DIGESTION (non ruminant) Flashcards
(50 cards)
1
Q
compare the digestive systems of carnivores, ruminants, simple stomach herbivores and birds
A
carnivore: large stomach, very long small intestine, short large intestine
ruminant: very large fore sttomach, small stomach, long small intestine and short/small large I
simple herbivore/hindgut: small stomach, medium small intestine, very large LI
bird: crop, long tube, pro-ventriculus, gizzard, small intestine, large intestine
2
Q
mechanisms of mechanical, chemical and enzymatic dig
A
M = chewing, muscular
C = acid, bile salts
E = Enzymes, microbes
3
Q
mechanisms of luminal dig (cavities)
A
- gastric secretions
- pancreatic secretions
purpose: large polymers to small polymers
4
Q
mechanisms of membrane dig
A
- enzymes on surface, in contact with end transprter
purpose: cleave smaller polymers to monomers
5
Q
what enzyme in saliva and what does it do? (non-ruminants)
A
amalyse -> starch digestion
6
Q
what is unique about a horse stomach
A
- very large non-glandular/squamous region -> hard to manage gastric ulceration and diet
- margo pliccatus = region between squamous and glandular = ulceration
7
Q
list the sections of the stomach and their purposes
A
cardia (within fundus) = mucous glands
fundus/body = parietal cells (HCL), chief cells (pesinogen - cleaved by HCL into pepsin), mucous neck cells, endocrine cells (histamine)
antrum = mucous neck cells, D cells (somatostatin - regulate HCL release), G-cells (gastrin)
8
Q
pepsinogen info
A
- optimal pH 2
- from chief cells
- HCL converts to pepsin (active)
- neutral pH in dudodenum inactivates it
- degrades proteins
- secretion stmulated by cholinergic vagal fibres, histamine and gastrin
9
Q
HCL info
A
- parietal cells
- intracellular carbonic anhydrase produces H+ and Bicarb
- bicarb moved out of cell which draws Cl- into cell
- Cl- moved out of cell along with H+ via a H+/K+ ATPase pump (uses ATP) - moves K+ into cell
10
Q
what stimulates and inhibits Gastric Acid secretion
A
stimualtors:
- gastrin from G cells (act on CCK-2 receptor to release histamine)
- histamine (act on H2 receptor to make cAMP)
- Acetylcholine (act on M3 receptor -> PSNS)
inhibitors:
- somatostatin (antral D cells - stop histamine)
- CCK (in duodenum)
- secretin (duodenum)
11
Q
mechanisms of protecting stomach from acids
A
- mucous (needs to mix with bicarb)
- bicarb - from parietal cells, secreted into mucus layer to make neutral pH next to epithelia)
- tight junctions to stop leakage of acid
- cell microcirculation -> maintain muccous layer -> if damaged, compormises blood supply
- glycoproteins and surface active phspholipids
12
Q
what are the digestion mechanisms of the stomach
A
- intrinsic factor -> glycoprotein from parietal cells -> for add intrinsic factor to B12 for absorption later in SI
- gastric lipase -> very active on milk TAG (dig of fats)
13
Q
ruminant omasum digestion
A
- Surface area 25% of rumen
- absorbs 25% of VFAs, ammonia, Na, K as the rumen
- chloride secretion, bicarb absorption
- fewer protozoa than rumen + smaller particles
14
Q
pancreatic enzymes (exocrine) -> release area,, activation process,
A
- made and released from acinar cells
- made as inactive zynogens -> activated once released
- secretes bicarb and mucous
15
Q
pancreatic enzymes and their actions /products -> converted to active once in SI
A
Proteolytic enzymes:
- trypsin(ogen) = oligopeptides
- chymotripsin(ogen) = oligopeptides
- (pro)carboxypeptidase = single aa
- (pro)elastase = single aa
lypolytic:
- lipase = fats
- (pro)phospholipase A2 = fats
amylolytic:
- alpha-amylase = monosacharides
16
Q
starch digestion steps:
A
- dietary polysaccharides converted to maltose by salivary and pancreatic amylase
- maltose, lactose and sucrose converted to monosaccharides by brush border enzymes
3, glucose and galactose absorbed across apical membrane by secondary transporter Na+ - fructose absorbed across apical membrane by facilitated diffusion (GLUT 5)
17
Q
how is glucose absorbed in small intestine
A
- into enterocyte (villi)
- driven by co-transprot mechanisms
- Uses Na+ gradient to concentrate glucose within cell
- diffusion from cell into capillary within the villi (passive)
- fructose is absrobed into cell by Na+ independent passive transport system (through GLUT 5)
no ATP needed
18
Q
how is trypsinogen converted to trypsin
A
enterokinase
19
Q
explain steps of protein digestion
A
- proteins hydrolysed by gastric pepsin and pancreatic proteolytic enzymes (trypsin, chymotrypsin, carboxypeptidase)
- simple amino acids absorbed across apical membrane (small intestine) by cotransport with Na+ (secondary active = energy dependnent)
- oligopeptides (big) broken into tri peptides or dipeptides and single peptides by brush border peptidases (aminopeptidases)
- some of these tri a d dipeptides can be absorbed across apical membrrane via H+/oligopeptide cotransporter
- Amino acids (single) can be moved across basolateral membrane via Na+ independnent transporters (into blood)
20
Q
how do intestinal phases influence pancreatic enzymes
A
- cephalic phase = when sense stimulated, vagal pathways regulate -> 25% enzymes secreted
- gastric -> stimulated by distension of stomach, vagal cholinergic system -> 10%-20% enzymes secreted
- intstinal phase -> stimulated by amino acids, fatty acids and H+ absorption/avaiability -> 50-80% secreted -> Has BIGGEST influence
21
Q
explain 4 phases of fat digestion in non-ruminants
A
- emulsification
- hydrolysis
- micelle formation
- absroption
- most digestion in small intestine from pancreatic lipase
- emulsification with bile salts before lipase digests
22
Q
Explain the process of fat digestion in non-ruminants
A
- large fat globules emulsified by bile salts
- pancreatic lipase hyrolyses triglycerides into monoglycerides and free fatty acids
- bile salts -> water-insoluble products transported to epithelial cells as micelles
- at brush border, monoglycerides and FFAs leave micelles and passively diffuse through cell membrane
- triglycerides aggregate and are covered by lipoproteins to form chylomicrons, which leave basal layer by exocytosis
- chylomicrons enter lymphatic vessles to be used
23
Q
how is fat digested in ruminants?
A
- rumen microbes hydrolyse tiglyceride into NEFA
- NEFA can be transported across enteroctye into micells
- inside enterocyte -> re-esterified to triglycerides (TAG) -> cholesterol added to form chylomicrons -> lympahtic vessels
24
Q
what is exocrine pancreatic insifficiency?
A
- inability of acinar cells of pancreas to make and secrete 3 enzymes to digest food -> amylase, lipases, trypsin
- treat -> enzyme supps
25
what does bile contain?:
- electrolytes (HCO3-, Na_, L-, K+, Ca2+)
- bile acids
- phospholipids
- excretion products (cholesterol, bilirubin)
26
bile acids -> formation and excretion
- synthesised from hepatocytes from cholesterol
- conjugate in liver with taurine OR glycine and then excreted in bile
- hydrophobic and hydrophilic sides to aid digestion of fat (wrap around)
- secreted into canaliculi as sodium salts
27
detailed bile acid action steps
1. emulsification by detergent action of acids decreasing surface tension of lipids and allow droplets to reduce in size -> colipase (from pancreas) allows lipase to reach triglycerides through bile products
2. soluble micelles allow lipids to diffuse through gut lumen into water layer and in close contact with absorptive surface of apical membrane
3. lipid components diffuse through apical membrane through special fatty acid binding proteins
*bile acids won't diffuse across they stay in lumen
28
explain bile acid sturcture and manufacture
- synthesised in liver
- bile made from cholesterol -> made into cholic acid or chendeoxycholic acid -> can be conjugated with taurine or glycine and then secreted into small intestine
29
explain bile acid storage and release
- only released when eaten food (sphincter of oddi closed)
- bile is concentrated in gallbladder -> epithelium absorbs Na, Cl, HCO3- and water into cells -> secretin signals release when bile is released so they mix
- when eaten food -> CCK (cholecystokinin) released to relax sphincter of Oddi -> releases bile
- when bile being recycled, indicates digestion occuring = positive feedback to release bile
30
bile pigments and how they are made
- pigment called bilirubin
- heme breakdown -> causes yellow pigment when enzymatic deflation of heme (in spleen, liver and kidney)
pigments then metabolised and released in bile -> cconjugated into water soluble glucuronides
1. old RBCs phagocytosed by macrophages, heme releases bilirubin
2. bilirubin transported attached to albumin into liver
3. bilirubin into gluronic acid and excreted into intestines as bile
31
what happens to bilirubin during conjugation processes
- once conjugated -> reduced by microbial enzymes in intestinal bacteria to form urobilinogen
- urobiligen can be excreted as feaces or absorbed into plasma (resecreted as bile) or absorbed into plasma and filtered by kidneys into urine
32
what is icterus or jaundice
- when increased bilirubin causes yellow plasma or tissues
*how yellow they aren't doesn't always signify how much bilirubin there is though*
33
explain the species differences in icterus
ruminants: elevated plasma bilirubin but don't present with icterus
horses: can have icterus without disease, often when fasting
dogs and cats -> icterus between horse and ruminant levels
34
what are the two possible impacts on bilirubin during disease
1. unconjugated: increased production of bilirubin (break down of RBCs increase) but hepatic uptake/conjugation decreases (can't be released so stays in blood/tissues)
2. conjugated (intrahepatic cholestasis) -> elevated when liver dysfunctioning, conjugated but can't metabolise it so can't excrete in feaces -> overflow then goes into plasma and excreted renally
35
what ends up in the large intestine
undigested carbs (fibre):
- non-starch polysaccharides
- resistant starch
- oligosaccharides
- undigested protein and intestinal secretions
- fermentation and production of VFA, CO2 and methane
36
non-starch polysacchairdes in LI types
Insoluble (cellulose etc):
- inccludes firbours foods, structural carbohydrates
- slow fermentation -> need long time in LI to digest
- minimal digestion in omnivores and carnivores
- decrease transit time
Soluble ( cereal, legumes etc):
- rapidly fermented in all species (VFAs)
- used to modify gut bacteria and change gut environment
usually negative effects in monogastrics
- increase transit time
37
resistant starch
- resistant to digestion in small intestine
- readily fermented -> bacteria change it to VFA
- can be a risk of acidosis -> very fast (horses)
38
oligossacharides in LI
- smaller polyosaccharides
- not attacked by animals enzymes -> readily fermented instead
- e.g. lactose
39
compare the intestinal cellulolytic activity of horse, pigs, sheep, dogs and cats
horse -> 30-60% nergy from VFA (high)
pigs -> some activity (9-20%)
sheep -> avg (8%) - have highly digestable diets
dogs -> basically none (2%)
40
what is the effect of fibre in pigs, dogs and chickens
- reduced nutrient digestibility
- can increase some bacterial infections and diarrhoea
- large intestine might adapt to it and increase fermentation
- highly soluble non-starch polysaccharides (NSP) will cause diarrhoea
- lower soluble NSP will increase stool volume and texture
- will be adventageous to dogs -> cheap, good stool quality
- too much of soluble NSP -> loss of nutrients
41
why would we get excessive fermentation in large intestine?
- high levels of resistant starch in
- poor starch digestion in SI
- rapid introduction to high starch diet (acidosis)
- high levels of oligossacharides
- high levels of soluble NSP
42
what happens in horse large intestine?
- pH is 6 -> good for anaerobic bacteria, fungi, protozoa
- hemicellulose and pectins are degraded, complex carbs are fermented for vit B and K synthesis
- essential amino acids synthesised
- all requires good motility
43
what happens when there's too much starch in horse LI?
- excessive fermentation = favours growth of amylolytic bacteria = acidosis -> causes laminittus
44
what happens to protein in the large intestine?
- fermented
- poteins in LI = incompletely digested plant proteins, endogenous proteins (from cell tunrover or abrasions)
- fermentation has no nutritional benefit -> instead protien used for microbial proliferation and microbes pass through feaces -> vitamins released can be digested though
45
impact of limiting fibre in protein metabolism
- ned carb breakdown to supply energy for protein breakdown
46
simple process of milk digestion in young ruminant
- casein protein of milk added to obamassum renin enzyme -> creates soluble components and a clot
- soluble componentns (called whey/liquid) have proteins, lactose and vitamins -> enter SI for digestion and absorption
clot broken down by pepsin and pre-gastric lipase into FFAs and diaglycerols -> go into SI for further digestion
*caesin proteins will be slightly denatured by acid of abomassum
47
simple process of colostrum digestion in young ruminant
- intact globulins (IgG) traverse the small intestine and transfer immunity to young
- need to get 2-12 hours
- has more protein, fat, and vitamins. sugars very easy to absorb
47
how do you tell if foal has adequate IgG
- failur of passive transfer (FPT test) -> take blood and measure
48
how do you know if colostrum is good quality?
- yellow, viscous
- specific gravity
- colostrometer
49
what pathogens cause neonatal diarrhoea and brief effects
- bovine rotavirus -> malabsorption, effects enterocytes -> produces enterotoxin to decrease the absorption of sodium and glucose, increases Cl- excretion
- cryptosporidium parvum -> malabsorptive diarrhoa -> invade illeum and damage vili -> less absorption. prostaglandin mediated anion secfetion (cl- and HCO3-) -> attack crypts too
- escherichia coli -> express K99 fimbria antigen and by secreting heat stable toxin on small intestine (chlorine secretion into lumen), an't absorb Na+ or H+ -> secretory diarrhoea -> can feed glucose to calf to help (increase Na+/ glucose transporter )
