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key principles in horse digestion
Hindgut-fermentative digestion
Non-rumiannt herbivore
Hindgut fermenter
Foregut enzymatic digestion
Ruminant vs non-ruminant
Rumiannt: uses rumen for fermientation, usually less picky
non-ruminant: After small intenstine fermentation (horse uses cecum), moresentitive
Note about enzymatic digestion in horses
dosnt really begin until the small intestine
Laminitess
High grain diet leads to too much sugar and startch
Also common in dairy cattle
Importance of pelvic flexure
Big diameter to small diameter
Leads to bottle neck
connects the left ventral colon to the left dorsal colon
Development of Gi tract
tract is small in neonatal foal
tract increases in size while liver remains the same
Small intestine increases until 4 weeks
Large intestine keeps growing
Mouth characterisitics for horse
Mechanical breakdown of food, saliva production, and initial digestion occurs.
Prehensile lips
Ingestine - slower than rumiannts, they graze longer
Mastication (chewing) higher for roughages vs concentrates
Why is the TMJ important
Joint that opens the mouth
What kind of teeth do horses have
hyposodont - continuesly growing teeth
Teeth in horses
condition of teeth affects feed efficiency
they chew in a circular motion
Salivarary glands
Helps lubricate
Less enzymatic digestion b/c no salivary amalase
why is saliva important
bicarbonate → helps neutralize and helps with grain digestion
lubricates
Parotid, sublingual and mandibular glands
10 gallons saliva / day
no enzymatic digestion
buffering capacity & lubrication
buffers unprotected upper stomach
allows bacteria in stomach to survive
Bicarbonate; NaCl; other electrolytes
Cardiac sphinctor
prevents regurgitation in horses
Between the esophagus and stomach
Esophagus
Transports food from mouth to stomach
4-5 feet long
Peristalisis
VERY muscular
Left side of trachea
Problems with esophagus
They can choke
eat to fast
dont chew food well
no salivia
nasal discharge
Group fed isnt good for pelleted feed unless you soak them to prevent chokcing
Equine Stomach
Very acidic environment
10% of GI capacity
ROP is fast: No abosprtion
Should not be empty
increase gas production → rupture
4 important parts of the stomach
Sphincters: cardiac + pyloric
Mucosal surfaces
Fundic region
Pyloric region
Mucosal surfaces
Squamous epithelial - non glandular - ½ of stomach
glandular epitheal - mucosal
fundic & pyloric
Fundic region
Parietal cells -HCL: helps prepare carboyhydrates + proteins to be broken down
Cheif cells - Pepsin: enzyme that digests protein
HCl activates zyomogen cells to secrete pepsin
Where does bile come from horses
Liver → they dont have a gallbladder
Pyloric region
Gastrin
Mucus
Extremely acidic
margo plicatus
a distinct dividing band inside a horse's stomach that separates the upper non-glandular region from the lower glandular region
separates squamous from glandular epithelium
Where is the primary site of non-glanudlar ulcers?
near the esophagus
Where is the primary site of ulcers in stomach
*NEED TO DOUBLE CHECK
Near the pyloric gland region (pylorous spynctor)
Very acidic (PH of 2.5)
Fermentative digestion in stomach
**write after office hours
Enzymatic Digestion in stomach
**write after office hours
Fundus/Body region characterists
PH decreases to 5.4 in distal end
Decreased fermentation
First site of enzymatic digestion of protein
Pyloric region characteristics
PH decreases to 2.6
Stops fermentation
Secretion of HCl increases
Ulcers
Esophageal area where ulcers occur → around margo plicatus
Gastric secretions constant even if stomach is empty → leads to ulcers
Equine Gastric Ulcer Syndrome (EGUS) causes
Bile secretions continual —> fasting increases chances
High grain; less hay/grass
Stress/excerise: Sloshing of stomach acid, cortisol decreases prostagladin (protects against ulcers)
Medications such as NSAIDs
Constant secretions
How common are ulcers
90% of racehorses
60% of performance horses
25-50% shown in foals
EGUS symptoms
Attitude changes: nervous or more tired
Changes in performance
Lots of laying down
Colic
Poor appetitie
Teeth grinding
Poor hair coat
Diffrent ulcer grades
Grade 0: No evidence
Grade 1 Inflammating: areas of reddening and hyperkeratonis
Grade 2 Erosion: small single or multiple ulcers
Grade 3 Progressive ulceration: Large single or extensive superficial lesions
Grade 4 Full ulceration
Most difinitive diagnosistic tool for ulcers
Gastroscopy with endoscope
Gastroscopy metholodgy
Gastroscopy preparation
Fasted - empty stomach. This alone can lead to ulcers
Measures severity and location
Examples of prescription medications for ulcers
Omeprazole
Sucralfate - bind to stomach ulcers
antacids - neutralize stomach PH
Other treatment alternatives for ulcers
acupuncture
herbals
food therapy
supplements
dietary management
decreasing grain
Ulcer prevention
Management
decrease grain, decreases gastrin which decreases HCL=l
increasing grazing time or hay, keeps gut full and increases salivia production
Oil supplmentation
Decrease workload
Known stressful situation - omeprazole (FDA, Gastrogard 28 day treatment)
Small intestine
30% of the tract
primary site of digestion and absorption
Fast ROP
No bacteria to detoxify
Small Intestine anatomy
Duodenum - Proximal
Disaccharidases
Bile duct
Pancreative duct for enzymes
Jejunum
Illeum - Distal
Important components/jobs of small intestines
Lactate prodicted in stomach is absorbed and coverted to VFA in LI
Amylase in SI increases with startchy feeds
Enterocytes have microvilli which increase surface area and absortpion
4 important Pancreatic Enzymes
Carbohydrases: 50-70% dig/absopred from pancreatic activity
Lipase: break down fat
Proteases: break down protein, 100%, Trypsin, chymotryripsin
Bicarbonate: Buffers the low pH from the stomach
Bile
Continuously funneled into duodenum from liver
fluxes into distal stomach for fat emulisification
Duodenum importance
Fat emulisification
Liver
Function → metabolism
glycogen storage
hormone production
protein metabolism
Bile production
portal vien
breaks down hemoglobin
Cecum
Large in the horse
Significant fermentation
VFA production
Microbes specific to feedstuff
ROP slow
Microbes in Cecum
specific to feedstuff: takes 3 weeks to change gut microbe population
Microbes produce vitamin k, B complex, protein and VFA
Large intestine
very large capacity
slow passage
colic possible at flexures… such as pelvic flexure
abosorption of fermentation products
Protozoa
Larger than bacteria
role in fiber digestion
defaunation not harmful - digestion wont suffer
bacteria
populations include amylotltic (lower PH, increase in grain leads to increase), cellulolytic (neutral pH) and proteolytic
Highest in cecum and ventral colon
Hindgut ulcers
right dorsal colon
44-63% of horses
Stress, hindgut acifosis, NSAIDS, parasites
Weight loss, diarrhea and colic are most common
Decreased performance and rough haircoat
Probiotics
Adding live microorganisms to the gastrointestinal tract of horses to improve microbial balance and digestive health.
Needed in time of stress
in feed products probiotics die as part as feed processing due to high heat
antibiotics strip gut of microbes
Common types of problems with teeth
Sharp enamal
Hooks
Where is the primary site of ulcers *true correct one
near the cardiac spynthictor
Where the esophagous ocnnects
Fermentatative Diestion in stoamch
very small amount
Starch and sugar are converted to lactic acid
Bicarbonate reversible formula
CO2 + H2O ←→ H2CO3
3 types of lipases
pancreatic lipase
hormone sensititve lipase
lipoprotein
What happens in the Duodenum
Fat emulsification
Fat is broken down from big glob into smaller globs
Micelles turn into chylomicrons which go into bloodstream
Sacculated and teniae
Terms to describe cecum and large intestine
sacculated: helps it stretch
tenaie: ribbon that aids in mobility
Amylolytic vs cellulolytic vs proteolytic
Amylotic more acidic conditions, thrives when there is alot of startch to break down
Cellulotic is the main one, more neutral PH, thrives with cellulose + fiber
Proteolytic enzymes function in all conditions, primarily breaking down proteins into amino acids.
What could cause acidicosis in horse
high grain diet
Diet affects if high in hay
Higher PH
High acetate
low proprionate
Diet affects if high in hay and concentrate
lowerish PH (still neutral)
very high acetate
slight increase in propionate
Diet affects if fasted
higher PH
lower acetate
higher propionate
Hindgut acidosis
Consuming a diet high in startch concentrates (grain)
Drop in pH below 6
Startch fermantation begins
we dont want this
Importantce of feed processing
Cracks seed holes open to allow carbohydrates through
cracking
steamed
hopped
Must be processed for effective digestiability
Pre-cecal startch digestion
we want this
Oat > barley > corn
corn needs to be processed
Mechanical, therman and hydrogethermal processing
increases prececal but not total tract digestability
benefitical in high grain diets
reduced hingut fermentation which can lead to health risks such as gas production, acidosis, leaky gut, ulcers and colic
Enzymatic vs fermentation products
Carbs → glyucose
Fiber/ structure carbohydrates → VFA