increased vascular permeability Bronchospasm |
|
|
What do COX pathway work on?
|
Prostanoids
|
|
|
COX --> PGE2, PGF2, PGI2, and thromboxane A2.
What are their effects? |
E --> fever (by resetting bodys thermostat)
F --> super sensitive to pain I --> vasodilation (its prostacyclin) Thromboxane A2 --> vasoconstriction |
|
|
With endotoxemia, the neutrophils csnt extravasate so they....
|
Marginate, causing neutropenia
|
|
|
When neutrophils marginate along the vessel wall, what do they do?
|
They vomit all over the endothelial cells, damaging the vessel walls
|
|
|
What two things activate neutrophils?
|
Selectins & integrins
|
|
|
Tumor factor (factor III) is exposed with endothelial damage, leading to what cascade?
|
Extrinsic (tissue = extrinsic)
|
|
|
LPS activates Hagemann factor (XII) leading to what cascade?
|
Intrinsic (11,9,8,12)
|
|
|
What is the hallmark of endotoxemia?
|
Vascular permeability
|
|
|
Where is all the blood in endotoxemic shock?
|
Its pooled in the floppy peripheral vessels instead of contributing to central circulstion and BP
|
|
|
Detrimental consequences caused by the upregulation of the immune system & inflammatory response culminates in the CS of (5):
|
Cardiovascular instability
Impaired hemostasis Organ fsilure (including laminitis) Shock Death |
|
|
Early hyperdynamic shock is what time frame?
|
Within the first hour of the hpbody "seeing" the endotoxin.
|
|
|
What are signs of early hyperdynamic shock?
|
Yawning!
bright red mm with FAST CRT Sweating Colic Muscle fasciculations Fever Recumbency |
|
|
After 90 minutes of endotoxemia, what are the CS.?
|
Diarrhea!
Dark red/purple mm with SLOW CRT 3rd spacing Coagulopathy OBTUNDED MENTATION hypothermia Circulatory failure --> MODS Abortion |
|
|
What will you see on bloodwork of a horse with endotoxemia?
|
Neutropenia
Lymphopenia Hyperglycemia (sympathetic system) Hyperlactatemia (hypoxia) Thrombocytopenia (DIC) prolonged aptt (intrinsic) Prolonged pT (extrinsic) Decreased fibrinogen (DIC) & therefore increased FDPs (D-dimer) |
|
|
What are the coag factors in the intrinsic pathway?
|
I love shopping at walmart cause everythings $11.98 instead of $12
|
|
|
Common pathway
|
1x2x5 = 10
|
|
|
Extrinsic pathway
|
XII
|
|
|
Remember hyperammonemic horses have what mental state?
|
Theyre obtunded (like end stage endotoxemia)
|
|
|
Whats one bright hope in the treatment of endotoxemia?
|
Activated protein C
|
|
|
Whats th side effect of activated protein C?
|
Fatal hemorrhaging (also its really expensive)
This is not currently a first line drug for endotox |
|
|
What are the 5 things were going to focus on in our end-goal resuscitation therapya.
|
CVS resuscitation
Preventing laminitis Removing the cause of the endotoxemia Neutralizing free circulating LPS Inhibition of LPs-mediated inflammation |
|
|
What are we going to administer to meet end-goals?
|
IVF
Oxygen Pressors Packed RBCs |
|
|
What so we ant sao2 to be?
|
95%
|
|
|
What does CVP represent and what level do we want?
|
Preload (pressure in the right atrium). We want it at least 10, so if its lower the horse needs more fluids
|
|
|
What is pressor therapy for?
|
BP
|
|
|
Why administer pRBCs?
|
To increase PCV
|
|
|
What is considered hyperlactatemia?
|
Idk, over 2 i guess
|
|
|
What do we want pAo2 to be?
|
>70mmHg
|
|
|
MAP?
|
Over 65
|
|
|
We want the oxygen saturation of venous blood to be...
|
Over 70
|
|
|
What might decrease COP?
|
Hypoproteinemia such as from diarrhea
|
|
|
What are amazing properties of hypertonic saline besides the fact that it povides CVS resuscitation?
|
Suppresses degranulation of neutrophils (remember theyre marginated and attacking the vessels), decreasing production of reactive oxygen species
Prevents neutrophils from adhering to the vessel endothelium (ie preventing margination of neutrophils) Blocks nuclear transcription of inflammatory cytokines Damn |
|
|
Which provides a higher
COP--hetastarch or plasma? |
Hetastarch
|
|
|
Which will result in higher refractometer readings--hetastarch or plasma?
|
Plasma
|
|
|
What is something you have to be aware of when dosing hetastarch?
|
Doses over 10 can cause increased aPTT --> bleeding
|
|
|
Can you give a higher dose of hetastarch or plasma?
|
Plasma cause its not synthetic and isnt associated with bleeding dyscrasias
|
|
|
Plasma is an excellent source of what 3 things?
|
Albumin
Anti-endotoxemic factors Clotting factors |
|
|
What are 4 disadvantages of plasma?
|
Takes time to thaw
Must be given slowly (no bolusing plasma!) Risk of hives/increased TPR if reaction $$ |
|
|
Because of hetastarch and plasmas disadvantages what do clinicians often do?
|
Give both (hetastarch bolus followed by plasma once its thawed)
|
|
|
Why are colloids so good for endotoxemic horses?
|
First of all they have leaky vessels so this wilo help plug up the holes.
Second, endotoxemic horses are often concurrently hypoproteinemic (because of leaky vessels? Diarrhea?) |
|
|
When using crystalloids how much do we give?
|
3-4x the volume we wish to put into the vessels cause 75% is gonna leak out into the interstitium
|
|
|
WHEN are we going to use cryotherapy and NSAIDs in the PREVENTION of laminitis"
|
Before they develop CS of laminitis
|
|
|
Whats cool ahotu low-dose banamine in horses with endotoxemia?
|
Prevemts LPS-associated prostanoid production
Minimizes early response to endotoxin |
|
|
Whats a deleterious effect of NSAID use?
|
Delayed mucosal healing
|
|
|
What can be given in conjunction with NSAIDs to counter the delayed mucosal healing?
|
2% lidocaine CRI
|
|
|
High dose banamine results in:
|
Good visceral analgesia Because it acts as a COX inhibitor
|
|
|
Broad spec Antibiotics are contraindicated in horses with diarrhea because they kill off normal colonic microbes.
When ARE yu going to give broad specs to a horse with diarrha? |
FPT (cause theyre severely neutropenic)
Clostridial doarrhea (flagyl) Degenerative left shift Really low lymphopenia |
|
|
What are your 2 options for neutralizing endotoxin?
|
Plasma
Polymyxin B |
|
|
What are the inhibitory effects of polymyxin B?
|
It suppresses NF-kb activity (nuclear signaling pathway) and therefore decreases production of pro-inflammatory cytokines
|
|
|
Polymyxin B (at higher doses) has what side effect?
|
Can be pretty nephrotoxic
|
|
|
What sre yur 5 drug options in inhibitipn of endotoxin-mediated inflammation?
|
2% lidocaine
NSAIDs Pentoxyfylline DMSO Ethyl pyruvate |
|
|
How does lidocaine lead to analgesia?
|
Anti-inflammatory effects on the bowel?
|
|
|
How do you administer lidocaine?
|
Slow bolus then CRI
|
|
|
When combined with abanamine, Lidocaine:
|
Prevents retardation of mucosal healing
|
|
|
Pentoxyfylline is a methylxanthine derivative that causes dose-dependent suppression of inflammatory cytokines. How does it do this?
|
Inhibits TNF...and peomotes PGI2??
|
|
|
Pentoxyfylline is a rheologic agent. What does that mean?
|
It changes the shape of RBCs, peomoting their deformation so they can get thru microvessels to supply oxygen to the tissues i guess?
|
|
|
DMSO must be given in less than a __% solution.
|
10
|
|
|
DMSO is an osmotic so it can result in
|
RBC lysis (hemolysis)
|
|
|
DMSO is a free radical scavenger and used for laminitis prophylaxis.
|
Yeah whatever
|
|
|
Whats our OTHER bright hope for the future in the treatment if endotoxemia?
|
Ethyl pyruvate
|
|
|
What does ethyl pyrivate do?
|
Decreases upregultion of inflammatory shit
|
|
|
Whats the bottom line when it comes to endotoxemia (4)
|
Recognize patients at risk for endotox
Restore perfusion/oxygenation Ameliorate CS Prevent laminitis |
|
|
LAMINITIS
|
LAMINITIS
|
|
|
What causes laminitis?
|
Inflamm NOT ISCHEMIA
|
|
|
What are MMPs normal function in the foot?
|
Normal remodeling
|
|
|
What happens to MMPS when inflammation hits the foot?
|
They upregulate, causing massive destruction of the basement membrane (detachment of the sens & insens laminae)
|
|
|
Why does decreased laminar energy delivery or protein synthesis cause laminitis?
|
Cause maintenance of the cytoskeleton is an energy-dependent process.
|
|
|
Treatments that facilitate _____ uptake into the foot are good for laminitis.
|
Glucose
(glucose = energy) |
|
|
What part of laminitis kills the horse?
|
Pressure necrosis. I dont know if i said that right
|
|
|
Whats the developmental stage of laminitis?
|
The 8-12 hours before CS arise when the laminae have separated--this is the time to treat, this is also the time you will start to feel bounding digital pulses.
|
|
|
T/F. Laminitis leads to (and is part of) MODS.
|
True
|
|
|
Tell me 6 risk factors for laminitis
|
Ndotoxemia
Metritis or RP Contralateral limb lameness Endocrinopathies Incomplete pre-cecal digestion Black walnut shavings |
|
|
What is the primary risk factor for laminitis in the ICU setting?
|
Endotoxemia
|
|
|
T/F. Endotoxin alone causes laminitis.
|
No--its the resulting inflammation that causes laminitis, NOT the actual endotoxin
|
|
|
What dietary changes lead to laminitis?
|
Increased amounts of readily digestible carbs
Grain overload/incomplete prececal digestion Lush spring grass (in ponies & EMS horses) |
|
|
Why do insulin resistant horses get laminitis?
|
Because the foot is hypoglycemic, ie has no energy; maintwnance of the cytoskeleton is an energy-dependent process
|
|
|
What endocrinopathies cause laminitis? (4)
|
PPID
EMS Insulin resistance Hyperinsulinemia |
|
|
Why must you check digital pulses frequently in a horse predisposed to laminitis?
|
Because you will feel the bounding pulses 8-12 hours before the horse starts showing any clinical signs of laminitis--this is the period (developmental stage) You need to ice the horse etc
|
|
|
Whats coeonary band edema (cleft) gonna result in?
|
Youll be able to push your thumb behind the hoof wall
|
|
|
Whats a horse with laminitis prob gonna stand like?
|
Shifting, rocking back on his HL. (normally the FL are affected)
|
|
|
Acutely laminitic horses have a lameness score of:
|
Obel 3 (usually)
|
|
|
Obel grade 3 =
|
Very reluctant to move, does NOT want to life his foot
|
|
|
During the developmental stage, laminar destruction occurs and it wont be for 8-12 hours before you start seeing CS.
At this stage, what will rads of the foot show? |
Possible thickening of the dorsal hoof wall--this may be THE only indicator of laminitis at this stage.
(= edema of laminar structures) |
|
|
What causes P3 detachment from the hoof wall?
|
Separation of the sensitive & insensitive laminae
|
|
|
Make 2 lines perpendicular to P3. If the distal line is longer, what has occurred?
|
Rotation, which is irreversible?
|
|
|
The angle between the bottom of P3 and the floor should be...
|
Less than five degrees
|
|
|
If the coffin joint doesnt line up with the coronary band, what peocess has occurred?
|
Sinking which is devastating for the animal
|
|
|
Can Sinking be reversed?
|
No way
|
|
|
What could a gas pocket on hoof rads represent?
|
Abscess from necrotic lamina
|
|
|
The toe hurts with laminitis. What hurts with navicular dz?
|
Heel
|
|
|
Why dont PD blocks improve laminitic pain?
|
Because they only get the heel
|
|
|
What block gets the whole foot?
|
Abaxial
|
|
|
What are your three main prophylactic treatments of laminitis?
|
Cryotherapy
Anti-inflammatories Sole support |
|
|
What are the general principles of therapy for acute laminitis?
|
Prophylaxis
Eliminate the primary cause Peomote digital circulation Reduce tension on te laminae Minimize digital inflammation and pain |
|
|
When is cryotherapy useful?
|
Only before CS are present.
|
|
|
Ice up to what joint?
|
Pastern
|
|
|
Whats the dosing range of Banamine?
|
0.5-1.1 mg/kg BID
|
|
|
What are the three levels of banamine dosing?
|
Anti-endotoxemia
Anti-inflammatory Analgesia |
|
|
Should NSAIDs be given IM?
|
No
|
|
|
What are the contraindications for NSAID use?
|
Renal or GI disease
|
|
|
What kins of sole support can we give a horse with laminitis?
|
Remove her shoes
Put deep bedding in her stall |
|
|
If your patient has developed
CS of laminitis what is critical?? |
Pain management
|
|
|
Mutlimodal therapy is important in treating pain of laminitis. What are your drug options?
|
NSAIDs
Opioids Alpha 2s (X& D) 2% lidocaine Ketamine Gabapentin Rwgional analgesia Caudal epidural |
|
|
What do you always have to remember about butorphanol when using it for treatment of laminitic pain?
|
That its analgesic effects wear off before sedative effects. A sedate horse does not equal a pian-free horse!
|
|
|
Why do you want to provide something like deep sand for the horse?
|
So he can stand on his tippy toes, reducing the pull of the DDF (and the pain)
|
|
|
Why give DMSO & Pentoxifylline to laminitic horses?
|
Cause theyre cheap and have minimal side effects--so why not
|
|
|
Effects of pentoxifylline?
|
Rheologic agent
Reduced production of cytokines, thromboxanes, TNF |
|
|
Acute laminitis might look like what in rads?
|
Normal +/- edema (aka thickeninf of the dorsal hoof wall)
|
|
|
What is very very important concerning exercise in the acutely laminitic horse?
|
He must be kept in a stall for at lwast a month--no forced exercise allowed
|
|
|
Why do chronic laminitic horses have such misshapen feet?
|
From chronic injury and abscessation and abnormal hoof growth
|
|
|
Why does ski foot occur?
|
Cause the hoof is growing from the toe rather than the coronary bans like its supposed to
|
|
|
What will a cheonic laminitic foot look like?
|
Misshapen (ski foot) with weird growth rings, bruised soles, cracks
|
|
|
If you have a horse with noemal rads but you still suspect hes laminitic what should you do?
|
Venogram--inject contrast into the digital vein
|
|
|
What does a venogram look like in a laminitic horse?
|
There is interruption of the vessels at the toe/dorsal laminae
|
|
|
What is a surgical method of trwating laminitis?
|
DDF tenotomy to reduce the pull on P3
|
|
|
The _______ the toe, the slower breakover.
|
Longer
|
|
|
Why do we want to ease breakover (shorten the toe) of laminitic horses?
|
Because the longer breakover is, the more strain on the DDF (and therefore pull on P3)
|
|
|
Hy might you groove the coronary band in a horse with chronic laminitis?
|
To encourage normal hoof growth (vs from the toe)
|
|
|
Why do we remove the entire hoof and keep reshaping the hoof?
|
Our goal is to reshape the entire hoof to make it more parallel to P3. (without changing any pressures or tension whatever that means)
|
|
|
Whats the prognosis for a sinker?
|
Only a 5% chance of being PASTURE SOUND =(
|
|
|
Whats the prognosis for a rotater?
|
Poor to guarded for return to previous level of performance
|
|
|
Is laminitis for life?
|
Yeah
|
|
|
THE GIT
|
THE GIT
|
|
|
What is the route on ingesta?
|
Cecum
RVC S LVC P LDC D RDC Transverse colon |
|
|
Horses stomachs rupture along the...
|
Greater curvature (cause thats where the pressure is the greatest)
|
|
|
The lesser curvature separates the...
|
Cardia from pylorus
|
|
|
T/F. The SI can do just about anything it wants, including custing thru the lesser omentum.
|
True
|
|
|
The gastrosplenic ligament comes off the back of the stomach. It is part of the _________ omentum
|
Lesser
|
|
|
Tell me about the duodenum when youre exploring the abdomen thru a ventral midline incision.
|
You have to dig way down to find it. You can visualize it but you CANNOT exteriorize it
(also, you cant feel it on rectal palp) |
|
|
The CBD empties into the ....
It contains enzymes from what two organs? |
Proximal duodenum
Liver and pancreas |
|
|
What is the most cranial part of the SI?
|
Duodenocolic ligament, which attaches the duodenum to transverse colon
|
|
|
What does the duodenocolic ligament attach?
|
Duod:transverse colon
|
|
|
The jejunum has a really long mesentery. Two results of this?
|
The SI can do anything it wants (go anywhere it wants), & you can easily exteriorize the jejunum during surgery
|
|
|
T/F. The jejunum has only one blood supply--the jejunal artery & vein, making R&As nearly impossible.
|
False. That statement describes the ileum.
The jejunum has great collateral circulation & is great for R&As (arborizing blood supply) |
|
|
The ileum is very ___________. Why?
|
Muscular! Because its job is to propel ingesta thru the ileocecal orifice (aka into the cecum)
|
|
|
The ileocecal fold is a surgical landmark. Explain.
|
The ileocecal fold is continuous with the dorsal cecum. It is easy to locate (since the cecum pops out at you during ventral celiotomy), and leads you to the small intestine!
|
|
|
Describe the antimesenteric band of the ileum
|
It is very thin and avascular
|
|
|
Describe blood supply to the ileum.
|
Limited blood supply--no collateral circulation, only an ileal artery & vein
|
|
|
How do you locate the SI during surgery?
|
Trace the dorsal cecal band to the ileocecal fold and you will land at the ileum!
|
|
|
What are the two vascular cecal bands?
Avascular? |
Lat & medial vascular bands
Dorsal & ventral are avascular |
|
|
Which vascular band extends all the way to the apex of the cecum?
|
Medial
(the lateral only extends like halfway up) |
|
|
What does the lateral cecal band become?
|
Cecocolic fold
|
|
|
What does the dorsal band of the cecum become?
|
Ileocecal fold
|
|
|
Describe the ileocecal fold
|
It is very thin fascia
|
|
|
The lateral cecal band communicates with the RVC thru which fold?
|
Cecocolic fold!
|
|
|
The cecocolic fold connects the:
|
Lateral cecum to the RVC
|
|
|
What three structures do you see when you open up a horse on its ventral midline?
|
(from cr to ca:)
RVC cecocolic fold Cecum |
|
|
What is the only cecal fold that is palpable on rectal palp?
|
Ventral band
|
|
|
So just to recap, give me a buzzword for each of the following cecal bands:
Lateral Medial Dorsal Ventral |
Lat = cecocolic fold
Medial extends all the way to the apex Dorsal = ileocecal fold Ventral palpated on rectal |
|
|
So which oart of the intestine does dorsal vs lateral cecal bands connect with?
|
Dorsal = ileum
Lateral = RVC |
|
|
Is the apex of the cecum dorsal or ventral?
|
Ventral, it runs towards the sternum (which ventral...touch yours. Thats ventral. This becomes important later)
|
|
|
Which part of the cecum is exteriorized with ventral midline celiotomy?
|
The apex, it pops right out st you
|
|
|
When you open the horses ventral midline, whats the first thing you see?
|
Cecum
|
|
|
The ______ colons are big & sacculated with 4 bands (like the cecum)
|
Ventral
|
|
|
What flexure separates the ventral colons?
|
Sternal (the sternum is ventral so it separates the ventral colons)
|
|
|
Which flexure separates the lefts?
|
Pelvic
|
|
|
Which flexure separates the Dorsals?
|
The Diaphragmatic flexure separates the Dorsal colons
|
|
|
So whats the order of flow thru the GIT?
|
Cecum
RVC sternal LVC pelvic LDC diaphragmatic RDC transverse! |
|
|
What three sites do NSAIDs target in the body? (negatively)
|
Gastric mucosa
RDC kidney |
|
|
Is the pelvic flexure sacculated?
|
No
|
|
|
Where is the pelvic flexure noemally located in the abdomen? Is it fixed there?
|
In the lower left quadrant and no its not fixed, when it becomes distended it floats up into the pelvic inlet
|
|
|
Tell me three things about the nephrosplenic ligament.
|
You should try to palpate it on rectal.
You should certainly palpate it during surgery. The colon can come up the left side of the abdomen and get stuck here |
|
|
Describe the small colons mesentery.
|
It is thick and fatty
|
|
|
What is important about the antimesenteric band of the small colon?
|
It is wide flat & raised--you can palpate it on rectal and it will tell you youre feeling the small colon, not the SI
|
|
|
The SI & the small colon are not sacculated, so how do you know what youre oakpating on rectal?
|
The small colon has a raised flat wide antimesenteric band--the SI doesnt have one
|
|
|
Should you ever be able to palpate SI on a normal rectal?
|
No
|
|
|
What kind of horse will classically show bruxism?
|
Foals with gastric ulers
|
|
|
What is a result of bloating/abdominal distention?
|
Dyspnea
|
|
|
Sand colic results in what kind of stool?
|
Really watery stool
|
|
|
What is a good indicator that a chronic disease is going on?
|
Weight loss
|
|
|
Muzzle deviated to the _______ would indicate left facial nerve paralysis
|
Right (the facial musckes are working on the right so theyre pulling the muzzle towards them)
|
|
|
What might cause stuff to come out of the nose?
|
Esophageal choke
(something about them being obligate nasal breathers and the oes should normally only be a potential space) |
|
|
Whats the most important part of rectal palpation?
|
Chemical sedation aka adequate restraint
|
|
|
What are the two drugs you should give before rectal palp?
|
Xylazine and buscopan
|
|
|
Why give xylazine for rectal palp instead of detomidine?
|
Well xylazine is very fast-acting, but the main point i got was that detomidine has been shown to MASK colic pain which isnt good
|
|
|
Why is buscopan so awesome?
|
It is a p-lytic, so i guess it slows down the GIT & reduces rectal pressures
|
|
|
What is a side effect of buscopan administration?
|
Transient increase in HR (like, 60, instead of 24-44 which is normal)
|
|
|
Increased rectal luminal pressure --> rectal tear.
What are the two ways we decrease rectal pressures? |
Buscopan and evacuating the rectum of feces
|
|
|
What is an important structure to palpate during a rectal on a stallion?
|
Inguinal rings....SI herniation can occur in these guys
|
|
|
What cecal band is palpable on a rectal?
|
Ventral band
|
|
|
You give a horse xylazine and buscopan prior to rectal palp. What are two die effects of xylazine?
|
Decreased HR & 2nd degree AV block
|
|
|
Can you palpate the duodenum on rectal?
|
No
|
|
|
Which kidney can you palpate on rectal?
|
Left only
|
|
|
Whats the first thing you do after a rectal exam?
|
Check your glove for blood
|
|
|
Holy horrors, there is blood on your glove. What will you do?
|
Hide it and leave ASAP. Just kidding, tell the owner
|
|
|
1st aid for rectal tears = "i couldnt have SED it BTR myself"
|
Sedate
Epidural Drugs Bare-handed exam Tampon Refer! |
|
|
What are your two good options for sedating a horse with rectal tear?
|
Xylazine +/- butorphanol
|
|
|
Why do you avoid using acepromazine for rectal tears?
|
Causes vasodilation and hypotension...which would potentiate the hypotension caused by endotoxemia
|
|
|
Why epidural for a horse with rectal tear?
|
So they dont strain
|
|
|
What do you use for epidural, and what space do you inject it?
|
Lidocaine & xylazine
Caudal sacral vertebral space (S6-ca1) |
|
|
Epidurals take 30min to effect so you want to administer one pronto. What are signs that the epidural is working?
|
Loss of tail and anal tone
|
|
|
What does a grade I rectal tear feel like on palpation?
|
A carpet...the mucosa and submucosa are torn
|
|
|
What does the mucosa feel like with grade II tear?
|
Mucosa feels noemal...its just the muscularis underneath it that is torn
|
|
|
How do you treat a grade I tear that is less than 3 cm long?
|
Medically!
Oral TMS Banamine (for inflammation and pain) Daily laxatives |
|
|
You have to monitor a rectal tea horse for...
|
Endotoxemia, fever, dyschezia
|
|
|
Grade II tears generally require no treatment, but they put the horse at risk for what?
|
Rectal impactions which ca lead to grade IV tear
|
|
|
Grade III tears affect which layers?
Where are IIIa vs IIIb tears located? |
All layers except serosa
IIIa arent close to the peritoneal cavity IIIbs are into the mesorectum, which is continuous with the peritoneum |
|
|
Grade III tears require immediate treatment. Describe treatment.
|
IV antibiotics
Anti-endotoxemic therapy Tetanus prophylaxis Rectal packing |
|
|
What IV antimicrobials do you use for grade III rectal tear?
|
GenPen & Metronidazole
|
|
|
You want to perform peritoneal paracentesis because changes occur immediately with a complete rectal tear. How do you perform?
|
Make incision thru linea alba, then insert teat cannula
|
|
|
Using centriduge and refractometer you can eval periotenal fluid.
Whats normal peritoneal fuid look like/contain? |
Clear transudate
Straw to yellow colored TP under 2 WBC under 5000 |
|
|
What would serosanguinous, green fluid, or thick orangle peritoneal fluid mean?
|
Serosanguinous = devitalized bowel (or splenic puncture or SQ blood vessel!)
Green = you stuck the intestine orrrr a bowel ruptured Thick orange = peritonitis |
|
|
Describe septic peritoneal fluid. Why is it this way?
|
Low BG, hig lactate, low pH
Bacteria eat glucose and make lactic acid, hence the above changes |
|
|
Whats the most distal portion of the GIT that can be visualized with endoscopy?
|
Peox duodenum
|
|
|
You have an adult horse that you want to do endoscopy on. What three things do you have to do before?
|
Fast
Sedate Distend stomach with air |
|
|
Do you have to fast foals for endoscopy?
|
Nah, milk leaves the stomach quick enough....with th adults, its that feed bolus you wanna get rid of
|
|
|
Is laparoscopy usually performed for acute or chronic disease?
|
Chronic
|
|
|
T/F. You can get intestinal bx via laparoscopy.
|
True
|
|
|
What is a contraindication for laparoscopy?
|
Acute intestinal distention (you dont want to go blindly poking into the abdomen with a distended intestine...you could easily rupture it)
|
|
|
Name two common reasons we do contrast rads in hrses.
|
Meconium impaction
Esophageal rupture |
|
|
MRI is only good for the
|
Head
|
|
|
To do an abdominal U/S on a horse, just squirt a little alcohol on their skin and throw a _________ probe on them.
|
Low frequency (3-5 mHz)
|
|
|
What two things are hyperechoic aka white on U/S?
|
Bone and gas!
Bone and gas! Bone and gas! |
|
|
Where is the stomach located (rib spaces)?
|
9-13
|
|
|
How do you know youre looking at the duodenum on U/S (give some landmarks).
|
Ventral to the caudal pole of the right kidney
Caudal to the liver |
|
|
The large colon nd cecum obscure the visceral organs, so you can see the small colon on U/S????
|
Can someone tell me if i wrote this correctly in my notes??
|
|
|
What is "sand flow"?
|
Collecting horse shit, mixing it with water in a glove, and letting it settle out. If there is sand in there, they will drop into the fingers of the glove
|
|
|
T/F. Rectal Mucosal biopsies suck
|
False! She said they are safe and easy, and she said they can often giive you a good idea of whats going on more proximally in the GIT
|
|
|
Dscribe how to do an "absorption test".
|
Fast them for 18-24 hours.
Get a baseline BG. Inject 10% D-xylose or D-glucose Take serial BGs & plot the curve |
|
|
You do an "absorption test" over the course of 4 hurs and thr BG remains stable. What does this tell you.
|
Malabsprptipn
|
|
|
With an "absorption test," when should BG peak in a normal horse?
|
At 60-120 minutes
|
|
|
What is the only thing that should be in a horses stomach?
|
A feed bolus--no reflux!
|
|
|
Is gastric reflux normal in the Horse
|
No, never, there shpuld only be a feed bolus in that stomach
|
|
|
Do hirses cough when an esophageal tube accidentally goes down their tracha?
|
No!
|
|
|
Can you palpate an esophageal tube in a horse?
|
No, horses have too many muscles in their neck
|
|
|
How do you know a stomach tube went down the esophagus?
|
Visualize it going down the left side of the neck
Negative pressure Auscult gas bubbles in the stomach when air is forced into the tube |
|
|
Where do rectal tears occur?
|
Dorsally**
|
|
|
Tell me 9 things you can palpate on rectal.
|
Spleen
Caudal pole of left kidney Nephrosplenic space Ventral cecal band Pelvic flexure Fecal balls in small colon Caudal abdominal aorta Ueogenital tract Inguinal rings in stallion |
|
|
STOMACH
|
STOMACH
|
|
|
Squamous epithelial cells in the stomach have few defenses against gastrix acid, but they are very impervious to pHs as low as...
|
2.5
(impervious = cant be penetrated. Thats right, I had to look it up) |
|
|
Why is the feed ball awesome at preventing ulcers?
|
Limits splashing of HCl& bile acids up to the squamous epithelium
|
|
|
What are two of the glandular mucosa's defenses against gastric acid?
|
Mucus secretion
HCO3 secretion Rapid regen & repair |
|
|
Reflux of ________ neutralizes stomach HCl
|
Duodenal secretions (from oancreas & liver)
|
|
|
*Which three receptors must be bound in order for HCl to be produced?
|
Gastrin
H2 ACh |
|
|
Glandular epithelium produces what three things?
|
Gastrin
Pepsinogen HCl |
|
|
PGE2 peoduces the
|
Mucus barrier
|
|
|
PGI2 produces
|
Vasodilation & therefore increased blood flow to the stomach
|
|
|
PGI2 aka
|
Prostacyclin, is a potent vasodiltor
|
|
|
Goblet cells produce what two things
|
Mucus and bicarb
|
|
|
Which epithelium is protected by the mucus barrier in the stomach?
|
Glandular
|
|
|
Why is meal feeding predisposing horses to gastric ulcers?
Grain feeding? |
Meal feeding = increased time periods that the stomach has a lower pH
Grains = decreased saliva (& thefore bicarb) & smaller feed balls. Results in increased VFA production & increased HCl damage to the squamous epithelium. |
|
|
What is an advantage of feeding legumes to horses in terms of EGUS?
|
Legumes have a good buffering effect and prevent the squamous epithelium from exposure to HCl.
|
|
|
Link between exercise & EGUS?
|
Meal feeding, high CHO meals more common in these horses.
Strenuous exercise decreases the pH in the squamous region of the stomach. HCl "sloshes up" into the squamous stomach |
|
|
Where are ulcers normally found in adults?
Foals? |
Adults = squamous, esp around the margo plicatus
Foals = glandular stomach and duodenum |
|
|
Are there breed and sex predilctions for EGUS?
|
There are technically breed predilections but its based on their work (eg thoroughbreds get EGUS because they are racing animals).
No sex predilection. |
|
|
In small animals, ulcers rwsult in anemia and hypoproteinemia.
What changes do you see in equine labwork? |
None
|
|
|
Name 6 true risk factora for EGUS.
|
Foals/weanlings
Stalls Stress High CHO diets Increased exercise NSAIDs (possibly helicobacter, but not pylori) |
|
|
Why do NSAIDs cause ulcers? Name two reasons.
|
Decreased PGE2 = decreased mucous production
Decreased PGI2 = decreased vasodilation = decrased blood flow to the stomach |
|
|
A horse is standing all "stretched out.". What two things could this indicate?
|
Urinary or gastric ulcer problem
|
|
|
CS of EGUS in adult horses =
|
Mild intermittent colic that worsens with feeding
Decreased appetite (especially for grain) Stops finishing his grain Loss of BCS, ugly coat, change in attitude |
|
|
High CHO meals --> increased HCl production --> ouchie during meals
|
Yah
|
|
|
Where do foals like to get ulcera?
|
Glandular stomach and duodenum
|
|
|
Qhat are your primary risk factors for ulcers in foals?
|
Hypoxemia
NSAIDs Stress/hospitalization Weaning (stress) |
|
|
T/F. In newborns and sick foals, hypoxemia is onw od the comkonest causws of EGUS.
|
True
|
|
|
T/F. Foals tend to show colic signs any time they have EGUS.
|
False--if CS are seen you know it is severe
|
|
|
Class signs of ulcers in foals with bad ulers?
|
Rolling & bruxism (adults with EGUS do not do this)
|
|
|
If. Clic workup is inconclusive via rectal, what else do you hsve to do?
|
Check for EGUS via endoscopy
(remember the story she told us about e mini horse that was taken to surgery for a damn ulcer cause they didnt do an endoscopy) |
|
|
How far down can the endoscope go in an adult horse?
|
Oly to the proximal duodenum
|
|
|
Sometimes with __________, you see huge ulers wit lots of fibrin deposition.
|
NSAID toxicity
|
|
|
Is there any correlation between squamous and glandular lesions?
|
No.
(i actually have no idea what that statement means) |
|
|
DDx for gastrix ulers =
|
Gastric obstruction (rare, but bad)
Gastric neoplasia (SCC) = totally different signalment |
|
|
Whats the different signalments for gastric ulcers vs gastric neoplasia?
|
Ulcers = young competitors
Neoplasia = old horses |
|
|
Do you trea horses with EGUS with antacids?
|
No, the volume youd have to give isnt practical
|
|
|
If you suspect EGUS & endoscopy isnt available, what could you base your diagnosis on?
|
Response to therapy
(possibly do an occult fecal blood test) |
|
|
Tell me about fecal occult blood tests
|
They arent very sensitive to GI bleeds In horses because they poop so much its hard to find the fecal ball that contains the blood... Anyway theyre looking for Ab @ Hb and albumin. Can get false positives with recent rectals
|
|
|
Whats the diet change youre gonna tey to get the owner to make in horses with EGUS?
|
Decreased CHO, increased roughage
|
|
|
Why is Ranitidine (H2 blocker) a pain in the butt to give horses for EGUS treatment?
|
Has to be given TID & takes like a month to work
|
|
|
What is the treatment of choice for ylcers?
|
Omeprazole (gastrogard) = peoton pump inhibitor!
|
|
|
Omeprazole dose for treatment of EGUS?
For ongoing maintenance/prevention? |
4 mg/kg
1 mg/kg |
|
|
How does Carafate work?
|
It leads to production of PGE2 which results in a mucus "bandaid" for the stomach.
|
|
|
What is a side effect of Carafate that doesnt make it as usefu of a drug?
|
It interferes with absorption of other drugs
|
|
|
EIPH protocol
|
Lasix
Clenbuterol Tribrissen (Bute?) |
|
|
T/F. RDC ulcers --> hypoproteinemia via PLE.
|
True
|
|
|
What are your 5 top differwntials for post-op colic?
|
post-op ileus
Peritonitis EGUS mechanical obstrution Adhesions |
|
|
T/F. You should consider Omeprazole as treatment for all patients that are going to be NPO'd or on reduced diets OR are in the hospital.
|
True
|
|
|
T/F. Squamous ulcers are harder to treat than pyloric ulcers.
|
False. Other way around
|
|
|
What is the only way to really get determine what a SI disease is?
|
Surgery
|
|
|
Acute vs chronic enteritis. Main difference?
|
Acute = colic
Chronic = weight loss |
|
|
With villous atrophy or destruction comes...
|
Malabsorption and weight loss
|
|
|
Acute SI enteritis -->
|
Dilated SI loops
Copious gastric reflux Rectal palp of many SI loops Increased TP in peritoneal fluid |
|
|
Chronic enteritis -->
|
Thickened SI walls +/- dilation
|
|
|
What is the hallmark of malabsorption?
|
Weight loss
|
|
|
What does IBD stand for?
|
Inflammatory bowel disease
|
|
|
What are the four types of IBD...and one weird surgical type of "IBD?"
|
GE
MEED LPE EE IFEE |
|
|
In horses, IBD is defined by granulocytic cells. What are these cells?
|
Macrophages
Eosinophils Lymphocytes |
|
|
What is the only way to get a definitive diagnosis of IBD?
|
Histopath
|
|
|
T/F. You can only truely diagnose IBD via full thicckness viopsies.
|
True
|
|
|
You are presented with a skinny horse with ravenous appetite. You are highly suspicious of IBD based on labwork showing hypoproteinemia and CS. What do you have to rule out before blaming the low protein on PLE?
|
PLN & liber disease....if no proteinuria or concurrent liver disease, then its PLE
|
|
|
T/F. Diarrhea is typical of IBD.F
|
False--diarrhea is not typical of SI disease
|
|
|
On bloodwork, almost all horses with IBD have
|
Hypoalbuminemia
|
|
|
How thick should a nomal intestinal wall be?
|
No thicker than 2-3 mm
|
|
|
What will abdomenocentesis of an IBD horse reveal?
|
Probably nothing--it should be normal
|
|
|
Rectal mucosal biopsies are...
|
Helpful for diagnosing IBD
|
|
|
Whens the only time horses really become hypoglycemic?
|
With malabsorption
|
|
|
What is the absorption test going to show in a normal horse? Horse with IBD?
|
A normal horse's BG will spike 60-120 min after receiving xylose or dextrose orally.
An IBD horse's BG remains flat |
|
|
Whats the only real treatment for IBD?
|
High (immunosuppressive doses) of CCS. But we dont like using this in horses because CCS --> enteritis & lameness
|
|
|
Who gets Granulomatous Enteritis?
|
Young standardbreds
|
|
|
What are the effector cells for the following diseases?
GE MEED LPE |
GE = macrophages
MEED = eosinophils LPE = lymphocytes, plasma cells |
|
|
How do horses with IFEE present?
|
Acute colic
|
|
|
IFEE presents acutely, like a horse with SI obstruction. What is the cndition of this horse?
|
No PLE, no chronicity, therefore its a normal healthy looking horse.
|
|
|
What will you do to correct IFEE?
|
Surgical decompression of SI, push all the contents of SI into cecum.
(they do great with this, and wake up normal) |
|
|
What caues proliferative enteropathy in foals and piglets?
|
Lawsonia intracellularis
|
|
|
What is the classic picture of a foal with lawsonia?
|
Ill thrift foal with ventral edema
|
|
|
What do we call lawsonia in piglets?
|
Garden hose gut
|
|
|
Where does lawsonia live?
|
Intracellular of course... Specifically in the crypt cells
|
|
|
What makes up the cranial esophageal sphincter?
|
Crixopharyngeus muscle
|
|
|
Twll me something about the caudal esophageal sphincter.
|
Its indistinct
|
|
|
Why can't horses vomit?
|
Because the lower esophagus has much higher pressures than the stomach
|
|
|
T/F. The esophagus obly has serosa within the cervical region.
|
False--only Within the abdomen (from the diaphragm to the stomach)
|
|
|
How is the esophagus able to move during swallowing/neck movement?
|
Because it is attached to the surrounding tissues
|
|
|
Describe the musculsture of the equine esophagus.
|
2/3 striated --> 1/3 smooth
|
|
|
The stratified squamous epithelium of the esophagus is continuous with...
|
The squamous epithelium of the cardia
|
|
|
Ptyalism can be a sign of difficulty with mastication or swallowing.
What CN are responsible for each of these functions? |
Mastication = V, VII, XII
Swallowing = V, IX, X |
|
|
Why are horses nasal obligate breathers?
|
Because their soft palate and epiglottis always touch unless they are swallowing (ie nothing can get from the mouth to the pharynx unlesd the horse is swallowing--nothing being "air")
|
|
|
What causea GP inflammation?
|
Idk i didnt go to class
|
|
|
If ptyalism, then...
|
Oral exam
|
|
|
With hypersalivation comes loss of which electrolytes? This leads to the horse prone to developing:
|
NaCl, K+
metabolic alkalosis |
|
|
Can you perform endoscopy of the guttural pouches?
|
Yes
|
|
|
Causes of primary oes choke?
|
A foreign body--usually roughage (possibly apple)
This is more likely to occur with oes trauma or difficulty chewing) |
|
|
What are causea of secondary intraluminal choke?
|
Tumor (SCC)
stricture Diverticula Cysts Vascular ring anomalies |
|
|
What are causes of secondary extraluminal choke?
|
Cervical/mediastinal/thoracic tumors
|
|
|
What are the four steps to examining the esophagus?
|
Palpation
Plain rads Contrast rads Endoscopy |
|
|
What are we palpating the esopahgeal region for?
|
Crepitus/subq emphysema <-- oes rupture
|
|
|
What kind of information about the oes do plain rads give us?
|
Look for an obstruction, or gas within fascial planes (indicating perf)
|
|
|
What are contrast rads good for?
|
The contrast will outline intraluminal obstructions or stricture
|
|
|
What is the best way to perform endoscopy of a horse's oes?
|
Advance the scope into the stomach.
Then, as you withdraw it, you will hsve your best views od the esophagus |
|
|
How do you observe the thoracic esophagus?
|
Thoracoscopy....which creates pneumothorax cause every tme you do a -scopy you hsve to distend the cavity with air...
|
|
|
Whats the #1 clinical sign of a horse with esophageal choke (something more specific for choke than ptyalism)?
|
Frothy nasal discharge contsining feed & saliva
|
|
|
Where might you be able to palpate an esophageal obstruction?
|
Left jugular furrow
|
|
|
If a horse has esophageal choke and he's extending his neck, wheres the most likely location of the obstruction?.
|
Proximal
|
|
|
What are three sequelae of esophageal rupture/perforation?
|
Crepitus
Pleural fluid (if thoracic oes) Tissue necrosis |
|
|
What are the most common sites of oes obstruction?
|
Cervical oes
Heart base/thoracic inlet Terminal oes |
|
|
What does U/S tell you about the esophagus?
|
Length and character of the obstruction
+/- info on the oes wall thickness & integrity |
|
|
What does passage of a NG tube tell you about an esophageal obstruction?
|
The location of the obstruction (but not the nsture of it)
|
|
|
Are CS of esophageal choke axute or chronic in onset?
|
Acute!
|
|
|
Why is sedation of a horse key when they have esophageal obstruction?
|
So they dont aspirate.
You want their head hanging lower than the point of their shoulder |
|
|
How do you relieve an esophageal obstruction?
|
Sedate then pass a NG tube and lavage to break up the impaction
+/- chemical relaxation of the oes |
|
|
Whats a good sedative combo for horses with esophaegal choke?
|
X (or detomidine) +/- butorphanol
|
|
|
What are two good drugs to relax the esophagus, making passage of the obstructiom easier?
|
Buscopan & oxytocin
|
|
|
As you're lavaging via NG tube, where is all the water coming out of?
|
The nose
(make sure the horses head hangs low to prevent aspiration) |
|
|
T/F. If initial relief of esophageal obstruction is a failure, horse should be euthanized.
|
False. Put him in a stall NPO'd and it is likely to resolve on its own
(with IVFs, oes relaxation drugs) |
|
|
Why do somw equinw practitioners use Sucralafate aka Carafate for cases of prolonged choke?
|
It may speed up oes healing sfter an obstruction
|
|
|
Why do some equine practitioners give NSAIDs to horses with choke?
|
They may decrease the chance of stricture development
|
|
|
What is a good broad spec antibiotic protocol for equine--parentwral vs oral?
|
Penzgen + Flagyl
TMS (oral) |
|
|
Contrast rads re most useful following resolution of choke for evaluation of...
|
Stricture formation as the oes heals
|
|
|
What are 4 causea of oea stricture?
|
Choke
Oral admin of corrosive substances Neck trauma Congenital |
|
|
What prognosis does oes stricture carry?
|
Guarded!
|
|
|
What 2 types of lesions can you get with oes stricture?
|
Circumferential or linear
|
|
|
If oes stricture lasts longer than ______, surgical treatment is peobably necessary
|
60 days (she talked about the bouganie or whatever)
|
|
|
Why do 40% of horses with oes choke reobstruct?
|
Because the oes proximal to the original obstruction is dilsted
Because of mucosal injury Due to esophagitis |
|
|
When should you refeed a horse after oes choke?
|
After confirmation of ucosal healing (via endoscopy)
|
|
|
How should you refeed a horse after oes choke?
|
Soft mash and fresh grass
|
|
|
Tell me some sequelae to oes perf.
|
Tissue necrosis (cause feed & saliva are draining theu the fascial planes yuck)
Sq emphysema Cellulitis Endotoxemia Horner's Left larpar |
|
|
An intrathoracic oes tear can result in...
|
Pleural fluid accumulation
|
|
|
You can use an esophageal wound for placement of...
|
Esophagotomy tube apparwntly
|
|
|
What percentage of horses with oes choke reobstruct?
|
40%
|
|
|
T/F. Choke can lead to irreversible megaesophagus if it isnt unobstructed quickly.
|
True. And therefore it can lead to reversible megaesophagus if they are unobstructed quickly.
|
|
|
How do you definitively diagnose functional motility problems of the esophagus?
|
Fluoroscopy
|
|
|
Whats the prognosis for motility dysfunction of the esophagus due to reflux esophagitis?
Congenital motility problem? |
Can be good
Poor |
|
|
Name some diseases that can cause megaesophagus in horse.
|
Reflux esophagitis
Neuro diseases (EPM, herpes-myeloencephalitis, idiopathic vagal neuropathy) |
|
|
How do you treat reflux esophagitis?
|
Metoclopramide or bethanecol to decrease lower oes tone, gastric emptying time (?), and GE reflux
|
|
|
Whats the only way to really dtermine what's causing SI disease?
|
Open them up
|
|
|
With villous destruction comes...
|
Malabsorption and weight loss
|
|
|
T/F. You see significant thickening of the SI with acute enteritis.
|
False--you see that (and weight loss) with chronic SI disease.
With acute enteritis you see significant colic signs |
|
|
What does acute vs chronic enteritis look like on U/S?
|
Acute = dilated SI loops
Chronic = Thickened SI walls |
|
|
T/F. Acute enteritis = colic. Chronic = weight loss
|
True
|
|
|
Is functional obstruction consistent with acute enteritis?
|
Yes
|
|
|
Tell me those 6 CS of acute enteritis on the first page of this packet.
|
Colic!
Functional obstruction Dilated loops of SI on U/S Copious gastrix reflux Rectal palpation of many loops of SI Increased TP in peritoneal fluid |
|
|
Tell me the CS of chronic enteritis
|
Weight loss
+/- colic Thickened SI wall on U/S |
|
|
What are the 4 "similar" types of IBD & the one "different" type?
|
Granulomatous
Multisystemix eosinophilic epitheliotropic Lymphocytic plasmacytic Eosinophilic Idiopathic focal eosinophilic enteritis |
|
|
T/F. In horses, IBD is typically defined by granulocytic cells (not neutrophiks)
|
True (eosins, macrophages, eosins)
|
|
|
What are the IBD effector cells in equins?
|
Eosins, macrophsges, lymphocytes (the granuloxytic cells)
|
|
|
How do you definitively diagnose IBD?
|
Full-thickness biopsy
|
|
|
What is the classic presentation of an .IBD horse?
|
Progressive weight loss despite a good appetite...possibly/probably with sme peripheral edema
|
|
|
Why do IBD horses tend to develop peripheral edema?
|
They are hypoalbuminemic due to their PLE
|
|
|
T/F. Diarrhea is typical of IBD & other SI disease in horses.
|
False
|
|
|
You U/S a horse's abdomen and see thickened SI walls with small lumens. Is this consistent with IBD or a more acute SI condition?
|
IBD & other chronic SI disease
|
|
|
T/F rectal biopsy, tho helpful for some disease diagnses, is not used for diagnosis of IBD.
|
False, it can be helpful for diagnosis of IBD!
|
|
|
How thick should a normal SI wall be?
|
No more than 2-3mm
|
|
|
What results does abdomenocentesis reveal in a horse ipwith IBD?
|
Normal
|
|
|
When do horses get hypoglycemic?
|
Really only with malabsorption
|
|
|
What is the typical result of IBD diagnosis?
|
Euthanasia
|
|
|
Why a horses with IBD typically euthanized?
|
Cause the only real treatment is immunosuppressive doses of CCS and thats gonna cause enteritis & laminitis....and isnt even that successful a treatment in the first place
|
|
|
Who is gonna get Granukomatous Enteritis?
|
Young Standardbreds! (packet 1)
|
|
|
A young Standardbred was diagnosed with granulomtous enteritis. What did the pathologist see on histology to determine this?
|
Lots of macrophages
(granulomas = macrophages) |
|
|
What is the only form of IBD that involves the skin?
|
MEED
|
|
|
With other IBDs, you can't see inflammatoey infiltrates anywhere but the SI. WHere can you find eosinophilia in horses with MEED?
|
Lots of tissues...liver, skin, blood, etc
|
|
|
A horse has dermatitis & diarrhea. Whats it got?
|
MEED
|
|
|
Whats the effector cell for MEED?
|
Eosins
|
|
|
Whats the effector cell for granulomstous enteritis?
|
Macrophages
|
|
|
How common is lymphocytic-plasmacytic enteritis?
|
It's rare
|
|
|
Why is idiopathic focal eosinophilic enteritis so different from other forms of IBD?
|
They present with acute colic
No PLE Therapy is surgical decompression (vs medical therapy/euthanasia with other forms of IBD) |
|
|
What does surgical decompression mean?
|
Dump the contents of the ?si Into the cecum
|
|
|
IFEE presents acutely, like a horse with...
|
An SI obstruction
|
|
|
Which form of IBD brings a noemal, healthy looking horse to your surgery table?
|
IFEE
|
|
|
Foals with ventral edema have...l
|
Lawsonia intracellularis
|
|
|
Lawsonia intracellularis is a ______ enteropathy
|
Proliferative
|
|
|
How do foals acquire lawsonia?
|
Idk, it is obviously caused by an infectious agent, but it doesnt noemally affect every foal on the farm so it cant be too too contagious
|
|
|
What other species gets Lawsonia intracellularis-induced proliferative enteropathy (and whats it called in them)?
|
Pigs get Garden Hose Gut!
|
|
|
T/F. Lawsonia is going to cause a herd outbreak.
|
False
|
|
|
Where does lawsonia INTRACELLularis live? Be more specific
|
In the crypt cells
|
|
|
Who does Lawsonia affect in the horse world?
|
Weanlings (4-6 mos)
|
|
|
What are risk factors for developing disease from Lawsonia?
|
Overcrowding
Dietary changes (weaning) Transport Weaning |
|
|
What do proliferative enteropathy foals look like?
|
They are all skinny and have ventral edema....(ill thrift, diminished stature)
|
|
|
What is the hallmark of PE?
|
Chronic wasting
|
|
|
L intracellulsris has affinity for crypt cells, leading to...
|
Villous atrophy
|
|
|
When you open up a SI affeced by L intracellularis, what will you see?
|
Red, ulcerated, corrugated mucosa
|
|
|
Is Lawsonia causing diarrhea?
|
Yes (and its a PLE)
|
|
|
What is the only foal colic disease that will cause edema?
|
PE (due to the malabsorption...so protein is shat out instead of absorbed)
|
|
|
What does the bloodwork of a foal with PE look like?
|
Hypoproteinemia (due to villous atrophy)
Mild anemia (anemia of chronic inflammation) Hyperfibrinogenemia (inflamm) Neutrophilia (infection) |
|
|
What is the gold standard in diagnosis of PE?
|
Isolation/cukture of Lawsonia with Warthin Starry silver stain
(this isnt really ever done) |
|
|
How do we actually diagnose PE in praxtixe?
|
PCR of the feces or tissue + IFA
|
|
|
Why mit PCR yield false positives?
|
Because PCR detects DNA whether the bacteria is dead or alive
|
|
|
Whats the treatment of Lawsonia?
|
Reduce intestinal inflamm via NSAIDs
IVFs (colloids!!) IV oxytet then Doxy PO (targets intracell orgs) |
|
|
Whats the prognosis for PE?
|
Pretty good, but keeo in mind this foal isn't going to grow as fast as the others and will not sell for as much at sale
|
|
|
What is the current term for anterior enteritis?
|
DPJ
|
|
|
Is DPJ contagious?
|
No. Despite possible infectious etiology, it is not contagious between horses
|
|
|
What is the hallmark CS of DPJ?
|
High volumes og enterogasteic reflux (which causes great relief to the horse when removed via NG tube)
|
|
|
Why is there such a huge volume of gastrix reflux with DPJ?
|
Cause there is so much inflammation & edema of the DPJ that lots of fluid (and elytes) are leaking into the lumen of the SI (& refluxing into the stomach)
|
|
|
Why can't the large volume of enterogastrix reflux continue being passed down the GIT?
|
Cause of a functional ileus--the inflammation affects the NMJs of the SI so it stops peristalsing
|
|
|
What might you see in peritoneal fluid of a horse with DPJ?
|
High TP (the intestines are sweating out proteins because theyre so inflamed & edematous the hydrostatic pressure is high)
|
|
|
Are fluids being absorbed from the lumen of the SI with DPJ?
|
No
|
|
|
What are the four sources of the accumulated fluid in DPJ?
|
Parotid salivary gland
Gastric secretions Pancreatic secretions Bile (from liver) |
|
|
What causes DPJ?
|
They don't know. Possible infectious etiology--C dificile?
|
|
|
Anytime you get fluid off a horse (gastric reflux, joint tap, abdomenocentesis, etc) what do you do with it?
|
Culture
|
|
|
What is an unfortunate reality of DPJ treatment?
|
High cost. These horses are losing 80-120 L a day to gastric reflux....& that doesn't include maintenance. Many of these horses are euthanized due to the fact that it costs thousands & thousands to treat
|
|
|
The gross lesions associated with DPJ are specifically found where?
|
Duodenum
|
|
|
What is our goal of DPJ therapy?
|
To rule out surgical disease!
DPJ is a medical disease and it responds to medical therapy! |
|
|
So our goal with DPJ is to rule out surgery. That being said, what is the only way to definitively diagnose DPJ?
|
At necropsy or surgery you will see serositis (bright red serosa) when you open up their abdomen.
Hyperemia/edema/hemorrhage Fibrinopurulent serosal exudation |
|
|
What is one CS of DPJ that will help you convince the surgeons to stay away?
|
Fever. Surgeons don't like to cut animals with fever.
|
|
|
Because DPJ is a duodenal disease, it often runs up the CBD. Which enzyme in horses is specific for th biliart tree?
|
biliary tree = GGT (it rhymes)
|
|
|
T/F. DPJ is an inflammatory syndrome
|
Trye
|
|
|
What is the major DDx for DPJ?
|
All SI obstructions (simple or strangulating)
|
|
|
When's the only time you'd take a DPJ horse to surgery?
|
Failure to improve with medical therapy or clinical deterioration
|
|
|
What do you feel on rectal palp of DPJ?
|
Dilsted loops of SI, which is what you feel with everyyyyy SI disease (ie rectals tell you there is SI disease but they don't really tell you what it is)
|
|
|
Whats the difference on rectal palpation between dilated SI bowels due to DPJ vs due to a surgical disease, eg strangulting obstruction?
|
DPJ= fluid-filled distention of SI bowels
Twist = tightly distended lollipops (ok so sometimes rectal palp will give you some information about what kind of SI disease it is) |
|
|
U/S of DPJ reveals what?
|
Large dilated, fluid-filled loops of SI due to poor motility, with increased wall thickness from all the inflammation and edema
|
|
|
Before we said you could get elevated TP on a DPJ belly tap. WhT other abnormalities will you see?
|
Dark yellow/orange
Normal or slightly elevated WBCs |
|
|
What is your initial therapy for DPJ?
|
Gastric decompression
|
|
|
T/F. DPJ peritoneal fluid is less than 10,000 WBCs, while surgical disease will result in WBCs over 10,000 with serosanguinous ....-ate (i never know what the fluids are termed)
|
True
|
|
|
What drugs will you give to treat DPJ after gastric decompression?
|
Anti-inflammatories (lido/NSAIDs)
Prokinetics (metoclopramide, bethanecol, erythromycin) Antimicrobials |
|
|
T/F. Laminitis peophylaxis is important in horses with DPJ because of the risk of endotoxemia.
|
True
|
|
|
What do you need to know about nutrition in a horse with DPJ?
|
NPO for 72 hours!!
Use TPN |
|
|
T/F. Esophageal rupture is a risk of DPJ.
|
True
|
|
|
SI: OBSTRUCTION OR STRANGULATION?
|
SI: OBSTRUCTION OR STRANGULATION?
|
|
|
What is the key difference between an obstruction & strangulation?
|
obstruction = luminal obstruction
strangulation = occlusion from serosal surface |
|
|
When the lumen & blood supply are interrupted (strangulation), the bowel becomes devitalized.
What are 3 sequelae of SI strangulation? |
endotoxemia
dehydration --> hemoconcentration CVS signs (shock) |
|
|
Are horses with SI obstruction shocky?
|
no!
|
|
|
Are horses with SI strangulation shocky?
|
yes!
|
|
|
Is the peritoneal fluid abnormal with simple luminal obstruction or with strangulation of the SI?
|
strangulation --> serosanguinous fluid with increased TP
|
|
|
Why must we differentiate between simple obstruction & strangulated SI?
|
cause we don't want to put a horse under GA & take him to surgery if it's a simple luminal obstruction that can be treated medically.
|
|
|
What are the 2 simple SI obstructions we learned about?
|
Ascarid impaction
Ileal impaction |
|
|
What are the 4 strangulating SI diseases we learned about?
|
Intussusception
SI volvulus Abdominal incarceration (thru a million different things) Pedunculated lipomas |
|
|
Which parasite causes ascarid impaction in foals & weanlings?
|
Parascaris equorum
|
|
|
What are some distinguishing characteristics of ascarids?
|
stout white worms with THREE prominent lips
(shut up pete, it's in board review questions) |
|
|
What's the PPP of P equorum & why is this clinically relevant?
|
8-12 weeks...cause by the time the baby is 3 months old, there are adult worms in the SI (which can cause SI obstruction if they're killed)
|
|
|
When should a foal first be dewormed?
|
by 8 weeks!
|
|
|
P. equorum lifecycle:
|
they eat L2, which bust thru the stomach --> peritoneum --> liver --> lungs --> trachea --> cough & swallow --> SI, where they become adults
|
|
|
How does P. equorum cause colic?
|
They live in the SI lumen...when they're killed all at once, they obstruct it.
|
|
|
What are two results of a massive die-off of P. equorum?
|
obstructive colic
inflammation --> endotoxemia (remember those suckers release toxic inflammatory shit when they're killed) |
|
|
What are CS of roundworms?
|
colic
depression endotoxemia (from the worms or from devitalized bowel) incr TPR gastric reflux (OF WORMS ahhhh ewwwww grossss) |
|
|
What's the history of a foal that's got obstructive colic from ascarids?
|
recent deworming following a shoddy deworming history
recent respiratory disease |
|
|
Why is respiratory disease associated with ascarids?
|
cause they migrate thru the lungs as part of their lifecycle
|
|
|
What do they call the respiratory disease caused by ascarids?
|
"summer colds"
|
|
|
What do worms in the stomach & SI look like on U/S?
|
they're white things
|
|
|
So how are you going to treat these foals that are obstructed with ascarids?
|
gastric decompression & lavage (flush those worms out)
anti-inflamms (NSAIDs, lidocaine) prokinetics anti-ulcer meds (omeprazole) |
|
|
Why don't we take foals with ascarid obstruction to surgery?
|
for whatever reason, surgery just has a really poor outcome with this disease (and we can relieve the obstruction medically so going to sx is dumb)
|
|
|
T/F If the bowel ruptures, the foal can't be saved.
|
True
|
|
|
What's the prognosis for ascarid obstruction?
|
GUARDED?! really?! foals die of roundworms cause they couldn't give them some dewormer?
sad. |
|
|
Why is the prognosis for ascarid impaction guarded?
|
not so much the SI obstruction itself, but the endotoxemia as a result of the toxins the dying worms release
|
|
|
T/F Ascardis (P. equorum) are showing resistance to Ivermectin.
|
True
|
|
|
If P. equorum has some resistance to ivermectin, when/why would you ever use it for them?
|
If a foal has a poor deworming history, we don't want to hit him with fenbendazole cause it'll result in a massive die-off of the worms which leads to obstruction...so you use ivermectin in these guys to slowly kill the worms =)
|
|
|
At which point in a horse's life is she officially resistant to ascarids?
|
by 2 years of age
|
|
|
What class of drug is fenbendazole?
|
benzimidazole
|
|
|
Just to review, what are the non-strangulating obstructions of the SI?
|
ascarid impaction & ileal impaction
|
|
|
What causes ascarid impaction?
|
P. equorum
|
|
|
What causes ileal impaction?
|
coastal bermuda grass
coarse fibrous feed tapeworms (Anoplocephala perfoliata) |
|
|
What do you feel on rectal palpation of an ileal impaction?
|
early on you can feel the ileal impaction, but as the disease progresses, shit becomes more distended proximal to the obstruction --> dilated SI loops on rectal palp (= very nonspecific)
|
|
|
Treatment of ileal impaction depends on how far along in the disease process the horse is...explain
|
early on you can give pain meds, IVF, maybe some mineral oil, and monitor her to see if she'll pass the obstruction
later on you have to do gastric decompression (surgery) |
|
|
With ileal impaction, the SI gets all distended with fluid. Will we do gastric lavage?
|
no! It's not advisable to give oral fluids when the SI is already distended!
|
|
|
When do you take an ileal impaction to surgery?
|
when the pain just keeps escalating (aka when the horse isn't getting better, she's getting worse)
|
|
|
What's the prognosis for ileal impaction?
|
good.
|
|
|
What's a post-op risk for ileal impaction? Why?
|
POI...you're running the bowel several times to strip its contents into the cecum. This can disrupt the bowel = inflammation --> ileus
|
|
|
Which intestinal parasite is known to perturb ileal motility?
|
tapeworm (anoplocephala perfoliata)
|
|
|
With strangulating diseases, what goes first--arterial or venous blood supply?
|
venous!
|
|
|
What are the SI strangulating diseases?
|
intussusception
SI volvulus abdominal incarceration pedunculated lipoma |
|
|
With strangulation, is there a change in TPR?
|
yeah they increase...and they get CVS compromise
|
|
|
When is there a change in peritoneal fluid?
|
with SI strangulation
|
|
|
What are signs of CVS deterioration?
|
endotoxemia
dehydration/hemoconcentration |
|
|
With strangulating disease, the venous supply is first occluded cause veins are so weak....what does this result in?
|
congestion
|
|
|
After venous congestion, what happens in strangulating diseases?
|
the arterial supply is cut off -> ischemia
|
|
|
Which two parasites cause intussusceptions?
|
ascarids & tapeworms
|
|
|
Where do tapeworms like to create problems?
|
ileum/ileocecal junction
|
|
|
What kind of intussusception do you get in a 1 yo horse with tapeworms?
|
ileo-cecal
|
|
|
What's the most common site of intussusception in horses?
|
ileo-cecal
|
|
|
Where do ascarids cause intussusception?
|
jejuno-jejunal
|
|
|
What's the "recepient" part of an intussusception called?
|
intussuscepciens = recipient...they sound the same kinda
|
|
|
What age group is most likely to get intussusception?
|
foals & weanlings due to dietary changes
|
|
|
What are inciting causes of intussusception?
|
deworming
abrupt dietary changes (eg weanlings) GI parasites (ascarids & tapes) |
|
|
What are the two sites tapes can cause intussusception?
|
ileo-cecal & ceco-colic
|
|
|
How does intussusception usually present?
|
acute colic
|
|
|
What do you feel on recta exam of a horse with intussusception?
|
dilated SI loops
|
|
|
Do you see abnormal peritoneal fluid with intussusception?
|
yes...
|
|
|
What's the treatment for intussusception?
|
R&A
|
|
|
When it comes to the different sites of intussusception, which has a guarded prognosis?
|
ileo-cecal (cause you have to perform a jejunocecostomy but leave the distal piece of the ileum....idk i guess the ileum likes to necrose & fuck everything up)
|
|
|
What's the dewormer for ascarids (P equorum)?
|
fenbendazole (ivermectin not so good, remember who it's used in)
|
|
|
What's the dewormer for tapeworms (Anoplocephala perfoliata)?
|
Praziquantel
|
|
|
What's the intermediate host for tapeworms & why is this clinically relevant?
|
orbatid mites....these nasty things live on pasture, so we deworm AFTER the first frost cause that means those suckers are dead & the horse won't be infected again this season
|
|
|
Poor deworming history is associated with which two SI diseases?
|
ascarid obstruction & intussusception
|
|
|
As a review, what are the strangulating obstructions of the SI?
|
intussusception
SI volvulus SI incarceration pedunculated/strangulating lipoma |
|
|
What's the SI twisting around when it becomes volvulused?
|
the root of the mesentery
|
|
|
With SI volvulus, what happens to the affected portion of the SI?
|
irreversible ischemia
|
|
|
Who does SI volvulus occur in?
|
foals/young horses
|
|
|
Which artery is occluded with SI volvulus?
|
cranial mesenteric artery
|
|
|
What are the two diseases we talk about the cranial mesenteric artery with?
|
SI volvulus
Thromboembolic colic |
|
|
Is SI volvulus an old horse disease?
|
NO! young horse dz!
|
|
|
T/F When bowel turns eggplant color, it's gonna take a lot to save it.
|
FALSE. When bowel turns eggplant color, it's dead forever
|
|
|
How much of the SI can we safely remove?
When do we euthanize on the table? |
under 50% of the SI
if we have to remove more than 50% of the SI the horse would have Short Bowel Syndrome = just euth. |
|
|
Describe anatomical location of the epiploic foramen using 3 words.
|
dorsal
cranial right |
|
|
Who gets incarceration of the SI thru the epiploic foramen?
|
cribbers
tall horses |
|
|
What are the borders of the epiploic foramen?
|
CaCaPP
caudate lobe of the liver caudal vena cava portal vein pancreas |
|
|
Can you extend the epiploic foramen?
|
no, 2 of its borders are major blood vessels, you can't go cutting into them
|
|
|
If you see a mesenteric rent as an incidental finding, what should you do and why?
|
close it or it will incarcerate a piece of the SI in the future
|
|
|
Which ligament is part of the lesser omentum?
|
gastrosplenic ligamet
|
|
|
T/F The epiploic foramen is a potential space.
|
true
|
|
|
Who gets direct inguinal hernias?
|
TN Walkers & Standardbreds
|
|
|
What's a hallmark finding of inguinal hernias?
|
cold balls
|
|
|
What does an "indirect" inguinal hernia mean?
|
that the vaginal ring remains intact...
|
|
|
What does a "direct" inguinal hernia mean?
|
the vaginal tunic has ruptured, and the SI is traveling subcutaneously
|
|
|
What part of the SI gets trapped in inguinal hernias?
epiploic foramen? |
distal jejunum/ileum in inguinal hernia
ileum in epiploic foramen |
|
|
What's the prognosis for SI disease?
|
pretty fair in most conditions
|
|
|
When do adhesions form?
|
within a week
|
|
|
Who gets the pedunculated lipomas?
|
arabians, ponies, geldings...but most importantly, OLD HORSES (>20 is classic)
|
|
|
Old horses get which 2 diseases?
|
dessicated feed impaction
pedunculated lipoma |
|
|
Will a horse with a feed impaction show CVS collapse?
|
NO, it's a luminal obstruction = NO CVS signs
|
|
|
Will a horse with a strangulating lipoma show CVS collapse?
|
YES, it's strangulating, therefore there will be CVS collapse!!!!!!!!!
|
