Gastrointestinal Flashcards
digestive organs:
* oesophagus
* stomach
* small intestine (SI)
* large intestine (LI)
accessory organs:
* pancreas
* liver
physiology of how digestion occurs
- motility - how food moves thru
- digestion
* digestion = chem breakdown by enzs
* absorption (once small enough units) - selective
* metabolism - what used for once in bloodstream
* egestion (defaecation)
stages digestion
- mechanical breakdown - prehension (food into mouth), mastication, motility
- chem breakdown - secretion, digestion
how do animals do prehension
tongue, lips, head movement
rough outline motility
move food gradually thru GI tract, absorb what want (once small enough), leave waste
which digestive process at each location
- teeth (mechanical)
- salivary glands - secretion
- stomach (motility, secretion)
- liver/gall bladder/pancreas - secretion
- SI - motility, digestion, absorption
- LI - motility, fermentation, absorption, egestion
what is secreted in saliva
mostly environ for enzs work - some species enzs asw (e.g. amylase) but often not there long enough
* plus mucous to lubricate food
egestion vs excretion
both getting rid waste substances
* egestion = allowing waste pass out
* excretion = removal once absorbed bloodstream
saliva types + where proded
- parotid = serous
- mandibular/buccal/sublingual = mucous + serous
- simple-stomached = mostly mucous, pH neutral
- complex-stomached = mainly serous for optimum fermentation, pH alkaline
serous vs mucous saliva
serous = more liquidy, balancing pH (ruminants more)
mucous for lubrication + conts amylase so for diets low starch (not ruminants)
why are digestive secretions reabsorbed
prevent dehydration
* not reabsorbed = diarrhoea
composition saliva
- mucin (+ water = mucous)
- amylase (omnivores + horses)
- bicarbonate - neutralisation + buffering
- phosphate (ruminants for alkaline)
- lysosome/antibodies reduce infection as food covered microbes
- prot-binding tannins (leaf + bud-eaters)
- urea (ruminants)
i.e. ions + pH appropriate action enzs, enzs + mucus
balance components depends diet + glands stimmed
saliva secretion non-ruminants in reference to blood
- primary secretion isotonic blood
- low flow (not eating) = hypotonic bc minerals reabsorbed blood
- high flow = remains isotonic bc no time + reabsorbs later
saliva secretion ruminants
always isotonic to blood - never time reabsorb bc E-low diet + constantly eating/digesting
* low flow rate saliva = PO4 predominates (mostly that)
* high flow rate = HCO3 predominates
how is salivary secretion regulated
under neural control ANS
* sympathetic = fight/flight = prod reduced
* parasymp = rest/digest = prod inc
reflex pathways salivary secretion types
- congenital = innate, from taste, afferent to salivary centre brain, efferent to salivary glands
- conditioned = learned, Pavlov, initiated cerebral cortex, then salivary centre in medulla oblongata
types motility movements digestion
- segmental contractions = mech breakdown
- peristaltic contractions
- anti-peristaltic contractions
- mass movement
peristaltic contractions =?
movement general aboral direction (away from mouth) at rate allow sufficient time digestion + absorption
how do segmental contractions work
mech breakdown at one place
anti-peristaltic contractions
movement food oral direction bc:
* slow transit digesta for sufficient digestion + absorption - longer in GI tract
* allow rumination
* protective - e.g. vomiting
what is mass movement
extended peristaltic contraction to empty sections GI tract + give space new food - e.g. colon for defaecation
* still aboral direction
how is motility regulated
chewing, swallowing, defaeaction (not horses) under voluntary control
intestinal contractions involuntary control (sm musc)
what causes chem breakdown
- secretion digestive juices
- salivary/liver/pancreas/stomach + intestinal wall glands
purpose mucus in digestive juices
- lubricate food
- protect mucosa from ulcerations - particularly stomach
important carb digestive enzs + where?
amylase + disaccharidases (to monosacchs)
* saliva
* pancreas
* intestinal mucosal surface
prot digestive enzs + where?
pepsin, trypsin, peptidases (-> small enough absorb)
* stomach glands
* pancreas
* intestinal mucosal surface
fat digestive enzs + where
lipase, phospholipase
* pancreas
* intestinal mucosal surface
how are nutrients absorbed
- mostly active transport against conc grad - mostly secondary, some primary
- passive transport facilitatively via transporter prot, or diff
layers abdominal wall
- skin - hair for insulation as traps air (dense = fur, wool = type)
- subcutaneous fascia
- muscles
layers subcutaneous fascia
- superficial fascia (all species)
conts adipose + cutaneous trunci musc (causes skin twitch, skin musc) - deep fascia (ox, horse) - big abdominal cavity w extra weight = need extra strength
4 muscles abdominal wall
LATERAL (outside to inside)
1. external abdominal oblique
2. internal abdominal oblique
3. transverse abdominal
VENTRAL:
rectus abdominis
functions abdominal wall
- enclose abdominal cavity
- contraction to inc intra-abdominal press for vomiting, defaecation
- larynx closed = contraction causes inc intra-thoracic press (via diaphragm, bc space dec) - breathing, coughing, sneezing
rectus abdominis
straight, originating sternum
* inserting on cranial border pubis via pre-pubic tendon
* L + R sepped linea alba (line middle 6 pack)
6 pack
external oblique abdominal musc
outermost lateral abdominal wall musc
* originates lateral caudal surfaces ribs 4+ + lumbodorsal fascia (part deep fascia of trunk)
* inserts on linea alba + prepubic tendon
* fibres run obliquely caudoventrally (from craniodorsal)
internal oblique abdominal musc
middle lateral abdominal wall musc
* originates on coxal tuber (hip bone) + lumbodorsal fascia
* inserts on linea alba, last rib + cartilages of caudal ribs
* fibres run obliquely cranioventrally (from caudo-dorsal)
transverse abdominal musc
innermost lateral abdominal wall musc
* originates on medial surfaces ventral parts caudal ribs + deep lumbodorsal fascia
* inserts on linea alba
* fibres run dorsal -> ventral
sheath rectus abdominis musc
formed from tendons lateral abdominal wall muscles, passing above/below rectus abdominis musc to join in midline
where sheath rectus abdominis joins midline+ how
aponeurosis + forms linea alba
how sheath rectus abdominis varies
int oblique abdominal musc inside + outside or just outside, transverse abd. musc inside or outside
* more spread out = strongest, least flexible - bearing more weight from rumen
* less spread out = more flexible, weaker
ox + horse keep same relationship entire length
how are abdominal wall muscles innervated
spinal nerves last thoracic vertebra + L1-L5
1. dorsal roots innervate dorsal musculature
2. ventral roots split 3 branches
3 branches vetral root innervation abdominal wall musc
- medial bet TA + IAO down to RA
- lateral bet IAO + EAO down to midway
- lateral cutaneous perforates EAO to innervate skin
what forms gut (embryologically)
endoderm = epithelium lining GI tract + associated exocrine glands
mesoderm = musc + CT
embryo develops + part yolk sac taken into bod - forms gut
how does yolk sac in bod form gut
- midgut sepped foregut/hindgut by cranial/caudal intestinal portals
- forgut/hindgut end blindly at oral/cloacal plates - will later perforate
which organs does foregut diff into
- pharynx
- oesophagus
- stomach
- initial duodenum
what does midgut diff into
- rest duodenum
- jejunum
- ileum
- caecum
- ascending/transverse colon
what does hindgut diff into
- descending colon
- rectum
how does foregut develop
- stomach rotates sideways + backwards + enlarges as storage organ
- pancreas develops - initially 2 sep organs, hence 2 secretory pts
blood supply to foregut
branches from celiac artery
development midgut
lots tubes looping + twisting increase SA massively for absorption
* rapid liver expansion = midgut pushed out abdominal cavity into umbilical cord to develop, then back into cavity b4 birth when more space due growth or die = physiological herniation
result midgut rotation
- colon quite cranial + caecum RHS
- twisted round central pt where CMA branches off aorta
blood supply to midgut
branches cranial mesenteric artery
general development hindgut
- bud from ventral part = allantoid (precursor umbilical cord)
- urorectal septum enlarges + divides 2 sep tubes
- = when born faecal + urinal waste can be sepped
blood supply to hindgut
branches caudal mesenteric artery
topographical anatomy
where something located in relation to space its in
peritoneum
single serous mem that lines abdominal cavity + envelops abdominal organs
* parietal closely adheres abdominal wall
* visceral closely adheres organ surface
* connecting bet the 2
connecting peritoneum types
- mesentery connects bowel (SI + LI) to body wall
- omentum connects stomach to something
- fold connects bowel to bowel
- ligament connects non-bowel to something
what defines abdominal cavity
peritoneal attachments - some organs tightly held in position, others loosely
what defines abdominal cavity
- diaphragm cranially
- abdominal wall laterally
- conts all organs inc peritoneum
define peritoneal cavity
- conts nothing, potential space bet parietal + visceral peritoneum
- small amount peritoneal fluid - lots = inflammation = peritonitis
structure + location diaphragm
- seps thorax + abdomen, attaching body wall at level last rib
- extends into thorax to level 5th intercostal rib
- musc outside, central tendon
holes in diaphragm
- aorta passes thru aortic hiatus bet L + R crura
- caudal vena cava thru caval foramen in central tendon
- oesophagus thru oesophagal hiatus
structure liver
4 lobes:
* L + R lobes - split medial + lateral sometimes
* caudate - split caudate + papillary processes
* quadrate
when do L + R lobes of liver split
if liver in centre abdomen bc has be able slide over self so diaphragm can move + contract to breathe - dogs, pigs
* displaced liver = no split
gall bladder role + parts
stores + concentrates (no synth) bile
has cystic, hepatic + common bile ducts
peritoneal attachments liver
- coronary ligament - circular around vena cava
- R + L trinagular ligaments = tight attachments to diaphragm
- falciform/round ligament to ventral body wall at umbilicus
* loose but liver so firmly attached elsewhere no matter
firmly attached diaphragm = hard access surgery
what does round ligament mean
foetal remnant - round ligament liver was umbilical vein
location + parts adult stomach
runs L -> R across abdomen
1. fundus = blind ending
2. corpus
3. pylorus (pyloric antrum)
peritoneal attachments stomach
- greater omentum = greater curvature stomach -> dorsal body wall
- lesser omentum = lesser curvature stomach -> liver (= hepato-gastric ligament)
- gastro-splenic ligament -> spleen
regions embryo that give rise stomach + epithelium types cause
- oesophageal -> stratified squamous
- cardiac -> glandular (mucous)
- fundic -> glandular (mucous/HCl/pepsinogen)
- pyloric -> glandular (mucous)
what areas of adult stomach derived from which embryological areas
table
omental bursa
potential space created when greater omentum folds back on itself
* stuff can go in by hole at end in development - shouldn’t but doess, esp jejenum in horses
where is spleen located + attached + purpose
LHS abdomen
* peritoneal attachment = gastro-splenic ligament
* blood reservoir
* v mobile + can get in way
duodenum is + what joins?
1st part SI
* exit bile duct/pancreatic duct on major duodenal papilla
* exit accessory duct on minor duodenal papilla - other part pancreas secretes contents here
peritoneal attachments duodenum
- mesoduodenum -> body wall
- duodeno-colic fold -> colon
- hepato-duodenal ligament (part lesser omentum) -> liver
pancreas structure
2 lobes:
* R running cranio-caudal
* L running medio-laterally
peritoneal attachments pancreas
- R lobe w/in mesoduodenum
- L lobe w/in deep fold (leaf) greater omentum
what is jejenum
middle part SI (80% of it), covered greater omentum
peritoneal attachment jejenum
meso-jejunum = mesentery
* attaches at single pt dorsal abdom wall + fans out along length
ileum
last part SI, enters LI at caeco-colic junction
peritoneal attachments ileum
- ileo-caecal fold - attached caecum
- meso-ileum (extension meso-jejunum)
caecum
1st part LI, blind-ending - for absorption water, electrolytes, breakdoan carbs
* dogs: ileum directly into colon, caecum attached side
* other species caecum continuous w colon + ileum enters
our species no have appendix
peritoneal attachments caecum
- ileo-caecal fold
- caeco-colic fold
colon structure
- ascending (right) = up right side
- transverse along
- descending (left) = down left side -> rectum
R + L colic flexures on either side where changes direction
what do sensory cells GI tract detect
- wall stretch
- nutrient conc
- metabolite conc
- osmolarity
- pH
- irritation of mucous mem
no pain receptors w/in abdomen
how are reflexes GI tract initiated
- stimulation sensory cells
- CNS at sight/smell food + in regulation appetite
how are digestive processes coordinated
neural + hormonal regulation
negative feedback mechanisms
enteric nervous sys (ENS)
GI tract’s own NS, entirely w/in its wall
= guts keep working independently w sensory + motor neurones in its wall
= short reflex arcs
what do sensory cells ENS respond to
- content lumen
- degree wall stretch
what do motor cells ENS stim
- smooth musc cells for motility
- epithelial cells to secrete digestive juices (-> lumen gut) + hormones (-> blood)
nerve plexus
intersecting bundle nerves
long reflex arcs of GI sys
part ANS, connect in CNS
* symp halts digestion
* parasymp promotes digestion (rest/digest)
reflex arcs illustrated
diagram
why short reflex arcs good
give GI tract extensive control of activities
types reflex arcs in ENS
- simple = single sensory cell, single motor cell - localised
- complex = simple connected by interneurons - impulse propagated wider
main transmitter in ENS
acetylcholine
inhibitory transmitters ENS
act on sphincters (these sep sections GI tract) to relax them
where do post-gang neurones ANS synapse
parasymp embed in wall GI tract + connect ENS
symp = synapse ENS or reduce ACh release at parasymp pre-synapses
NTs for ANS digestive sys
all parasymp cholinergic
symp pre-gang fibres cholinergic
symp post-gang adrenergic (NT noradrenaline)
action noradrenaline in symp ANS reponse
- inhibit secretion + motility
- decrease blood supply to GI tract
entero-enteric reflexes
coordinate activity bet diff parts GI tract
* e.g. mastication stims release saliva, gastric juices, bile
* stretching stomach relaxes ileo-solic sphincter = food out SI (poop) in prep new food into SI from stomach (=gastro-colic reflex)
main regulatory hormones digestive sys + where proded
- gastrin - stomach
- secretin - duodenum
- cholecystokinin (CCK) - duodenum
- gastric inhibitory peptide (GIP) - SI
stim for + effect of gastrin
peptides, aas, Ach
HCl production
stim for + effect of secretin
HCl
pancreatic HCO3-
stim for + effect of CCK
FAs, monoglycerides, aas, peptides
pancreatic enzs, gall bladder contract
stim for + effect of GIP
fat, glucose, aas
INHIBITS HCl, STIMS insulin production
phases of digestion regulation
- cephalic
- gastric
- intestinal
cephalic phase digestive reg
pertains to head, e.g. anticipation food, emotion
* coordinated by ANS
gastric phase digestive reg
pertains to stomach, e.g. distension, presence peptides
* coordinated ANS, ENS, hormones (gastrin)
intestinal phase digestive reg
pertains intestins, e.g. distension, lumen contents
* coordinated ANS, ENS, hormones (secretin, CCK, GIP)
how is appetite regulated
controlled hypothalamus
1. appetite centre causes food searching, direct affect behaviour
2. satiety centre causes refusal food + inhibits appetite centre
theories for mechanism appetite regulation
- glucostat = by levels glucose
- CCK = by levels CCK
- lipostat = by levels fat, leptin hormone
motility defn
coordinated contraction sm musc in GI tract
control contractions GI tract
pacemaker cells = interstitial cells of Cajal, located bet longitudinal + circular sm musc
* repetitive + spontaneous oscillations in mem pot
* no stim = depol too weak reach threshold = no contraction
* stim (neural/hormonal) = depol reaches threshold = a pot = sm musc contract
* frequency a pots determines contraction strength = temporal summation
how are sm musc contractions in GI tract synchronised
oscillations from pacemaker cells transferred to (+ bet) sm musc via gap junctions
leaves greater omentum
1st runs caudally to bladder = superficial leaf
then runs cranially my back to the stomach = deep leaf
then runs dorsally to body wall
limbs pancreas
R runs cranial -> caudal on right, w/in mesoduodenum
L runs R -> L across abdomen w/in deep leaf
major duodenal papilla
where pancreatic duct empties secretions
major duodenal papilla
where pancreatic duct empties secretions
structures duodenum
cranial flexure, descending duodenum, caudal flexure, ascending duodenum
connecting peritonea duodenum
mesoduodenum -> body wall
hepato-duodenal ligament
ileal bvs
mesenteric: run parallel to ileum at mesenteric attachment
anti-mesenteric: run parallel to ileum on opp side to mesenteric attachment
how view hollow GI organs radiograph
feed radio-opaque meal (barium)
deglutition
= swallowing = propulsion food oral cavity -> oesophagus
1. food molded bolus by tongue
2. moved upwards + backwards to pharynx
initially under voluntary control until reaches back pharynx
swallowing reflex
press-sensitive sensory cells stimmed + swallowing centre medulla initiates = involuntary
how food prevented entering trachea
- movement food back in mouth forces soft palette up to seal off nasal cavity
- movement tongue pushes epiglottis shut seal off trachea
horse can’t breathe thru mouth
how does food enter oesophagus
peristalsis = contraction/relaxation muscles
what happens in oesophagus
no digestion, just movement food to stomach
swallowing disorders
- failure soft palette close off nasal cavity
- failure epiglottis close off trachea = choking
- pharyngeal paralysis - nerve/muscle injury so can’t control/just can’t swallow
- botulism
- myaestheania gravis
botulism
clostridial toxins block ACh release = can’t initiate contractions = can’t swallow
myaestheania gravis
antibodies formed against ACh receptors = ACh can’t bind = no contractions initiated = no swallow
anaesthesia relation swallowing
- anaesthetic agents induce vomiting
- swallowing process impaired bc reflexes reduced (anaesthetised)
= inhalational pneumonia = food/liquid down trachea into lungs
oesophagus anatomy
- mucosal layer stratified squamous = protective inside
- submucosal layer - bvs + CT
- muscular layer
- serosal layer
muscular layer oesophagus
- inner circular + outer longitudinal
- sk + sm musc
- both under involuntary control
serosal layer oesophagus
NECK = only adventitia (loose CT) = slow healing
THORAX = true serosal layer, tight so can be cut + heal well
so never surgery neck, thorax avoid = stuck oes: pull out/ push stomach
innervation oesophagus
SYMP via cervical sympathetic chain
PARASYMP:
* SVE/AA via recurrent laryngeal to cranial cervical oesophagus
* AE/AA via vagus to caudal cervical/thoracic oesophagus
sk musc still innervated parasymp in caudal bc involuntary control
after food enters oesophagus
- upper oesophageal sphincter closes behind bolus so at contraction food no back to mouth
- epiglottis opens to allow resp
- peristaltic contractions move food down - inc against gravity, e.g. horse grazing
- lower oesophageal sphincter opens allow food pass into stomach
lower oesophageal sphincter
= cardiac sphincter, seps bottom oes + stomach
* physiological sphincter = not anatomically obvious
* always closed except in swallowing or gastric acid come up + cause heartburn
how is acidic stomach content further prevented re-entering oes
oes enters abdomen + stomach at oblique angle = as stom fills shuts off lower oes by exerting press diaphragm to compress at hole wher oes passes thru
emesis is + how?
vomiting = active propulsion stom/top SI contents into oral cavity
1. deep inspiration w closure trachea/nasal cavity
2. = incr intra-abdominal press via diaphragm
3. contract abdominal musc (not gastric)
4. cardiac sphincter opens
5. anti=peristalsis for food up oes
6. upper oesophageal sphincter opens
protective - quicker way get rid toxin than wait pass thru sys (closer)
how is vomiting controlled
vomiting centre in medulla
what stims emesis
- pharyngeal/gastric distension (prevent rupture)
- pharyngeal/gastric irritation
why can’t horses (+ rats) vomit
- lack vomiting reflex
- v well developed cardiac sphincter
- exaggerated oblique entry oes thru diaphragm
stom usually ruptures b4 vom occurs = stomach tube + suck
gastric torsion
stom rotates 90-360 = cardiac sphincter sealed off = can’t vom
* stom distends further w gas
* rotation can compromise blood supply gastric tiss = oedematous/hypoxic (not enough O2)/necrotic
* stom dilatation can squish caudal vena cava = not enough blood return heart = hypovolemic shock
most common horses + barrel-chested dogs
functions simple stom
- digestion - continuation starch, start prot
- protection - acid kills bac came w food
- storage - food delivered SI controlled rate
- mech breakdown + mix w gastric juices -> semi-liquid chyme
rumen equiv simple stom
abomasum
4 anatomical regions stom
- cardia = entrance, physiological valve
- fundus = blind-ending part
- corpus = bod
- pylorus = exit
cell types in stom mucosa
- mucous (goblet) - secrete mucus as barrier protect against HCl
- parietal (oxyntic) - secrete HCl to digest prot
- chief (peptic) - secrete pepsinogen (inactive form pepsin) to digest prot
- entero-endocrine - secrete hormones
how are cells arranged in mucosa
cylindrical glands
why do chief cells secrete pepsinogen
all cells in mucosa etc made up prot so need inactive form pepsin then once reaches stom lumen can be converted to active pepsin
role motility in stom
- prep stom to receive meal
- mechanically break down chyme
- empty stom contents gradually into SI (gives time digestive process 1st)
- prevent regurgutation stom contents into oes
receptive relaxation
initial relaxation stom sm musc when animal starts eating
* regulated swallowing centre via vagus
* transmitter = vasoactive intestinal peptide
motility process in stom
- starts in fundus - weak contractions, move through
- propogated down corpus
- pyloric sphincter opens = chyme -> duodenum
- contractions reach pylorus = pyloric sphincter closes = food forced back into corpus, helping mixing
MAINLY PERISTALSIS
what regs stom emptying
- strength contraction (for how much passes out)
- opening/closing pyloric sphincter
stimulation stom emptying
NEURAL REG:
expansion stom walls = inc strength contraction
HORMONAL REG:
release gastrin into blood -> brain -> ANS parasymp -> motor neurones = incr strength contractions + dilation pyloric sphincter
inhibition stom emptying
incr press duodenal walls, low pH, high fat/peptide conc, high osmolarity = inhibit gastric contractions
NEURAL REG via incr symp activity/decr parasymp
HORMONAL REG via secretin, CCK + GIP
topography abdomen
digestion offcial defn
enzymatic breakdown nutrient macromols into smaller units that can be absorbed
breakdown starch
complex carbs amylose + amylopectin by amylase from saliva (in stom) + pancreas (in SI) @ pH >6
hydrolysable carb
can be digested by mammalion enzs - those w α-glycosidic bonds, not w β (= non-hydrolysable)
breakdown prot
by pepsin @ low pH
how is hydrolysable carb still digested in stom
gradual pH decline from centre stom to edge = amylase stays active for a while
comparative starch digestion stom
based levels starch diet
1. omnivores high = pigs adapted bigger fundus from cardiac region embryo w glandular mucosal (no acid) = conts longer
2. herbivorous low but working horses adapted higher - fundus derived oesophageal region no prod acid = conts longer
3. carnivorous low = no amylase in saliva
comparative salivary amylase levels
- pigs = high
- horses = low as diet no usually cont starch
- nope in carnivores + ruminants
- v high humans as stom not adapted starch digestion
main components gastric juice
- HCl
- pepsinogen - inactive form pepsin as organs made prot so needs reach stom lumen b4 converted
stomach mucosa
v thick layer mucous = protective barrier, v resistant digestion to prevent ulcers
functions HCl
- convert pepsinogen -> pepsin
- provide acidic environ for pepsin work
- kill microbes + prevent fermentation - so some fermentation (starch -> VFAs) in horse/pig as part stom no prod acid
- breaks down prot, CT + musc -> more digestible particles
secretion HCl process
-> 2-2.5pH
alkaline tide
HCl secretion = HCO3- -> blood = pH incr = excreted urine = urine pH incr just after meal
* once food in SI pancreas neutralises blood so due delay food passing stom -> SI
pepsin working
initiates degradation prot + collagen by breaking peptide links = -> smaller chunks
* peptides stim further HCl secretion = more pepsinogen -> pepsin = pos feedback
* pepsin activates pepsinogen = auto-catalysis
auto-catalysis
enz activating own inactive slef
stimulation secretion stom
long (vagus) + short (local) reflex arcs
3 substances work alone but amplify each other
1. ACh/histamine bind receptors directly on cells: chief (pepsinogen), parietal (HCl) + mucin (mucous)
2. Gastrin stims ECL cells prod histamine to stim mainly parietal (HCl)
cephalic phase stim secretion in stom
neural due sight, smell, taste
* direct stim via ACh
* indirect stim via gastrin in blood
secretion gastric juice: pepsinogen, HCl, mucous
gastric phase stim secretion in stom
neural after food entered stom due expansion + peptide in lumen
* direct stim via ACh
* indirect stim via gastrin in blood
secretion gastric juice: pepsinogen, HCl, mucous
effect food entering duodenum on secretion gastric juice stom
stim or inhib depensing acidity chyme + food components
* neural stim (cholinergic)
* hormonal stim (gastrin/cholecystokinin)
normally inhib
role CCK in secretion gastric juices
dogs = partial agonist (low H+) or strong antagonist (high H+)
cats = strong agonist
hormonal stim release gastric juice
gastrin released blood in response peptides in stom
duodenal inhibition secrtion gastric juice
same signals that inhibit stom motility
* neuronal via vagus = parasymp
* hormonal - secretin, CCK, GIP
localised stom inhib gastric juice secretion
pH <2 = stop gastrin release protect mucosa from damage
1. no food in stom = H+ low but not buffered = gastrin inhibed
2. food in stom = buffers (prot) = H+ reduced = gastrin released
more prot in diet = more gastrin release
how is stom mucosa protected ulceration
- secretion thick mucous layer
- cell mem w interconnecting tight junctions impenetrable by H+
- epithelial cells replaced 2-3 days
what causes ulcers stom + duodenum
HCl + pepsin damage epithelial cells + underlying tiss:
* incr acid prod = duodenal
* weakened mucosal layer = gastric
damaged cells prod histamine = stims acid secr = worse
result ulceration
incr secretion, incr damage, decr absorption as villi damaged
* eventually prot broken down as far as blood supply = blood in gut lumen, digested -> dark red = faeces almost black
pathophysiology
how normal physiology goes wrong
causes ulcers
- Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synth - these stim prod mucous + HCO3- so protective mechs reduced
- mast cell tumours = prod excess histamine = incr HCl prod
- gastrin-proding tumours = prod excess gastrin = incr HCl prod
general idea behind treatment ulcers
- reduce HCl secr
* anti-histamines to block it binding
* proton pump inhibitors stop H+ -> gut lumen in secr = less HCl secr - protect ulcerated mucosa
* antacids neutralise acid
* mucosal binding agents bind damaged tiss = protective layer so no further acid damage
4 food grps digested where
hydrolysable carbs: dig mouth, stom, SI; absorb SI
prot: dig stom, SI; absorb SI
lipids: dig SI, abdorb SI
non-hydrolysable carb: dig LI, absorb LI
absorption
selective process via specific transporter prots by diff down conc grad + 2 AT
when are diff substances absorbedin relation body requirements
- organic nutrients + monovalent ions absorbed irrespective body requirements
- divalent ions + trace els toxic high concs + absorbed depending body requirements
which nutrients absorbed where SI
- most nutrients absorbed entire length
- some (B12 + bile salts) only ileum - no transporter prots for them elsewhere
phases digestion SI
- luminal - enzs secreted by salivary glands + pancreas
- membranous - enzs attached epithelial surface intestinal cells
how is SA SI incr
- walls folded = mucosal folds
- cells folded = villi
- villi folded = microvilli (brush border)
intestinal epithelial cell types
- goblet cells secr mucous - lube + protect - + HCO3- neutralise stom acid
- Paneth cells defend against microbial penetration
- eneterocytes responsible absorption via transporter prots = brush border enzs attached for dig
- enteroendocrine cells control digestion via sensory mechs + release hormones
turnover SI cells
migrate from crypts up villus + sloughed off at tip into lumen gut = digested
purpose SI motility
- mix contents w segmental (digestive period)
- move contents down SI w peristaltic (inter-digestive period)
how does SI empty
- motility stom incr after eating
- gastro-ileal reflex = ileal contractions incr
- circular musc at ileo-colic junction = physiological valve = sphincter relaxes
to give space for food from stom
segmental contractions SI - how work
- circular contractions along intestine = contents divided segments
- new contractions in centre distended segment
- repeated = contents mixed dig juices + moved towards mucosal surface for dig + absorp
pattern segmental contractions SI
- intense when stom empties
- short periods weak allow weak peristaltic so food moves along
- chyme reaches distal SI + feedback mech inhibits proximal SI contractions
coordinates transit for max dig + absorp
inter-digestive period
period when dig/absorp complete
peristaltic contraction pattern SI
- irregular moderate activity = short distance + dies out = food no too fast
- regular strong activity = long dist, each contraction starting slightly further along food into LI
* reaches ileum = next starts duodenum = Migrating Myo-electric Complex (MMC), further prevent food LI -> SI
how does peristalsis work SI
distension segment =
1. longitudinal musc relax/circ musc contract behind chyme + vice versa in front
* motor neurons ENS secr ACh stim contraction sm musc
how is contraction type determined
coordination longitudinal + circular musc layers
cause contractions SI
interstital cells of Cajal = pacemaker cells
* always spontaneous oscillations - slow waves highest frequency duoden, declining to ileum
* sufficient depol = a pot spikes = sm musc contract
* propagate cell-to-cell via gap junctions
* strength contraction determined no. a pots
what regs motility SI
ENS = carries on always
* chyme in duoden = short reflex arcs dependent degree distension
* strength contraction depends ANS parasymp vs symp = long reflex arcs
major function ANS = coordinate motility diff parts GI tract
diff bet hydrolysable + non-hydrolysable carbs
α-glycosidic bonds digestble by mammalian enzs
β not + requires microbial fermentation
carb digestion in luminal phase
- starch -> maltose
- salivary amylase continues digestion in stom until acid inhibits
- amylase digestion in SI w pancreatic amylase
carb digestion membranous phase
enzs attached enterocytes
1. maltose (maltase) -> glucose + glucose
2. sucrose (sucrase) -> glucose + fructose
3. lactose (lactase) -> glucose + galactose
= disaccharidases
disaccharidase rate function
maltase + sucrase v fast: Roabsorption limiting factor for how much in blood
lactase slower: Rodigestion limiting factor
disaccharidase levels varying w age
neonate = high lactase, low maltase bc lots lactose from milk
adult = low lactase, high maltase bc not normally much milk in diet once weaned
ruminants = NO sucrase
how are glucose + galactose absorbed SI
sodium-glucose co-transporter (SGLT1)
1. Na+ + sugar bind on luminal side
2. high Na+ digest juice, low cell = down conc grad + E used co-transport sugar = 2 AT
3. conformational change moves sugar into cell + release into cytosol
4. conc dugar high cytosol so fac diff into blood via facilitative transporter GLUT2
how is Na+ conc grad maintained gut lumen -> enterocyte
Na+/K+ATPase on basolateral mem
* 3Na+ out cell into ISF, 2K+ in
* needs ATP = 1AT
how is fructose absorbed SI
- down conc grad -> cell by facilitative transporter GLUT5 = passive
- down conc grad -> blood via GLUT2
what happens to monosacchs once in blood
-> liver via hepatic portal vein: regs everything so toxins removed/detoxed
stored as glycogen or in circulation to be metabolised for E
do digestive functions adapt to diet
some reged by diet: monosacc transport prots, sucrase, maltase
* incr levels nutrient = incr levels enz to deal w (takes time to adapt)
some enzs pre-programmed appear at certain phase life, disappear other regardless - lactase
how is omnivore SI adapted to diet
diet conts high levels hCHO (hydrolysable carb) = SGLT1 levels high throughout
how does ruminant SI adapt diet
- SGLT1 expression high lambs: lots lactose milk
- rumen develops = less hCHO SI = SGLT1 declines to negligible in adults (down-regulated)
how is horse SI adapted diet
SGLT1 highest young, low old but competing fed more hCHO = SI adapts more SGLT1 overall (esp proximally)
what causes lactose intolerance + its effects
all except human caucasian low lactase after weaning
* lactose accumulates gut lumen = decr water absorption due osmotic force
* = incr water gut lumen = diarrhoea
* LI = fermented -> lactic acid = pH decr = upset microbial balance
* lactic acid poorly absorbed = osmotic effect = less water absorption = diarrhoea
* gas products = distension + disomfort/pain
prot digestion SI
pancreatic proteases in luminal digestion -> di/tri-peptides bod can absorb
* prot from diet carnivores/omnivores
* herbivores low prot diet but lots microbial prot from rumen
no membranous digestion; lots enzs needed as lots diff aas
absorption products prot digestion
- aas into enterocytes via Na+ co-transport (2AT)
- di/tri-peptides into enterocytes via H+ co-transport
- enterocyte -> blood via facilitative transporters
enzymatic dig v fast so Roabsorption limiting
why can’t prots be absorbed as intact prot
would be regarded as foreign mat + evoke immune reaction
which species have placental transfer maternal antibodies
primates, rodents, dogs, cats
not pigs, ruminants, horses - colostrum
how do neonates allow absorption intact antibodies
- epithelial cells intestine permeable intact prot = holey
- stom prods negligible amounts HCl
- pancreatic enz secretion low
- colostrum conts trypsin inhibitors
== no digest antibodies as prot
only 1st 24hrs!!!! then normal function + no more passive immunity
relative fat content diff diets
carnivore/omnivore high
herbivores low (still have capacity digest)
sources fats
triglycerides
* plants also have galacto-glycerides + phospholipids
* animal tiss conts cholesterol + phospholipids
what does lipase breakdown fats to
monoglycerides + free fatty acids (FFAs)
where is lipase from
low amounts from saliva/ stom (fat dig starts SI)
most secreted in pancreatic juice
function bile salts
- emulsify fat droplets to smaller size, incr SA for digestion
- lipase water soluble + fats water insoluble so need water/fat interface
- stop fat droplets re-coalescing
how do bile salts work
water soluble (neg charge) + fat soluble component
* lipid soluble part dissolves in fat droplet
* water soluble part protrudes outside fat droplet
- segmental contractions break fat droplets smaller droplets + neg charges repel so stay as small droplets - no bile = re-coalesce into larger droplets
- lipase attaches water soluble part emulsified droplet + digests lipids w/in
what are micelles + why needed
aggregated bile salts that absorb monoglycerides + FFAs from emulsified fats come in contact w
* small enough enter space bet microvilli but emulsified fats to large fit between for absorption
* micelles in contact w cell mem + monoglycerides/FFAs diff into enterocyte
* micelles return luminal content to absorb more
metabolism of fat in cells
same for fat soluble vits
- ER: monoglycerides + FFAs re-esterified form triglycerides
- coalesce w cholesterol + phospholipids make chylomicrons w prot coat = can be transported lymph + blood (aqueous sol)
- packaged in G app
- transferred basolateral mem + released ECF in exocytosis
- too large enter caps = -> lymph (bypasses liver) -> blood
only nutrient that bypasses liver, otherwise regs all to protect bod
absorption water SI routes
- para-cellular = across tight junctions bet epithelial cells
- trans-cellular = across cell mem via transporter prots
* aquaporins in luminal mem
* osmosis thru Na+/glucose or aa transporters (they move thru, water w)
effects chylecystokinin
- stims gallbladder contract + release bile
- stims release pancreatic enzs
- supresses gastric emptying
- supresses appetite
- triggers peristalsis
all in SI
what water is absorbed + where
reabsorption digestive juice secretions + water from food
mostly SI, some LI more maximum reabsorption to prevent dehydration
horses = most water absorption in LI
how is Na+ absorbed
via many transporters to provide E for 2AT
how are K+ + Cl- absorbed
diffusion, usually associated w other ions, e.g. Na+
how is bicarbonate absorbed + why
lost secreted in digestive juices SI so need reabsorb prevent metabolic acidosis
* HCO3-/Cl- counter transporter
how is H3PO4 absorbed
- simple-stomached duoden, pH = 6, mostly absorbed divalent form (HPO42-)
- ruminant duoden, pH = 4, mostly absorbed monovalent form (H2PO4-)
- recycled in gut absorption/salivary secretion
function phosphate in gut
- rumen buffer w HCO3- to maintain pH
- important source nutrition ruminal microbes
how is iron absorbed
2AT coupled w H+ via divalent metal transporter 1
1. iron low = transferrin unsaturated = Fe2+ -> blood, binds transferrin, circulation round bod
2. iron high = transferrin saturated = remains cell boundw apoferritin form ferritin = intracellular storage
Fe3+ poorly absorbed so reduced to Fe2+ by vit C or brush border enz in lumen ferri-reductase
regulated according to requirements bc too much = toxic
how is Ca2+ absorbed
- passive transport - high dietary incr rate
- body Ca2+ low/requirement high (growth/lactation) = AT stimmed by calcitrol (hormone)
* incr vit-D-dependent synth Ca2+-binding prots (calbindin) - ATs Ca2+ into bod
cell -> blood = pumped by Ca2+ ATPase
absorbed according body requirements
functions LI
- absorption water + ions
- fermentation non-hydrolysable carbs - degree depends amount fibre diet - loads horses, no carnivores, some ruminants
what do glands mucosa LI secrete
- mucous for protection/lubrication
- HCO3- to neutralise VFAs
only microbial digestion so no digestive enzs
which part colon varies bet species + how
ascending colon:
* simple carnivores
* omnivores/ruminants = moderate
* horses = extensive
rectum
terminal part colon for storage faeces b4 egestion
main cell types LI
- colonocytes = absorptive but no villi, just crypts (invaginates lining) + less microvilli - less absorption so smaller SA
- goblet cells: mucous + HCO3- for lubrication hard stuff in lumen (water absorbed)
fermentation
of fibre by microbes -> volatile FAs (VFAs) = E source as absorbed (not wanted by microbes)
role VFAs
- E source
- maintain homeostasis colonic epithelium by regulating genes controlling proliferation, apoptosis, differentiation
main VFAs
- acetate - used liver, oxed other cells to gen ATP, source acetyl CoA for lipid synth
- propionate = substrate gluconeogenesis
- butyrate = E production, cellular homeostasis so not enough fibre = more prone colon cancer
how are VFAs absorbed LI
VFAs = short chain FAs (SCFAs)
absorbed by SCFA/HCO3- exchanger
how is Na+ absorbed LI
Na+ channs + Na+/H+ exchanger - enhanced by aldosterone
how is Cl- absorbed LI
bicarbonate/hydroxyl exchange
how is water absorbed LI
- osmmotic press
- hydrostatic press
- solvent drag - taken up w other nutrients
most water re-absorption horse in LI bc extensive fermentation + that requires lots water so lots pumped in = diarrhoea more dangerous as more water lost + dehydrated faster
diarrhoea is?
water lost in faeces thru incr secretion + decr absorption
* incr water content = distension = incr motility = absorption further reduced
causes diarrhoea
- nutritional, e.g. change composition diet too fast = gut can’t absorb (wrong enzs) = osmotic flow water into gut lumen
- infections, e.g. E. Coli bac secrete enterotoxins bind cell mem epithelia stimming cAMP in glands = hyper-secretion
- stress = strong activation parasymp sys = incr secr + motility
how to treat diarrhoea
- intravenous fluids maintain blood vol + press w ions replace from excessive secretion/insufficient reabsorption + HCO3- counteract metabolic acidosis bc not reabsorbed - for EXTREME DEHYDRATION
- oral rehydration therapy = drink sol cont NaCl + glucose as absorption nutrients w water causes more efficient water absorption than declining grad from drinking water alonE: incr osmotic grad + solvent drag thru transporter channs - MODERATE DEHYDRATION
contractions in LI
- segmental in caecum/colon, lower frequency than SI
- peristaltic
- anti-peristaltic, most prominent proximal colon w mat back to caecum
- mass movement, only in LI towards rectum for evac
intrinsic regulation motility
slow oscillations controlled pacemaker cells
* pacemaker region in centre colon secnding waves both directions = peristaltic + anti-peristaltic
* pacemaker region distal end colon only sends waves aborally = peristaltic towards rectum
contractions strongest pacemaker regions, hindering transit mat past
extrinsic reg motility
LI under stronger neural influence
* transit faster after meal as expansion stom/duoden initiates gastro-colic reflex so sphincter bet SI + LI opens + food forced further down
* gastrin + CCK play role incr motility after meal
what is constipation
abnormal accumulation food mat in gut, usually colon
* common if dogs eaten bones or dry food that expands
* inflammation/pain from prostate/anal glands = inhibition motility (hold it in, more water absorbed, even harder to pass)
* megacolon = sm musc in wall weak = colonic contractions weak
distension colon causes pain
how do we treat constipation
- oral fluids to soften faecal mat
- non-digestible mat like paraffin oils to lubricate
- drugs to strengthen contractions - usually enemas
how do we defaecate
- press sensitive cells in rectum stim defaecation reflex
- terminal colon + rectum contract
- inner anal sphincter sm musc relaxes
- outer anal sphincter sk musc relaxes if involuntary - can be heald closed some species (not horses, ruminants)
contraction abdominal musc = incr abdom press =helps evac
structure exocrine pancreas
- grps acini (clusters epithelial cells)
- simple cuboidal epithelium around excretory duct
- lots ducts combine to pancreatic/accessory pancreatic duct
structure endocrine pancreas
isolated clumps cells around capillary = islets of Langerhans
functions pancreas
- digestion (exocrine) -> dig enzs + bicarbonates neutralise stom acid = protect intestinal mucosa + provide pH enzs work
- reg metabolism (endocrine) -> insulin + glucagon
relative amounts pancreatic juice proded diff species
horse/pig = lots for suitable intestinal environ for fermentation
* equiv saliva production ruminants
ionic composition pancreatic juice
similar blood
* HCO3- AT -> duct lumen in exchange Cl-
* water follows by osmosis
* = H+ -> bloodstream (corresponding)
NORMAL FLOW RATE: HCO3- reabsorbed into acinar cells
HIGH FLOW RATE (e.g. in dig): no time reabsorb = juice v alkaline
* Na+/K+ constant (all flow rates)
how is alkaline tide negated
H+ transported bloodstream from pancreatic duct when water blood -> duct (osmosis) = blood normal
which dig enzs secreted by pancreas
- proteases secreted inactive form prevent autodigestion (pancreas made up prot) - trypsin(ogen), chymotrypsin(ogen), (pro)elastase, (pro)carboxypeptidase
- amylase to break down starch
- lipases/phospholipases fat -> glycerol/FAs
- ribo/deoxyribo-nuclease break down RNA/DNA
how are proteases activated from pancreas
- duodenal epithelial surface conts enteropeptidase: trypsinogen -> trypsin
- trypsin autocatalyses itself + activates other proteases
pancreatic cells prod trypsin inhibitor = precaution against autodigestion
which dig phases cause pancreatic juice secretion
all 3
how do dig phases reg pancreatic secretion
CEPHALIC/GASTRIC: mediated by vagus/gastrin
* carnivores = only enzymatic component
* horse/pig = ionic component asw (for LI fermentation)
INTESTINAL: mediated by secretin/CCK
* = large incr secretion
* vasoactive inhibitory peptide (VIP) inhibits effect secretin
how does secretin work
released from duodenum in response H+ + incr HCO3- secr = neg feedback mech (as acid neutralised stim for secr decr)
how does cholecystokinin work
released duoden in response fat/prot metabolites (stuff from their breakdown)
* incr enz secr + gall bladder contract (release bile)
* pos feedback mech (incr enz secr = more metabolites….)
diffs in pancreatic secr bet species
RUMINANTS: continuous flow rumen -> abomasum/SI = constant secr regardless eating
CARNIVORES/OMNIVORES: intermittent flow stom -> SI = intermittent secr
HORSES: continuous flow stom -> SI = constant secr but also incr after eating
why is horse pancreatic juice diff
low HCO3- = only able neutralise acidic stom contents bc ileum secretes loads HCO3- (also neutralises VFAs from fermentation in LI
types cells in islets Langerhands + which hormones prod
- β -> insulin
- α -> glucagon
- δ (delta) -> somatostatin, inhibits insu + gluca (paracrine so only has effect in area secreted) = pancreas self-reg
where are pancreatic hormones proded + where go
secreted in bloodstream -> liver (via hepatic portal vein) -> other tissues to effect
how + why is insulin proded
synthed as pre-pro-hormone, converted pro-insulin (inactive due c-peptide), secreted as active by cleavage c-peptide
* released in response incr plasma levels glucose + aas
* anabolic effect = build up stores glycogen/musc
deactivated in liver
reg insulin locally
direct feedback mech from levels glucose + aas - want constant low level gluc
bi-phasic secretion:
1. initial immediate secretion stored insulin (5-15mins)
2. more prolonged secr newly-synthed adjusted plasma levels gluc
also stimmed GI hormones (e.g. GIP) released when food enters duoden = secreted in anticipation absorption in SI = greater secr when gluc administered orally vs intravenously
how does ANS reg insulin secr
parasymp activity (via vagus) = incr secr from long-reflex arc
symp activity+ adrenaline = decr secr
insulin action target cells
binds receptor on cells, activated = functions as tyrosine kinase
phosphorylation intracellular prots mediates insulin action
1. stims cell uptake nutrients from blood (gluc + aas)
2. anabolic mediator = causes build up mols
3. mobilises glucose transporter GLUT4 to cell mems = gluc uptake enhanced (esp sk musc + adipose tiss)
4. incr conc/activity intracellular enzs involved metabolism gluc/aas/adipose
GLUT transporters diff brain, liver, intestines, kidney + mammary tiss
what metabolism is caused by insulin + where
- glycogenesis in liver/sk musc (+ decr gluconeogenesis)
- formation glycerol/FFAs for triglyceride synth
- inhibits enzs that breakdown triglycerides, e.g. hormone sensitive lipase
- synth prots for E source
diabetes mellitus
plsma gluc incr (hyperglycaemia) bc decr cell uptake
= kidney capacity reabsorb gluc exceeded (glucosuria)
types diabetes
Type I = insulin-dependent (IDDM) = insulin production impaired = give insulin injections
Type II = non-insulin-dependent (NIDDM) = insulin production normal but cells resistant (receptors no work)
IDDM most common
what causes IDDM
- pancreatic inflammation
- hypersecretion hormones antagonistic to insulin (cortisol, growth hormone)
- obesity
hyperglycaemia results in?
- polyuria + polydipsia = expect urine dilute so urine specific gravity low but artificially normal/high due glucosuria
- incr lipid degradation = incr plasma FFAs = not all metabolised = production ketone bodies (normally oxed to CO2/H2O) = metabolic acidosis = impaired brain function -> diabetic coma/death
polyuria
excessive urine vol
polydipsia
excessive thirst
hypoglycaemia
plasma gluc < 5mM, usually due insulin overdose (e.g. owner injects even if animal no eaten) or insulinoma (tumour β cells)
* treated oral/intravenous gluc
ruminants less sensitive to it
glucagon production
peptide hormone released in response decr levels gluc + aas w catabolic effect
* synthed as pre-pro-hormone, converted pro-glucagon, secreted as active glucagon
* deactivated by metabolism in liver + kidneys
glucagon action
- stimmed by decr plasma glucose + incr plasma aas (substrate for gluconeogenesis) + incr symp activity
- binds receptors on target cells to activate adenyl cyclase
- acts opp insulin w net effect dependent ratio
- incr plasma gluc by stimming liver glycogenolysis + gluconeogenesis (substrate propionate VFA + aas)
why is liver lobated/not
located under dome diaphragm - impedes movement during resp bc touching
* centrally located = L + R lobated
* horses = turned to R so only L side touching = only L side lobated
* ruminants = turned further so neither sides touching so neither side lobated
overall cellular structure
liver surrounded capsule CT that extends into liver as v branched septae
* septae create structural units = hepatic lobules around central vein (hexagonal)
functional cells liver
hepatocytes
how do hepatocytes absorb
mols move out sinusoid through endothelial fenestrations into ‘Space of Disse’ then across cell mem into hepatocytes
space of Disse = bet hepatocyte mem + sinusoid endothelium
how biliary sys works
bile: liver -> duodenal lumen
1. across hepatocyte mem into bile caniculus (dilated intercellular space)
2. flows canaliculi -> small bile ducts = ductules
3. anastomose into larger ducts
4. coalesce to form hepatic bile ducts (now extrahepatic)
5. lead into common bile duct
6. enters duoden at ‘Sphincter of Oddi’
function gall bladder
bile into gall bladder from common bile duct b4 enters duoden for storage + concentrating (remove water) in animals w intermittent eating
* constant eating = constant flow (horses no gall bladder)
* then when eat, bile goes back into common bile duct (via cystic duct)
blood in + out liver
hepatic artery brings blood from aorta, hepatic veins take blood to caudal vena cava
hepatic portal vein brings blood from GI sys to remove toxins
how does blood mix in liver + where does it go inside
hepatic portal vein = 75% of blood in, hepatic artery = 25% so press from arteries not so high that venous blood can’t enter (also conts blood from all of GI)
-> mixed in sinusoids -> central veins -> hepatic veins
where are vessels located in liver structure
portal tracts (triads) bile duct, hepatic artery + portal vein bet lobules
then blood goes into liver down sinusoids to central vein
hepatic acinus
functional unit liver
* liver in zones corresponding distance arterial blood supply (from O2 supply)
* zone 1 = closest
* pattern death inwards from zone 3
endothelium + contents sinusoids
- fenestrated for mols enter hepatocytes
- Kupffer cells = macrophages to patrol + destroy
general function + what stuff goes where
blood in sinusoids
1. bad stuff -> hepatocytes -> bile duct
2. normal stuff stays -> central vein
functions liver
- detox body waste, drugs
- synth cholesterol + bile acids
functions hepatocytes
- synth plasma prots
- breakdown rbcs
- carb, lipid + aa metabolism
- removal bac
- production clotting factors
- storage glycogen, Fe, Cu, vits
carb metabolism in liver
- glycogenesis
- glycogenolysis
- gluconeogenesis (maintain blood gluc)
lipid metabolism in liver
- oxidation FAs + ketone body formation
- synth cholesterol, phospholipids, bile acids
prot metabolism in liver
- deamination + transamination aas
- synth non-essent aas
what does liver do to toxins
generic phase: coenz cytochrome P450 oxidises
specific phase: further degradation -> aas, sulfate -> urinary/biliary sys
= conversion to less toxic compounds
which things detoxed in liver
- drugs
- toxins
- endogenous metabolites - NH3 from prot breakdown, hormones once done, haem
example plant toxin
digitalis from foxglove = heartbeat faster + stronger
degradation of rbcs
rbcs removed from blood by macrophages spleen + liver (Kupffer cells)
-> yield haem from Hb
-> biliverdin (green) in macrophage
-> bilirubin (yellow)
-> liver
-> binds albumin (finite amount, build up bilirubin = jaundice)
-> conjugated w glucoronic acid = conjugated bilirubin
-> excreted in bile
-> glucoronic acid removed by intestinal bac in gut
-> metabolised to stercobilin (brown)
= bile pigments
what makes urine yellow
in intestines conjugated bilirubin -> urobilinogen (yellow) -> kidney
layers of lining GI tract
inside to outside
- mucosa = mucous epithelium -> lamina propria -> muscularis mucosae (sm musc, no in rumen)
- submucosa = loose CT w bvs, nerve plexuses
- muscularis = circular (inner) + longitudinal (outer)
- serosa = CT layer + peritoneum
what are papillae
small outgrowths dorsal surface tongue
* filiform = long, threadlike
* circumvallate + fungiform = cushion-shaped
* foliate = succession of folds
keratinised stratified squamous epithelium studded w tastebuds
how does mucosa change down GI tract
- stratified squamous oesophagus w mucous glands
- thicker, folded in stom w mucous glands, parietal cells (in lamina propria), simple columnar
- pyloric region = less chief + parietal + gastric glands to start buffering acid for duoden
- way way thicker single layer epithelium on v long villi duoden
- jejunum = villi get more slender
- ileum = villi get shorter
- colon = more even thickness w loads goblet cells for loads mucus move stuff along, now even sized colonic crypts not villi
how does muscle type change down GI tract
sk in oesophagus -> sm
* dogs = changes at oesophagus stom junction
* pigs = as passes thru diaphragm
* horses = @ caudal 1/3 oesophagus
Brunner’s glands
secrete alkaline mucous in duoden (found submucosa) to protect from stom acid
what distinguishes ileum lining from rest GI tract
Peyer’s patches = lymphoid associated tiss (so purple w H&E bc lymphocytes)
reticulum inner lining
papillae w muscularis mucosae extending into it - arranged honeycomb appearance - + keratinised stratified squamous
where is ENS located
nerve plexuses bet inner + outer muscularis layers + smaller plexuses in submucosa
purpose muscularis mucosae
sm musc to keep epithelium in contact w lumen contents + allow contents glands empty out
bile functions
- emulsify lipids so accessible pancreatic lipases
- makes micelles so lipids soluble + intestine can uptake
- exit route waste products, drugs, excess cholesterol
components bile
- water
- electrolytes - HCO3- makes it alkaline
- biliary prots
- bile pigments
- cholesterol
- phospholipids
- bile acids
synth + development bile acids
from x to y …. thru GI tract
how are bile acids secreted
- AT into bile canaliculus by transporter prot Bile Salt Excretory Pump (BSEP) - canaliculi isolated hepatocytes mem w tight junctions so no leakage
- canaliculi feed into large canals
- emptied into duodenum at major duodenal papilla, controlled Sphincter of Oddi (sm musc contracts circularly)
- not fat soluble = stay in SI until ileum where transport prots reabsorption
or goes gall bladder for storage + later release
enterohepatic circulation
- bile acids reabsorbed AT terminal ileum
- transported in hepatic portal vein -> liver
- captured from bloodstream via Na+-dependent Taurocholate Co-transporting Polypeptide (NTCP)
- recycled (95%)
how is bile secretion regulated
parasymp sys (vagus)
* CCK released response fat duoden, causes contraction gall bladder + relax Sphincter Oddi
* secretin released response acid chyme duoden, incr HCO3- production liver -> bile
+ amount bile salts (= bile acids) returning to liver via enterohepatic circ - more return = more secretion
secretin less effect than CCK, mainly stims release pancreatic juice
sphincter of oddi in animals w/o gall bladder
inactive so constant flow bile into duoden - horses constantly eating
causes liver disease + problems
infection, poisoning, tumours
affects bile acid recycling, detoxification, metabolic functions
liver can regenerate so some disease reversible
clinical signs liver disease
- stunting (liver important growth process)
- weight loss + diarrhoea (fat not digested)
- vomiting (toxins still circling, bod trying remove)
- ascites = accumulation fluid abdomen
- changed liver size - ultrasound, radiography, palpation (normally shouldnt feel liver bc hidden under diaphragm)
- icterus (= jaundice) (incr levels bilirubin in blood)
- tendency bleed (liver prods clotting agents)
polyuria + polydipsia (PU/PD)
incr/decr liver size
incr = hepatomegaly
decr = microhepatica
liver enzs released when liver damaged
cats/dogs:
* alanine aminotransferase (ALT)
* aspartate aminotransferase (AST)
horses/ruminants:
* gamma glutamyl transferase (GGT)
* alkaline phosphatase (ALP/ALKP) - lots other orgs secrete in response damage
how measure liver function
detect levels liver metabolites:
* pre- + post-prandial (= meal) bile acid levels blood - 0, dramatic incr after, slowly decr - lower if can’t recycle/synth
* serum bilirubin - v low (excreted)
* serum prots (e.g. albumin) - made liver so disease = lower levels
cholestasis
intrahepatic:
* decr secretion bile by hepatocytes
* decr bile flow + backflow biliary constituents
* = impaired normal biochem processes w/in hepatocytes
extrahepatic in connecting tubes:
* obstruction gall bladder, bile ducts
* e.g. tumour, gallstones (= cholelithiasis), inflammation gall bladder (cholangiohepatitis)
* = jaundice (whites eyes, mucous mems)
disease biliary sys
porto-systemic shunts are?
aberrant vessel(s) connect hepatic portal vein to caudal vena cava = blood bypasses liver
1. congenital = single = ligate
2. acquired = multiple, usually due portal hypertension so diversion as liver overwhelmed = hard treat
it’s route least resistance = all blood ends up bypassing liver
clinical signs porto-systemic shunts
liver can’t detox waste products = hepatic encephalopathy–>
1. hyperammoniaemia due breakdown prots
2. NH3 affects brain so depression, tremors, head pressing (can’t get out corner)
3. PU/PD
4. worse after eating
methods diagnosis porto-systemic shunts
- ultrasound
- fluoroscopy = x-rays thru bod over period time to get video movements inside
- exploratory laparotomy = find bvs + see if connected
exocrine gland
secretes products into duct that delivers to lumen of organ or free surface of epithelium (e.g. skin)
endocrine gland
secfetes product into extracellular space where quickly taken up by blood
no duct
zymogen granules
in pancreatic acinar (exocrine) cells - where enzs + proenzs stored before release
stain brightly
what do serous cells pancreas secrete
isotonic fluid cont (pre)enzs, enz inhibitors + HCO3-
* by exocytosis into duct = merocrine
microscopic structure exocrine pancreas/salivary duct
v similar
- simple cuboidal epithelium around excretory duct
- several ducts combine make pancreatic, accessory pancreatic, mandibular etc
- nuclei close outer surface cells, zymogen granules grped apical end near to duct
- exocrine tiss lobular
how are endocrine + exocrine arranged in pancreas
islets Langerhans (endocrine) scattered thruout lobules exocrine tiss (majority, 80%)
endocrine stained a bit lighter + near caps for hormones enter
which salivary glands secrete which saliva types
parotid = serous (w enzs, bicarb etc in)
mandibular, buccal, sublingual = mix mucous + serous
serous vs mucous saliva in simple-stomach vs complex stomach animals
simple = mainly mucous
* lubricate passage food
* pH neutral for amylase action
complex (ruminants) = copious, mainly serous
* provide optimum conditions fermentation
* pH alklaine buffer forestomach for fermentation
purpose myoepithelial cells in salivary gland
contract to squeeze saliva from duct upon nerve stim
ito cells
== stellate cells in space of Disse
* store vit A - visible vacuole cont lipid
direction bile flow
opp from direction blood flow
* duct runs from near central vein to portal triad w portal vein + hepatic artery
gall bladder epithelium
- simple columnar lining
- v vascular lamina propria
- external musc layer of randomly oriented sm musc
- folded so can expand + retract as required
absorptive + post-absorptive state
absorptive = eating + nutrients flowing into bloodstream to provide E
post = stopped eating, no fresh nutrients, E requirements still same so derived stored nutrients
herbivores = nutrition continuous (food less E dense) = no distinction
what happens in absorptive state
- cells use nutrients source E + prot synth
- galactose/fructose converted glucose in liver
- liver fills glycogen stores + synths lipids for export other tissues
- excess carb, fat, prot stored as lipid/glycogen (sk musc = glycogen storage)
- all cells net synth prot
ruminants = carb fermented to VFAs - don’t absorb glucose intact
lipid not as efficient as glucose at releasing E
what happens to glucose in liver
stored as glycogen until reps ~5% mass then remaining converted triglycerides
* some stored liver - less efficient source E
* most exported blood as VLDL
very low density lipoprot
what happens glucose in adipose tiss
taken up + converted glycerol for synth triglycerides as reserve source E
* excess = some converted FFAs
its the FFAs taken up
how are lipids made water soluble for transport in blood
binding to prots
1. FFAs bound albumin
2. others bound apoprots = lipoprots
apoprots = interface bet lipid core + aqueous environ = can be transported
types lipoprot + where transport lipids
- chylomicrons = fat absorbed GI tract -> rest bod
- VLDL = synthed liver -> elsewhere
- LDL = synthed liver from VLDL -> transport cholesterol other cells
- HDL = synthed liver, transports apoprots for lipid uptake, then cholesterol -> liver
very low/low/high density lipoprot
what happens chylomicrons + VLDL
- converted FFA by lipoprotein lipase in cap wall
- taken up adipose tiss (stored as triglycerides)/ musc (oxed for E)
- remnants taken up by liver + metabolised
- remaining VLDL remnants converted LDL - transfer cholesterol -> cells
when can musc metabolise lipids
in aerobic environ - FFAs
why do cells need cholesterol
lil bit to make phospholipid mems
what does HDL do
- apoprots -> chylomicrons + VLDL, incr lipid uptake
- remove cholesterol cells + transfer liver = cholesterol-rich HDL - degraded release cholesterol converted bile salts/excreted in bile
what happens aas absorbed
- 75% taken up liver for prot synth + converted keto acids
- 25% bypass liver + enter systemic circulation - prot synth, E if glucose low (gluconeogenesis), -> fat/glycogen for storage
role keto acids
- provide E liver cells (Krebs cycle)
- converted glucose/glycogen
- converted FAs for lipid synth
- used synth non-essential aas
what happens to degraded aas
leads NH3, converted urea liver, excreted kidneys
HERBIVORES:
* urea transferred fore-stom/LI via diffusion across epithelium (also secreted saliva ruminants)
* source N for microbial prot synth
* excess secreted by kidneys
how does bod provide E in post-absorptive state
- liver mobilises glycogen stores (finite)
- liver prods glucose other sources - gluconeogenesis mostly w aas precursor (propionate in herbivores)
- use glucose for E reserved brain, erythrocytes, kidneys, sk musc if anaerobic (can’t use other sources)
- other tissues E from lipids (glucose-sparing)
how is post-absorptive state requirements different in pregnancy/lactation
glucose essential (other sources no se va) for foetal metabolism + lactose syth
== maintenance plasma glucose levels extra important
how does liver respond reducing plasma glucose levels
- reduces anabolic activities (overall activity)
- mobilising glycogen stores to release glucose (only sufficient maintain few hrs)
gluconeogenesis
glucose synthed non-carb sources by liver + kidneys
* substrate pyruvate from lactate, glycerol, aas
* diff animals rely on it diff amounts
1. omnivores absorb sufficient glucose
2. carnivores diet v low so v dependent
3. herbivores = carbs fermented VFAs (not as efficient at yielding E) - only propionic acid = precursor
glucose conc determines glucose -> pyruvate or vice versa
sk musc in post-absorptive state
glycogenolysis but can’t dephosphorylate glucose phosphate = no free glucose -> bloodstream so:
1. glucose oxed to pyruvate/lactate
2. converted -> glucose by liver
3. enters bloodstream
== Cori cycle
glycogen stores depleted (starvation etc) = aas from prot degradation precursors for gluconeogenesis
what happens FFAs in post-absorptive state
VLDL synthed from plasma FFA
= FFA transport capacity increased (bc albumin limits)
= important mobilisation triglycerides from adipose tiss to be broken down by hormone-dependent lipase
* glycerol used gluconeogenesis
* FFA oxed for E production (glucose-sparing)
nervous tiss has low uptake FFAs = v depensent glucose for E
what happens FFAs taken up by liver
converted acetyl CoA = liver E source (citric acid cycle)
* most acetyl CoA surplus + converted ketone bodies (can’t reconvert -> acetyl CoA for E prod but other tissues can)
* monogastric = brain can switch to use as E source so prots can last longer (not in ruminants)
* pigs + horses = most FFAs reesterified to triglycerides so low levels ket bods
alternative source ket bods ruminants + why important
synthed from VFA butyrate in epithelial cells - v important bc butyrate inhibits gluconeogenesis
ketosis if levels ket bods too high
what regs carb metabolism
- insulin - incr uptake gluc, stim glycogenesis, incr gluc use, inhibit gluconeo
- glucagon opp
- adrenaline
- glucocorticoids have role in gluconeogenesis
effect adrenaline in carb metabolism
- stims glycogenolysis in liver
- released in anticipation high gluc usage = maintains plasma glucose constant despite incr consumption
stress = adrenaline = more gluc released but not used = hyperglycaemia (cats at vet)
regulation prot metabolism
insulin works on lots cells:
* incr aa uptake
* incr prot synth liver + musc = anabolysis
glucagon works mostly on liver:
* incr aa uptake
* prots degraded into aas used gluconeogenesis
regulation fat metabolism
Insulin (absorptive state):
* triglycerides synthed from glycerophosphates/FFAs + stored
* inhibition FFA release into blood
glucagon (post-absorptive + exercise):
* incr lipolysis in adipose tiss
* mobilises triglycerides for ATP production
when does gluconeogenesis occur ruminants
absorptive state = propionic acid/aas precursors
post-absorptive = aas/glycerol
insulin:glucagon ratio constant + gluconeogenesis always required as glucose fermented to VFAs by microbes not absorbed
where does fermentation occur diff species
carnivores = small degree stom
omnivores = lil bit LI
herbivores = fore-stom or LI (= hindgut fermenters)
fermentation
degradation non-hydrolysable carb β-glycosidic bonds by microbes - anaerobic
* long + slow
* GI tract adapted for antiperistalsis so slow transit food + for microbial pop thrive
what happens to stuff from fermentation in fore-gut fermenters
- VFAs (fermentation produucts) absorbed in stom
- microbial prot passes abomasum + SI for dig + absorp = main source prot
what happens stuff from fermentation hindgut fermenters
LI = fermentation chamber
* VFAs absorbed in colon
* microbial prot lost faeces - rabbits do coprophagy (eat poop)
fore-gut vs hindgut fermentation
hindgut less efficient bc:
1. microbes less efficient
2. lower degree amylolytic fermentation
3. lose microbial prot in faeces
BUT gut transit time can be decreased to consume more in hindgut whereas dependent rate fermentation in foregut
* poor nutrient quality fibre = faster = eat more = get more nutrient
* = more efficient on abundant poor quality forage (rare)
ruminant nutritional strategies
- browsers (concentrate selectors), e.g. deer = select fruit, seeds, buds high hydrolysable carb (simple sugars)
- grazers (grass/roughage eaters), e.g. cow = eat fibrous
- intermediates (adaptable feeders), e.g. goats
simple sugars vs VFAs as source E
simple sugars more efficient source E
browser vs grazer adaptations
in a table
oesophageal/ventricular groove
groove w lips forms tube oes -> reticulo-omasal orifice (-> abomasum) present all ruminants so milk can bypass fermentation chamber for lactose be used E
* sucking + chemoreceptors in pharynx sensitive to warm milk = reflex closure groove
* kept grazers so simple sugars bypass + glucose can be used E - digestion yields more E than fermentation
can be stimmed salt cols used prep oral medication to bypass fermentatio
what happens if cold milk suckled
prevents complete curling over oesophageal groove = spills reticulo-rumen
= lactose fermented to lactic/other organic acids
= adverse effect on developing microbes (=diarrhoea)
also if too much milk + spills over into reticulo-rumen
dig enzs diff species types
CARNS:
* no salivary amylase bc v lil hydr carb diet
* lots enz for stom/pancreas dig prots + fat
OMNIS:
* lots salivary amylas bc lots hydr carb diet
* lots enzs stom/pancreas for carb, prot + fat
SIMPLE-STOM HERBIS:
* moderate enzs dig carb b4 fermentation LI = can dig gluc (= can be worked harder)
RUMINANT HERBIS:
* low levels enzs dig carb after fermentation (all -> VFAs)
* moderate enzs for prot dig microbial prot abomasum/SI
need feed horse more prot than ruminant bc microbial lost
where is stuff absorbed diff species
CARNIS/OMNIS:
monosacchs, peptides, monoglycerides, FAs in SI
SIMPLE-STOM HERBIS:
* monosacchs, peptides in SI
* VFAs in LI
RUMINANT HERBIS:
* VFAs in fore-stom
* peptides in SI
deglutition
swallowing
regurgitation
passive transfer stom contents to oral cavity for remastication
re-mastication
additional chewing fibrous mat that was regurgitated
rumination
process re-gurgitation, re-mastication, re-deglutition
adaptation rumen stom + structure
for fermentation roughage/fibre
1. oesophageal area enlarged = forestom (stratified squamous to protect rough grass) = reticulum + rumen + omasum
2. abomasum = 4th compartment similar to stom
where does fermentation occur ruminants
fore-stom (most) + LI (anything that escaped in rumen)
overall strcuture reticulum + rumen
diagram from left side
reticulum structure
- inner surface raised into ridges (honeycomb)
- wall lots sm musc
10-20L capacity
rumen structure
- divided dorsal + ventral sac by longitudinal groove
- coronary pillars define caudal-dorsal + caudo-ventral blind sacs
- walls cont sm musc for contraction
- papillae incr SA (esp caudo-dorsal/ventral) for absorption H2O, VFAs, ions - on bottom bc that’s where settle (VFAs dense) - no sm musc
- neural plexuses reg contraction - short + long
histology fore-stom wall
stratified squamous epithelium
1. keratinised layer - stratum corneum
2. layer w tight junctions limit diffusion - selective - stratum granulosum
3. stratum basale = layer where cell division occurs b4 cells migrate -> lumen
4. lots caps for absorption
stratum corneum = inside w bac on it
omasum function + structure
lil bit fermentation but main role passage fermented mat rumen -> abomasum
* reged by reticulo-omasal orifice
papillae incr SA = can expand + contract to squeeze mat out
* more in grazers
On R side
structure abomasum
columnar epithelium w glands
1. HCl
2. pepsinogen
3. rennin (young) to precipitate casein (milk prot) + retain milk longer for pepsin act
regulation movement stuff -> + out of abomasum
receives constant flow fermented mat from omasum
* distension inhibits rumino-reticular contractions = flow slows
* regulation emptying same as simple stom
how is abomasum pH diff from simple stom
pH slightly higher due alkilinity fermentation fluid
* still acidic - kill bac, ruminal microbes for digestion
where are digestive components distributed
depends on density
* v dense like stones, wire fall straight into reticulum + remain (for life)
* gas from fermentation at top dorsal sac
* large particles have more gas associated from fermentation that surrounds = float at bottom dorsal sac at level oes
* more dense = more fermented particles sink into reticulum/cranio-dorsal blind sac/ventral sac
types rumino-reticulum contractions
- primary (mixing contents)
- secondary (eructation)
- rumination
how many primary ruminal contractions should there be at diff stages eating
EATING: 5-8 strong contractions/5mins
RUMINATING: 4-5 contractions/5mins
FASTING: 0-1 weak contractions/5mins
how often do secondary ruminal contractions occur
after every 2-3 primary contractions
process primary rumino-reticulum contractions
- 1st reticular = coarse mat -> central/dorsal rumen
- 2nd reticular = fermented mat -> cranial blind sac + small vol (50-100ml) fermented mat thru reticulo-omasal orifice -> omasum
- cranial blind sac = moderately fermented mat -> dorsal sac + well fermented -> reticulum
- dorsal sac = backwards contraction (caudal -> cranial) w overall circular movement contents in dorsal sac + some exchange w ventral sac
- ventral sac = backwards w overall circular movement contents ventral sac (fine mat), some exchange w dorsal + well-fermented -> cranial blind
thing named contracts
rumination contractions when + why
occurs when coarse mat stims oesophageal opening
* extra reticular contraction then normal primary
* occurs when resting after eaten
ruminants have to ruminate
process rumination contraction
- newly swallowed mat forced -> dorsal sac + replaced partially fermented mat (that’s what goes back up)
- thorax expands, gening neg press in thorax
- lower oesophageal sphincter opens
- diaphragmatic musc contracts = forces mat into oes (NOT abdominal wall muscs)
- antiperistalsis in oes = food -> oral cavity
- liquid immediately reswallowed
- rest mat rechewed w extra salivary secretion + reswallowed
why require secondary contractions
2000 litres gas from fermentation a day + oesophageal opening usually below level gas so can’t escape during rumination
can’t occur w animal on side so standing surgery or mech to remove gas
eructation process
(secondary contractions)
- caudal-dorsal blind sac contracts forward = contents -> cranial blind sac + ventral sac
- dorsal sac conts contracting = gas at top -> oesophageal opening
- incr neg press in thorax = oes expands
- cardiac sphincter opens + gas -> oes, antiperistalsis = -> oral cavity
- some escapes via mouth, most inhaled
- ventral sac contraction = gas collecting in caudo-ventral sac blind sac escape -> top dorsal sac
after every 2-3 primary contractions
bloat causes
due failure to eructate bc:
* complete oesophageal obstruction, e.g. potato
* partial obstruction, e.g. neck abscess, tumour
* fresh clover = small bubbles, can’t coalesce = foam that doesn’t collect in dorsal sac = can’t be eructated (= frothy bloat)
results of bloat
- incr ruminal press = respiratory + cardiac distress
- stretching rumen reduces/stops rumen contractions (mechanoreceptors)
what regs fore-stom motility
mainly autonomic long reflexes - afferent + efferent fibres in vagus (= vago-vagal reflex)
* tension, mechano + chemoreceptors play off to reg
stimulation + inhibition rumen motility
STIM: tension receptors respond stretch rumen walls
* in series w sm musc walls around oesophageal opening, oesophageal groove, reticulum wall, rumen pillars, cranio-dorsal blind sac wall
* INCREASE MOTILITY
inhib: mechanoreceptors sensitive severe stress
chemoreceptors respond decr pH, incr osmolarity + incr VFA conc
* in basal layer rumen epithelium (= epithelial receptors)
* decrease motility
result increased motility
food particles broken down faster + sub-grp sensors round reticulo-omasal orifice:
* release VIP (vasoactive intestinal peptide)
* = relaxation reticulo-omasal sphincter during 2nd reticular contraction
= incr rate passage food
result decr motility
rumination decr = food particles broken down more slowly = decr rate passage food
where is rumen motility controlled
vagal centre in medulla - 2 centres nerve clusters reg:
* frequency ruminal contractions
* force ruminal contractions
receive input rumen receptors, olfactory organ, taste-buds, oral cavity stretch receptors
stress = sever decr motility
stregnth + frequncy contractions indicator wellbeing - disease, stressed
GI situation at birth + initial development after
- abomasum developed but not fore-stom
- fore-stom developed when starts eat roughage (2-3wks)
- lamb dependant milk for nutrition + microbes for fermentation received from mother as licks
microbial fermentation
chem breakdown of substance (non-hydr carb) by microbes under anaerobic conds for own growth, cell division + motility
* end prods used by host - at rumen pH mainly ionic form (acetate, butyrate, propionate) - VFAs
what is retained longest in rumen
lignified roughage retained longer than succulent herbage bc harder breakdown - needs longer to be fermented
why rumen anaerobic
O2 can gain entry rumino-reticulum from blood supply (diffusion) + swallowed air
* aerobic = food broken down -> CO2 + H2O - no E to host
* anaerobic = total degradation prevented - fermentation stops at VFAs - can be used for E
how is rumen made anaerobic
facultative anaerobes = anaerobic bac + can use O2 - adhere luminal surface + remove all O2
micro-organisms present in rumen
bac = amylolytic (ferment hydr carb) + cellulolytic (non-hydr)
protozoa
fungi
how long are diff microbes retained rumen
- amylolytic bac short lifespan + exist fluid phase = ejected w contents
- cellulolytic bac/protozoa/fungi longer lifespan = need stay longer to establish, proliferate, work = attach luminal wall or fibre
how is sterile rumen made microbial
initially sterile - microbes have be ingested
* all environmental ingested but ruminal establish (adapted to environ = competitive advantage)
* mother ruminates so oral cavity conts representative pop ruminal microbes - transferred when licks
neonate isolated = gradually establish bac but not protozoa or fungi = enough but not as efficient
so bonding v important
types bac in rumen
- amylolytic = hydr carb, break α-glycosidic -> monosacchs - high tolerance low pH + can proliferate fast
- cellulolytic = cellulose, hemi-cellulose, fructosans, pectin, break β-glycosid -> monosacchs - low tolerance low pH
- proteolytic = prot -> peptides -> aas for microbial prot synth/fermentation -> VFAs + NH4+
- methanogenic = CO2 -> CH4
- lactate-utilisers = lactate -> propionate
protozoa in rumen
- prod VFAs, lactate, CO2 + H2
- store glucose as glycogen - recovered when digested in SI
proliferate w high starch diets - gradually incr amount by gradual incr hydr carb in diet
* reduced w high fibre diets
can survive w/o but fermentation more efficient w
fungi in rumen
spores attach lignin + split apart = susceptible cellulolytic digestion but only work aerobically + rumen anaerobic so we don’t get that one
reprod by free-swimming flagellated spores + proliferate w diets high lignin (e.g. straw) - slowly so pops time readjust
homeostasis rumen environ
food fermented -> VFAs + NH4+ = osmolarity incr, pH decr = water -> rumen (osmosis)
* NH4+ taken up by microbes
* VFAs absorbed by host
= incr rumination, incr HCO3- (from saliva + blood)
= osmolarity decr, pH incr
= water reabsorbed to bloodstream = no net loss
how does rumen acidosis happen
incr consumption hydr carb = VFAs incr = pH decr
* too much = acid-resistant lactate-producers proliferate at expense lactate-utilisers
* lactate poorly absorbed = pH decr
* too low pH injures rumen epithelium = water in
* = dehydration + hypovolaemic shock
how treat rumen acidosis
IV alkaline fluids - correct dehydration + acidosis
prevented by introducing hydr carb slowly over 2-3 weeks = lactate utilisers incr levels
* gradual so microbial pop has time adjust + keep up
what determines Rofermentation
- feedstuff type - starch fermented more rapidly than fibre
- vol feedstuff
- microbial balance - amylolytic bac ferment faster than cellulolytic
why are fore-gut fermenters more resitant to toxins than hind-gut
rumen microbes can degrade toxins before absorption = can cope w higher levels before problem
e.g. foxglove, ragwort
carb metabolism ruminants
- bac surface enzs break down -> monosacchs/short-chain polysacchs
- dissolved rumen fluid + taken up microbes + metabolised (glycolysis) to provide E for microbes
- anaerobic so glycolysis only -> VFAs
- waste product for microbes but source E for ruminants
- propionate from anaerobic glycolysis pyruvate + from lactate
diet high starch = more lactate-utilisers = more VFA AND more propionate
why prod methane
glycolysis = NAD+ -> NADH
need regen NAD+ (aerobic = resp chain) so methane-producers reduce CO2 -> CH4 via oxidation NADH -> NAD+
* = NAD+ replenished for bac glycolysis
* reduces H+ ions = maintain ideal rumen pH
worth waste E-rich CH4
how else can NAD+ be regened in rumen
reduction sulphate/nitrates by other ruminant bac
how is fat metabolised rumen
long-chain fatty acids in 3 forms:
1. free form, e.g. in oil seed plants
2. triglycerides, e.g. commercial feed
3. galacto-lipids, e.g. grass
hydrolysed + galactose/glycerol parts fermented -> VFAs (mostly propionic acid)
why does ruminant body fat differ other species
unsaturated FAs synthed as stereoisomeric cis form in animal tiss but ruminal bac hydrogenation also gens some trans unsaturated FAs
how is prot metabolised rumen
degraded by ruminal bac ->
* peptides
* aas
* NH3 + organic acids
* branched FAs
rumen microbial proliferation
high Roprot synth
* mostly from inorganic N
* also from non-prot nitrogen (NPN) in food + additives, e.g. urea
cellulolytic require NH4+
amylolytic use NH4+ + aas
what is NPN w examples
N sources from mols not building blocks prot
* amides
* amines
* peptides
* aas
* nucleic acids
* urea
* nitrates
* ammonium ions
microbes but no animals can use for prot synth (indirect ruminants can)
how is NPN metabolised
microbes: NPN -> NH3 -> aas -> prot
microbial prot digested stom/SI as in simple stom
why do we need NPN + examples good sources
essential healthy microbial pop
* grass/grain 5-15%
* silage 70% (due microbial fermentation)
extra prot dairy cow diet
bc require more when lactating than from NPN
- urea added to incr NPN = incr microbial pop - need more E to proliferate (usually form hCHO, e.g. molasses)
- ‘by-pass’ prots added diet - poorly soluble, e.g. corn prot, so escape fermentation -> abomasum/SI for dig
* or thru oesophageal groove if functional still
what happens surplus prot ruminants
recycled into urea (liver) + secreted saliva
excess urea excreted kidneys = E costly so don’t overshoot NPN in diet
absorption defn
selective transfer useful nutrients into host’s bloodstream
absorption in rumen
- papillae in reticulo-rumen incr SA - most dense in ventral sac + cranial/caudo-dorsal blind sacs (most absorp)
- specific transport prots + E source
- feed mat digested to suitable size - mostly VFAs
which parts rumen permeable what
stratum corneum = anion (-ate) + undissociated acid (-ic acid)
stratum granulosum = only undissociated acid
* pH 7 anion form predominates = poorly absorbed
* H+ secr exchange Na+ -> blood = pH decr in fermen = undissociated form conc incr = incr absorption
what happens to VFAs as absorbed
- acetic acid absorbed unchanged
- some propionic acid metabed -> lactic acid
- all butyric acid -> β-hydroxybutyric acid
what happens to water in rumen
moves bet rumen + ECF depending osmotic grad
what happens lactic acid in rumen
stronger acid = more poorly absorbed than VFAs = remains rumen lowering pH
* when absorbed liver converts -> glucose
what happens NH3 in rumen
rapidly absorbed so equilibrium constantly shifting so NH4+ -> NH3
* absorbed = converted -> urea by liver
inorganic ion movement bet rumen + blood
rumen neg compared blood = hard absorb pos ions
1. Na+ + Mg2+ AT -> blood
2. Cl- absorbed -> blood in exchange HCO3-
3. Ca2+ + PO43- absorbed SI
what happens in omasum as passing -> abomasum
- lil bit fermentation
- absorption more VFAs so just 10% -> abomasum
- water + Na+ absorbed = ingesta more solid
- conts less HCO3- = abomasum has secrete less H+
SA incr bc papillae
omasal canal
allows mat pass straight rumen -> abomasum
parts colon in horse
ascending = large = fermentation chamber
1. ileo-caecal valve -> caecum -> caeco-colic valve
2. ventral colon -> narrow pelvic flexure
3. dorsal colon -> narrowing transverse colon (short)
–> small colon (descending colon)
muscle in horse LI
circular slay
longitudinal not continuous - in taenial bands (= taenia)
* diff parts have diff no.
* shorter than LI = sacculations (haustra) = pockets for stuff move into = delayed transit time
how much fermentation in LI diff species
CARNIS: most dig/absorp already done = minimal fermen
RUMIS/OMNIS: moderate
HORSES: most non-hydr carb -> LI so extensive
what happens products fermentation horses
VFAs absorbed LI muscosa -> blood
gases CH4 + CO2 -> rectum (peristalsis) + expelled (flatulence)
last stage so some VFAs + all microbial prot wasted
metabolism + role VFAs horse
ACETATE
* used in liver
* oxed in other cells to gen ATP
* sources acetyl CoA for lipid synth
PROPIONATE
* substrate gluconeogenesis
BUTYRATE
* E production
* homeostasis colonic epithelium - regs genes controlling proliferation, apoptosis, differentiation cells
== why need eat fibre
how are VFAs absorbed horse
SCFA/HCO3- exchanger in LI
how is Na+ absorbed horse
Na+ channs + Na+/H+ exchanger in LI
* enhanced by aldosterone
how is Cl- absorbed horse
bicarbonate or hydroxyl exchange in LI
maintains pH at suitable level fermentation
water absorption horses
extensive in LI - lots still in bc kept for fermentation, gone by:
* osmotic press
* hydrostatic press
* solvent drag - VFAs absorbed = Cl- + Na+ -> blood = net absorption NaCl (also creates osmotic press)
benefit horse dig sys compared ruminants
hCHO digested in SI -> glucose (more efficient E source) as passes there first
* if lots hCHO + enzs + transporters in SI no time up-regulate = passes -> LI = upset microbial balance
fibre fermentation + response horses
+ what happens when fails
microbial fermen = -> VFAs = decr pH
* neutralised by copious pancreatic secretion HCO3-
* goblet cells in LI secr mucous + HCO3-
* ileum secr HCO3-
too many VFAs = too much H+ = no neutr = pH decr = multiplication acid resistant microbes favoured (amylolytic + lactate producers) = more lactic acid, less well absorbed = pH decr…..
also hCHO substrate amylolytic bac = proliferate = upset balance - but intro slowly so dig for more gluc SI
difference prot fermentation horses compared ruminants
equine hindgut more capable absorbing aas/peptides = less taken up by microbes = good bc microbial prot lost
how are microbial N requirements met horse
urea secreted by ileum/LI -(microbial urease)> NH3 = NPN source microbial prot synth
difference in how prots absorbed horse vs ruminant
absorbed intact not metabed as absorbed
* so prop propionic acid for gluconeogenesis incr w incr hCHO -> LI
diffs in microbes present horse LI compared rumen
food mat -> LI less hCHO (done SI, not rlly stom not much amylase saliva) = amylolytic pop lower = fermen slower
still ciliate protozoa in both but diff species - smaller no. but larger (similar total mass)
fungi v similar
all lost in faeces so no digested for prot like in ruminants
how + why caecum diff in horses
sepped colon by caeco-colic valve (other species = continuous) = sep fermen compartment AND when antiperistalsis to slow movement in colon no distension (so no pain) where food backed up against closed ileo-caecal valve (we don’t want food returning to SI)
caecal contractions horse
- segmental = high microbial activity = high fermen + absorp
- mass so all -> colon every 3-5mins = sm musc whole caecum contracts longer
colon contractions most species
- segmental + peristaltic
- anti-peristaltic prominent proximal colon
- chyme colon -> caecum
- mass descending -> rectum (+ out caecum)
colonic contractions horse different how?
- no retrograde colon -> caecum
- anti-peristaltic mostly in distal part ventral colon
- passage chyme slowed by v narrow pelvic flexure (only small well fermented mat can pass)
= slow transit + efficient fermentation
mass descending colon -> rectum
still have mass movement out caecum (only place mass)
equine colic
= clinical sign abdominal pain
1. true colic relates GI pain
2. false colic relates other abdominal pain - e.g. bladder, kidney, uterus
diagnose by rectal exam (most useful method)
results highest levels equine morbidity (illness) + mortality
normal sounds/locations horse auscultation
L dorsal = SI/small colon = fluidy = high pitch
L ventral = pelvic flexure = often something stuck
R dorsal/ventral = caecum = loud, toilet flushing = emptying via caeco-colic valve
always use L + R, ventral + dorsal to refer segments
abnormal sounds abdominal auscultation horse
- incr frequency = enteritis/ spasmodic colic (SI overdrive, sm musc relaxant)
- tympanitic = hollow, drum-like = gut distension w gas = obstruction
- decr frequency = ileus (surgeon handles guts + stop working)/obstruction (can’t get thru = movement slowed)
normal rectal exam horse
diagram
rectal exam if SI obstruction
surgical colic = needs referral
rectal exam ileal impaction
= blocked as going into caecum
* don’t feel SI distension if catch early
rectal exam caecal impaction
PRIMARY = impaction w ingesta
SECONDARY = due obstruction large colon
rectal exam colonic impaction
most commonly at pelvic flexure bc narrows
* large colon also feels enlarged
* can usually be treated medically at 1st opinion (not so much if secondary impaction)
impaction defn
blockage, abnormal accumulation food mat
rectal exam: left dorsal displacement
== nephro/reno-splenic entrapment
= large colon to L of spleen + trapped over NSL in NS space
* bc so mobile as only attached self
refer for surgery
SI also mobile so goes in space but can then get out
rectal exam: right dorsal displacement
large colon lateral to caecum
torsion vs volvulus
torsion = twisting of organ round its own axis
volvulus = twisting of organ round axis perpendicular to own
rectal exam: large colon volvulus/torsion
volvulus 1st but often associated w torsion
* then all abdo bvs trapped = no blood back heart = hypovolaemic shock
rectal exam: small colon impaction
how identify spinal nerves
nerve running behind last rib = T13 (thoracic) then caudally from there = L1 - L4 (lumbar) + cranially = T12 ->
T13 in dogs, T15 in pigs, T18 in horses
tight + loose stom attachments
- greater omentum = loose (folds etc)
- lesser omentum = tight to liver _ liver firmly attached diaphragm = no movement
- gastro-splenic ligament = tight but spleen no attached = can move w stom
- tightly attached oes
stom can’t move much, only really rotate: normally volvululs
why extra doubly shouldn’t handle pancreas
handle = damage
damage a cell = releases its contents
pancreas cells cont loads proteases = cells break down = much more discomfort than damage other organs
how distinguish bet 3 parts SI
- duoden only one w Brunner’s glands to secr mucous
- ileum only one w Peyer’s patches as part IS
- jejunum has neither
- jejunum = bvs hit at right angles
- ileum = bvs run along its length
purpose caecum
reserve space = slow digestion colon w reserve space w/o distension or food returning ileum
why so many diff bvs to each organ
in normal movement if right side squished + bvs squished blood supply to that organ still continues
what is CT scan
radiography but lots images put together make 3D image
what are MRI scans used for
mostly looking at nervous sys
v expensive
why ultrasonography no good for looking at GI sys
too much motility = can’t really see
